MD3 Cardiovascular System Physiology Practice

A set of 44 PRACTICE flashcards based on the cardiovascular physiology lecture, covering action potentials, cardiac cycle, hemodynamics, and blood pressure regulation, and hypertension.

What are the two types of cardiac cells and their primary functions?

Ventricular myocytes (non-pacemaker) are responsible for fast, powerful contraction with a stable resting potential; Pacemaker cells (SA node, AV node, Purkinje) possess automaticity for spontaneous depolarization to set the heart rate.

What ion is responsible for Phase 0 (Depolarization) in ventricular myocytes, and at what threshold?

Fast $Na^+$ influx ($I_{Na}$) starting at a threshold of $-70\,mV$ and spiking to $+30\,mV$.

What occurs during Phase 2 (Plateau) of the ventricular action potential?

L-type $Ca^{2+}$ influx balances $K^+$ efflux, a phase unique to cardiac muscle that triggers calcium-induced calcium release (CICR).

Why is the absolute refractory period (ARP) essential in cardiac muscle?

The ARP spans Phases 0 to 3, ensuring no stimulus can re-fire the cell regardless of strength, which prevents fatal tetanic contractions.

How do Class III antiarrhythmics affect the action potential?

They block rapid $K^+$ efflux during Phase 3 repolarization, which prolongs the action potential duration and the QT interval.

Which specific current is responsible for the spontaneous depolarization (Phase 4) in the SA node?

The 'funny' current ($I_f$, HCN channels) along with a decrease in $I_K$ and an increase in $I_{CaT}$.

How does the parasympathetic nervous system (M2 receptors) affect the SA node?

It decreases the slope of Phase 4 and hyperpolarizes the cell, thereby slowing the heart rate.

Which cardiac tissue has the fastest intrinsic rate, and why does it act as the dominant pacemaker?

The SA node ($60-100\,bpm$) is the dominant pacemaker because its fastest rate suppresses all others via overdrive suppression.

What is the sequence of Calcium-Induced Calcium Release (CICR)?

AP arrives at sarcolemma → L-type $Ca^{2+}$ channels (DHPR) open → small $Ca^{2+}$ influx triggers Ryanodine Receptors (RyR2) on the SR → large (~80-90%) $Ca^{2+}$ release into the cytoplasm.

What is the mechanism behind the Frank-Starling law of the heart?

Increased stretch (preload) leads to more optimal actin-myosin overlap (~2.2 $\mu m$), allowing for maximum cross-bridge formation and greater force/stroke volume.

How does Digoxin increase cardiac contractility?

It inhibits the $Na^+/K^+$ ATPase, increasing intracellular $Na^+$ which reverses the NCX exchanger, leading to higher intracellular $Ca^{2+}$ levels.

Which phase of the cardiac cycle has the highest myocardial oxygen demand?

Isovolumetric contraction, when the ventricular pressure rises rapidly with all valves closed.

What is the clinical significance of chordae tendineae and papillary muscles?

They prevent AV valve leaflet eversion into the atrium during systole; rupture (e.g., post-MI) can cause acute mitral regurgitation and flash pulmonary edema.

In the Wiggers diagram, what events define S1 and S2 heart sounds?

S1 ('lub') is caused by the closure of the Mitral and Tricuspid valves at the start of systole; S2 ('dub') is caused by the closure of the Aortic and Pulmonic valves at the end of systole.

Under what conditions is an S3 heart sound (ventricular gallop) considered pathologic?

In adults over 40 years old, it indicates heart failure, dilated cardiomyopathy, or mitral regurgitation due to rapid filling of a volume-overloaded ventricle.

What does an S4 heart sound (atrial gallop) indicate?

It indicates late diastolic atrial kick into a stiff, non-compliant ventricle, commonly seen in HTN, aortic stenosis, or hypertrophic cardiomyopathy.

What does the JVP 'a wave' represent, and when is it absent?

It represents atrial contraction; it is absent in Atrial Fibrillation (AF) because there is no coordinated atrial contraction.

What is the pathognomonic JVP finding for Tricuspid Regurgitation (TR)?

Giant v-waves, caused by venous filling of the RA while the TV is closed or incompetent during systole.

What defines Kussmaul sign?

The JVP rises on inspiration rather than falling, which is characteristic of constrictive pericarditis.

On a Pressure-Volume (PV) loop, what does the width of the loop represent?

The Stroke Volume ($SV = EDV - ESV$).

How does increased afterload affect the Pressure-Volume (PV) loop?

The loop shifts UP and LEFT, resulting in higher pressure, a smaller SV, and a larger ESV.

What is the formula for Mean Arterial Pressure (MAP) and why is it not simply the average of SBP and DBP?

$MAP = DBP + 1/3(SBP - DBP)$; it accounts for the fact that at rest, two-thirds of the cardiac cycle is spent in diastole.

What are common causes of an increased Pulse Pressure (PP)?

Aortic regurgitation (AR), hyperthyroidism, AV fistula, aging, and high fever.

What is the formula for Ohm's Law for systemic circulation?

$CO = (MAP - CVP) / TPR \approx MAP / TPR$.

What are the primary resistance vessels in the systemic circulation?

Arterioles, which account for approximately 60% of total peripheral resistance (TPR).

According to Poiseuille's Law, what happens to resistance if the vessel radius is halved?

Resistance increases 16-fold ($r^4$ relationship; $0.5^4 = 1/16$).

What is the advantage of organs being arranged in parallel in the systemic circulation?

It allows each organ to receive blood simultaneously and reduces the overall total peripheral resistance (TPR).

Which blood vessels have the largest total cross-sectional area and the slowest blood flow velocity?

Capillaries; the slow velocity allows for maximum contact time for nutrient and gas exchange.

What factors increase the Reynolds Number ($Re$), predisposing blood flow to turbulence?

Increased velocity, increased diameter, and decreased viscosity (as seen in anemia).

Which vessels are the high-compliance capacitance vessels of the body?

Veins, which hold approximately 70% of the blood volume with minimal pressure change.

What is the Windkessel effect?

The ability of elastic arteries like the aorta to buffer systolic ejection through their moderate compliance, ensuring continuous blood flow during diastole.

In Starling forces, which pressure is responsible for pulling fluid into the capillary?

Plasma oncotic pressure ($\pi_c$), which is primarily determined by albumin levels.

What is the primary determinant of blood viscosity?

Hematocrit (red blood cell concentration).

Which nerves carry afferent signals from the carotid sinus and aortic arch baroreceptors?

The glossopharyngeal nerve (CN IX, Hering's nerve) from the carotid sinus and the vagus nerve (CN X) from the aortic arch.

What is the baroreceptor reflex response to a decrease in blood pressure?

Decrease in firing leads to increased sympathetic output ($\beta_1$ for contractility/HR and $\alpha_1$ for vasoconstriction) and decreased parasympathetic output to increase MAP.

What is the evidence for dominant parasympathetic (vagal) tone on the heart at rest?

The administration of atropine (a muscarinic blocker) causes the resting heart rate to rise from ~70 to ~100+ bpm.

What is the primary stimulus detected by peripheral chemoreceptors (carotid and aortic bodies)?

Hypoxia (specifically P_aO_2 < 60\,mmHg).

What are the three components of the Cushing Triad found in patients with increased intracranial pressure?

Hypertension, Bradycardia (reflex), and irregular breathing.

Why are baroreceptors unable to regulate blood pressure long-term?

They adapt or 'reset' to sustained pressure changes, accepting the new elevated BP as the normal set point.

Which enzyme does ACE inhibitors target, and what is a common side effect related to its secondary function?

ACE (which converts Angiotensin I to II); blocking it leads to bradykinin accumulation, causing a dry cough or angioedema.

How do ANP and BNP lower blood pressure?

They bind to the NPR-A receptor to increase $cGMP$, leading to vasodilation, decreased renin/aldosterone, and increased natriuresis ($Na^+$ excretion).

What are the laboratory findings in Conn syndrome (Primary hyperaldosteronism)?

Low renin and high aldosterone; clinically presents with HTN, hypokalemia, and metabolic alkalosis.

What physical exam finding is characteristic of coarctation of the aorta?

Hypertension in the upper extremities with weak femoral pulses and decreased perfusion to the lower extremities.

What is the definitive cure for preeclampsia (toxemia of pregnancy)?

Delivery of the placenta.