This summary integrates essential cardiovascular physiology topics, structured around the 12 key learning objectives, from circulatory pathways and blood flow regulation to electrophysiology and autonomic control.
The cardiovascular system functions as a dual-circuit network with pulmonary and systemic circulations:
Pulmonary Circulation: Blood flows from the right atrium and right ventricle to the lungs for gas exchange. Pulmonary arteries transport deoxygenated blood to the lungs, while pulmonary veins return oxygenated blood to the heart’s left atrium.
Systemic Circulation: Oxygenated blood from the left atrium flows through the left ventricle and is pumped via the aorta to the body’s organs. This systemic circuit includes branching arteries, arterioles, and capillaries for nutrient and gas exchange, returning deoxygenated blood via veins to the heart.
Blood flow (
In the vascular network:
Pressure is generated by the heart and maintained by large elastic arteries, like the aorta.
Resistance varies with vessel radius, length, and blood viscosity, with arterioles providing significant resistance and flow control.
Mean Arterial Pressure (MAP) reflects the average arterial pressure throughout one cardiac cycle and is crucial for assessing circulatory health. MAP, calculated as:
weights diastolic pressure more heavily due to its longer duration, ensuring consistent blood flow during diastole.
Cardiac output (CO) is the total blood volume pumped by a ventricle per minute, calculated by multiplying stroke volume (SV) by heart rate (HR):
Cardiac output varies with physical demands and distributes blood flow based on tissue metabolic needs. Systemic venous blood is a major reservoir, containing about 65-70% of the total blood volume due to high venous capacitance.
TPR represents the cumulative resistance of systemic circulation and is a key determinant of blood pressure. TPR can be calculated with Ohm’s Law applied to the entire vascular system:
where MAP is the arterial pressure, Pv is venous pressure (often negligible), and CO is cardiac output.
Fluid exchange in capillaries follows Starling forces, balancing hydrostatic pressure (P) and oncotic pressure (π):
This balance allows for proper fluid exchange across capillary walls:
Positive Qf (hydrostatic pressure > oncotic pressure) pushes fluid into tissues.
Negative Qf (oncotic pressure > hydrostatic pressure) pulls fluid into capillaries.
When these forces are unbalanced, edema or dehydration can occur.
The cardiac cycle includes five primary phases:
Atrial Systole: Atria contract to push blood into ventricles.
Isovolumetric Contraction: Ventricles contract with all valves closed, increasing pressure.
Ventricular Ejection: Blood is ejected from the ventricles as pressure exceeds that in the arteries.
Isovolumetric Relaxation: Ventricles relax, reducing pressure while valves remain closed.
Ventricular Filling: Blood fills ventricles passively, restarting the cycle.
The Pressure-Volume (P-V) Loop depicts left ventricular pressure and volume changes throughout the cardiac cycle. Alterations in the loop can indicate conditions like valve stenosis, regurgitation, or heart failure:
A to B: Diastolic filling.
B to C: Isovolumetric contraction.
C to D: Ejection.
D to A: Isovolumetric relaxation.
The cardiac action potential is regulated by multiple ion channels:
Na⁺ channels rapidly depolarize the cell membrane.
Ca²⁺ channels sustain depolarization in pacemaker cells.
K⁺ channels repolarize the membrane, restoring the resting potential.
HCN ("funny") channels contribute to pacemaker potential, especially in the SA node.
The baroreflex stabilizes blood pressure through a rapid feedback loop:
High BP stretches baroreceptors, activating signals to reduce sympathetic tone, lower heart rate, and cause vasodilation.
Low BP reduces baroreceptor firing, which increases sympathetic tone, elevating heart rate and causing vasoconstriction.
The sympathetic nervous system (SNS) influences cardiovascular dynamics by:
Increasing heart rate and contractility: SNS activation increases cardiac output through β₁ adrenergic receptors.
Inducing vasoconstriction: α₁ adrenergic receptors cause arteriolar constriction, raising TPR and blood pressure.
Endothelial cells release vasoactive substances to regulate vascular tone:
Vasodilators:
Nitric Oxide (NO): Relaxes smooth muscle.
Prostacyclin (PGI₂): Inhibits platelet aggregation and dilates vessels.
Vasoconstrictors:
Endothelin: Strong vasoconstrictor associated with hypertension.
Thromboxane A₂ (TXA₂): Promotes vasoconstriction and clot formation.
This structured summary provides an integrated view of cardiovascular function, emphasizing the physiological mechanisms that maintain homeostasis and respond to varying physiological demands.
Blood moves through a closed-loop system comprising two circuits: the pulmonary and systemic circulations.
Pulmonary Circulation: Blood enters the right atrium via the vena cavae, passes through the right ventricle, and is pumped to the lungs via the pulmonary arteries. In the lungs, gas exchange occurs, oxygenating the blood.
Systemic Circulation: Oxygenated blood returns to the left atrium, moves into the left ventricle, and is pumped through the aorta into systemic arteries, arterioles, and capillaries, where nutrient and gas exchange occurs. Deoxygenated blood returns via venules and veins to the right atrium.
Blood flow (
Here:
Pressure (
Resistance (
Mean Arterial Pressure (MAP) is an average pressure in the arteries, not the mean of systolic and diastolic pressures since diastole occupies more of the cardiac cycle:
Where:
SBP is systolic blood pressure
DBP is diastolic blood pressure
For a BP of 120/80, for example:
Cardiac output is the volume of blood pumped by a ventricle per minute. It is calculated as:
Where:
SV is stroke volume (volume per beat)
HR is heart rate (beats per minute)
For example, if
Total Peripheral Resistance (TPR) represents the systemic vascular resistance and is derived from Ohm’s law adapted for the entire systemic circuit:
Where:
MAP is mean arterial pressure
Pv is venous pressure (usually negligible)
CO is cardiac output
The Starling Equation describes fluid movement across capillary membranes, balancing hydrostatic pressure (P) and oncotic pressure (π):
Where:
If hydrostatic pressure exceeds oncotic pressure, fluid moves into the interstitium, potentially causing edema. Conversely, if oncotic pressure is too high, fluid retention in capillaries can cause tissue dehydration.
The cardiac cycle consists of:
Atrial Systole: Atria contract, pushing blood into ventricles.
Isovolumetric Contraction: Ventricles begin contraction, increasing pressure but with no volume change.
Ventricular Ejection: Ventricular pressure exceeds aortic/pulmonary pressure, ejecting blood.
Isovolumetric Relaxation: Ventricles relax, reducing pressure without changing volume.
Ventricular Filling: Ventricles fill passively as atrial pressure exceeds ventricular pressure.
A Pressure-Volume (P-V) Loop represents changes in ventricular volume and pressure throughout the cardiac cycle, typically for the left ventricle:
Point A to B: Diastolic filling
Point B to C: Isovolumetric contraction (no volume change, pressure rise)
Point C to D: Ejection (volume decreases, pressure rises then falls)
Point D to A: Isovolumetric relaxation (pressure drops, no volume change)
Abnormal P-V loops can indicate conditions like stenosis (narrowing) or insufficiency (valve regurgitation).
Cardiac action potentials involve distinct phases mediated by ion channels:
Phase 0 (Depolarization): Na⁺ channels open, Na⁺ influx causes rapid depolarization.
Phase 1 (Initial Repolarization): Transient K⁺ channels open, small K⁺ efflux.
Phase 2 (Plateau): L-type Ca²⁺ channels open, Ca²⁺ influx balances K⁺ efflux.
Phase 3 (Repolarization): K⁺ channels dominate, causing repolarization.
Phase 4 (Resting): Resting membrane potential maintained by K⁺ leakage channels.
The baroreflex is a feedback mechanism regulating blood pressure:
Increased BP stretches baroreceptors, activating afferent signals to the brainstem, resulting in decreased sympathetic and increased parasympathetic tone to lower heart rate and dilate vessels.
Decreased BP reduces baroreceptor activation, increasing sympathetic tone, elevating heart rate and vasoconstriction to restore pressure.
The sympathetic nervous system (SNS) primarily regulates:
Heart rate and contractility: SNS activation releases norepinephrine, which binds β₁ receptors to increase heart rate and force.
Vasoconstriction: SNS causes arteriolar vasoconstriction via α₁ receptors, raising TPR and blood pressure.
Vasodilators:
Nitric Oxide (NO): Produced by endothelial nitric oxide synthase (eNOS); relaxes vascular smooth muscle.
Prostacyclin (PGI₂): Inhibits platelet aggregation and dilates blood vessels.
Vasoconstrictors:
Endothelin: Potent vasoconstrictor, often upregulated in hypertension.
Thromboxane A₂ (TXA₂): Promotes vasoconstriction and platelet aggregation.