Physiology: Cardiovascular Physiology

Cardiovascular physiology explains how the heart and blood vessels work together to deliver oxygen and nutrients, remove metabolic waste, and maintain stable internal conditions. It connects cellular metabolism to organ function through circulation, and it becomes clinically tangible through measurements like the electrocardiogram (ECG), blood pressure, and indicators of blood flow. Understanding the cardiac cycle, ECG interpretation, blood pressure regulation, and hemodynamics provides a practical framework for reasoning about both normal physiology and common disease patterns.

The cardiovascular system as a pump-and-pipe network

At its core, the cardiovascular system is a pressure-driven flow circuit. The heart generates pressure, and the vessels distribute flow. Flow through any segment depends on a pressure gradient and resistance. Clinically, this concept appears in everyday situations: a narrowed artery increases resistance and reduces flow distal to the obstruction; vasodilation decreases resistance and increases flow.

A useful organizing relationship is:

• Pressure drives flow
• Resistance opposes flow
• The heart’s pumping determines how much blood enters the system per minute (cardiac output)

Cardiac output is defined as: $CO=HR\times SV$

where $HR$ is heart rate and $SV$ is stroke volume. Many compensatory responses in illness can be understood as attempts to preserve cardiac output when either heart rate or stroke volume falls.

The cardiac cycle: coordinated pressure and volume changes

The cardiac cycle is the repeating sequence of electrical activation, mechanical contraction, valve movement, and blood flow. It is easiest to understand by tracking what is happening in the ventricles, which provide the force for systemic and pulmonary circulation.

Key phases of the cardiac cycle

1. Ventricular filling (diastole)

• The ventricles relax and fill from the atria.
• Most filling is passive early in diastole; atrial contraction contributes an extra “atrial kick” late in diastole, which becomes more important when ventricular relaxation is impaired.

1. Isovolumetric contraction

• Ventricular pressure rises sharply after electrical activation.
• Both the atrioventricular (AV) valves and semilunar valves are closed, so volume does not change.
• The first heart sound (S1) is associated with AV valve closure at the onset of systole.

1. Ventricular ejection

• When ventricular pressure exceeds aortic or pulmonary artery pressure, semilunar valves open and blood is ejected.
• Stroke volume depends on preload (filling), afterload (pressure the ventricle must overcome), and contractility (intrinsic strength of contraction).

1. Isovolumetric relaxation

• Ventricular pressure falls after ejection.
• All valves are closed again; volume remains constant.
• The second heart sound (S2) is associated with semilunar valve closure.

Preload, afterload, and contractility in practical terms

• Preload reflects ventricular filling and is related to end-diastolic volume. Increased venous return generally increases preload and stroke volume through the Frank-Starling mechanism.
• Afterload is the load the ventricle must eject against, closely tied to arterial pressure. Higher afterload tends to reduce stroke volume if contractility does not change.
• Contractility changes stroke volume at a given preload and afterload, influenced by sympathetic activity and certain medications.

These concepts help interpret real situations. For example, dehydration reduces venous return and preload, lowering stroke volume and potentially blood pressure. Chronic hypertension increases afterload, increasing the work of the left ventricle.

ECG interpretation: linking electrical activity to cardiac function

The ECG is a surface recording of the heart’s electrical activity. It does not measure contraction directly, but electrical events precede mechanical events in a predictable way.

Major ECG components and what they represent

• P wave: atrial depolarization
• PR interval: time from atrial depolarization to ventricular depolarization, reflecting conduction through the AV node and His-Purkinje system
• QRS complex: ventricular depolarization (rapid because the Purkinje system conducts quickly)
• ST segment and T wave: ventricular repolarization (recovery phase)

A foundational approach to ECG interpretation begins with rhythm and rate, then evaluates intervals and waveform morphology. Even without diagnosing specific pathologies, physiology guides interpretation:

• Conduction delays prolong intervals.
• Abnormal depolarization pathways widen the QRS.
• Changes in repolarization can shift ST segments and alter T wave patterns.

Because mechanical contraction follows depolarization, disturbances in rhythm can impair cardiac output. A very fast rate can reduce diastolic filling time; a very slow rate can reduce cardiac output even if stroke volume is preserved.

Blood pressure regulation: short-term control and long-term balance

Arterial blood pressure is a regulated variable because it determines organ perfusion. It is not constant beat-to-beat, but it is tightly controlled through integrated neural, hormonal, and renal mechanisms.

A practical approximation is: $MAP\approx CO\times TPR$

where $MAP$ is mean arterial pressure and $TPR$ is total peripheral resistance.

Short-term regulation: baroreceptor reflexes

The fastest control comes from arterial baroreceptors in the carotid sinus and aortic arch:

• If blood pressure falls, baroreceptor firing decreases.
• The autonomic nervous system responds by increasing sympathetic tone and reducing parasympathetic tone.
• Heart rate rises, contractility increases, and arterioles constrict, raising blood pressure.

This mechanism is evident when standing up quickly. Gravity reduces venous return and transiently lowers blood pressure; reflex responses prevent fainting by increasing heart rate and vascular tone.

Long-term regulation: kidneys and volume control

Over hours to days, the kidneys set the long-term baseline by adjusting sodium and water excretion, influencing blood volume and venous return. Hormonal systems modify this balance:

• The renin-angiotensin-aldosterone system supports blood pressure by promoting vasoconstriction and sodium retention.
• Antidiuretic hormone increases water retention, especially when volume is low or plasma osmolality is high.

Long-term regulation explains why chronic hypertension often involves sustained changes in vascular resistance and volume handling rather than moment-to-moment autonomic shifts alone.

Hemodynamics: how blood flows through vessels

Hemodynamics applies physical principles to circulation. Flow is influenced by vessel radius, length, viscosity, and pressure gradients. In physiology, the most important controllable factor is vessel radius, especially at the level of arterioles.

Resistance and the role of arterioles

Arterioles are the primary resistance vessels. Small changes in arteriolar diameter markedly change resistance and therefore affect:

• Systemic vascular resistance
• Tissue perfusion
• Blood pressure distribution between organs

Local metabolic demand can trigger vasodilation in active tissues, improving oxygen delivery where it is most needed. Meanwhile, sympathetic tone can constrict vessels in other regions to preserve blood pressure during stress.

Capillary exchange and fluid balance

Capillaries are designed for exchange. Movement of fluid across capillary walls depends on the balance between hydrostatic pressure (pushing fluid out) and oncotic pressure (pulling fluid in), driven largely by plasma proteins. When this balance shifts, edema can develop. Clinically, this helps make sense of swelling in situations where venous pressure is elevated or plasma protein levels are low.

Venous return: the other half of cardiac output

The cardiovascular system is a closed loop, so cardiac output must match venous return. Veins act as capacitance vessels, storing a large fraction of blood volume. Venous return is supported by:

• Skeletal muscle pump during movement
• Venous valves that prevent backflow
• Respiratory pressure changes that assist flow toward the thorax
• Sympathetic venoconstriction that shifts blood toward the heart

When venous return drops, preload falls and stroke volume decreases, often triggering compensatory increases in heart rate and vascular resistance.

Bringing it together: physiology at the bedside

Cardiovascular physiology becomes most useful when it links measurements to mechanisms:

• ECG provides insight into rhythm and conduction, which influence filling time and pumping effectiveness.
• Blood pressure reflects the interaction between cardiac output and vascular resistance, modulated by neural reflexes and long-term renal control.
• Hemodynamics explains why vessel tone, blood volume, and regional flow distribution matter as much as heart function itself.

A coherent understanding of the cardiac cycle, ECG fundamentals, blood pressure regulation, and hemodynamics helps interpret everyday clinical patterns, from orthostatic symptoms to the consequences of sustained high afterload. It also grounds more advanced topics in a consistent framework: the heart generates pressure, the vessels distribute flow, and the body continuously adjusts both to meet changing demands.