crdclctrphyslgy
During cardiac depolarization, which ion channel primarily determines the slope of phase 0, and how does this relate to conduction velocity?
Sodium channels; the slope of phase 0 determines the speed of depolarization and thus the conduction velocity through the myocardium
A rhythm strip shows P waves before every QRS with a regular rhythm and rate of 70 bpm. What is this rhythm?
Normal sinus rhythm
When mean arterial pressure decreases, what is the immediate reflex response, and which nerves carry the signal?
Decreased baroreceptor firing increases sympathetic output; signal carried via CN IX (carotid) and CN X (aortic)
What determines whether fluid is filtered out or absorbed at a capillary bed?
The balance of hydrostatic and oncotic pressures—summed as Net Filtration Pressure (NFP = Pc - Pif - πp + πif)
A patient receives phenylephrine for nasal congestion. What receptor does it act on, and what is its vascular effect?
Alpha₁ receptor; vasoconstriction of arterioles increases MAP
Why does myocardial ischemia slow cardiac conduction and predispose to arrhythmias?
Ischemia keeps Na⁺ channels in an inactivated state, forcing depolarization via slower Ca²⁺ influx
An ECG reveals a “sawtooth” baseline between QRS complexes. What is the underlying mechanism?
Atrial flutter due to reentrant circuits within the atria
Which mechanisms maintain short-term and long-term control of arterial pressure, respectively?
Short-term: baroreceptors; long-term: renal blood-volume control
Arteriolar constriction reduces capillary hydrostatic pressure. What effect does this have on fluid movement?
Promotes absorption into the capillary
Explain how clonidine lowers blood pressure, emphasizing the alpha₂ receptor’s function
Alpha₂ receptor activation decreases norepinephrine release, reducing sympathetic tone, heart rate, and vascular resistance
If a patient receives a β-adrenergic agonist, how will calcium influx during phase 2 of the ventricular action potential be affected, and what is the consequence for contractility?
β-agonists increase Ca²⁺ influx via L-type channels, enhancing intracellular Ca²⁺ and thus increasing contractility
A patient has irregularly irregular RR intervals with absent P waves. What are two possible hemodynamic consequences?
Loss of atrial kick and variable ventricular filling, potentially leading to reduced cardiac output
Explain how the muscle pump aids venous return and under what conditions it is most important.
Skeletal muscle contraction compresses veins, promoting venous return—especially during standing and exercise
A patient with protein malnutrition develops edema. Explain the mechanism
Decreased plasma oncotic pressure (from hypoalbuminemia) favors filtration and fluid accumulation in tissues
Why does epinephrine cause skeletal muscle vasodilation but cutaneous vasoconstriction?
Beta₂ receptors predominate in skeletal muscle and heart arterioles (vasodilation), while alpha₁ receptors dominate in skin and GI (vasoconstriction)
A drug that inhibits the “funny current” (If) would primarily affect which phase of the SA node action potential and have what effect on heart rate
Phase 4 depolarization; it would slow spontaneous depolarization and reduce heart rate
How would you distinguish between a Second- and Third-Degree AV block on ECG?
Second-degree block shows intermittent dropped QRS with some conduction; third-degree shows complete atrial–ventricular dissociation
During mild pain, blood pressure rises, yet during severe pain, it drops. Why?
Mild pain increases sympathetic tone; severe pain triggers parasympathetic dominance and cardiovascular collapse
Why does hypertension predispose to edema formation despite normal lymphatic function?
Elevated capillary hydrostatic pressure increases filtration beyond lymphatic removal capacity
Compare the hemodynamic responses to epinephrine versus norepinephrine infusion
Epinephrine increases pulse pressure without changing MAP due to beta₂ dilation (no vagal reflex); norepinephrine increases MAP and triggers baroreflex bradycardia
Why would hyperkalemia slow the firing rate of the SA node?
Elevated extracellular K⁺ reduces the resting membrane potential negativity, decreasing excitability and slowing pacemaker activity
Explain why ventricular tachycardia is more life-threatening than supraventricular tachycardia
VT originates below the AV node with wide QRS complexes and inefficient contraction, which can rapidly degenerate into ventricular fibrillation
A patient with heart failure has impaired cardiopulmonary baroreceptor function. What compensatory neurohormonal changes occur, and what are their hemodynamic consequences?
Increased sympathetic tone, vasoconstriction, and blood volume retention—raising afterload and worsening heart failure
Explain the physiological “safety factors” that prevent edema despite transient increases in capillary pressure
Myogenic constriction, interstitial pressure rise, and enhanced lymphatic drainage compensate to limit net filtration
A patient on MAO inhibitors eats cheese and experiences hypertensive crisis. Explain the mechanism and identify the molecule responsible
Tyramine escapes metabolism by MAO, enters nerve terminals, releases excess NE → massive sympathetic activation → hypertensive crisis