Costanzo | Physiology | Chapter 4 | Cardiovascular Physiology | Study Guide
Chapter 4: Cardiovascular Physiology Notes
I. Circuitry of the Cardiovascular System
Heart as a Pump: The heart generates pressure to drive blood through the vasculature. Arteries carry oxygenated blood to tissues under high pressure (stressed volume), while veins return deoxygenated blood to the heart under low pressure (unstressed volume).
Systemic and Pulmonary Circulations:
The left heart pumps blood to all organs except the lungs (systemic circulation).
The right heart pumps blood to the lungs (pulmonary circulation).
These circulations operate in series, meaning the output of one equals the input of the other (Cardiac Output = Venous Return).
Parallel Arrangement: Within the systemic circulation, blood is distributed simultaneously to various organ systems in parallel, allowing independent regulation of regional blood flow.
II. Hemodynamics
Velocity, Flow, and Area: Velocity (v) is inversely proportional to the total cross-sectional area (A) of the vessels (v=Q/A). Velocity is lowest in the capillaries, which have the largest total cross-sectional area, facilitating nutrient exchange.
Resistance (Poiseuille Equation): Resistance is determined by blood viscosity, vessel length, and—most critically—the vessel radius (r). A twofold decrease in radius increases resistance 16-fold (r4 relationship).
Laminar vs. Turbulent Flow: Laminar flow is streamlined and silent. Turbulent flow (high Reynolds number) causes murmurs and can be triggered by high blood velocity, low viscosity (anemia), or vessel narrowing (thrombus).
Compliance: Describes the volume a vessel can hold at a given pressure. Veins have high compliance (capacitance vessels), while arteries have low compliance. Arterial compliance decreases with aging, leading to higher systolic pressures.
III. Cardiac Electrophysiology
Action Potentials (AP):
Ventricles, Atria, and Purkinje system: Feature a long duration and a plateau phase (Phase 2) caused by an inward Ca2+ current.
SA Node: The normal pacemaker. It features an unstable resting potential and spontaneous Phase 4 depolarization driven by the If current (Na+ influx).
Conduction Velocity: Fastest in the Purkinje system (allows rapid ventricular contraction) and slowest in the AV node (allows time for ventricular filling).
Electrocardiogram (ECG):
P wave: Atrial depolarization.
QRS complex: Ventricular depolarization.
T wave: Ventricular repolarization.
PR interval: Correlates with AV node conduction time.
IV. Cardiac Muscle Contraction
Excitation-Contraction Coupling: An action potential leads to Ca2+ entry via L-type channels, which triggers a massive release of Ca2+ from the sarcoplasmic reticulum (SR) (Ca2+-induced Ca2+ release). Ca2+ binds to troponin C to initiate contraction.
Inotropism (Contractility): Positive inotropic agents (e.g., sympathetic stimulation, cardiac glycosides like digoxin) increase the force of contraction by increasing intracellular Ca2+.
Frank-Starling Law: States that the volume of blood ejected (stroke volume) depends on the volume present at the end of diastole (preload).
V. Regulation of Arterial Pressure
Baroreceptor Reflex: A fast, neural reflex. A decrease in arterial pressure (Pa) is sensed by receptors in the carotid sinus, leading to increased sympathetic outflow to increase heart rate, contractility, and TPR.
Renin-Angiotensin II-Aldosterone System (RAAS): A slow, hormonal system. Activated by decreased renal perfusion, it results in the production of Angiotensin II (vasoconstriction) and Aldosterone (increased Na+ reabsorption and blood volume).
VI. Microcirculation and Starling Forces
Fluid Exchange: Governed by the balance of hydrostatic and oncotic pressures. Filtration is favored by capillary hydrostatic pressure (Pc) and interstitial oncotic pressure. Edema occurs when filtration exceeds lymphatic drainage.
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Chapter 4 Study Guide
I. Glossary of Key Terms
Afterload: The pressure against which the heart must pump (aortic pressure).
Chronotropic effect: A change in heart rate.
Compliance: The distensibility of blood vessels; ΔV/ΔP.
Dromotropic effect: A change in conduction velocity (usually in the AV node).
Ejection Fraction: The fraction of end-diastolic volume ejected per beat (normally 55%).
Inotropic effect: A change in myocardial contractility.
Preload: The resting fiber length/volume from which the heart contracts (end-diastolic volume).
Stressed Volume: The volume of blood in the arteries under high pressure.
Total Peripheral Resistance (TPR): The combined resistance of all systemic peripheral vasculature.
II. 50 Question-and-Answer Quiz
Which vessels have the highest resistance? Arterioles.
Which vessels have the largest total cross-sectional area? Capillaries.
What is the formula for Cardiac Output? Stroke Volume×Heart Rate.
What defines 'normal sinus rhythm'? AP originates in the SA node, occurs regularly (60-100 bpm), and follows the correct sequence.
Which ion is responsible for the Phase 0 upstroke in ventricles? Na+.
Which ion is responsible for the Phase 0 upstroke in the SA node? Ca2+.
What is Phase 2 of the ventricular AP? The plateau phase (Ca2+ influx).
What effect does sympathetic stimulation have on Phase 4 of the SA node? Increases the rate of depolarization (increases If), raising heart rate.
Which current is responsible for the unstable resting potential in the SA node? If.
Where is conduction velocity the slowest? AV node.
Where is conduction velocity the fastest? Purkinje system.
What does the P wave represent? Atrial depolarization.
What does the PR interval represent? AV node conduction time.
What does the QRS complex represent? Ventricular depolarization.
What does the T wave represent? Ventricular repolarization.
How does digitalis increase contractility? It inhibits Na+-K+ ATPase, leading to higher intracellular Ca2+.
What is the effect of increased afterload on stroke volume? It decreases stroke volume.
What is the effect of increased preload on stroke volume? It increases stroke volume (Frank-Starling).
What defines the 'Absolute Refractory Period'? The period when no new AP can be elicited regardless of stimulus strength.
Which receptor mediates increased heart rate? β1 adrenoreceptors.
Which receptor mediates vasoconstriction in the skin? α1 adrenoreceptors.
Which receptor mediates vasodilation in skeletal muscle? β2 adrenoreceptors.
What does a high Reynolds number indicate? Turbulent flow.
In the Starling equation, which pressure favors absorption? Capillary oncotic pressure.
What is the effect of aging on pulse pressure? It increases pulse pressure due to decreased arterial compliance.
Which organ receives the highest percentage of cardiac output? Kidneys/GI tract (approx. 25% each at rest).
Which organ receives the highest percentage of CO during exercise? Skeletal muscle.
What is the primary factor controlling coronary blood flow? Local metabolites (hypoxia, adenosine).
What is 'active hyperemia'? Increased blood flow proportional to metabolic activity.
Where are baroreceptors located? Carotid sinus and aortic arch.
What nerve carries baroreceptor signals from the carotid sinus? CN IX (glossopharyngeal).
What nerve carries baroreceptor signals from the aortic arch? CN X (vagus).
What is the response of the baroreceptor reflex to hemorrhage? Increased sympathetic and decreased parasympathetic outflow.
What enzyme catalyzes the conversion of Angiotensin I to II? ACE.
What is the action of Aldosterone on the kidney? Increases Na+ reabsorption.
What is the primary stimulus for the RAAS? Decreased renal perfusion pressure.
How does Angiotensin II affect TPR? It causes potent vasoconstriction, increasing TPR.
Which heart sound is associated with AV valve closure? First heart sound (S1).
Which heart sound is associated with semilunar valve closure? Second heart sound (S2).
What is 'isovolumetric contraction'? All valves are closed; ventricular pressure rises at a constant volume.
What is the 'Dicrotic notch'? A brief dip in aortic pressure when the aortic valve closes.
What is the effect of increased heart rate on the cardiac cycle? Shortens the time for diastole (filling).
What defines the 'Mean Systemic Pressure'? The pressure when blood flow is zero throughout the system.
What shifts the vascular function curve to the right? Increased blood volume or decreased venous compliance.
What is the 'Fick Principle' used to measure? Cardiac output.
How does the body increase heat dissipation? Arteriolar vasodilation in the skin.
What is 'orthostatic hypotension'? A drop in blood pressure upon standing.
How does the heart compensate for chronic hypertension? Left ventricular hypertrophy.
Which ion channel does the parasympathetic Gi protein act on directly? K+ channels (to slow HR).
What is the 'Staircase effect' (Treppe)? Stepwise increase in tension as heart rate increases.
III. Short Answer Questions
Explain the inverse relationship between vessel diameter and blood flow velocity.
Answer: Since flow (Q) is constant, v=Q/A. As diameter increases (especially in the capillary bed), the total cross-sectional area increases, forcing velocity to decrease to maintain the same total flow.
Describe how decreased arterial compliance affects pulse pressure.
Answer: Compliance is ΔV/ΔP. If compliance is low, a fixed stroke volume (ΔV) ejected into the artery causes a much larger increase in pressure (ΔP), thus increasing the difference between systolic and diastolic pressure (pulse pressure).
Why is the AV node delay physiologically important?
Answer: It ensures that the atria have sufficient time to contract and fully fill the ventricles with blood before ventricular contraction begins.
How does hyperkalemia lead to muscle weakness?
Answer: Elevated serum K+ depolarizes the resting membrane potential. This closes Na+ inactivation gates, making them unavailable for the upstroke of the action potential, thus blocking muscle activation.
IV. Essay Questions
Describe the coordinated cardiovascular compensatory responses to acute hemorrhage.
Answer: Hemorrhage causes a decrease in Pa due to lost blood volume. Baroreceptors detect this and trigger increased sympathetic outflow, leading to: (1) Increased heart rate and contractility (to increase CO); (2) Arteriolar constriction (to increase TPR); and (3) Venoconstriction (to increase venous return). Simultaneously, the RAAS is activated by low renal perfusion, producing Angiotensin II for vasoconstriction and Aldosterone for Na+ and water retention to restore blood volume.
Compare the effects of the sympathetic and parasympathetic nervous systems on cardiac function.
Answer: Sympathetic stimulation (β1 receptors) increases heart rate (positive chronotropic), conduction velocity (positive dromotropic), and contractility (positive inotropic) by increasing Ca2+ and If currents. Parasympathetic stimulation (M2 receptors) decreases heart rate and AV conduction velocity by increasing K+ conductance and decreasing If and Ca2+ currents, but has minimal effect on ventricular contractility.
