19.4 Cardiac Physiology

Cardiac Physiology

Cardiac physiology explains how the heart adjusts its output to match the body's constantly shifting demands. Whether you're sprinting, sleeping, or standing up from a chair, the heart fine-tunes its rate and force of contraction through a combination of nervous system signals, hormones, and intrinsic mechanical properties.

Heart Rate and Cardiac Output

Heart rate is simply the number of times the heart contracts per minute. At rest, this is typically 60–100 beats per minute (bpm).

Cardiac output (CO) is the total volume of blood the heart pumps per minute. It's calculated with a straightforward formula:

$CO = HR \times SV$

where $HR$ is heart rate and $SV$ is stroke volume (the amount of blood ejected per beat).

A typical resting CO is about 5 L/min (e.g., 72 bpm × ~70 mL per beat). If you double heart rate while stroke volume stays the same, cardiac output doubles proportionally. During heavy exercise, CO can increase to 20–25 L/min or more.

Exercise Effects on Cardiovascular Function

Exercise ramps up the body's demand for oxygen and nutrients, and the cardiovascular system has to keep pace. Here's how it adapts:

1. The sympathetic nervous system activates and releases norepinephrine, which binds to beta-1 adrenergic receptors on the heart.

2. This produces two effects:

   • Positive chronotropy: increased heart rate
   • Positive inotropy: increased force of contraction (contractility)

3. At the same time, venous return increases because of the skeletal muscle pump (contracting leg muscles squeeze blood back toward the heart) and the respiratory pump (deeper breathing creates pressure changes that pull blood into the thorax).

4. Greater venous return stretches the ventricles more before contraction, which increases stroke volume through the Frank-Starling mechanism (more on this below).

The net result is a large increase in cardiac output from both a faster heart rate and a larger stroke volume.

Cardiovascular Control Mechanisms

The cardiovascular center in the medulla oblongata is the brain's command hub for heart regulation. It contains two functional areas:

• Cardioacceleratory center: sends sympathetic signals to increase heart rate and contractility
• Cardioinhibitory center: sends parasympathetic signals (via the vagus nerve) to decrease heart rate

At rest, parasympathetic (vagal) tone dominates, which is why resting heart rate sits well below the heart's intrinsic pacemaker rate of ~100 bpm.

The Baroreceptor Reflex

Baroreceptors are stretch-sensitive receptors located in the aortic arch and carotid sinuses. They continuously monitor blood pressure and trigger rapid corrections:

• Blood pressure rises → baroreceptors fire more frequently → the cardiovascular center increases parasympathetic output and decreases sympathetic output → heart rate and contractility drop → blood pressure falls back toward normal
• Blood pressure drops → baroreceptor firing decreases → sympathetic output increases, parasympathetic output decreases → heart rate and contractility rise → blood pressure is restored

This reflex is a classic negative feedback loop and one of the fastest mechanisms for short-term blood pressure regulation.

Factors in Heart Rate Regulation

Several factors beyond the autonomic nervous system influence how fast and how forcefully the heart beats:

Autonomic Nervous System (review)

• Sympathetic stimulation (norepinephrine at beta-1 receptors) increases heart rate and contractility
• Parasympathetic stimulation (acetylcholine at muscarinic receptors) decreases heart rate

Hormones

• Epinephrine and norepinephrine (catecholamines from the adrenal medulla) mimic sympathetic effects, raising heart rate and contractility
• Thyroid hormones ($T_3$ and $T_4$) upregulate beta-1 receptors on the heart, making it more responsive to catecholamines. Hyperthyroidism can cause tachycardia for this reason.

Ions

• Calcium ($Ca^{2+}$) is essential for myocardial contraction. Increased extracellular $Ca^{2+}$ enhances contractility; decreased $Ca^{2+}$ weakens it.
• Abnormal levels of potassium ($K^+$) can disrupt the heart's electrical activity. Hyperkalemia is particularly dangerous because it can depolarize the resting membrane potential and lead to arrhythmias.

Medications

• Beta-blockers (e.g., propranolol) block beta-1 receptors, reducing heart rate and contractility. These are commonly prescribed for hypertension and certain arrhythmias.
• Digitalis (digoxin) increases contractility by raising intracellular $Ca^{2+}$ concentration. It's used in heart failure to strengthen each contraction.

Inotropic Agents and Heart Function

An inotropic agent is any substance that changes the force of myocardial contraction. The term comes from ino- (fiber) and -tropic (turning/changing).

Positive inotropic agents increase contractility:

• Digitalis, $Ca^{2+}$, epinephrine, norepinephrine
• They work by increasing intracellular $Ca^{2+}$ concentration or by making the contractile proteins (myofilaments) more sensitive to $Ca^{2+}$

Negative inotropic agents decrease contractility:

• Beta-blockers, calcium channel blockers (e.g., verapamil), barbiturates
• They work by reducing intracellular $Ca^{2+}$ or decreasing myofilament sensitivity to $Ca^{2+}$

A useful way to remember this: positive inotropes push more calcium toward the contractile machinery, while negative inotropes pull it away or block its effects.

Determinants of Cardiac Performance

Stroke volume is the volume of blood ejected from the left ventricle per beat. Three factors determine it:

• Preload: the degree of ventricular stretch at the end of diastole (filling). More blood in the ventricle = more stretch = stronger contraction. This is the Frank-Starling mechanism.
• Afterload: the resistance the ventricle must overcome to eject blood. In practice, this is largely determined by arterial blood pressure. Higher afterload means the ventricle has to work harder, and stroke volume tends to decrease.
• Contractility: the intrinsic strength of contraction independent of preload and afterload. Positive inotropic agents increase contractility; negative inotropic agents decrease it.

To summarize the relationships:

Cardiac output remains the product of heart rate and stroke volume: $CO = HR \times SV$

The ventricular pressure-volume loop is a graph that plots ventricular pressure against ventricular volume throughout one complete cardiac cycle. It visually shows the phases of filling, isovolumetric contraction, ejection, and isovolumetric relaxation, and changes in preload, afterload, or contractility shift the shape of the loop in predictable ways.

Heart's Response to Hemodynamic Changes

The heart has several built-in responses to handle sudden changes in blood flow and pressure:

Autoregulation of Coronary Blood Flow The coronary circulation adjusts its own resistance to maintain relatively constant blood flow to the heart muscle across a range of perfusion pressures. When myocardial oxygen demand increases, coronary arterioles dilate to deliver more blood.

Anrep Effect When afterload suddenly increases (e.g., a spike in blood pressure), the ventricle initially ejects less blood. Over the next few beats, contractility gradually increases to compensate, helping restore stroke volume despite the higher resistance. This is the Anrep effect.

Bainbridge Reflex When venous return increases rapidly (e.g., during IV fluid administration), stretch receptors in the right atrium and vena cavae trigger an increase in heart rate. This prevents blood from pooling in the venous system and helps the heart accommodate the extra volume.

Cardiac Electrical Activity and Monitoring

The cardiac action potential is the electrical event that triggers each heartbeat. Pacemaker cells in the SA node generate action potentials spontaneously, and these signals spread through the conduction system to coordinate contraction of the atria and ventricles.

The electrocardiogram (ECG/EKG) records this electrical activity from the body surface over time. Each wave and interval on the ECG tracing corresponds to a specific electrical event in the heart, making it a valuable diagnostic tool.

Heart sounds are produced primarily by the closing of heart valves:

• S1 ("lub"): closure of the AV valves (mitral and tricuspid) at the start of ventricular systole
• S2 ("dub"): closure of the semilunar valves (aortic and pulmonary) at the start of ventricular diastole

Abnormal heart sounds, called murmurs, can indicate valve dysfunction or other structural problems. Listening to heart sounds with a stethoscope (auscultation) is one of the most basic and informative clinical assessments of cardiac function.