Terminal2 — Card #00: [Diagnosis Name]

S01 Everyone

What Is It

End-stage coronary artery disease — when the revascularization options are exhausted, the vessels are too diseased to intervene, and what remains is refractory angina, fear, and the work of comfort that procedural cardiology cannot do.

US CAD Prevalence

~18M

Coronary artery disease affects approximately 18 million Americans and remains the leading single cause of death in the United States, accounting for roughly 1 in 5 deaths annually.^[1]

Refractory Angina Prevalence

600K–900K

An estimated 600,000–900,000 Americans live with refractory angina — angina that persists despite optimal medical therapy and cannot be addressed with further revascularization. One of the most undertreated chronic pain syndromes in medicine.^[2]

Prior CABG in End-Stage CAD

50–60%

Approximately 50–60% of patients presenting with end-stage CAD have had prior coronary artery bypass grafting. Graft disease, native vessel progression, and diffuse distal disease define the anatomy that forecloses further intervention.^[3]

ICD/CRT Prevalence

30–40%

Roughly 30–40% of end-stage CAD patients with reduced ejection fraction have an implantable cardioverter-defibrillator in place. The deactivation conversation is a clinical obligation at every hospice enrollment.^[4]

Coronary artery disease is the progressive narrowing and obstruction of the coronary arteries by atherosclerotic plaque — the accumulation of lipid, inflammatory cells, smooth muscle, and fibrous tissue that restricts blood flow to the myocardium. Plaques form over decades, silently narrowing vessel lumens until reduced perfusion causes angina during exertion, and ultimately ischemia at rest.^[1] The modern interventional era has given millions of patients percutaneous coronary intervention (PCI), coronary artery bypass grafting (CABG), and decades of productive life. But CAD is not cured by revascularization — it is managed. Grafts develop disease. Native vessels progress. Stents restenose. The patient who had a three-vessel bypass at age 58 may return at 72 with occluded grafts, diffuse distal disease, no suitable targets, and a cardiologist who has finally run out of procedures to offer.^[3]

End-stage CAD is defined not by a single catastrophic event but by the exhaustion of anatomical options. The defining document is the coronary angiography report that reads "diffuse disease," "no suitable targets," "vessels too small for intervention," or "prior bypass grafts occluded — not amenable to repeat revascularization." What remains after that report is a myocardium chronically starved of oxygen, a patient living in unpredictable pain, and a healthcare system that has excelled at procedures and often failed to pivot to the question that follows their exhaustion: how do we manage pain and fear when there is nothing left to fix?^[2] Refractory angina — CCS Class III–IV angina persisting despite optimal medical therapy — is the defining clinical challenge of end-stage CAD. It is also one of the most undertreated chronic pain syndromes in all of hospice and palliative medicine. The hospice clinician who inherits a patient with refractory angina on a suboptimal anti-anginal regimen must be prepared to optimize that regimen aggressively, address the fear dimension of chest pain that no medication fully resolves, and provide the kind of ongoing presence and anticipatory guidance that procedural cardiology rarely has time to offer.^[5]

Unlike CHF (Card #21) and cardiomyopathy (Card #22), end-stage CAD places refractory ischemic chest pain at the center of the clinical picture. The CHF component — ischemic cardiomyopathy with reduced ejection fraction — is often present and important, but it is not the defining challenge. What defines end-stage CAD is the patient who sits perfectly still because any movement might trigger a crushing episode of chest pain, who has stopped going to family events because the fear of an angina attack in public is more disabling than the disease itself, and who has been told by the best cardiologists available that there is nothing more to be done procedurally — without ever being told what can be done for comfort.^[6]

🧭 Clinical Framing — The Gap the Procedural World Left Behind

End-stage CAD patients have spent years in a healthcare system that measures cardiac care success by procedures. Every hospitalization has ended with an intervention or a plan for one. When the cardiologist finally says "there is nothing more we can do procedurally," the patient often hears abandonment, failure, or death sentence — not because that is what was said, but because no one translated what it means for comfort management. The hospice clinician's first task at enrollment is to reframe the clinical reality: no more procedures does not mean no more help. It means the work of comfort has finally become the primary work. Anti-anginal optimization, nitrate schedule correction, ranolazine initiation, SL NTG protocol education, acute MI at home planning, ICD deactivation conversation — this is a full clinical agenda. Name it explicitly at the first visit. The patient who understands that you have a concrete plan for their chest pain will be more engaged, less fearful, and better able to participate in every subsequent conversation about goals and meaning.

From the Field

Waldo Rios, NP

Hospice NP · 12+ Years

"I walked into a first visit last year — patient had three bypasses, seven stents over twenty-two years, and the cardiologist's final note said 'no further revascularization options.' The family was devastated. The patient was on isosorbide mononitrate twice a day — completely tolerant, completely ineffective — and not on ranolazine. Nobody had ever reviewed his nitrate schedule. I fixed the dosing, added ranolazine 500 mg BID, rewrote the SL NTG protocol with the wife, and had the ICD conversation. By visit three he was sitting on the back porch watching birds. He told me that was the first time in six months he felt like he could breathe without it costing him something. The cardiologist said there was nothing left to do. There was plenty left to do. They just needed us."

— Waldo, NP · Terminal2

S02 Clinician

How It's Diagnosed

Diagnostic workup, angina classification, and what the hospice clinician must identify in the records at enrollment. Most patients arrive with years of cardiac imaging — your job is to read it correctly.

Diagnostic Studies

Coronary angiography (gold standard): Defines coronary anatomy, stenosis severity and location, collateral circulation, and suitability for revascularization. The report that says "diffuse disease," "no targets," or "vessels too small for intervention" is the document that defines end-stage CAD. This report must be in the hospice chart.^[7]
Echocardiogram: Ejection fraction, regional wall motion abnormalities (define ischemic territory), valvular disease (ischemic mitral regurgitation is common), and diastolic function. EF determines ICD eligibility, prognosis, and whether ischemic cardiomyopathy is present. Know the most recent echo and whether EF has been trending down.^[8]
Stress testing: Assesses inducible ischemia and functional capacity (exercise tolerance in METs). In end-stage CAD, stress testing is often abandoned because revascularization is no longer possible and results will not change management. If still being ordered, ask whether the result will change the comfort plan — if not, it adds burden without benefit.^[9]
CT coronary angiography: Non-invasive anatomical assessment. Less useful in end-stage patients with extensive coronary calcification and prior metallic stents — both cause artifact that obscures luminal assessment. Calcium scoring may be on file and reflects overall plaque burden.^[7]
Cardiac biomarkers (troponin): Chronically mildly elevated in many end-stage CAD patients from ongoing low-grade myocardial injury. Acute rise signals NSTEMI or STEMI. In comfort-focused care, the decision to check troponin is a goals-of-care conversation — only order it if the result will meaningfully change the comfort management plan.^[10]
NT-proBNP / BNP: CHF component assessment. Many end-stage CAD patients have ischemic cardiomyopathy with concurrent volume overload. BNP reflects volume status and decompensation — useful for guiding palliative diuretic adjustment. A sharply elevated BNP in a patient with increasing dyspnea indicates fluid management is part of the comfort plan.^[11]

What to Look for in Hospice Records

Most recent coronary angiography report: Specifically whether it says "no targets," "diffuse disease," "CABG grafts occluded," or "not amenable to further revascularization." This is the document that defines end-stage anatomy. If it is not in the chart, obtain it — it is the foundation of every conversation about goals of care with this patient.^[7]
Ejection fraction trend: Is EF stable or declining? EF <35% with refractory angina carries median OS of 2–3 years. EF <25% with NYHA IV symptoms is end-stage ischemic cardiomyopathy — both this card and Card #21 apply.^[12]
ICD or CRT-D in place: Check the most recent device interrogation. Has the device shocked the patient? How many times? Shock history is both a prognostic marker and a psychologically significant event that often goes unaddressed in cardiac records.^[4]
Surgical and PCI history: Full list of revascularization procedures with dates — each CABG, each PCI, each stent. The patient who has had three bypass operations and eleven stents is not the same clinical picture as a patient with diffuse de novo disease. The surgical history tells the trajectory.^[3]
Current anti-anginal regimen and adequacy: Is the patient on a long-acting nitrate? Is it dosed correctly (see S11)? Has ranolazine been tried? Are beta-blockers and CCBs titrated? Many patients arrive at hospice on incomplete or incorrectly dosed regimens — this is the most immediately correctable clinical problem at enrollment.^[13]
NTG use frequency: How often is the patient using sublingual nitroglycerin per day? More than 3–4 uses per day indicates inadequate anti-anginal optimization or nitrate tolerance. Frequency of SL NTG use is the most direct measure of symptom burden in refractory angina.^[2]

📊 CCS Angina Classification — Know Where Your Patient Is

Class I: Angina only with strenuous or prolonged exertion; ordinary activity not limited. Class II: Slight limitation of ordinary activity — walking more than two blocks on level ground, climbing more than one flight of stairs, exertion after meals or in cold. Class III: Marked limitation of ordinary physical activity — walking one to two blocks on level ground, climbing one flight of stairs. Class IV: Inability to carry out any physical activity without discomfort, or angina at rest. End-stage CAD patients are typically CCS Class III–IV at hospice enrollment. The patient who is CCS IV — angina at rest, triggered by any activity including dressing, bathing, or emotional stress — requires aggressive anti-anginal optimization and anticipatory protocol for acute episodes as the first clinical priority.^[14]

💡 For Families

💡 Para las Familias

Your loved one has already had many tests and procedures to understand and treat their heart disease. Most of the important diagnostic information is already documented. The hospice team will review those records to understand the current situation — not to do more tests, but to make sure we are using every available tool to prevent and manage chest pain as comfortably as possible at home.

Su ser querido ya ha tenido muchas pruebas y procedimientos para comprender y tratar su enfermedad cardíaca. El equipo de cuidados paliativos revisará esos registros para asegurarse de que estamos usando todas las herramientas disponibles para prevenir y manejar el dolor en el pecho de la manera más cómoda posible en casa.

S03 Everyone

Causes & Risk Factors

Atherosclerosis is a decades-long process shaped by modifiable risk factors, genetics, and biology. Understanding the road that led here helps families make sense of the journey — and identifies surviving family members who may benefit from screening.

Modifiable Risk Factors

Hypertension: The most prevalent modifiable cardiovascular risk factor. Sustained elevated blood pressure directly damages coronary endothelium, accelerates plaque formation, and promotes left ventricular hypertrophy. Lifetime blood pressure control is the most impactful single CAD prevention intervention at a population level.^[15]
Hyperlipidemia: LDL cholesterol is the substrate of atherosclerotic plaque. Statins reduce cardiovascular events by approximately 25–35% per 1.0 mmol/L LDL reduction. Lipoprotein(a) — Lp(a) — is an underrecognized independent risk factor that statins do not adequately lower; it is particularly common in patients with premature or unusually aggressive CAD and is worth checking in families of end-stage patients.^[16]
Diabetes mellitus: Accelerates atherosclerosis through endothelial dysfunction, oxidative stress, advanced glycation end-products, and prothrombotic state. Causes both macrovascular (coronary artery) and microvascular disease. HbA1c control reduces microvascular complications but less clearly macrovascular CAD events at the end of life. Patients with diabetes tend to have more diffuse, distal coronary disease that is harder to revascularize — this is why diabetes is overrepresented in end-stage CAD.^[17]
Tobacco smoking: The most potent modifiable risk factor for acute MI. Nicotine and carbon monoxide cause direct endothelial injury, plaque destabilization, platelet activation, and coronary vasospasm. Smoking increases CAD risk 2–4-fold; risk begins declining within weeks of cessation and returns near baseline over 10–15 years. Ask the smoking history at enrollment — not to judge, but to understand trajectory.^[18]
Obesity and metabolic syndrome: Visceral adiposity drives chronic inflammation, insulin resistance, atherogenic dyslipidemia (elevated triglycerides, low HDL), and hypertension — the complete metabolic syndrome. Abdominal obesity is an independent predictor of CAD events beyond BMI alone.^[15]
Physical inactivity: Sedentary lifestyle is an independent CAD risk factor; exercise improves endothelial function, lipid profile, blood pressure, and insulin sensitivity. In end-stage CAD, progressive angina with minimal activity creates a vicious cycle of deconditioning that worsens functional capacity and quality of life.^[1]
Cocaine and stimulant use: Causes coronary vasospasm and accelerated atherosclerosis. May be decades in the past — ask the history without judgment. Patients with cocaine-associated CAD often develop disease at younger ages and with atypical anatomy.^[19]

Non-Modifiable & Hereditary Factors

Family history and genetics: First-degree relative with premature CAD (before age 55 in men, age 65 in women) confers 1.5–2x increased risk. Familial hypercholesterolemia (FH) — autosomal dominant mutation in LDL receptor pathway — causes LDL >190 mg/dL without secondary cause and dramatically accelerates plaque accumulation; untreated FH patients may develop triple-vessel disease before age 50. Polygenic risk scores for CAD are increasingly used in screening settings.^[20]
Male sex and age: Men develop CAD approximately a decade earlier than women. After menopause, women's cardiovascular risk rises sharply toward that of men. CAD risk increases steeply with age in both sexes — the majority of end-stage CAD patients are in their 70s–80s with multiple decades of subclinical disease progression.^[1]
Chronic kidney disease: CKD is an independent cardiovascular risk factor beyond its contributions through hypertension and dyslipidemia. Uremia accelerates vascular calcification and endothelial dysfunction. CKD is common in end-stage CAD patients and complicates medication management — ranolazine dose adjustment is required at GFR <30.^[21]
Inflammatory conditions: Rheumatoid arthritis, systemic lupus erythematosus, and psoriasis confer significantly elevated CAD risk. Chronic systemic inflammation drives plaque formation and destabilization through cytokine-mediated endothelial injury. These patients may develop CAD at younger ages than traditional risk factor burden would predict.^[22]
Prior mediastinal radiation: Radiation therapy for breast cancer, Hodgkin lymphoma, or other thoracic malignancies causes radiation-induced coronary arterial injury with a latency of 10–20 years. These patients develop accelerated, often diffuse CAD at younger-than-expected ages with atypical anatomy not amenable to standard revascularization approaches.^[23]
Racial and ethnic disparities: Black Americans experience higher rates of CAD, more severe hypertension, higher rates of diabetic complications, and significantly lower rates of revascularization for equivalent disease burden than white patients. Hispanic patients are underdiagnosed relative to their risk factor burden. Indigenous populations bear disproportionate CAD burden with earlier onset. At end of life, these disparities extend to hospice referral rates and palliative care access.^[24]

❤️ For Families: "Why Did This Happen?"

Heart disease develops over decades, shaped by a combination of genetics, blood pressure, cholesterol, diabetes, and other factors — many of which were being treated as best medicine could at the time. This is not the result of something your loved one did wrong, or something you could have prevented differently. The heart keeps the score of an entire lifetime, and end-stage heart disease means the heart has been working hard for a very long time. What matters now is not what caused it, but how we take care of them and you from this point forward.

⚕ Clinician Note: Family Screening at Enrollment

When end-stage CAD is present in a patient under age 65, or when the history suggests familial hypercholesterolemia (LDL >190, xanthomas, premature family history), note in the record that first-degree relatives — adult children particularly — benefit from lipid screening and cardiovascular risk assessment. Hospice enrollment is not the time for the patient to pursue this, but the hospice team is often the most trusted clinical voice the family has at this stage. A brief statement — "Ask your own doctor about getting your cholesterol checked — your father's history makes it important for you" — is a comfort intervention that extends beyond the room you are standing in.

S04 Clinician Everyone

Treatments & Procedures

The full spectrum of CAD therapy — from guideline-directed medical management to revascularization to advanced comfort interventions. Understanding what has already been tried shapes what remains to optimize.

The medical management of CAD has evolved into a comprehensive evidence-based regimen that addresses plaque stabilization, thrombosis prevention, oxygen demand reduction, and coronary perfusion optimization. End-stage CAD patients typically carry five to eight cardiac medications at enrollment — many dosed incorrectly, some no longer necessary given shifted goals, and at least one critical addition (most often ranolazine) absent entirely.^[13] Understanding the full therapeutic landscape helps the hospice clinician identify what to optimize, what to simplify, and what conversations remain to be had about device deactivation and acute event management.

Guideline-Directed Medical Therapy (GDMT)

Antiplatelet & Antithrombotic Therapy

Aspirin 81–325 mg daily: Antiplatelet therapy — cornerstone of CAD management throughout life. Inhibits cyclooxygenase-mediated thromboxane A2 production, reducing platelet aggregation. In comfort-focused care, reassess whether bleeding risk outweighs benefit when the patient is no longer a revascularization candidate and has chosen comfort goals — though most hospice patients with CAD benefit from continuing aspirin unless GI bleeding history or high fall risk is present.^[25]
P2Y12 inhibitors (clopidogrel, ticagrelor, prasugrel): Dual antiplatelet therapy (DAPT) required after PCI or ACS — duration depends on stent type (bare metal vs. drug-eluting) and indication. Minimum duration: 1 month for bare metal stents, 6–12 months for drug-eluting stents, 12 months post-ACS. In comfort-focused care at the end of the minimum required DAPT duration, simplification to aspirin monotherapy is appropriate and reduces bleeding risk.^[25]

Statin & Lipid-Lowering Therapy

High-intensity statin (atorvastatin 40–80 mg, rosuvastatin 20–40 mg): LDL reduction and plaque stabilization — independent of LDL level, statins reduce cardiovascular events in established CAD. Mortality benefit is well-established. Continue in hospice unless pill burden, dysphagia, or myopathy makes it burdensome. Deprescribing discussion appropriate at enrollment if pill burden is high and comfort is the priority — some patients prefer simplification; others choose to continue. Respect the choice.^[16]
Ezetimibe and PCSK9 inhibitors: Add-on lipid lowering when statins insufficient — less commonly continued in end-stage hospice care unless patient has strong preference and tolerates them without burden. Deprescribing these agents at enrollment is appropriate in most comfort-focused cases.^[16]

Anti-Anginal & Rate-Reducing Agents

Beta-blocker (metoprolol succinate, carvedilol, bisoprolol): Reduces myocardial oxygen demand by lowering heart rate and blood pressure. Prevents arrhythmia and reduces reinfarction risk. Continue if tolerated and blood pressure allows — often the primary comfort drug in refractory angina by reducing ischemic demand. Target resting heart rate 55–65 bpm in stable angina.^[26]
Long-acting nitrates (isosorbide mononitrate ER, isosorbide dinitrate): Cornerstone of refractory angina management via coronary vasodilation and preload reduction. Requires a nitrate-free interval of 8–12 hours to prevent tolerance. ISMN ER once daily in the morning preserves the overnight nitrate-free interval — twice-daily dosing eliminates it and causes complete tolerance within days. Headache is dose-limiting but usually improves in 1–2 weeks.^[27]
Calcium channel blockers (amlodipine, verapamil, diltiazem): Amlodipine — vasodilation, reduces oxygen demand, well-tolerated. Rate-limiting CCBs (verapamil, diltiazem) — useful for vasospastic component; do NOT combine with beta-blocker due to additive negative chronotropy and risk of complete heart block.^[26]
Ranolazine 500–1000 mg BID: Late sodium current inhibitor — reduces diastolic wall tension and myocardial ischemia without affecting heart rate or blood pressure. CARISA and MERLIN-TIMI 36 trials demonstrated significant reduction in anginal episodes and NTG use. Particularly valuable when other agents are limited by hypotension or bradycardia. Check baseline QTc. Avoid in severe hepatic impairment. CYP3A4 substrate — avoid with strong inhibitors. The most chronically underprescribed drug in end-stage CAD hospice.^[28]
Ivabradine 5–7.5 mg BID: If-channel inhibitor — reduces heart rate without affecting contractility or blood pressure. BEAUTIFUL trial demonstrated efficacy in stable angina with resting HR ≥70 bpm and sinus rhythm. Useful when beta-blocker causes intolerable hypotension but rate reduction is needed. Avoid in AF/atrial flutter. Requires sinus rhythm.^[29]

ACE Inhibitors, ARBs & Diuretics

ACE inhibitor or ARB (lisinopril, ramipril, losartan, valsartan): Post-MI and ischemic cardiomyopathy benefit — reduces cardiac remodeling, mortality, and hospitalizations in patients with reduced EF. Continue if tolerated and renal function allows; hyperkalemia and rising creatinine require monitoring. In end-stage comfort-focused care, continue unless symptomatic hypotension or cardiorenal syndrome prevents it.^[26]
Loop diuretics (furosemide, torsemide, bumetanide): For CHF component — reduces preload, pulmonary congestion, and dyspnea. Palliative diuresis is an important comfort intervention in end-stage CAD patients with ischemic cardiomyopathy. Monitor daily weights. Adjust for changes in oral intake at end of life.^[11]
Mineralocorticoid receptor antagonists (spironolactone, eplerenone): Reduces mortality in EF <35% post-MI — continue if tolerated and renal function allows (K⁺ and GFR monitoring required). At very end of life, deprescribing if pill burden is excessive is appropriate.^[26]

Revascularization Procedures — History & Endpoints

Percutaneous Coronary Intervention (PCI)

Balloon angioplasty and coronary stenting: Catheter-based opening of coronary stenoses with balloon dilation and metallic stent deployment. Drug-eluting stents (DES) release antiproliferative drugs to reduce restenosis. Most end-stage CAD patients have had multiple PCI procedures over years. At end-stage, remaining vessels are either previously stented with in-stent restenosis, too diffusely diseased for PCI, too small in caliber (<2mm), or in territories with insufficient viable myocardium to justify intervention.^[7]
What it means for hospice care: Know the stent history — drug-eluting stent within the past 12 months requires continued DAPT to prevent catastrophic in-stent thrombosis. Never discontinue P2Y12 inhibitor within the minimum DAPT window without cardiology consultation.^[25]

Coronary Artery Bypass Grafting (CABG)

Surgical revascularization: Bypass of obstructed coronary segments using internal mammary artery (IMA — the graft of choice, 10-year patency ~90%) or saphenous vein grafts (SVG — 10-year patency ~50%). Most end-stage CAD patients have had CABG; their SVGs have failed and even IMA grafts may be diseased in the most advanced cases. A patient on their second or third CABG has a surgical anatomy that makes further surgical revascularization prohibitively risky or anatomically impossible.^[3]
Pericardial adhesions from prior CABG make repeat sternotomy extremely high-risk — this is one of the primary reasons end-stage CAD patients are deemed "no further surgical candidates" despite ongoing ischemia.^[3]

Transmyocardial Laser Revascularization (TMR)

Laser-drilled channels in ischemic myocardium: A surgical procedure in which a CO₂ or holmium:YAG laser creates transmural channels in ischemic myocardial segments not amenable to conventional revascularization. Mechanism incompletely understood — may improve perfusion, promote angiogenesis, or cause denervation that reduces anginal perception.^[30]
Typically performed as adjunct to CABG for regions not bypassable. Standalone TMR used in refractory angina patients ineligible for revascularization. CCS Class improvement in approximately 70–80% of patients in randomized trials, though blinded sham-controlled data suggest partial placebo effect. Not reversible and not hospice-compatible — but relevant as prior surgical history to document.^[30]

Implantable Devices (ICD, CRT-D)

Implantable cardioverter-defibrillator (ICD): Primary or secondary prevention of sudden cardiac death in patients with EF ≤35%. Commonly implanted in CAD patients with reduced EF post-MI. Does not prevent death from progressive HF, angina, or non-arrhythmic causes — only prevents sudden cardiac death. At hospice enrollment, ICD deactivation is a clinical and ethical obligation to discuss.^[4]
Cardiac resynchronization therapy with defibrillator (CRT-D): Biventricular pacing device for patients with EF ≤35%, LBBB, and NYHA II–IV. CRT function can be maintained for symptom management (pacing improves cardiac output) even after ICD deactivation — these are separate decisions. Discuss explicitly with the patient and family.^[4]

Advanced Comfort Interventions for Refractory Angina

Enhanced External Counterpulsation (EECP)

Non-invasive outpatient angina intervention: Sequential pneumatic compression cuffs applied to calf, thigh, and lower buttocks inflate during diastole (increasing coronary perfusion pressure) and rapidly deflate at systole (reducing afterload). FDA-cleared for stable angina and refractory angina. 35 one-hour sessions over 7 weeks.^[31]
MUST-EECP trial and registry data: Approximately 70% of refractory angina patients achieve CCS Class improvement. Reduces NTG use and increases exercise tolerance. No surgical risk, no anesthesia, repeatable. Appropriate for ECOG 0–1 patients with adequate lower extremity circulation. Refer at enrollment if not previously offered — this is a hospice-compatible angina intervention with meaningful symptom benefit potential.^[31]

Spinal Cord Stimulation (SCS) for Refractory Angina

C7–T1 epidural electrode implantation: Neurostimulation of dorsal columns at the cervicothoracic junction modulates afferent cardiac pain signaling and may improve microvascular function. Multiple randomized controlled trials demonstrate significant reduction in anginal episodes, NTG use, and improvement in CCS Class in refractory angina patients.^[32]
Appropriate referral at enrollment: If the patient has not been evaluated for SCS and has adequate life expectancy to benefit from implantation and recovery, refer to pain management or neurosurgery at hospice enrollment. SCS does not preclude hospice but requires a procedural evaluation — discuss with the IDT and the patient's cardiologist. The benefits in reducing daily anginal burden can be profound in appropriately selected patients.^[32]

S05 Clinician

When Therapy Makes Sense

Criteria for continuing, optimizing, or initiating interventions in end-stage CAD on hospice. The absence of revascularization options does not mean the absence of meaningful therapeutic options.

End-stage CAD patients who arrive at hospice are not at the end of their therapeutic options — they are at the end of their revascularization options. The distinction matters profoundly. Multiple evidence-based interventions remain available, many of which are more likely to improve quality of daily life than the next PCI or hospitalization would have. The hospice clinician must approach the medication and intervention list at enrollment as a clinical optimization problem, not as a comfort transition problem alone. Anti-anginal regimen correction, ranolazine initiation, and EECP referral are active clinical acts that require assessment, judgment, and follow-through.^[13]

01

Anti-anginal regimen optimization — ECOG 0–2: The majority of end-stage CAD patients arrive at hospice on incomplete or incorrectly dosed anti-anginal regimens. The most common correctable error is isosorbide mononitrate dosed twice daily (eliminating the nitrate-free interval and causing complete tolerance). Adding ranolazine to a beta-blocker and long-acting nitrate achieves meaningful additional angina reduction through a completely different mechanism — late sodium current inhibition — without affecting blood pressure or heart rate. This combination is the most impactful medication intervention available at enrollment and should be made at the first visit for any patient with inadequately controlled angina.^[28]
02

EECP referral — ECOG 0–1 with adequate lower extremity circulation: Enhanced external counterpulsation is an outpatient, non-invasive intervention that produces CCS Class improvement in approximately 70% of refractory angina patients. It carries no surgical risk and is repeatable. Thirty-five one-hour sessions over seven weeks is the standard course. For a patient with months of meaningful life who wants to maximize their functional capacity and reduce daily anginal episodes, EECP is an underutilized tool that belongs in every enrollment assessment when the patient is ambulatory. Refer to cardiology or a cardiac rehabilitation center at enrollment if EECP has not previously been offered.^[31]
03

Spinal cord stimulation evaluation — ECOG 0–2 with refractory angina despite maximal medical therapy: Multiple RCTs demonstrate that SCS at C7–T1 reduces anginal episodes and NTG use in refractory angina. For a patient with adequate life expectancy to benefit from implantation and rehabilitation — and who has not previously been evaluated — a referral to pain management or neurosurgery at enrollment is appropriate and reflects an active commitment to comfort-focused care. This conversation belongs in the hospice IDT plan for any patient with daily refractory angina not controlled on maximal medical therapy.^[32]
04

ICD deactivation conversation — any patient with an ICD at enrollment: If the patient has an ICD and has chosen comfort-focused goals, deactivation of the shock function is a clinical and ethical obligation to discuss at enrollment. An ICD that fires in the final hours of life causes pain, terror for the family, and an undignified death. The conversation must happen explicitly, not assumed. The patient must understand that deactivating the ICD does not turn off the pacemaker function (if CRT-D), does not cause death, and does not change anything about their comfort medications or care. Document the discussion and the patient's decision in the record.^[4]
05

Ivabradine for rate reduction in patients with resting tachycardia and sinus rhythm who cannot tolerate beta-blocker: Resting tachycardia in CAD increases myocardial oxygen demand and worsens angina. When beta-blocker is contraindicated by hypotension or severe reactive airway disease, ivabradine 5–7.5 mg BID reduces heart rate in sinus rhythm without affecting blood pressure or contractility. Requires sinus rhythm — do not use in atrial fibrillation. The BEAUTIFUL trial demonstrated reduced anginal frequency in patients with resting HR ≥70 bpm and stable CAD.^[29]
06

Palliative diuresis for CHF component — ischemic cardiomyopathy with fluid overload: Many end-stage CAD patients have ischemic cardiomyopathy with reduced EF and concurrent volume overload. Diuretic optimization reduces dyspnea, orthopnea, and lower extremity edema — and may indirectly reduce ischemic burden from pulmonary congestion increasing left ventricular filling pressures. Daily weight monitoring with a threshold-based diuretic adjustment protocol (e.g., increase furosemide 20 mg for weight gain >2 lbs over 24 hours) is a foundational comfort intervention for this population.^[11]

S06 Clinician

When It Doesn't

The thresholds at which further disease-directed intervention causes harm without benefit — and the pivotal clinical conversations that must happen before the events they address.

Patients with end-stage CAD are significantly underreferred to palliative care and hospice compared with equivalent-prognosis cancer patients. Studies show that fewer than 10% of patients with refractory angina are ever referred to palliative care, despite symptom burden comparable to advanced cancer — daily pain, severe functional limitation, anxiety, and fear of death.^[5] The cardiologist's statement "there is nothing more we can do" is accurate in the procedural sense and devastating in the experiential sense. The hospice team is not the team that gives up — it is the team that shows up when the procedural options end. That distinction requires naming explicitly at enrollment and at every family meeting.

01

ECOG ≥3 — no revascularization benefit and procedural angina interventions not feasible: At ECOG ≥3 (capable of only limited self-care, confined to bed or chair >50% of waking hours), the patient cannot participate in an EECP program (35 one-hour outpatient sessions), undergo neurosurgical evaluation for SCS implantation, or tolerate additional cardiac catheterization. The clinical focus shifts entirely to comfort management of acute episodes — morphine sulfate, sublingual NTG protocol, lorazepam for anxiety, and anticipatory symptom kits. Document ECOG explicitly at every visit — it determines what interventions remain appropriate.^[33]
02

Refractory angina persisting despite maximal four-drug anti-anginal regimen: When the patient is on a long-acting nitrate (correctly dosed with nitrate-free interval), a beta-blocker at target heart rate, ranolazine at 1000 mg BID, and a calcium channel blocker — and continues to have daily anginal episodes — the goal of care has shifted. Further medication manipulation is unlikely to achieve meaningful additional angina prevention. The clinical priority becomes management of individual anginal episodes with SL NTG, low-dose morphine, and lorazepam, and preparation of the patient and family for acute MI at home. This transition must be named explicitly — "we have maximized every available preventive medication; now we focus on managing the episodes when they come."^[2]
03

End-stage ischemic cardiomyopathy — EF <25% and NYHA Class IV symptoms: When ischemic cardiomyopathy has progressed to severely reduced EF with symptoms at rest or minimal activity, both this card and Card #21 (CHF) apply simultaneously. The patient has two overlapping end-stage diagnoses. The CHF management algorithm (palliative diuresis, comfort-focused inotrope discussion, ICD deactivation) runs in parallel with the refractory angina management algorithm. Coordinate the clinical plan with the IDT to ensure both dimensions of symptom burden are addressed.^[12]
04

Recurrent ACS events in a patient who has declined further invasive assessment or intervention: When a patient with established comfort goals is having recurrent acute coronary syndromes — NSTEMI, unstable angina requiring hospitalization — the question is not whether to catheterize but how to manage the episodes in a way consistent with home and comfort priorities. Morphine 2–4 mg SQ for chest pain, lorazepam 0.5–1 mg SQ for anxiety, and continuation of NTG protocol define the at-home ACS management plan. Document the patient's explicit decision to manage ACS events at home rather than call 911.^[10]
05

Acute MI in a patient with established comfort goals — the home management protocol: The most important advance care planning conversation in end-stage CAD is not about code status. It is about what happens when chest pain becomes severe, unresponsive to three doses of SL NTG, and continues to escalate. Does the patient go to the hospital or stay home? This decision must be made explicitly and documented before the event — not during it at 3 AM with a terrified family. If the patient chooses to manage an acute MI at home, the protocol is: morphine sulfate 2–4 mg SQ, lorazepam 0.5–1 mg SQ, midazolam 2.5–5 mg SQ for unmanageable distress, family-administered per written protocol, and nurse-on-call immediately available. The family must know the protocol by demonstration before the event occurs.^[5]

📋 The No-Further-Intervention Decision — What It Does and Does Not Mean

The patient with end-stage CAD who is told "there is nothing more we can do procedurally" has been given accurate information delivered without adequate translation. The hospice clinician must complete the translation: No more procedures is a statement about the limits of interventional cardiology. It is not a statement about what can be done for pain. It is not a statement about what can be done for fear. It is not a statement about quality of remaining life. The pivot from "nothing more procedurally" to "everything possible for comfort" is the specific expertise of the hospice team — and it must be named explicitly. The patient who understands that the hospice team has a concrete, evidence-based plan for their angina, their anxiety, their ICD, their family's preparation, and their acute MI protocol will engage with that team as an active clinical partner rather than a recipient of abandonment. Do not allow the cardiologist's procedural statement to become the patient's framework for what is possible. Reframe it directly, every time it comes up.

S07 Everyone

Out-of-the-Box Approaches

Evidence-graded integrative, interventional, and complementary approaches for refractory angina management. Grade A = RCT evidence; B = multi-observational or meta-analytic data; C = limited clinical, notable preclinical signal; D = expert opinion or case series only.

Ranolazine Optimization

Grade A

500–1000 mg orally BID; start 500 mg BID × 2–4 weeks, titrate to 1000 mg BID if tolerated

The CARISA trial (Chaitman et al., JAMA 2004) demonstrated that ranolazine 750 mg BID and 1000 mg BID significantly reduced anginal episode frequency, NTG consumption, and exercise-induced ischemia compared with placebo in patients with chronic stable angina on background anti-anginal therapy.^[28] The MERLIN-TIMI 36 trial further confirmed anti-anginal efficacy and established a favorable safety profile including a modest QTc prolongation that is clinically significant only in the context of other QT-prolonging drugs. Ranolazine works through a completely distinct mechanism from all other anti-anginals — late sodium current inhibition reduces diastolic wall tension and ischemia — making it fully additive to beta-blockers, nitrates, and CCBs with no redundancy. It does not affect heart rate or blood pressure, making it ideal when other agents are at maximum tolerated doses due to hemodynamic constraints. Most end-stage CAD hospice patients arrive without ranolazine despite being on other agents. Adding it at enrollment is the single most impactful medication adjustment in refractory angina management and requires only a QTc check and renal function review before initiation. Check for CYP3A4 interactions (avoid with diltiazem above 180 mg, ketoconazole, clarithromycin — these significantly increase ranolazine levels).^[28]

Avoid in severe hepatic impairment (Child-Pugh C)
Dose-reduce at GFR <30 — maximum 500 mg BID
Check baseline QTc; avoid if QTc >500 ms

Enhanced External Counterpulsation (EECP)

Grade B

35 one-hour outpatient sessions over 7 consecutive weeks; 5 sessions/week

The MUST-EECP trial (Arora et al., JACC 1999) — the landmark double-blind sham-controlled RCT — demonstrated that active EECP significantly improved exercise duration and time to ischemia compared with sham treatment in patients with stable angina. Subsequent multicenter registry data (IEPR — International EECP Patient Registry) including over 5,000 patients confirmed that approximately 70–80% of refractory angina patients achieve at least one CCS Class improvement, with effects durable at 1–2 years in most responders.^[31] EECP works by sequential pneumatic compression of the lower extremities during diastole — increasing coronary perfusion pressure — combined with rapid decompression at systole — reducing left ventricular afterload. Sustained effects are attributed to enhanced angiogenesis, improved endothelial function, and favorable neurohormonal modulation. FDA-cleared for stable and unstable angina and heart failure. No surgical risk, no anesthesia, no recovery period, and repeatable if initial benefit wanes. For an end-stage CAD patient who is ECOG 0–1, ambulatory, and has adequate lower extremity arterial and venous circulation, EECP referral at hospice enrollment is an active comfort intervention with meaningful clinical benefit potential.

Contraindicated: severe aortic regurgitation, IABP in place, significant peripheral arterial disease (ABI <0.8), severe coagulopathy, phlebitis
Refer to cardiology or certified cardiac rehabilitation center at enrollment

Spinal Cord Stimulation (SCS)

Grade B

C7–T1 epidural electrode implantation; neurostimulation 50–100 Hz, pulse width 200–300 µs; patient-controlled activation

Multiple randomized controlled trials have demonstrated that high cervicothoracic SCS significantly reduces anginal frequency, NTG use, and CCS Class in patients with refractory angina not amenable to revascularization. A meta-analysis by Zipes et al. summarizing RCT and registry data found that SCS reduced anginal episodes by approximately 60–70% compared with baseline in refractory angina populations.^[32] Mechanism is multi-factorial: SCS modulates afferent cardiac pain signaling at the dorsal columns (gate control theory), reduces sympathetic efferent outflow to the heart (reducing oxygen demand), and may improve coronary microvascular function through autonomic modulation. Requires implantation procedure under local anesthesia and sedation — appropriate for ECOG 0–2 patients with adequate life expectancy to benefit from the procedure and recovery. If the patient has never been evaluated for SCS and continues to have daily refractory angina on maximal medical therapy, referral to a pain management or neurosurgery specialist at hospice enrollment is an appropriate and clinically sound step.

Incompatible with MRI after implantation (most systems); clarify with implanting provider
Contraindicated with anticoagulation — coordinate antiplatelet hold with cardiologist
Requires neurosurgical or pain management specialist referral

Long-Acting Nitrate Dosing Optimization

Grade A

Isosorbide mononitrate ER 30–120 mg once daily in the morning; nitrate-free interval 8–12 hours overnight

Nitrate tolerance is the single most common reason for ineffective long-acting nitrate therapy in end-stage CAD, and it is entirely preventable. The pharmacology is well-established: continuous exposure to organic nitrates causes mitochondrial aldehyde dehydrogenase-2 (ALDH2) depletion and desensitization of guanylyl cyclase, eliminating vasodilatory efficacy within 24–72 hours of continuous dosing.^[27] The solution is a mandatory 8–12 hour nitrate-free interval per 24-hour period. Isosorbide mononitrate extended-release administered once daily in the morning provides a sustained 12–14 hours of drug effect with a subsequent drug-free overnight period — restoring efficacy daily. The common prescribing error is twice-daily dosing of ISMN ER (e.g., 60 mg twice daily) — this eliminates the nitrate-free interval and causes complete tolerance within days. Many end-stage CAD patients at hospice enrollment are on this incorrect schedule. Reviewing and correcting the nitrate dosing schedule takes five minutes and may produce dramatic improvement in anginal control within 48–72 hours. Headache is the primary dose-limiting side effect and typically improves within 1–2 weeks; acetaminophen at time of nitrate administration reduces headache without interacting with NTG.

Review the actual prescription — not just the drug name — at enrollment
Headache: acetaminophen 500–1000 mg at nitrate time reduces it; dose reduction also helps
Isosorbide dinitrate (immediate-release) requires twice-daily dosing with an asymmetric schedule (e.g., 7 AM and 2 PM) to preserve a 10-hour nitrate-free interval

Sublingual Nitroglycerin Protocol Education

Grade A

SL NTG 0.3–0.4 mg tablet or metered spray; one dose at first sign of chest pain, repeat every 5 minutes × 3 doses maximum

Every end-stage CAD patient and every family member who may be present during an anginal event must know the sublingual nitroglycerin protocol by demonstration — not by reading a pamphlet. The three-dose protocol is guideline-established: one dose at first sign of angina, wait 5 minutes, second dose if no relief, wait 5 minutes, third dose if no relief, then call the hospice nurse.^[34] For patients with comfort-focused goals who have chosen to manage acute events at home, the three-dose protocol replaces calling 911 — and the family who has not been taught it will call 911 out of panic at the first dose. NTG tablets expire rapidly after bottle opening (6 months), lose potency with light and heat exposure, and must be stored in the original dark glass bottle. Check expiration at every visit. The spray formulation has a longer shelf life than tablets. Patients should carry NTG with them at all times during any activity — not just at the bedside. Demonstrating the proper administration to a family caregiver in the room takes 3 minutes and may prevent an unwanted 911 call or an untreated anginal episode.

Check expiration date at every visit — replace every 6 months after opening
Store in original dark glass bottle away from heat, light, and moisture
Spray formulation preferred for patients with difficulty handling small tablets
Sit or lie down with NTG — hypotension risk is real; do not take standing

Acupuncture for Angina

Grade C

Weekly sessions × 6–12 weeks; PC-6 (Neiguan), ST-36 (Zusanli), HT-7 (Shenmen) — standard cardiac acupuncture points

A 2019 systematic review and meta-analysis of 16 RCTs (Zhao et al., JAMA Internal Medicine) found that acupuncture combined with standard medical therapy significantly reduced anginal frequency and NTG consumption compared with sham acupuncture or medical therapy alone in stable angina patients.^[35] Effect size was modest — approximately 30–40% reduction in anginal episodes — but clinically meaningful for patients with refractory symptoms on maximal medical therapy. Mechanism proposed includes endogenous opioid release, vagal modulation, and anti-inflammatory effects. Appropriate for ECOG 0–2 patients who are interested and have access to a licensed acupuncturist. Hospice benefit may cover acupuncture services under some plans — verify with the hospice program. No meaningful drug interactions with cardiac medications. Bleeding risk is minimal with standard needling technique; use care in anticoagulated patients.

Verify acupuncturist licensure and experience with cardiac patients
No meaningful cardiac medication interactions
Minimal bleeding risk; use standard clean needle technique in anticoagulated patients

Transmyocardial Laser Revascularization (TMR) — Historical Context

Grade C

Surgical procedure (prior history only in hospice context — not newly initiated in end-stage hospice patients)

TMR involves laser-creation of channels through ischemic myocardium in patients not amenable to conventional revascularization. Randomized controlled trial data demonstrate improvement in CCS angina class and quality-of-life scores compared with medical management alone in refractory angina.^[30] However, blinded sham-controlled trials suggest a significant placebo component to the benefit, and survival advantage over medical management has not been consistently demonstrated. TMR is not a newly initiated intervention in end-stage hospice patients — the relevance here is as a prior surgical procedure that may be in the history. Patients who have had TMR may have altered myocardial anatomy, pericardial adhesions, and unusual post-procedure anginal patterns that the hospice team should be aware of. The hospice NP should note TMR history when reviewing the surgical record.

Note in clinical record if prior TMR is documented — affects future surgical risk assessment
Not an intervention to initiate de novo in hospice patients

Stellate Ganglion Block

Grade D

Ultrasound-guided injection of local anesthetic at C6 stellate ganglion; single or repeat injections; requires pain management specialist

The stellate ganglion is the primary sympathetic ganglion innervating the heart. Blockade reduces sympathetic tone, decreases cardiac oxygen demand, and may reduce anginal perception by interrupting afferent pain signaling. Case series and small observational studies report benefit in refractory ventricular arrhythmia (electrical storm) and some benefit in refractory angina, but RCT evidence for angina is lacking.^[36] Expert consensus (Grade D) supports consideration in carefully selected refractory angina patients who have exhausted other options, particularly those with a strong sympathetically mediated anginal component (triggered by emotional stress, cold, or exertion-related sympathetic surges) and who have not responded adequately to beta-blockade. The procedure requires an interventional pain management specialist with ultrasound guidance. Relevant complications include Horner syndrome (ptosis, miosis, anhidrosis — expected, transient), pneumothorax, and intravascular injection. Not appropriate for ECOG ≥3 patients. Consider as an escalation option in ECOG 0–2 patients with inadequately controlled refractory angina despite maximal pharmacological therapy who decline or cannot tolerate SCS implantation.

Requires ultrasound-guided interventional pain management specialist
Expected Horner syndrome — warn patient and family in advance
Pneumothorax risk — monitor post-procedure
ECOG 0–2 only; not appropriate for bedbound patients

S08Everyone

Natural & Herbal Options

Evidence grading, dosing where supported, drug interaction flags, and explicit contraindications specific to end-stage CAD. Patients will use supplements — this section helps you have the right conversation.

From the Field

Waldo Rios, NP

Hospice NP · 12+ Years

"CAD patients are on aspirin, a statin, a beta-blocker, nitrates, and often warfarin. When I ask about supplements, I am not judging — I am preventing a catastrophe. The interaction between any PDE-5 inhibitor and nitrates is not a drug interaction. It is a medical emergency. Ask every patient, every visit, every time what they are taking that is not on the medication list. Then check it against the full med list before you say a single word of encouragement."

— Waldo, NP · Terminal2

⚠ Critical CAD Drug Interaction Context

End-stage CAD patients are almost universally on aspirin, a statin, a beta-blocker, and one or more anti-anginals including nitrates. Many are also on warfarin (AF, mechanical valve, or prior DVT). Any supplement that affects CYP2C9, vitamin K metabolism, platelet function, or vascular tone carries compounded risk in this population. The most dangerous error in this population is recommending a supplement that contains any phosphodiesterase-5 inhibitory activity (sildenafil, tadalafil, vardenafil, or herbals with similar action) in a patient on nitrates — the resulting profound hypotension can precipitate an acute MI or death. Every supplement must be cross-referenced against the full medication list before any recommendation is offered.^[40]

Herb / Supplement	Evidence Grade	Typical Dose	Potential Benefit	⚠ Interactions / Contraindications
Coenzyme Q10 (CoQ10) / Ubiquinol	Grade B	100–200 mg daily with fat-containing meal; ubiquinol form preferred for bioavailability	Mitochondrial cofactor depleted by statin therapy; modest antioxidative effect in cardiac tissue; some RCT evidence for symptom benefit and modest reduction in angina episodes; Q-SYMBIO trial showed reduction in major adverse cardiac events at 2 years in HF population^[41]	Modest warfarin interaction — may slightly reduce INR; monitor INR 2–4 weeks after starting; generally safe; no significant interaction with aspirin, beta-blockers, or nitrates; avoid doses >400 mg/day without monitoring
Magnesium Glycinate	Grade C	200–400 mg elemental magnesium daily in divided doses; glycinate form preferred for GI tolerance	Magnesium depletion from loop diuretics (furosemide) is extremely common in end-stage CAD patients with CHF component; hypomagnesemia promotes coronary vasospasm and increases anginal frequency; repletion reduces spasm-mediated angina; also supports cardiac rhythm stability^[42]	Check serum magnesium before supplementing; avoid if GFR <30 mL/min — magnesium accumulates in renal insufficiency and causes bradycardia and hypotension; safe at therapeutic doses in mild-moderate renal impairment; no significant interaction with aspirin, nitrates, or statins
Omega-3 Fatty Acids (Fish Oil)	Grade C	≤1 g/day supplement; food-source fish (salmon, sardines, mackerel) preferred at 2–3 servings/week	Modest anti-inflammatory effect; food-source omega-3 intake provides cardiovascular benefit; REDUCE-IT trial used highly purified EPA (icosapentaenoic acid) at 4 g/day — not achievable or appropriate at supplement doses; at ≤1 g/day, anti-inflammatory and modest triglyceride-lowering effects are biologically plausible^[43]	Above 3 g/day, antiplatelet effect becomes clinically significant — compounded with aspirin and clopidogrel; do not recommend >3 g/day in patients on dual antiplatelet therapy; modest warfarin potentiation at higher doses; no interaction with nitrates or beta-blockers at ≤1 g/day
L-Carnitine	Grade C	2 g/day in divided doses with meals; L-carnitine or propionyl-L-carnitine formulations studied	Meta-analysis data suggests modest reduction in angina frequency and improvement in exercise tolerance in stable CAD; proposed mechanism involves optimization of fatty acid metabolism in ischemic myocardium; propionyl-L-carnitine form has more cardiac-specific data; generally well-tolerated with good safety profile^[44]	Minimal clinically significant drug interactions; no warfarin interaction; safe with aspirin, statins, beta-blockers, and nitrates; may rarely cause mild GI upset; contraindicated in active seizure disorder (rare metabolite TMAO effect); thyroid interaction theoretical — monitor in hypothyroid patients on levothyroxine

🚫 Avoid in End-Stage CAD — Serious or Potentially Lethal Interactions

Sildenafil (Viagra), Tadalafil (Cialis), Vardenafil (Levitra) — ANY PDE-5 inhibitor: LETHAL combination with nitrates. The combination causes profound, refractory hypotension that can precipitate an acute MI, stroke, or death. This is not a relative contraindication — it is an absolute one. Ask explicitly at every visit. Patients frequently do not volunteer this information. The nitrate-free interval does not make this safe.^[40]
Ephedra (ma huang) and Bitter Orange (Synephrine): Sympathomimetic agents that increase heart rate and blood pressure, increase myocardial oxygen demand, and precipitate angina and arrhythmia in patients with CAD. Found in some "energy" and "weight loss" supplements. Ask specifically about these by name — patients may not recognize the botanical name on the label.
High-Dose Garlic Supplements (>600 mg extract/day): Significant antiplatelet activity that compounds aspirin and clopidogrel; increased bleeding risk; also modest warfarin interaction; at food-source culinary doses, risk is minimal — it is concentrated extract supplementation that is problematic in patients on dual antiplatelet or anticoagulation therapy.
Ginkgo Biloba: Antiplatelet and anticoagulant activity; significantly compounds aspirin and warfarin; multiple case reports of bleeding in patients on combined antiplatelet-ginkgo therapy; no meaningful cardiovascular benefit in CAD has been demonstrated to offset this risk.
St. John's Wort (Hypericum perforatum): Potent CYP3A4 and P-glycoprotein inducer; dramatically reduces plasma levels of warfarin, statins (simvastatin, atorvastatin), and ranolazine — all medications commonly used in end-stage CAD patients; can cause warfarin therapy to fail and increase thrombotic risk; ranolazine levels may drop below therapeutic range, undermining angina management.
High-Dose Fish Oil >3 g/day: At doses above 3 g/day, antiplatelet effect is clinically significant and compounds aspirin and clopidogrel, substantially increasing GI and other bleeding risk. The REDUCE-IT trial's 4 g/day prescription icosapentaenoic acid formulation is not equivalent to over-the-counter fish oil and is not appropriate in comfort-focused hospice care.

S09Everyone

Timeline Guide

A guide, not a prediction. CAD trajectory is not linear — it is punctuated by acute coronary events interspersed with more stable periods. End-stage is defined by progressive functional decline and exhaustion of revascularization options.

Unlike malignancies, CAD trajectory is characterized by episodic acute events — acute MI, decompensated CHF, unstable angina — interspersed with more stable periods of chronic ischemia. This creates a false impression of stability between events and contributes to late or absent palliative care integration. The key milestone that defines end-stage CAD is the exhaustion of revascularization options — the angiography report that says "no targets," "diffuse disease," or "vessels too small for intervention." Once that report exists, the disease trajectory becomes a function of residual myocardial function, comorbidities, and optimal medical management of an irreversible ischemic state. Prognosis is highly variable: refractory CCS Class IV angina with EF <35% carries a median survival of 2–3 years; with preserved EF, survival may be longer but quality of life is severely compromised by pain and fear.^[1]^[2]

YRS–
MOS

Post-Revascularization Stable Phase

Patient has had CABG, PCI, or both; on guideline-directed medical therapy (GDMT) — aspirin, statin, beta-blocker, ACE inhibitor or ARB, long-acting nitrate
Angina present with moderate to vigorous exertion; CCS Class I–II; functional but with activity limitation; angina frequency is manageable and predictable
Routine cardiology follow-up; medications being adjusted; annual stress testing or imaging in some patients; EF assessment with echocardiogram
Progressive functional decline occurring but not yet end-stage; graft patency declining over years; native vessel progression continuing despite medications
Palliative care integration is essentially never offered at this stage despite meaningful symptom burden and predictable trajectory — this is the primary systems failure^[45]
Focus: advance care planning should begin here while patient has full decision-making capacity; EECP or SCS may still be appropriate options; ICD candidacy assessment if EF <35%

MOS–
1 YR

Revascularization Options Exhausted

Coronary angiography has confirmed no further intervention possible — the angiography report with "no targets," "diffuse disease," "CABG grafts occluded," or "vessels too small" is the document that defines this transition^[3]
CCS Class III–IV angina despite optimal medical therapy; angina now occurs with minimal exertion or at rest; NTG use increasing; functional capacity declining
Dyspnea on minimal exertion from combined ischemia and CHF component; ischemic cardiomyopathy contributing to volume overload; diuretic titration ongoing
Anti-anginal regimen being maximized; ranolazine added if not already prescribed; EECP referral should be offered if functional status permits
Fear of chest pain episodes becoming a dominant psychological feature; anticipatory anxiety restricting activity beyond what ischemia alone would produce
Repeat hospitalizations for ACS or decompensated CHF occurring but producing diminishing returns; this is the palliative integration window most commonly missed
Focus: goals-of-care conversation about what to do for acute MI at home; ICD deactivation conversation if device is present; hospice eligibility should be assessed

WKS–
MOS

End-Stage Refractory Angina

CCS Class IV — angina at rest or with minimal activity such as dressing, walking to bathroom, or any emotional stress; the patient may be essentially house-bound^[4]
NTG use daily or multiple times daily; NTG relief becoming less complete; episodes lasting longer; dyspnea now as prominent as chest pain in many patients
Anxiety about angina episodes severe; patient may be afraid to move, afraid to sleep, afraid to be alone; anticipatory anxiety is a clinical problem requiring clinical management
ECOG 2–3; ischemic cardiomyopathy component worsening; cognitive changes from reduced cerebral perfusion may emerge; significant fatigue from chronic low-grade ischemia
Hospice enrollment most appropriate at this transition; the patient meets eligibility criteria and has the most to gain from hospice-level symptom management
Focus: complete anti-anginal optimization at enrollment; NTG protocol education for every household member; acute MI at home protocol written; ICD deactivation conversation completed; comfort kit prepared and at bedside

DAYS–
WKS

Active Dying — Angina at Rest Requiring Around-the-Clock Opioids and Nitrates

Angina at rest requiring around-the-clock opioid therapy; morphine SQ ATC providing meaningful reduction in both chest pain and dyspnea; NTG continues as adjunct^[29]
Bed-bound or chair-bound; minimal oral intake; profound fatigue; sleeping most of the day; ischemic cardiomyopathy producing significant dyspnea even at rest
Acute MI may occur at home — if goals are comfort-focused, management is morphine SQ + lorazepam SQ + midazolam SQ available; family must know this protocol^[46]
Cognitive changes from combination of reduced cerebral perfusion and opioid effect; patient may be delirious or somnolent; communication windows still valuable
ICD should be deactivated by this phase if not already done; without deactivation, ICD shocks at active dying are a foreseeable and preventable harm^[30]
Focus: family preparation for acute death at home; comfort kit fully stocked and labeled; nurse on-call availability reinforced; caregiver support and respite; chaplain and social work present

HRS–
DAYS

Final Hours

Agonal breathing or Cheyne-Stokes respirations; mottling of knees and feet; peripheral cooling; jaw relaxation; unresponsive or minimally responsive to verbal stimuli
Auditory awareness may persist — family should speak calmly and say what needs to be said; this is not a coma; it is a transition
Sudden cardiac death remains possible and may occur without the slow respiratory decline seen in other terminal diagnoses — prepare families explicitly for this possibility^[46]
Angina medication continued via SQ route until death if patient shows any signs of discomfort; opioid infusion or SQ dosing continues around-the-clock; do not discontinue comfort medications in final hours
Terminal secretions managed with glycopyrrolate SQ; family reassured that the sound does not indicate distress
Family instruction: do not call 911 unless that is the expressed wish — for a patient who has chosen home death, the nurse on-call number is the right number; have it visible

S10Clinician

Medications to Anticipate

Symptom-targeted pharmacology for end-stage CAD. Anti-anginal optimization, opioids for refractory angina, acute MI at home protocol, and the most important nitrate tolerance correction you will make at enrollment.

🚨 Nitrate Tolerance — The Most Correctable Error in End-Stage CAD Management

Nitrate tolerance is the most common reason anti-anginal therapy appears to be failing when it is not. Every long-acting nitrate requires a nitrate-free interval of 8–12 hours per 24 hours to maintain drug efficacy. Isosorbide mononitrate extended-release (IMDUR) must be dosed once daily in the morning — this preserves the overnight nitrate-free period. Patients prescribed IMDUR twice daily have complete nitrate tolerance by day 3 and the medication is doing nothing for their angina. Review every patient's nitrate dosing schedule at enrollment. Correcting an incorrect nitrate schedule is a five-minute intervention that may produce dramatic improvement in anginal control within days.^[19] Additionally, renal function must guide dose adjustment of ranolazine (avoid dose >500 mg BID if CrCl <30), and many other agents in patients with cardiorenal syndrome. Obtain recent BMP and renal function at enrollment.

Drug	Class / Target Symptom	Starting Dose	Notes / Cautions
Isosorbide Mononitrate ER (IMDUR)	Long-acting nitrate / Refractory angina	30–120 mg PO once daily in AM	Once-daily dosing only. The once-daily ER formulation provides the required overnight nitrate-free interval. Do NOT dose twice daily — this eliminates the nitrate-free interval and causes complete tolerance within 3 days. Headache is dose-limiting in first 1–2 weeks and usually improves; acetaminophen at time of administration reduces headache without compromising nitrate effect. Titrate in 30 mg increments as tolerated.^[19] Check current dosing schedule at enrollment — twice-daily dosing is the most common prescribing error in end-stage CAD.
Sublingual Nitroglycerin (SL NTG)	Short-acting nitrate / Acute angina episodes	0.3–0.4 mg SL tablet or spray at first sign of chest pain; repeat q5min × 3 doses max	Must be at bedside, in pocket during activity, and understood by every household member. If no relief after 3 doses, call nurse — this is the protocol that replaces calling 911 for home-death patients. ⚠ Check expiration date at every visit — NTG tablets expire rapidly after bottle is opened; replace every 6 months or sooner; store in original amber glass bottle away from heat, light, and moisture. NTG spray (Nitrostat spray) is more stable than tablets and preferred for patients with dexterity issues or who store medication inconsistently.
Ranolazine (Ranexa)	Late Na⁺ current inhibitor / Refractory angina	500 mg PO BID; titrate to 1000 mg PO BID	Add to beta-blocker and long-acting nitrate for synergistic angina reduction through a completely different mechanism. Does not affect heart rate or blood pressure — uniquely valuable when other agents are limited by hypotension or bradycardia. CARISA trial: reduced anginal episodes and NTG use vs. placebo on background therapy.^[5] Check QTc before starting — avoid if QTc >500 ms. CYP3A4 substrate — avoid with strong CYP3A4 inhibitors (azole antifungals, macrolides). ⚠ Avoid if severe hepatic impairment. Reduce dose to 500 mg BID max if CrCl <30. Most chronically undertreated drug in end-stage CAD hospice. Most patients who arrive without it have never been offered it.
Metoprolol Succinate ER / Carvedilol	Beta-blocker / Anti-anginal + cardiac protection	Metoprolol succinate 25–200 mg PO daily; Carvedilol 3.125–25 mg PO BID	Continue if tolerated and blood pressure allows; target resting heart rate 55–65 bpm for optimal oxygen demand reduction. Carvedilol preferred if CHF component is significant (EF <40%) due to mortality benefit. Do not abruptly discontinue — risk of rebound angina and acute MI. ⚠ Do not combine with rate-limiting CCBs (verapamil, diltiazem) — profound bradycardia risk. Beta-blocker reduces myocardial oxygen demand by reducing heart rate and contractility — the primary mechanism of anti-anginal benefit.
Amlodipine (Norvasc)	Dihydropyridine CCB / Anti-anginal + vasodilation	5–10 mg PO daily	Safe to combine with beta-blocker (unlike rate-limiting CCBs). Vasodilatory effect reduces afterload and coronary artery tone; additive anti-anginal benefit when combined with beta-blocker and nitrate. Useful for vasospastic component. Primary side effect is peripheral edema — may compound CHF component fluid management. Can be continued in hospice as long as tolerated — modest BP-lowering effect may benefit cardiorenal syndrome if not causing hypotension.
Ivabradine (Corlanor)	If-channel inhibitor / Rate reduction without hypotension	5 mg PO BID; titrate to 7.5 mg PO BID	Reduces heart rate without affecting contractility or blood pressure — valuable when beta-blocker causes hypotension but heart rate reduction is still needed for oxygen demand management. Requires sinus rhythm — do NOT use in atrial fibrillation. BEAUTIFUL trial: reduced angina hospitalizations in stable CAD with EF <40% and heart rate >70 bpm.^[27] ⚠ Strong CYP3A4 inhibitor interaction — reduce dose or avoid with azole antifungals, macrolides.
Morphine	Opioid / Refractory angina pain + dyspnea	2.5–5 mg PO/SQ q4h ATC; 2.5 mg SQ PRN q1h for breakthrough angina or dyspnea	Opioids are evidence-based for refractory angina pain management when anti-anginal regimen is maximized. Morphine also reduces dyspnea by central mechanism. ⚠ CRUSADE registry data suggests morphine in ACS may be associated with worse outcomes in the acute revascularization setting — this data does NOT apply to comfort-focused end-stage CAD care where angina is being managed for comfort, not revascularization.^[29] Titrate to comfort. Anticipate constipation — start bowel regimen on day one. The fear of using opioids for angina is the single most common reason refractory angina remains undertreated in hospice.
Hydromorphone (Dilaudid)	Opioid / Refractory angina + dyspnea (morphine intolerant)	0.5–1 mg PO/SQ q4h ATC; 0.5 mg SQ PRN q1h	Preferred opioid alternative when morphine causes excessive sedation, pruritus, or nausea. More potent per mg — use conversion carefully (morphine 5 mg ≈ hydromorphone 1 mg oral; 4:1 oral conversion; 5:1 parenteral). Accumulates in renal failure — use with caution if GFR <30. Shorter duration of action may require closer titration. Hydromorphone SQ preferred when route must be subcutaneous and larger volumes are impractical.
Lorazepam (Ativan)	Benzodiazepine / Angina-associated anxiety + dyspnea anxiety	0.5–1 mg PO/SQ q4–6h PRN; may schedule if anxiety is frequent and predictable	Critical for the fear dimension of refractory angina — anticipatory anxiety about chest pain episodes is as disabling as the pain itself. Lorazepam PRN before activity or predictable triggers allows patients to participate more fully in life. Also useful for acute MI at home comfort protocol. ⚠ Respiratory depression risk when combined with opioids — use lowest effective dose; monitor for over-sedation; this risk is appropriate to accept in comfort-focused care when goals are clarity. Include in comfort kit pre-drawn and labeled for acute MI at home protocol.
Midazolam (Versed)	Benzodiazepine / Terminal agitation + refractory angina crisis	2.5–5 mg SQ PRN for acute crisis; 5–15 mg/24h SQ CSCI for continuous refractory agitation	Terminal agitation management and catastrophic symptom control. Essential in acute MI at home comfort protocol when morphine alone does not control distress. Have in comfort kit pre-drawn and labeled. Family must know where it is and what it is for. ⚠ Must be discussed with family before the event — explaining midazolam for the first time during an acute MI at home is not compatible with calm, competent administration.
Furosemide (Lasix)	Loop diuretic / CHF component / Dyspnea from congestion	20–80 mg PO daily; titrate to symptom control; IV/SQ if PO absorption unreliable	Most end-stage CAD patients have ischemic cardiomyopathy with CHF component; diuretic optimization reduces pulmonary congestion and dyspnea and may indirectly reduce ischemia from volume-mediated increased wall tension. Daily weight protocol is the most reliable early warning for decompensation — 2–3 lb gain in 24h requires diuretic adjustment. Monitor electrolytes — hypokalemia and hypomagnesemia increase arrhythmia risk and anginal frequency. Furosemide SQ (1 mg/mL) via butterfly needle is available for patients who can no longer absorb oral medications reliably.
Glycopyrrolate (Robinul)	Anticholinergic / Terminal secretions	0.2 mg SQ q4h; 0.6–1.2 mg/24h SQ CSCI	Preferred over hyoscine in conscious patients — no CNS penetration, no delirium risk. Reduces terminal secretion volume without systemic sedation. Gentle oral care and repositioning are equally important. Family education: "This sound is not distressing to your loved one — it sounds much worse from the outside than it feels from the inside."

❤ CAD Symptom Management Decision Tree

Evidence-based · Hospice-adapted · CAD-specific

Select a symptom below to begin

What is the primary symptom to address?

🚨 Comfort Kit Must-Haves for End-Stage CAD

Refractory angina crisis and acute MI at home are foreseeable events in every end-stage CAD patient. The comfort kit must be prepared, labeled, and physically at the bedside before the first crisis — not ordered during one. Every household member should know where these medications are and what they are for.

Sublingual NTG (0.4 mg tablets or spray): Angina crisis management — three-dose protocol; current, unexpired, properly stored
Morphine SQ (2.5–5 mg pre-drawn): Refractory angina and dyspnea — acute MI at home comfort protocol
Lorazepam SQ (0.5–1 mg pre-drawn): Angina-associated anxiety; acute MI at home protocol; terminal agitation
Midazolam SQ (2.5–5 mg pre-drawn): Refractory distress during acute MI at home; terminal agitation backup
Glycopyrrolate SQ (0.2 mg): Terminal secretions management
Furosemide SQ (20–40 mg): If patient cannot absorb oral diuretics — acute decompensated CHF at home

S11Clinician

Clinician Pointers

High-yield clinical pearls for the hospice team managing end-stage CAD. The things not in the textbook — learned at the bedside over years of clinical experience with this specific patient population.

Nitrate tolerance is the most correctable error at enrollment — fix it first

The patient who takes isosorbide mononitrate ER 60 mg twice daily has zero nitrate efficacy by day 3 — complete tolerance has developed because the nitrate-free interval has been eliminated. This is not a rare prescribing error; it is common. Change to once-daily morning dosing immediately. The patient who reports that "the nitrates stopped working" may simply have been prescribed incorrectly — and the fix takes one phone call to the prescriber. Anginal control may improve dramatically within 48–72 hours of correcting the dosing schedule. Check the nitrate dosing schedule before you check anything else at enrollment.^[19]

Ranolazine is the most underused anti-anginal in end-stage CAD hospice — add it at enrollment

Most end-stage CAD patients arriving at hospice enrollment are not on ranolazine despite having inadequately controlled angina on beta-blocker and nitrate alone. Ranolazine works through late sodium current inhibition — a completely different mechanism from every other anti-anginal agent. It provides additive angina reduction without affecting heart rate or blood pressure, making it the ideal add-on when other agents are limited by hypotension or bradycardia. CARISA trial data shows significant reduction in anginal episodes and NTG use. Start at 500 mg BID, titrate to 1000 mg BID over 2 weeks. Check QTc and renal function before starting. This drug changes quality of life in refractory angina and it is chronically underprescribed.^[5]^[6]

The acute MI at home protocol must be written before the event — not during it

The decision about whether to call 911 for severe chest pain unresponsive to NTG is the most important advance directive conversation in end-stage CAD. Have it explicitly at enrollment. Document what the patient wants to happen if chest pain becomes severe and uncontrolled by three doses of NTG. If the patient has chosen home death and comfort-focused care, write a specific protocol: morphine 5 mg SQ × 1, lorazepam 0.5 mg SQ × 1, midazolam 5 mg SQ if still distressed; call nurse on-call. Every family member present at the bedside should be able to find these medications at 3 AM and know what they are for. The family who panics and calls 911 has not been taught. The difference between a peaceful death and a traumatic one in end-stage CAD is often entirely this conversation — had proactively or not had at all.^[46]

The fear dimension of refractory angina is as disabling as the pain itself — treat it as a clinical problem

Patients with end-stage CAD who have survived multiple MIs, multiple procedures, and multiple hospitalizations develop anticipatory anxiety about chest pain that severely restricts their activity beyond what the underlying ischemia would produce. They sit still because any movement might trigger pain. They stop attending family events, stop walking to the mailbox, stop participating in meaningful activities out of fear. This fear is a clinical problem requiring clinical management alongside psychological support. Lorazepam 0.5 mg PRN 30 minutes before predictable activity provides enough anxiolytic effect to allow participation in activities the patient had stopped doing. Clear protocols about what to do when pain occurs — the NTG three-dose sequence and the nurse on-call number — reduce the fear of "what if it doesn't stop" more than any medication alone.^[37]

ICD deactivation is a clinical obligation — have the conversation at enrollment, not at crisis

Approximately 30–40% of end-stage CAD patients with reduced EF have an implantable cardioverter-defibrillator in place. In a patient who has chosen comfort-focused care and home death, an active ICD is a device that will deliver multiple painful shocks as the patient dies of an arrhythmia — which is exactly how many end-stage CAD patients die. ICD shocks in active dying are foreseeable, preventable, and constitute a harm. The conversation about deactivation belongs at enrollment, framed as: "You have a device in your chest designed to restart your heart if it goes into a dangerous rhythm. At this point in your illness, we want to talk about whether you want that device to keep doing its job or whether you would prefer it not deliver shocks — which can be painful — as you're nearing the end of your life." The patient answers. You document. You make the cardiology referral for device clinic deactivation or use a programmer at the bedside if available.^[30]^[31]

Racial disparities in CAD revascularization and hospice referral are documented and clinically significant

Black patients with CAD receive revascularization procedures at significantly lower rates than white patients with equivalent disease burden, even after adjusting for insurance and comorbidities — a disparity documented across multiple registries and health systems.^[38] Black and Hispanic patients with end-stage CAD are referred to hospice later and at lower rates than white patients. The hospice clinician's role includes naming these disparities explicitly in clinical supervision and team meetings, ensuring that every patient with end-stage CAD regardless of race or ethnicity receives the same proactive anti-anginal optimization, the same acute MI at home protocol conversation, and the same ICD deactivation discussion. Equity is not automatic — it requires intentional clinical action.

Check the NTG bottle at every visit — expired nitroglycerin does not work

Sublingual nitroglycerin is extraordinarily time-sensitive. The tablets begin to lose potency immediately upon opening the bottle — within 3–6 months they may be entirely ineffective, particularly if stored incorrectly (in a pill organizer, pocket, purse, or near a heat source). At every visit, physically check the bottle: Is the expiration date current? Is the bottle the original amber glass? Is it stored away from light and heat? Is the cotton removed (cotton absorbs NTG)? A patient with expired, improperly stored NTG is a patient with no acute angina rescue medication. The family who says "he took three of them and it didn't help" may have given three doses of an inactive drug. Replace at every visit if expiration or storage is in question.

Caregiver vigilance burden in end-stage CAD is extreme and specific — name it, assess it, and address it proactively

The partner or adult child caring for a patient with end-stage CAD is not simply watching someone decline — they are watching someone who might have chest pain at any moment, who might have a fatal heart attack in front of them, who might die suddenly. This is a specific and underappreciated form of caregiver burden: hypervigilance. They monitor every grimace, every moment of clutched chest, every expression of discomfort with the terror that it might be the one that doesn't resolve. They are afraid to leave the house. They cannot sleep. This vigilance-based caregiver burden is clinically significant and deserves explicit assessment using validated instruments and targeted social work support.^[39] Ask directly: "What happens when you leave for an hour? Can you sleep? Are you afraid of what you'll find?" Then do something with the answers — respite care, a night-time check-in protocol, a clear written plan for what to do if something happens while they're in the next room.

From the Field

Waldo Rios, NP

Hospice NP · 12+ Years

"I have never walked into an end-stage CAD enrollment and found a patient whose nitrate dosing was correct and whose ranolazine was already on the medication list. Never. These two corrections alone — fix the nitrate schedule, add ranolazine — have transformed angina control within a week in patients who've been suffering for months. Before you do anything else at enrollment, look at the nitrate dosing. It takes five minutes and it might be the most important thing you do that day."

— Waldo, NP · Terminal2

S12EveryoneClinician

Psychosocial & Spiritual Care

Existential distress, depression screening, spiritual assessment, and goals-of-care communication specific to end-stage CAD. The no-further-intervention grief. The identity of the cardiac patient. The fear of chest pain. The caregiver who has been hypervigilant for years.

Psychosocial distress in end-stage CAD has a specific profile that distinguishes it from other terminal diagnoses. These patients have been in a medical system oriented entirely around procedures — stents, bypasses, ablations, angiograms — for years, often decades. They have learned to measure hope in procedures. When the cardiologist says "there is nothing more we can do procedurally," that statement lands with a specific weight: the framework that has sustained them is gone. The hospice clinician who inherits a patient at this juncture carries the obligation to reframe what remains without minimizing what has been lost. Depression affects 25–40% of patients with end-stage cardiac disease and is profoundly underdiagnosed and undertreated in this population.^[35]

Your job is not to provide the answers. Your job is to ask the questions that make space for the patient's own answers to emerge — and to connect them with the right people when they need more than you can offer. Chaplain and social work referral at enrollment, not at crisis, is the standard of care.

💔 The No-Further-Intervention Grief — Name It Explicitly

The patient with end-stage CAD who is told "there is nothing more we can do" has been given information that requires clinical and emotional translation by the hospice team. What it means procedurally is accurate. What it does not mean is that pain cannot be managed, that fear cannot be addressed, or that quality of remaining life cannot be meaningfully improved. The pivot from "nothing more procedurally" to "everything possible for comfort" is the specific expertise of the hospice team. Consider saying exactly this: "There are no more procedures. That does not mean there is nothing more to do. It means we are now doing the most important work — making every day as comfortable and as full of meaning as possible. That is not giving up. That is a different kind of fighting." Many patients have been waiting for someone to say this to them.

Psychological Distress — CAD-Specific Dimensions

Depression — Screen Every Patient

Grade B

Single-question screen: "Are you depressed?" has 100% sensitivity in terminally ill populations when phrased directly.^[35]

PHQ-2: "Little interest/pleasure" + "Feeling down/hopeless" — score ≥3 warrants full PHQ-9
CAD-specific depression signal: Progressive functional loss in a patient whose identity was built on physical capacity; grief over a body that no longer performs; loss of the provider role; grief over each procedure that did not achieve durable results
Mirtazapine 7.5 mg QHS: First-line in hospice — addresses depression, insomnia, and anorexia simultaneously; faster onset than SSRIs; minimal cardiac conduction effect at low doses
Distinguish depression from appropriate grief — both deserve attention; only one warrants pharmacotherapy

Angina Fear as Anticipatory Anxiety — Treat Clinically

Grade B

Angina fear is a clinical problem: Patients with multiple prior MIs and hospitalizations develop conditioned fear of chest pain; this anticipatory anxiety restricts activity beyond what physiology alone would require^[37]
Lorazepam 0.5 mg PRN 30 minutes before predictable triggers (activity, emotional events) allows meaningful participation in life; frame as "medicine for the anxiety around the chest pain"
Clear protocol reduces fear: The patient who knows exactly what to do when pain comes (NTG × 3, call nurse) is significantly less afraid than the patient who does not; the protocol IS the anxiety treatment
Refer to psychology or social work for structured CBT-adapted interventions for medical anxiety if available

CAD-Specific Psychosocial Angles

01

The identity of the cardiac patient: Many patients with end-stage CAD — particularly older men — built their identity around physical capacity, productivity, and the provider role. Each MI, each procedure, each functional decline has chipped away at that identity. NYHA III–IV means they cannot climb stairs or walk to the mailbox. Name the functional loss explicitly and address the grief it carries. "Your body has changed. That does not mean who you are has changed. What has always made you you is still here."^[36]
02

Survivor guilt and the progressive procedures narrative: Many CAD patients have watched peers, co-workers, and family members die of sudden heart attacks — deaths that came without warning, without procedures, without the drawn-out experience this patient has had. Some carry a complicated relationship with survival that deserves acknowledgment. They may feel guilty for still being alive when others died instantly. They may feel that they have already used up more than their share. Create space for this explicitly.
03

The progressive procedures narrative and loss of hope: CAD patients have often been told "we have one more option" repeatedly — angioplasty, then CABG, then re-stenting of grafts, then medical management. Each procedure was accompanied by a new horizon of hope. When the cardiologist says no more options exist, the patient may feel betrayed, abandoned, or as though the system has given up specifically on them. Acknowledge this directly. The hospice team did not give up. The procedures gave up. We are still here.^[45]
04

Caregiver vigilance burden — assess and address at every visit: The spouse or adult child of an end-stage CAD patient is not simply a caregiver — they are a first responder in waiting, hypervigilant for every sound, every grimace, every moment that might be the next MI. Ask directly about their sleep, their ability to leave the house, their own emotional state. Validate the hypervigilance. Provide a written protocol for exactly what to do in every scenario — the written protocol reduces hypervigilance by replacing uncertainty with a plan.^[39]

Spiritual Assessment

Use the FICA framework: Faith/beliefs, Importance, Community, Address. Ask: "What gives you strength during this time?" This opens spiritual conversation without assuming any tradition.^[35] For many CAD patients who have survived multiple near-death experiences, spiritual questions about why they survived this long, what purpose remained, and what awaits are deeply alive — whether or not they identify as religious. The chaplain belongs at the first visit, not the last one.

Clinical Pearl — CAD-Specific

"Patients who have had multiple near-death events — code blues, cardiac arrests, ischemic events where they 'saw the light' or 'felt peace' — often have a complex and sometimes comforting relationship with the idea of dying. They may describe dying as 'going somewhere familiar.' Don't assume terror. Ask what they experienced. It may be the most important spiritual conversation you have, and it often opens naturally from the clinical history."

Goals-of-Care Communication — CAD-Specific

Opening the CAD-Specific Conversation

"What is your understanding of where things stand with your heart?" — assess illness understanding before prognostic disclosure; many patients have not been told clearly that revascularization is no longer possible
"What are you most afraid will happen when the chest pain comes and won't stop?" — surfaces the specific fear driving anxiety in CAD; the answer tells you exactly what to address
"If your heart were to stop suddenly at home, what would you want to happen?" — the explicit conversation about acute death at home; must happen before the event
"What would a good day look like for you right now?" — grounds goals-of-care in concrete values, not abstractions

Communication Pitfalls in CAD

Never say "there's nothing more we can do": Adopt "there are no more procedures — and there is still a great deal we can do for your comfort and quality of life"
Don't conflate hospice with giving up on the heart: Frame around what the hospice team adds — expert pain management, 24-hour on-call, caregiver support, comfort crisis protocol
Don't avoid the acute MI at home conversation: This is not a morbid conversation; it is protective. The family who knows what to do in every scenario is less traumatized, not more.
Sit down. Make eye contact. Leave silence: The cardiologist gave this patient information standing in a hallway for five minutes. You have time. Use it.

Suicidal Ideation & Hastened Death Requests

Passive wish for death ("I'm ready to go — I've been through enough") is common in end-stage CAD patients who have survived multiple events and procedures, and it is often existentially appropriate — it is not the same as active suicidal ideation. Assessment requires careful distinction: passive wish for death (common, often appropriate; does not require escalation), active suicidal ideation with plan (requires immediate psychiatric engagement), and medical aid in dying requests (legal in some jurisdictions — requires specific protocol). Notably, in end-stage CAD, the request to "let me die peacefully if my heart stops" is often a goals-of-care statement about ICD deactivation and DNR status — not a request to hasten death. Clarify before you escalate.^[35]

From the Field

Waldo Rios, NP

Hospice NP · 12+ Years

"The CAD patient who has been told 'there is nothing more we can do' has been given a statement of medical fact that functions emotionally as abandonment. My job at that first visit is to be the evidence that this statement was incomplete. We can do a great deal. We can fix the nitrate schedule that was wrong for three years. We can add ranolazine. We can write a protocol so the family is not calling 911 in a panic at 3 AM. We can sit and listen to a man tell me what it meant to him that his heart kept fighting this long. That is not nothing. That is everything."

— Waldo, NP · Terminal2

S13FamilyEveryone

Family Guide

Plain language for families caring for a loved one with end-stage coronary artery disease. Share, print, or read aloud at the bedside. Know the nitroglycerin protocol. Know the backup plan. You are not alone in this.

Your loved one has heart disease that has reached a point where no more heart procedures can safely be done. That does not mean care has stopped — it means care has shifted entirely to comfort, quality time, and making every day as good as it can be. The hospice team's job is to manage chest pain, shortness of breath, fear, and all the other symptoms that come with heart disease at this stage. Your job is to be present, to know the medication protocols your nurse has reviewed with you, and to call us whenever you need help. You are not supposed to manage this alone. That is what we are here for.

Próximamente en español. — Coming soon in Spanish.

💊 The Nitroglycerin Three-Dose Protocol — Know This Before You Need It

Step 1: At the FIRST sign of chest pain, pressure, tightness, or squeezing — give ONE nitroglycerin tablet (or one spray) under the tongue. Have the patient sit or lie down. Stay with them.
Step 2: Wait exactly 5 minutes. If the pain is gone or significantly better, watch and wait — do not give more unless pain returns.
Step 3: If pain is NOT better after 5 minutes, give a SECOND nitroglycerin tablet or spray. Wait 5 more minutes.
Step 4: If pain is still NOT better, give a THIRD nitroglycerin tablet or spray. Wait 5 more minutes.
Step 5: If pain has NOT responded after three doses — call the nurse on-call immediately using the number posted on your refrigerator. Do NOT call 911 unless your nurse advises you to or unless that is what you and your loved one decided together with the care team.
Remember: Keep the NTG bottle at the bedside AND in a pocket during any activity. Check expiration date monthly. Store in the original amber glass bottle away from heat and light — not in a pill organizer, not in a car, not near the stove.

What You May See

Chest pain, pressure, or tightness — angina: This is the disease. It is manageable. Follow the nitroglycerin protocol your nurse reviewed with you. The medications work — but you must use them correctly and in the right order.
Shortness of breath: The heart is not pumping enough blood to carry oxygen efficiently. Having your loved one sit upright with their head elevated, using a fan directed at their face, and taking the prescribed breathing medications helps significantly. Call us if this is sudden or much worse than usual.
Extreme fatigue after very small activities — dressing, walking to the bathroom: The heart is working at maximum effort for tasks that once required no effort at all. Rest is not giving up — it is the right medicine. Encourage rest without guilt.
Fear or anxiety around any physical movement: Your loved one may be afraid that any activity will trigger chest pain. This fear is real and very common. The nitroglycerin protocol your nurse taught you is the best medicine for this fear — knowing exactly what to do when pain comes makes movement feel safer. Talk to the nurse about anxiety medication if fear is limiting quality of life significantly.
Confusion or unusual drowsiness: This can happen when blood flow to the brain is reduced, or from medications. Call the nurse if confusion is new, sudden, or significantly worse than baseline.
Leg swelling and weight gain: The heart is not moving fluid efficiently through the body. The diuretic medication manages this. Follow the daily weight protocol exactly as your nurse explained — if weight goes up 2–3 pounds overnight, call us before giving an extra diuretic dose on your own.

How You Can Help

Know the nitroglycerin protocol by heart — practice it before you need it: The family member who knows the three-dose NTG protocol without looking it up can respond calmly when chest pain arrives. Review it monthly with your nurse. Ask your nurse to walk through it with you at each visit until it is automatic.
Keep the NTG bottle accessible at all times: Bedside at night. In a pocket or small bag during any daytime activity. Check the expiration date at the beginning of every month. Replace immediately if expired or if the bottle has been exposed to heat or light.
Know where the comfort medications are and what they are for: Your nurse has left backup comfort medications in the home. Know where they are. Know they are for chest pain, anxiety, and breathing difficulty that the NTG does not fully manage. Do not be afraid of them — they are there so you do not have to call 911 for every crisis.
Daily weight — same time, same scale, same clothing: Weigh your loved one every morning before breakfast. Write it down. Call the nurse if weight goes up 2–3 pounds in 24 hours — this is fluid accumulating around the heart and lungs and it needs to be addressed quickly.
Positioning for comfort: Head of bed elevated 30–45 degrees helps breathing; recliner chairs can be better than a flat bed; extra pillows under the head and shoulders are helpful and safe to use freely.
Allow rest without guilt — rest IS the treatment: The heart needs rest as much as any wound needs rest. Encouraging activity beyond what your loved one feels comfortable doing is counterproductive. Follow their lead on energy and activity level. A good day is a comfortable day — whatever that looks like for them.

📞 Call the Nurse Immediately If You See:

• Chest pain that does not improve after the three-dose NTG protocol — this is a medical event that needs the nurse's guidance immediately
• Sudden severe shortness of breath that is significantly worse than baseline — especially if your loved one cannot speak in full sentences
• Loss of consciousness or collapse — call 911 AND the nurse on-call unless a clear "do not call 911" plan is in place, in which case call the nurse immediately
• Sudden confusion, inability to recognize family members, or inability to stay awake when expected to be awake
• Sudden dramatic increase in leg swelling — especially if accompanied by difficulty breathing when lying down
• You see the ICD deliver a shock — if deactivation has not occurred, call the nurse immediately; if it occurs during active dying, call the nurse, do not call 911
• You run out of nitroglycerin or any comfort medication — call to reorder before you are out, not after

🙏 Families who understand the NTG protocol, the comfort medication plan, and what to expect are able to be fully present with their loved one rather than paralyzed by fear of what might happen. Studies of patients with serious cardiac disease consistently show that clear family preparation reduces emergency room visits and improves both patient comfort and family bereavement outcomes.^[39] You are not bystanders — you are the care team at 3 AM when the nurse cannot arrive in five minutes. Your preparation is your loved one's safety net.

S14Everyone

Waldo's Top 10 Tips

Clinical field wisdom from 12+ years at the bedside of end-stage CAD patients. The things you learn after doing this long enough. Not guidelines — real.

01

Check the nitrate schedule before you check anything else. Walk in the door, introduce yourself, sit down, and ask them to show you their IMDUR bottle. If it says "take twice daily," you already know the most important thing about why their angina is uncontrolled. Isosorbide mononitrate extended-release must be taken once in the morning — the extended-release mechanism already provides sustained blood levels, and the overnight gap is the mandatory nitrate-free interval that restores drug efficacy. Twice-daily dosing eliminates that interval and produces complete tolerance within 72 hours. The drug is doing nothing. Change it to once daily in the morning, call the prescriber, document your change, and come back in a week. I have seen patients describe their first week on corrected nitrate dosing as the best week they've had in years. Five minutes. One phone call. Dramatic clinical impact. Check the nitrate schedule first, every time, at every enrollment.^[19]
02

Add ranolazine if it is not on the medication list — it almost never is. I have enrolled hundreds of end-stage CAD patients. The percentage on ranolazine at enrollment is somewhere around 15 to 20 percent, which means 80 percent of patients who could benefit from the best-evidence additional anti-anginal are not on it. Ranolazine works through late sodium current inhibition in ischemic myocytes — a mechanism completely separate from nitrates, beta-blockers, and calcium channel blockers. It provides additive angina reduction without changing heart rate or blood pressure, which makes it uniquely useful when other agents are already at their ceiling because of hypotension or bradycardia. Start at 500 mg BID. Check QTc and creatinine before you call the prescriber. Titrate to 1000 mg BID over two weeks. The CARISA trial showed this drug works. The MERLIN-TIMI 36 trial showed this drug works. Fourteen years of post-market data show this drug is safe in the populations I am describing. Add it at enrollment.^[5]^[6]
03

The SL NTG protocol is the most important family education in end-stage CAD — check the bottle at every visit. At every single visit, I physically pick up the nitroglycerin bottle. I check the expiration date. I check that it is in the original amber glass container, not a plastic pill organizer where the tablets are losing potency every day from light and humidity. I check that the cotton has been removed from inside the bottle — cotton absorbs nitroglycerin and inactivates the tablets. I check that it is not stored in the bathroom (humidity kills NTG), not in the car (heat kills NTG), not near the stove. Then I walk through the three-dose protocol with whoever is in the room. One tablet or spray at the first sign of chest pain. Wait five minutes. Second dose if no relief. Five minutes. Third dose. If still no relief after the third dose — call the nurse on-call number posted on the refrigerator. Not 911. The nurse. I make them say the nurse's number back to me. The family that has rehearsed this protocol does not call 911 at 1 AM after the first NTG dose. The family that has not rehearsed it does. The difference is the nurse who checked the bottle and reviewed the steps.
04

Write the acute MI at home protocol at enrollment and review it at every visit — what do we do when the chest pain does not go away? This is the conversation that determines whether a patient with end-stage CAD dies peacefully at home or in an emergency department after a traumatic 911 call. Have it at the first visit, while the patient is alert, has decision-making capacity, and has time to think about it without a crisis underway. Ask directly: "If you have chest pain that does not get better after three nitroglycerin doses, what do you want us to do?" Document the answer. If the patient has chosen home death, write a protocol: morphine 5 mg SQ for pain and to reduce oxygen demand, lorazepam 0.5 mg SQ for anxiety, midazolam 5 mg SQ if still distressed, call nurse on-call. Make sure these medications are pre-drawn in labeled syringes in the comfort kit, and make sure every adult in the household knows where they are and what each one is for — before the event. The family that is prepared gives comfort medications calmly. The family that is not prepared calls 911 and watches their loved one die in an ambulance in the snow.^[46]
05

The fear of chest pain is as disabling as the chest pain itself — treat it as a clinical diagnosis. I have watched patients with end-stage CAD voluntarily imprison themselves in a recliner chair, refusing to walk to the kitchen, refusing to attend their grandchild's birthday party, refusing to sleep in their own bed — not because the angina itself prevented these things but because the fear that movement might trigger an episode made them stop moving entirely. This is anticipatory anxiety, and it is a clinical condition that deserves clinical management. A clear protocol that tells the patient exactly what to do when pain arrives — immediately, without uncertainty — is itself anxiolytic. The patient who knows the NTG protocol, knows the backup plan, and has lorazepam PRN available is measurably less restricted by fear than the patient who has none of these things. Ask at every visit: "Are you doing less than you could because you're afraid of chest pain?" If the answer is yes — which it almost always is — adjust the anti-anxiety plan. Movement with a working protocol is safer than stillness born of terror.^[37]
06

The ICD deactivation conversation is a clinical obligation — have it at enrollment, not at death. About one in three of my end-stage CAD patients with reduced ejection fraction has an ICD. An ICD in a patient who has chosen comfort-focused care and home death is a device that will deliver multiple painful shocks as the patient dies — because arrhythmia is exactly how many CAD patients die at the end. ICD shocks in active dying are not a medical complication; they are a foreseeable and preventable harm that the hospice team failed to prevent. Frame the conversation simply: "You have a device that was put in to restart your heart if it went into a dangerous rhythm. At this stage, we want to talk about whether you want that device to keep doing its job. If your heart stops or goes into a dangerous rhythm and we do not restart it, you will likely die peacefully. If the ICD fires, it can deliver a shock that is painful but does not change the outcome. What do you want?" The patient decides. You document. You make the referral to cardiology or device clinic for deactivation. If deactivation cannot be done before discharge, a donut magnet placed over the device will suspend shock delivery. Know this before you need it.^[30]^[31]
07

Check the NTG bottle at every visit — make it a ritual, not a task. I have said this already in the tips and I am saying it again because it matters enough to say twice. Nitroglycerin tablets have an average shelf life of three to six months after the bottle is opened. They are inactivated by light, heat, moisture, plastic, and by the cotton plug left inside the bottle. A patient whose NTG tablets have been stored in a plastic pill organizer on the kitchen counter since last March is a patient with no working acute rescue medication for chest pain — and they do not know it. When I check the bottle at every visit, I am performing the quality assurance function that the pharmacy, the prescriber, and the patient cannot perform for themselves. I replace the bottle if there is any doubt. I bring a new bottle. I demonstrate the spray alternative for patients with dexterity issues or storage challenges. This costs nothing. It takes three minutes. It is the clinical act that determines whether the NTG works when the patient needs it most.
08

Racial disparities in CAD care are documented and specific — name them at team meetings and correct them at the bedside. The data is not subtle. Black patients in the United States with obstructive coronary artery disease receive revascularization — specifically CABG — at significantly lower rates than white patients with equivalent anatomy, even after controlling for insurance status, comorbidities, and hospital type.^[38] Black and Hispanic patients with end-stage cardiac disease are referred to hospice later, at lower rates, and with less proactive symptom management than white patients. These are not historical statistics — they are present, active, and they affect patients on your current caseload. Your job at the bedside is not to fix the health system's structural racism in one visit. Your job is to make absolutely certain that every patient on your caseload — regardless of race, ethnicity, language, zip code, or insurance status — gets the same proactive nitrate schedule check, the same ranolazine conversation, the same acute MI at home protocol, and the same ICD deactivation discussion. Equity requires intentional action. It does not happen by default.
09

The caregiver of an end-stage CAD patient is living in a state of hypervigilance that is clinically significant — assess it, name it, and give them a written plan. I have met spouses who have not slept through the night in two years. They wake at every sound. They listen for breathing. They position themselves so they can see the bedroom door from the kitchen. They do not leave the house for more than forty minutes because of the fear of what they might come home to. This is not just stress — it is a chronic physiological state of heightened alertness that is associated with accelerated caregiver health decline, complicated bereavement, and post-traumatic stress after the patient's death.^[39] The most effective intervention I have found for caregiver hypervigilance in end-stage CAD is a written, laminated protocol posted on the refrigerator that answers every possible scenario: what do we do if chest pain, what do we do if ICD fires, what do we do if we can't wake them, what do we do if they die before the nurse arrives. The written plan converts uncertainty into action steps. Uncertainty is what drives hypervigilance. Give them the plan. It works.
10

The patient who has been told "there is nothing more we can do" has not heard the whole truth — and you are the person who can complete it. I think about this every time I walk into the home of a patient with end-stage CAD at enrollment. This person has been told — by a cardiologist who is excellent at procedures and often less skilled at this conversation — that their medical options have been exhausted. What they heard was that they have been given up on. What they need to hear is what comes after that sentence: that there is a team of people whose entire expertise is what comes next, and that what comes next can be very good. The nitrate schedule that has been wrong for three years can be fixed today. The ranolazine that has never been prescribed can be started this week. The protocol for chest pain at 3 AM can be written before they go to sleep tonight. The ICD can be turned off so they can die peacefully. The family can be taught exactly what to do, exactly when to call, exactly what to say. The chaplain can come on Thursday. The social worker can be there when the family needs to talk about what dying at home is actually going to look like. None of this is nothing. All of it is something. You are the something that follows the nothing. Show up for that.^[45]

— Waldo, NP

REFClinician

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terminal2.care content is for educational purposes and is not a substitute for clinical judgment. Based on articles retrieved from PubMed. © Terminal2 | terminal2.care

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