Hemodynamics, Murmurs, and Ischemia

Cardiovascular Reasoning Map

A strong cardiovascular answer usually comes from deciding which variable changed first. Preload is ventricular filling before contraction, approximated by end-diastolic volume or pressure. It rises with venous return, blood volume, venoconstriction, and longer diastolic filling time. By the Frank-Starling mechanism, moderate increases in preload improve actin-myosin overlap, increase stroke volume, and widen the pressure-volume loop. Afterload is the force the ventricle must overcome to eject blood.

For the left ventricle, it tracks aortic pressure, systemic vascular resistance, and arterial stiffness; for the right ventricle, it tracks pulmonary vascular resistance. Increasing afterload raises systolic pressure, leaves more blood behind at end-systole, narrows stroke volume acutely, and increases myocardial oxygen demand. Contractility is load-independent inotropy. Increasing contractility makes the ventricle eject more completely at a given afterload, decreasing end-systolic volume, increasing stroke volume, and increasing ejection fraction.

On the pressure-volume loop, the end-systolic pressure-volume relationship shifts up and left. Decreased contractility, as after a large myocardial infarction or with systolic heart failure, shifts it down and right, increasing end-systolic volume and reducing ejection fraction. A normal left ventricular pressure-volume loop begins with mitral valve opening and passive filling, then atrial contraction adds the final end-diastolic volume. Mitral valve closure starts isovolumetric contraction and produces S1. Aortic valve opening begins ejection.

Aortic valve closure ends ejection, produces A2, and begins isovolumetric relaxation. Mitral valve opening restarts filling. S2 splitting comes from the interval between A2 and P2. Inspiration increases venous return to the right heart and transiently delays pulmonic valve closure, so physiologic splitting widens. Fixed splitting suggests an atrial septal defect because left-to-right shunting equalizes right-sided filling across respiration. Paradoxical splitting, classically in left bundle branch block or severe aortic stenosis, means A2 is delayed and the split narrows with inspiration.

Murmurs are best understood by flow direction and pressure gradient. Aortic stenosis is a crescendo-decrescendo systolic ejection murmur at the right upper sternal border that radiates to the carotids. The left ventricle develops concentric hypertrophy from pressure overload, and a late-peaking murmur implies a large obstruction. Aortic regurgitation is an early diastolic decrescendo murmur from backflow into the left ventricle; chronic disease causes volume overload, eccentric hypertrophy, widened pulse pressure, and bounding pulses.

Mitral regurgitation is a holosystolic murmur at the apex radiating to the axilla; left atrial pressure rises during systole and the v wave is accentuated. Mitral stenosis is a low-pitched diastolic rumble with an opening snap, often due to rheumatic scarring, and it predisposes to left atrial enlargement, atrial fibrillation, and pulmonary hypertension. Tricuspid regurgitation is holosystolic at the lower left sternal border and increases with inspiration. Ventricular septal defect is also holosystolic at the left lower sternal border, often harsh because a high-pressure left-to-right jet crosses the septum.

Hypertrophic obstructive cardiomyopathy is a dynamic systolic ejection murmur from septal hypertrophy and systolic anterior motion of the mitral valve. Anything that shrinks the left ventricular cavity, such as standing, Valsalva strain, or decreased preload, worsens obstruction and increases the murmur. Squatting, passive leg raise, and handgrip increase preload or afterload, enlarge the cavity or oppose outflow, and usually decrease the murmur. Mitral valve prolapse is also louder with reduced left ventricular volume; the click moves earlier with standing or Valsalva and later with squatting.

Most other murmurs decrease when venous return falls. Handgrip increases afterload, so it augments regurgitant murmurs such as mitral regurgitation, aortic regurgitation, and ventricular septal defect while reducing forward-flow murmurs such as hypertrophic obstructive cardiomyopathy and many cases of aortic stenosis. Shock questions require matching hemodynamics to the initiating problem. Hypovolemic shock has low preload, low pulmonary capillary wedge pressure, low cardiac output, compensatory high systemic vascular resistance, cool skin, tachycardia, and high oxygen extraction.

Cardiogenic shock has pump failure, low cardiac output, high systemic vascular resistance, and elevated filling pressures; pulmonary edema supports left-sided failure. Obstructive shock includes tamponade, tension pneumothorax, massive pulmonary embolism, and severe pulmonary hypertension. Tamponade impairs diastolic filling, equalizes diastolic pressures, produces hypotension, jugular venous distention, muffled heart sounds, pulsus paradoxus, and a small quiet heart on imaging.

Pulmonary embolism raises right ventricular afterload, causing acute right heart strain, high jugular venous pressure, clear lungs, and sometimes syncope. Distributive shock, as in sepsis or anaphylaxis, has low systemic vascular resistance with high or normal early cardiac output, warm skin early, and impaired oxygen extraction. Neurogenic shock combines vasodilation with bradycardia because sympathetic tone is lost. Coronary perfusion of the left ventricle occurs mainly during diastole because systolic intramyocardial pressure compresses the coronary vessels.

Tachycardia worsens ischemia by reducing diastolic filling time and increasing oxygen demand. Myocardial oxygen demand rises with heart rate, contractility, wall tension, and afterload. Wall tension is proportional to pressure times radius and inversely proportional to wall thickness, explaining why ventricular dilation raises demand and why concentric hypertrophy initially reduces wall stress but eventually becomes maladaptive. Stable angina reflects fixed atherosclerotic narrowing with exertional supply-demand mismatch.

Variant angina reflects coronary vasospasm and transient transmural ischemia, often with episodic ST elevation. Unstable angina and myocardial infarction typically reflect plaque rupture with platelet activation and thrombus formation. Subendocardial infarcts are especially vulnerable to global hypoperfusion because the inner myocardium has the highest wall stress and poorest perfusion reserve. Transmural infarction is more often due to complete epicardial coronary occlusion and produces regional ST elevation in the affected leads.

Irreversible ischemic injury begins with ATP depletion, impaired ion pumps, cell swelling, lactic acidosis, and loss of contractility. Troponin I and T are highly specific markers of myocardial injury and rise after myocyte membrane damage; CK-MB is less specific but can help identify reinfarction because it returns to baseline sooner. Infarct complications follow tissue biology. Arrhythmias can occur early because ischemic myocardium is electrically unstable. Fibrinous pericarditis can occur over the first several days.

Macrophage-mediated tissue digestion makes the wall weakest around days 3 to 7, when papillary muscle rupture, free wall rupture with tamponade, and interventricular septal rupture are classic risks. Later granulation tissue and collagen deposition create scar, and chronic remodeling can lead to ventricular aneurysm, mural thrombus, and heart failure.