Chapter 3 of 5 - Physiology Course
Cardiovascular Physiology
The heart generates flow; the vessels distribute it. This chapter connects the cardiac cycle to pressure-volume thinking and whole-body perfusion.
Cardiovascular physiology questions often reward linking pump function (how much blood leaves the heart per minute) with vascular resistance (how hard arterioles oppose flow) and venous return (what refills the ventricle before the next beat). The figures below summarize the cardiac-output relationship and a prototypical short-loop pressure reflex.
Cardiac Cycle Essentials
Systole ejects blood; diastole fills the ventricles. Key intervals include isovolumetric contraction and relaxation (valves closed, volume fixed) versus ejection and filling phases. Heart sounds correlate with valve motion and turbulent flow (for example mitral closure at S1, aortic closure at S2).
Pressure-volume loops integrate valve timing with ventricular work: widening of the loop can reflect increased afterload or contractility changes; shifts along the volume axis often reflect preload. Murmurs are interpreted by knowing when pressures cross between chambers or great vessels - systolic versus diastolic timing on the cycle diagram is high yield when paired with clinical vignettes.
CO and SVR interact with compliance and venous tone; the baroreflex adjusts HR and vascular resistance acutely.
Venous return & filling
Blood returns to the atrium; EDV sets preload.
Stroke volume
Frank-Starling, contractility, afterload determine SV.
Cardiac output
CO = HR × SV supplies systemic circulation.
Mean arterial pressure
MAP trends with CO × SVR (conceptually) plus compliance effects.
Perfusion of organs
Autoregulation and local metabolites modulate regional flow.
Aligning ECG timing, valve events, and ventricular pressure-volume changes clarifies murmurs and hemodynamic panels.
Stroke Volume and the Frank-Starling Law
Preload (end-diastolic fiber length) increases contractile force so that, in healthy hearts, more filling yields a stronger beat. Afterload opposes ejection (arterial pressure and vascular impedance). Contractility shifts the force-length relationship (sympathetic stimulation, inotropes).
Ejection fraction (stroke volume divided by end-diastolic volume) is a common clinical index of systolic function but does not alone define CO - tachycardia with modest EF can still yield inadequate output if SV falls. Heart failure phenotypes often separate reduced versus preserved EF; physiology explains why diastolic stiffness raises filling pressures even when systolic contraction looks near normal on imaging.
| Determinant | Clinical lever (examples) |
|---|---|
| Preload | IV fluids, venous tone, regurgitant lesions (volume overload) |
| Afterload | Hypertension, aortic stenosis, systemic vasoconstriction |
| Contractility | Catecholamines, ischemia, acidosis, beta-blockade |
Quick Check
Which equation correctly relates cardiac output to heart rate and stroke volume?
Fill in the Blank
The Frank-Starling mechanism describes increased stroke volume when ventricular ________ increases (greater end-diastolic fiber length).
Vascular Physiology and Blood Pressure
Arterioles are the main resistance vessels. The baroreflex buffers acute pressure changes via carotid and aortic arch sensors, adjusting sympathetic and parasympathetic outflow to heart and vessels.
Capillary hydrostatic and oncotic pressures govern fluid shift between plasma and interstitium - Starling forces connect cardiovascular physiology to edema formation in heart failure, liver disease, and nephrotic states. Long-term blood pressure regulation adds renal salt and water handling, RAAS activity, and volume status on top of neural reflex arcs.
Carotid sinus and aortic arch baroreceptors fire more when stretch increases; the medulla shifts autonomic balance to stabilize MAP.
MAP changes stretch on arterial wall
Increased MAP increases baroreceptor firing (typical pattern).
Afferents to medullary centers
Nucleus tractus solitarius integrates the signal.
Adjusted autonomic outflow
Parasympathetic tone to SA node and sympathetic tone to heart/vessels.
HR and SVR respond
Opposes the initial pressure change (negative feedback).
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