Pressure Points
Which two variables determine mean arterial blood pressure?
Cardiac Output × Total Peripheral Resistance (MAP = CO × TPR)
In hypovolemic shock, what is the first compensatory reflex to activate?
Baroreceptor-mediated sympathetic stimulation → tachycardia and vasoconstriction.
List the four Starling forces that govern capillary fluid exchange.
Capillary hydrostatic, interstitial hydrostatic, plasma oncotic, interstitial oncotic.
Define cardiac reserve and explain how it changes in heart failure.
Difference between resting and max CO; markedly reduced → poor exercise tolerance.
Which cartilage forms the rostral boundary of the laryngeal inlet?
Epiglottic cartilage.
According to Ohm’s Law, an increase in TPR will have what effect on BP if CO stays constant?
BP increases because flow (Q) must overcome greater resistance.
Which hormone system is stimulated by renal hypoperfusion to restore arterial pressure?
Renin–Angiotensin–Aldosterone System (RAAS).
In right-sided heart failure, which body cavity commonly accumulates fluid and why?
Abdomen (ascites) due to increased systemic venous pressure raising capillary hydrostatic pressure.
What two mechanisms provide immediate compensation after sudden myocardial weakening?
Increased preload (venous return) and increased sympathetic activity (β₁ inotropy & chronotropy).
Which muscle is the only abductor of the arytenoid cartilage?
Cricoarytenoideus dorsalis muscle.
Which factor most directly aids venous return during inspiration?
The thoracic pump — negative intrapleural pressure draws venous blood toward the heart.
Which anesthetic-related mechanism causes hypotension during surgery?
Anesthetic-induced vasodilation and loss of sympathetic tone → decreased venous return & CO.
What distinguishes inflammatory vs non-inflammatory edema at the capillary level?
Inflammatory = increased endothelial permeability (gap formation); non-inflammatory = increased hydrostatic or decreased oncotic pressure without endothelial injury.
Why is mild fluid retention initially beneficial but later harmful in decompensated HF?
Restores CO via Frank-Starling; prolonged retention → volume overload, edema, ventricular dilation, decreased contractility.
Dorsal displacement of the soft palate in horses causes what main clinical sign?
Respiratory obstruction and exercise intolerance (“gurgling/roaring” noise during work).
During hemorrhage, both baroreceptor and chemoreceptor reflexes activate.
Which autonomic adjustments occur simultaneously in arterioles and the heart, and how do these maintain perfusion of vital organs?
Sympathetic outflow → arteriolar vasoconstriction (↑ TPR) and ↑ HR/contractility (β₁). These shunt blood to brain & heart while limiting cutaneous flow.
Compare neurogenic, anaphylactic, and hypovolemic shock in terms of vascular resistance and venous return, and identify one drug you’d use in each.
Neurogenic = ↓ sympathetic tone → massive vasodilation → use norepinephrine.
Anaphylactic = histamine-mediated vasodilation + ↑ permeability → use epinephrine.
Hypovolemic = low preload from fluid loss → use IV fluids ± dopamine if refractory.
A dog with severe hypoalbuminemia (0.7 g/dL) has ascites and ventral edema.
Explain the sequence from hypoalbuminemia to edema formation and name two diagnostic tests to identify the underlying cause.
Decreased plasma oncotic pressure → net filtration out of capillaries → fluid accumulates interstitially.
Test for protein-losing enteropathy (fecal α₁-PI, ultrasound) and protein-losing nephropathy (UPC ratio).
A dog with decompensated HF receives an ACE-inhibitor and pimobendan. Explain how each drug alters the Frank-Starling curve and ventricular wall stress, and why excessive diuresis can reverse these benefits.
ACE-I decreases afterload → less wall tension (LaPlace); pimobendan increases contractility → shifts curve up/left. Too much diuresis decreases preload below optimal sarcomere length → reduced CO.
A Thoroughbred presents with exercise-induced noise and poor performance. Describe the neuroanatomical basis of this condition
Degeneration of left recurrent laryngeal nerve → atrophy of cricoarytenoideus dorsalis → laryngeal hemiplegia. Diagnose via endoscopy
Which reflex restores normal BP after a sudden drop, what cranial nerves carry its afferents, and what happens to firing frequency, sympathetic tone, and vagal tone during hypotension?
Baroreceptor reflex via CN IX (glossopharyngeal) and CN X (vagus); decreased baroreceptor firing → ↑ sympathetic (vasoconstrict + tachycardia) and ↓ vagal activity → BP restoration.
Hypertensive cats often present with retinal detachment. Explain the pathophysiology of the lesion and why calcium-channel blockers like amlodipine are first-line therapy.
Sustained ↑ arterial pressure → end-arteriole damage → retinal arteriolar rupture & exudation.
Amlodipine blocks L-type Ca²⁺ channels → arteriolar dilation ↓ afterload & protects microvasculature.
Compare the pathogenesis and fluid composition of cardiogenic vs non-cardiogenic pulmonary edema, and indicate one drug that targets each mechanism.
Cardiogenic (L HF): increased hydrostatic pressure → transudate low protein → treat with furosemide.
Non-cardiogenic (ARDS): increased permeability → protein-rich exudate → treat underlying cause + O₂ support.
Differentiate compensated vs decompensated heart failure in terms of renal response and fluid balance, and propose one short-term and one long-term therapeutic strategy for each.
Compensated: kidneys retain modest Na⁺/H₂O → normal CO at rest but low reserve. Tx = ACE-I (long-term) + controlled diuretic (short-term).
Decompensated: persistent renal retention → volume overload, pulmonary edema. Tx = IV furosemide (short-term) + pimobendan & dietary Na restriction (long-term).
In horses, explain why the soft palate always lies beneath the epiglottis and what physiological advantage this provides.
This arrangement makes the horse an obligate nasal breather, preventing oral airflow during rest and exercise and ensuring efficient oxygen delivery during high-performance activity.