Pathophysiology: Cardiovascular Disorders

Cardiovascular disorders share a common theme: the heart and blood vessels are forced to work under conditions that impair oxygen delivery to tissues. Whether the initiating problem is a narrowed coronary artery, a stiffened aorta, an abnormal heart rhythm, or a sudden drop in circulating volume, the downstream pathophysiology often converges on reduced cardiac output, altered vascular resistance, and tissue hypoxia. Understanding these mechanisms is essential because clinical signs, diagnostic findings, and treatment strategies all trace back to the underlying physiology.

This article reviews the disease mechanisms of five major cardiovascular conditions: ischemic heart disease, heart failure, arrhythmias, hypertension, and shock.

Core physiological concepts

At a systems level, tissue perfusion depends on blood flow and oxygen content. Blood flow is driven by pressure gradients and limited by resistance. A useful relationship is:

$$\text{Blood pressure (MAP)}\approx \text{Cardiac output (CO)}\times \text{Systemic vascular resistance (SVR)}$$

Cardiac output is the product of heart rate and stroke volume:

$$CO=HR\times SV$$

Stroke volume is influenced by preload (ventricular filling), afterload (the pressure the ventricle must pump against), and contractility (myocardial force generation). Many cardiovascular disorders can be understood as disruptions in one or more of these variables, followed by compensatory responses such as sympathetic activation and neurohormonal signaling (notably the renin-angiotensin-aldosterone system), which may stabilize perfusion in the short term but worsen disease over time.

Ischemic heart disease: oxygen supply-demand mismatch

Ischemic heart disease results when myocardial oxygen demand exceeds supply. The most common mechanism is reduced coronary blood flow due to atherosclerotic plaque that narrows the arterial lumen. Plaque rupture can trigger thrombosis and abruptly occlude flow, producing acute coronary syndromes.

Atherosclerosis and plaque instability

Atherosclerotic disease develops within the arterial intima. Over time, lipid accumulation and inflammation lead to plaque formation. Stable plaques primarily limit flow during increased demand, while unstable plaques are prone to rupture. Rupture exposes thrombogenic material, promoting platelet aggregation and clot formation. The key pathophysiologic pivot is the transition from a fixed stenosis to a dynamic obstruction.

Consequences of myocardial ischemia

Ischemia rapidly impairs myocardial relaxation and contraction because cardiomyocytes depend on continuous aerobic metabolism. ATP depletion disrupts ion pumps, leading to:

• Diastolic dysfunction early (impaired relaxation)
• Systolic dysfunction if ischemia persists
• Electrical instability due to altered membrane potentials, predisposing to arrhythmias

If ischemia is prolonged, myocyte necrosis occurs. The damaged myocardium is replaced by scar tissue, which does not contract and can impair overall ventricular function. Even without infarction, repeated ischemia can cause chronic remodeling and reduced reserve.

Heart failure: impaired pumping and maladaptive compensation

Heart failure is a clinical syndrome caused by the heart’s inability to meet metabolic demands, either because it cannot pump effectively (systolic dysfunction) or cannot fill properly (diastolic dysfunction). The pathophysiology is less about a single lesion and more about a feedback loop of reduced output and compensatory mechanisms that eventually become harmful.

Systolic versus diastolic dysfunction

• Systolic dysfunction: reduced contractility lowers stroke volume and ejection fraction. Common upstream causes include ischemic injury, cardiomyopathy, and long-standing pressure overload.
• Diastolic dysfunction: a stiff ventricle impairs filling, raising filling pressures even when ejection fraction is preserved. Hypertension and aging-related myocardial changes often contribute, as do infiltrative processes.

Both forms can lead to pulmonary congestion (left-sided failure) or systemic venous congestion (right-sided failure). Importantly, congestion is driven by elevated filling pressures, not just low output.

Neurohormonal activation and remodeling

When cardiac output falls, the body responds as if it is facing volume depletion:

• Sympathetic activation increases heart rate and contractility and constricts vessels to maintain blood pressure.
• The renin-angiotensin-aldosterone system increases sodium and water retention, raising preload.
• Vasoconstriction increases afterload, making it harder for the ventricle to eject blood.

These responses can temporarily improve perfusion, but chronically they promote ventricular hypertrophy, dilation, fibrosis, and worsening pump efficiency. This remodeling increases oxygen demand and creates a substrate for arrhythmias.

Arrhythmias: abnormal impulse formation or conduction

Arrhythmias arise from disturbances in electrical impulse generation, impulse conduction, or both. The heart’s coordinated contraction depends on organized depolarization. When timing or pathways are disrupted, mechanical performance and perfusion can deteriorate.

Mechanisms of arrhythmia

1. Abnormal automaticity: cells outside the normal pacemaker regions develop spontaneous depolarization, creating ectopic beats or tachyarrhythmias.
2. Triggered activity: afterdepolarizations occur during or after repolarization, often influenced by electrolyte abnormalities or ischemia.
3. Reentry circuits: an impulse travels in a loop due to unidirectional block and slow conduction, sustaining tachycardia. Scar tissue after myocardial infarction is a classic substrate.

Hemodynamic impact

The clinical significance of an arrhythmia depends on heart rate, rhythm regularity, and atrioventricular synchrony:

• Very fast rates reduce diastolic filling time, lowering stroke volume.
• Loss of coordinated atrial contraction can reduce ventricular filling, especially in stiff ventricles.
• Ventricular arrhythmias can cause abrupt loss of effective cardiac output and lead to collapse.

Ischemia and heart failure both increase arrhythmia risk, creating a tight pathophysiologic link among these conditions.

Hypertension: chronic pressure load and vascular dysfunction

Hypertension is sustained elevation of arterial pressure and is a major driver of cardiovascular morbidity. The underlying mechanisms typically involve increased systemic vascular resistance, altered renal handling of sodium and water, and vascular structural changes.

Vascular resistance and endothelial function

Small arteries and arterioles govern SVR. Persistent vasoconstriction and structural remodeling increase resistance. Endothelial dysfunction reduces the availability of vasodilators and favors vasoconstrictive, pro-inflammatory signaling. Over time, vessel walls thicken and stiffen, locking in higher resistance and widening pulse pressure.

Cardiac and organ consequences

The left ventricle must generate higher pressure to overcome afterload. The response is concentric hypertrophy, which initially normalizes wall stress but reduces compliance and raises diastolic filling pressures. This contributes to diastolic heart failure and increases myocardial oxygen demand, which can worsen ischemia. Hypertension also accelerates atherosclerosis and predisposes to stroke and kidney disease through chronic vascular injury.

Shock: failure of perfusion at the systemic level

Shock is a state of inadequate tissue perfusion leading to cellular dysfunction. While blood pressure is often low, the defining issue is insufficient oxygen delivery relative to tissue needs. Mechanistically, shock can result from decreased cardiac output, decreased vascular tone, reduced circulating volume, or impaired oxygen utilization.

Major shock patterns and hemodynamics

• Cardiogenic shock: the heart cannot pump effectively, often due to large myocardial infarction or severe heart failure. Cardiac output falls, filling pressures rise, and tissues become hypoxic despite adequate volume.
• Hypovolemic shock: loss of intravascular volume reduces preload, leading to reduced stroke volume and cardiac output. Compensatory vasoconstriction may maintain SVR initially.
• Distributive shock: pathologic vasodilation causes low SVR and maldistribution of flow. Even if cardiac output is high, perfusion can be ineffective because vascular tone is inadequate.
• Obstructive shock: mechanical impediment to filling or ejection reduces cardiac output (for example, conditions that limit venous return or block outflow).

Cellular consequences

When oxygen delivery drops, cells shift toward anaerobic metabolism, generating lactate and failing to maintain ion gradients. Microcirculatory dysfunction can compound the problem: even when large-vessel pressures are corrected, capillary flow may remain abnormal. Without reversal, shock progresses from compensated to decompensated states with multi-organ failure.

How these disorders intersect in practice

Cardiovascular conditions rarely occur in isolation. Hypertension increases afterload and promotes hypertrophy, raising the risk of diastolic heart failure and ischemia. Ischemic injury weakens contractility and introduces scar-based reentry circuits that foster arrhythmias. Heart failure amplifies neurohormonal activation, worsening vascular resistance and fluid retention, and severe decompensation can culminate in cardiogenic shock. These links explain why treatment strategies often target shared pathways: improving perfusion, reducing maladaptive neurohormonal drive, restoring rhythm, and reducing the workload of the heart.

A mechanistic view of cardiovascular pathophysiology ties symptoms to root causes. Chest pain reflects ischemia, dyspnea often reflects elevated filling pressures, syncope may reflect transient loss of output from arrhythmia, and cool clammy extremities can signal compensatory vasoconstriction in shock. Understanding the “why” behind these findings is what turns clinical data into effective decisions.