What are the key factors, clinical presentations, and treatment options for patients with cardiac disease, including left and right heart failure, ischemic heart disease, and acute myocardial infarction (AMI)?

Cardiac Disease: Comprehensive Overview

A. Factors Affecting Cardiac Function and Stroke Volume

Stroke volume is determined by three primary factors: preload, afterload, and myocardial contractility, with myocardial oxygen supply being critical for maintaining contractile function. 1

Preload

• Preload represents ventricular end-diastolic volume and pressure, reflecting the degree of myocardial fiber stretch before contraction. 1
• In right ventricular failure, elevated systemic venous pressure increases RV preload, while in left ventricular failure, elevated pulmonary venous pressure increases LV preload. 2
• The right ventricle is particularly preload-dependent compared to the left ventricle, requiring adequate filling pressures to maintain cardiac output. 2

Afterload

• Afterload is the resistance against which the ventricle must eject blood, determined by systemic vascular resistance for the LV and pulmonary vascular resistance for the RV. 1
• The RV is exceptionally sensitive to afterload increases, with steep declines in stroke volume when faced with pressure elevations, unlike the more afterload-tolerant LV. 2
• Pulmonary vasoconstriction from hypoxia and inflammation increases biventricular afterload and myocardial oxygen demand. 1

Myocardial Oxygen Supply

• Coronary perfusion pressure (aortic diastolic pressure minus ventricular end-diastolic pressure) determines myocardial oxygen delivery. 1
• Impaired cardiac output and progressive diastolic dysfunction raise ventricular end-diastolic pressures, which reduce coronary perfusion pressure, myocardial contractility, and stroke volume. 1
• In acute myocardial infarction, coronary artery flow can be compromised by an expanding false lumen or dissection flap extension into the coronary ostium. 1

B. Left and Right Heart Failure

Left-Sided Heart Failure

Causes

• Coronary artery disease, hypertension, valvular disease, and cardiomyopathies are the primary causes of left-sided heart failure. 3
• Ischemic cardiomyopathy represents the most common cause of heart failure worldwide, resulting from obstructive coronary artery disease with systolic left ventricular dysfunction. 4

Clinical Presentation

• Dyspnea (especially with exertion), paroxysmal nocturnal dyspnea, and orthopnea are the predominant respiratory symptoms. 5
• Pulmonary rales/crackles on auscultation indicate fluid accumulation in the lungs. 5
• Tachycardia occurs as a compensatory mechanism to maintain cardiac output. 5
• Fatigue and decreased exercise tolerance result from reduced cardiac output and skeletal muscle perfusion. 5
• Advanced cases may present with Cheyne-Stokes respiration and cachexia. 5

Hemodynamic Effects

• Left ventricular dysfunction leads to increased left ventricular filling pressures, which elevate left atrial pressure and cause pulmonary venous congestion. 5
• Cardiac remodeling with chamber dilation and/or hypertrophy occurs as the disease progresses. 5
• The myocardium undergoes geometric and structural changes, with the chamber dilating and/or hypertrophying and becoming more spherical. 1

Treatment

• ACE inhibitors and β-blockers are first-line therapy for all patients with left ventricular systolic dysfunction regardless of symptom severity. 3
• Diuretics provide fluid retention relief and symptom management. 3
• Aldosterone antagonists are indicated for selected patients. 1
• Cardiac resynchronization therapy is recommended for patients with LVEF <35% and QRS duration ≥150 ms. 3
• Implantable cardioverter-defibrillators for patients meeting specific criteria. 3

Right-Sided Heart Failure

Causes

• Right-sided heart failure often occurs secondary to left-sided heart failure but can result from pulmonary hypertension, right ventricular infarction, or pulmonary embolism. 3
• Acute proximal right coronary artery occlusion classically causes RV failure, though RV dysfunction may also occur after larger left coronary artery infarctions. 6
• Chronic lung disease, congenital heart disease, infiltrative disease, infectious disease, and valvular abnormalities are additional causes. 7

Clinical Presentation

• Elevated jugular venous pressure, peripheral edema, and hepatomegaly are the most reliable clinical indicators. 2
• Hypotension and elevated jugular pressure in the presence of clear lung fields are hallmark signs. 6
• RV heave, loud P2 sound of pulmonary valve closure, and S3 or S4 gallop over the RV are characteristic findings. 2
• Early satiety and epigastric fullness/pain occur due to hepatic congestion and ascites. 2
• Oliguria results from decreased renal perfusion. 2
• Advanced cases present with hypoxia, peripheral cyanosis, and confusion. 2

Hemodynamic Effects

• Right ventricular dysfunction leads directly to systemic venous hypertension, causing fluid accumulation in peripheral tissues, abdomen, and liver. 2
• Decreased cardiac output causes tissue hypoperfusion. 2
• Ventricular interdependence occurs when RV dilation causes leftward shift of the interventricular septum, impairing LV filling. 2
• Renal perfusion decreases, triggering salt and water retention that manifests as peripheral edema and ascites. 2

Treatment

• Loop diuretics are first-line therapy for fluid overload, with spironolactone added to enhance diuresis. 2
• Management of pulmonary hypertension with calcium channel blockers, nitric oxide, or prostaglandins when appropriate. 2, 3
• Anticoagulation for pulmonary embolism if present. 2
• Antibiotics when pulmonary infection or endocarditis is the underlying cause. 2
• Inotropic support with dobutamine for short-term use in end-stage disease. 2
• Oxygen therapy to maintain saturation above 90% in hypoxemic patients. 2
• Careful fluid management is critical to prevent worsening venous congestion while maintaining adequate preload. 3

Critical Pitfall: Right-sided heart failure requires higher diuretic doses and combination therapy compared to left-sided failure, with aggressive diuresis targeting elimination of jugular venous pressure elevation even if mild hypotension or azotemia develops. 2

C. Ischemic Heart Disease

Epidemiology and Causes

• Coronary heart disease is the underlying cause in most patients with heart failure due to left ventricular systolic dysfunction. 8
• The estimated direct and indirect costs of coronary heart disease in the United States exceeded $177 billion in 2010. 1
• Atherosclerotic disease, hypertension, diabetes, obesity, metabolic syndrome, and family history of cardiomyopathy increase risk. 1

Autonomic Nervous System Response to Ischemia

• In response to tissue ischemia and necrosis, released inflammatory mediators impair tissue metabolism and induce nitric oxide production, causing systemic vasodilation and exacerbating hypotension. 1
• This maladaptive neurohormonal response stresses an already dysfunctional myocardium. 1
• The response may be acute in AMI-CS or superimposed on chronic neurohormonal activation in ADHF-CS. 1

Pathophysiology

• Ischemic cardiomyopathy results from the combination of irreversible loss of viable mass following acute myocardial infarction with dysfunctional but viable myocardium in the context of chronically reduced myocardial blood flow and reduced coronary reserve. 4
• Coronary artery flow compromise leads to myocardial ischemia or infarction, present in up to 19% of patients with acute aortic dissection. 1
• The dissection-related cardiac malperfusion syndrome may present with ECG changes indistinguishable from primary myocardial ischemia or infarction. 1

Angina Pectoris

• Angina represents myocardial ischemia manifesting as chest discomfort, typically precipitated by exertion or stress and relieved by rest or nitroglycerin. 1
• Patients may present with atypical symptoms, particularly women, elderly, and diabetics. 1
• Shared decision-making involving the patient and provider should guide diagnostic and therapeutic options, with explanation of risks, benefits, and costs. 1

Hemodynamic Effects of Ischemia

• Ischemia impairs myocardial contractility, reducing stroke volume and cardiac output. 1
• Diastolic dysfunction develops, raising ventricular end-diastolic pressures and reducing coronary perfusion pressure. 1
• Maladaptive cycles of ischemia, inflammation, vasoconstriction, and volume overload culminate in multiorgan system failure. 1

D. Acute Myocardial Infarction

Pathophysiology

• The central pathophysiologic derangement is diminished cardiac output leading to systemic hypoperfusion. 1
• AMI-CS is typically associated with >40% loss of left ventricular myocardium. 1
• Mechanical complications include free wall rupture, ventricular septal defect, and papillary muscle rupture. 1
• Impaired cardiac output and progressive diastolic dysfunction raise ventricular end-diastolic pressures, reducing coronary perfusion pressure, myocardial contractility, and stroke volume. 1

Patient Presentation

• Acute chest pain, elevated cardiac enzymes, and abnormal electrocardiogram are typical presentations. 1
• Heart failure may be categorized by Killip classification: class 1 (no rales or third heart sound), class 2 (pulmonary congestion with rales over <50% of lung fields or third heart sound), class 3 (pulmonary edema with rales over 50% of lung fields), class 4 (shock). 1
• Acute free wall rupture presents with cardiovascular collapse and electromechanical dissociation, usually fatal within minutes. 1
• Subacute free wall rupture (25% of cases) presents with sudden hemodynamic deterioration, recurrence of pain, and re-elevation of ST-segments. 1

Hemodynamic Profile

• Cardiogenic shock is characterized by clinical signs of poor tissue perfusion (oliguria, decreased mentation), hypotension, small pulse pressure, tachycardia, and pulmonary edema. 1
• Right ventricular infarction presents with high jugular venous pressure, poor tissue perfusion or shock, bradycardia, and hypotension. 1
• Hyperdynamic state shows tachycardia, loud heart sounds, and good peripheral circulation. 1
• Pump failure manifests as tachycardia, tachypnea, and basal rales. 1

Diagnostics

• Twelve-lead electrocardiogram and cardiac troponin testing should be performed immediately to identify ACS precipitating acute HF decompensation. 1
• Two-dimensional echocardiography with Doppler assesses LVEF, left ventricular size, wall thickness, and valve function. 1
• Coronary arteriography is indicated for patients with angina or significant ischemia unless ineligible for revascularization. 1
• Chest radiography identifies pulmonary congestion and cardiomegaly. 1
• Blood gases should be checked regularly in severe heart failure and shock. 1

Treatment

• Early revascularization (thrombolysis or primary percutaneous coronary intervention) improves short- and long-term outcomes and reduces progression to heart failure. 8, 6
• HF patients hospitalized with fluid overload should receive intravenous diuretics at doses greater than or equal to their chronic oral daily dose. 1
• Beta-blocker therapy at low dose should be initiated after optimization of volume status and discontinuation of intravenous agents. 1
• Patients on guideline-directed medical therapy should continue treatment except in cases of hemodynamic instability. 1
• Oxygen administration with pulse oximetry monitoring, with continuous positive airway pressure or endotracheal intubation for severe cases. 1
• Thrombosis/thromboembolism prophylaxis is recommended for all hospitalized patients. 1
• Coronary artery bypass graft may be indicated after failed PCI, coronary occlusion not amenable for PCI, cardiogenic shock, or mechanical complications. 1
• Intra-aortic balloon pump placement for most patients requiring emergency surgery. 1

Critical Management Algorithm for AMI with Heart Failure:

1. Immediate ECG and cardiac biomarkers 1
2. Assess Killip class and hemodynamic status 1
3. Emergent revascularization (PCI or thrombolysis) 8, 6
4. Initiate IV diuretics for fluid overload 1
5. Continue GDMT unless hemodynamically unstable 1
6. Echocardiography to assess extent of damage and complications 1
7. Consider mechanical circulatory support for cardiogenic shock 1
8. Monitor serum electrolytes, renal function during diuretic titration 1

Common Pitfall: Patients with AMI complicated by heart failure are often atypical in presentation, frequently presenting in shock but less likely to complain of chest pain, and when present, pain is more often mild and less abrupt in onset, leading to delayed diagnosis. 1