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VM 565 Exam 1: Learning Objectives | Complete Solutions (Verified Answers)

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VM 565 Exam 1: Learning Objectives | Complete Solutions (Verified Answers) What is heart disease? structural/functional abnormality What is heart failure inadequate output or needs high filling pressures. Compliance definition? ΔV/ΔP (distensibility); stiffness = 1/compliance. What is passive compliance? the inherent elasticity and distensibility of blood vessels or heart chambers, allowing them to expand and store blood without active muscle contraction what is active compliance? the dynamic ability of arteries to expand and contract, which can be altered or regulated by smooth muscles in their walls. What determines pressure in a segment? ≈ Volume ÷ Compliance (or Volume × Stiffness). Equation for flow? ≈ ΔPressure ÷ Resistance. Where is resistance clinically meaningful? Precapillary arterioles (small radii). Biggest determinant of resistance? Radius^−4. Normal valves → resistance? Essentially negligible. Preload mainly reflects... Ventricular end-diastolic volume (filling). Afterload approximated by... (Systolic pressure × Radius) ÷ Wall thickness. ↑ Afterload → ESV? Increases. ↑ Contractility → ESV? Decreases. Cardiac output equation? SV × HR SV equation? EDV – ESV Effect of ↑ HR on diastolic filling? Decreases (less time). A-fib effect on pulses? Irregular rate with variable/weak pulses due to variable filling. Where is most blood volume? Systemic veins. Why do veins hold the most blood? High compliance + large capacity. Venoconstriction effect on RA flow? ↑ Venous pressure → ↑ VR to RA. Angiotensin II effect on venous system? ↓ Compliance (↑ stiffness) → ↑ venous pressures. Why do high venous pressures cause edema? ↑ Capillary hydrostatic pressure → ↑ filtration. Left-sided failure edema location? Lungs (pulmonary edema). Right-sided failure edema location? Systemic (legs/abdomen—ascites). Lymphatics prevent edema until... Filtration > lymph drainage capacity. Concentric hypertrophy stimulus? Pressure overload (↑ afterload). Eccentric hypertrophy stimulus? Volume overload (↑ preload). Concentric outcome? Wall thickening, relatively normal chamber size; normalizes wall stress. Eccentric outcome? Chamber dilation with proportional wall mass increase. MMVD (dogs) primary lesion → sequence? Mitral regurg → volume overload → eccentric LV hypertrophy. DCM core defect? Primary contractile weakness → dilation + low forward output. HCM core defect? Primary myocardial thickening → diastolic dysfunction. How DCM breaks compensation? Fails to generate pressure; dilation worsens MR/volume overload → neurohormonal drive. Major systems in chronic HF? RAAS, SNS, vasopressin. Short term effects of neuroendocrine activation? maintains BP Long term effects of neuroendocrine activation? fibrosis, Na/H2O retention, vasoconstriction. Hypovolemia (dehydration) hemodynamics? ↓ Preload → ↓ SV/CO → hypotension. Rapid fluid bolus effect on pressures? Increases venous/arterial pressures (if compliance unchanged). Renal hypoperfusion: two causes? ↓ Arterial pressure gradient or ↑ renal arteriolar resistance. High venous pressures risk? Edema upstream of the failing side. Diuretics main hemodynamic effect? ↓ Volume → ↓ venous pressures → relieve edema ACE inhibitors key effects? ↓ Ang II → vasodilation, ↓ venous stiffness, ↓ remodeling Arteriolar vasodilators lower BP by... ↓ Precapillary resistance → ↓ arterial volume/pressure. If SV is low with normal HR, suspect? Low preload, high afterload, or low contractility. Beta-blockers helpful because... ↓ HR (↑ filling time), ↓ O2 demand, blunt SNS If arterial pressure ↑, two mechanistic buckets? ↑ Volume or ↓ Compliance (↑ stiffness) If afterload chronically high, structural response? Concentric hypertrophy. If chronic MR, structural response? Eccentric LV hypertrophy If venous compliance acutely ↓, RA filling? Increases (↑ VR), can raise CO if heart tolerates What are "myocardial depressant factors"? Circulating mediators that acutely depress relaxation and contraction—reversible when the cause resolves. Two major consequences of interstitial fibrosis? ↑ Diastolic stiffness (↓ compliance) and electrical heterogeneity → arrhythmia risk. Common drivers of cardiac fibrosis? Aging, chronic inflammation, high workloads, chronic SNS/RAAS, toxins, myocyte death. Diastolic P-V curve change with fibrosis? Upward/steeper shift (higher pressure at any volume). Define hypertrophy at the cell level. Myocyte gets bigger (more contractile elements/mitochondria), not more myocytes. What is eccentric hypertrophy? = cells lengthen (chamber dilates) What is concentric hypertrophy? = cells widen (wall thickens, chamber shrinks). What is "remodeling"? changes in size, shape, structure (cells, interstitium, chamber geometry). When can remodeling be adaptive? Short-term SNS/RAAS responses, concentric LVH normalizing wall stress in aortic stenosis. Key trade-offs of concentric LVH in AS? ↓ Wall stress but ↑ diastolic stiffness and ↑ myocardial O₂ demand. Chronic SNS/RAAS—good or bad? Helpful acutely (maintain BP/CO); chronically → fibrosis, Na/H₂O retention, adverse remodeling. How does cell loss raise afterload? Thinner wall (↓ thickness) + larger radius → ↑ wall stress (afterload term). Bedside signs of cardiomegaly? Strong precordial impulse; radiographic cardiomegaly; echo chamber/wall changes. ECG clue to chamber enlargement? Wide QRS (more mass → longer depolarization). Biomarkers used for cardiomegaly? (NT-)proBNP (dogs/cats), troponin for myocyte injury. Why ACEi/ARB in chronic HF? Blunt RAAS → ↓ vasoconstriction/fibrosis/volume → slow remodeling. Role of aldosterone blockers? Block mineralocorticoid effects → anti-fibrotic, natriuresis. Beta-blockers help by... ↓ SNS drive → ↓ HR/O₂ demand, anti-arrhythmic, allow reverse remodeling Diuretics fix which failure axis? Venous pressure (relieve congestion/edema), not mortality disease-modifying If fibrosis increases, what happens to EDV and filling pressures? EDV ↓; LV/LA diastolic pressures ↑ If pressure overload persists, expected structural change? Concentric hypertrophy If chronic MR, expected structural change? Eccentric LV hypertrophy (↑ mass with dilation) If LA huge in a cat with dyspnea, most likely diagnosis? HCM with high LA pressure ± thrombus If sudden venodilation (e.g., anaphylaxis), arterial pressure initially... Falls (↓ venous return → ↓ preload/SV) If doxorubicin (toxin) exposure, long-term risk? Myocyte injury → fibrosis → DCM-like failure How are murmurs classified? By timing, location, and intensity What does timing mean for murmurs? systolic, diastolic, or continuous What does location mean for murmurs? apex/base, left/right, or armpit What does intensity mean for murmurs? grade I-VI Where is a left apical murmur usually heard? Mitral valve Where is a left basilar murmur usually heard? Aortic or pulmonic valve What murmur is best heard in the left axilla/armpit? PDA (patent ductus arteriosus) What murmur is best heard on the right side? Tricuspid valve murmurs Does louder always mean worse? Usually yes, except: Stenosis: narrower = louder. VSD: larger hole = softer murmur but worse disease. Innocent murmur features in puppies? Grade ≤2-3, systolic, left basilar, disappears by ~6 months. Innocent murmurs in cats? NONE When should a puppy murmur be investigated further? If >6 months old or >grade 3, or if not left basilar Are diastolic or right-sided murmurs ever innocent? NO What other conditions may cause non-cardiac murmurs? Anemia, hypoproteinemia (turbulence without structural defect). What determines femoral pulse quality? Pulse pressure = systolic - diastolic pressure Bounding (water hammer) pulses are seen in? PDA, aortic regurgitation, sometimes AV fistula, thyrotoxicosis, chronic bradycardia. Slow-rising pulse is seen in? Severe subaortic stenosis What causes a pulse deficit? Arrhythmias Why does AFib cause pulse deficits? Variable filling time → some beats don't generate palpable output What does jugular vein assessment indicate? Right atrial pressures and right-sided heart disease Jugular distension beyond ⅓ up the neck suggests? Elevated right atrial pressure or tricuspid regurgitation What is the hepatojugular reflex? Pressing the liver → jugular distension if RA pressures are high What is S3? Early diastolic vibration during rapid filling What is S4? Late diastolic vibration during atrial contraction Gallops in cats signify? Diastolic dysfunction, almost always cardiomyopathy (esp. HCM) Gallops in big dogs may indicate? DCM with diastolic dysfunction Gallops in small dogs often mean? Early mitral valve disease (systolic click, not as serious as feline gallop). Can gallops be seen on ECG? No, they are auscultatory findings, not electrical. What is the LA:Ao ratio and its significance? Left atrial : aortic root ratio; >1.5 = LA enlargement (bad prognosis). How is systolic function often measured? Fractional shortening (FS%) using M-mode. Normal FS% in dogs/cats? ~25-45% What echo view is used to measure LA:Ao? Right parasternal short-axis at heart base What does color Doppler show? Flow direction and turbulence (red = toward probe, blue = away) What does spectral Doppler allow? Measurement of velocity → pressure gradient Most common acquired canine heart disease? MMVD (mitral valve disease) Most common feline cardiomyopathy? HCM (hypertrophic cardiomyopathy) Which breeds are predisposed to subaortic stenosis? Large breeds (Golden Retriever, Boxer, Newfie) Why must all cats with murmurs be considered for echo? No truly innocent murmurs in cats; 30% may have no pathology, but can't know without echo What three steps should you always follow when reading thoracic radiographs for the heart? (1) Assess heart size (big/small, cardiac vs non-cardiac) (2) Assess pulmonary vessels (arteries & veins) (3) Assess lung fields (normal vs abnormal). What's an example of a non-cardiac cause of an enlarged cardiac silhouette? Pericardial effusion On lateral view, which chamber forms the apex of the heart? Left ventricle How is VHS measured? Draw a line from carina → apex, then a perpendicular line across the widest part. Walk each line against vertebral bodies starting at T4, add both values. What's a normal VHS in most dogs? About 8.5-10.5, but breed-dependent What additional vertebral measurement can assess LA size? Vertebral left atrial size (VLAS) On lateral, what is the hallmark of left atrial enlargement? Loss of caudal cardiac waist What causes tracheal carina elevation on lateral view? Severe LA enlargement pushing it dorsally What is mainstem bronchial compression? LA enlargement pressing on mainstem bronchi at the carina On DV/VD, what clock position corresponds to the LA appendage? 2-3 o'clock What two signs of LA enlargement are seen on DV/VD? 2-3 o'clock bulge (appendage) and "cowboy legs" (splayed mainstem bronchi) What is the "double wall" appearance? Superimposition of a large LA creating two visible borders on DV/VD How does LV enlargement appear on lateral view? Heart becomes taller How does LV enlargement appear on DV/VD? Apex displaced further left What indicates RV enlargement on lateral view? Increased sternal contact (>3 sternebrae) What indicates RV enlargement on DV/VD? Bulge at ~10-11 o'clock, or apex pushed leftward by RV On lateral view, what is the order of artery, bronchus, and vein (dorsal → ventral)? Artery, Bronchus, Vein What do you compare pulmonary vessel size to on lateral? Neck of the 4th rib On DV/VD, how do you identify pulmonary artery vs vein? Artery lateral to bronchus, vein medial What do enlarged pulmonary veins suggest? Left-sided CHF What do enlarged pulmonary arteries suggest? Pulmonary hypertension or heartworm disease What three findings are needed to diagnose left-sided CHF on radiographs in dogs? Enlarged LA, enlarged pulmonary veins, and pulmonary edema Where is pulmonary edema usually seen in dogs with CHF? Perihilar and caudodorsal lung fields In cats, what are the radiographic rules for CHF? Cardiomegaly may or may not be present, pulmonary vessels may or may not be enlarged, and edema can be patchy, anywhere in lungs. What non-cardiac diseases can mimic CHF signs in cats? Asthma, bronchitis, pneumonia, idiopathic pulmonary fibrosis What biomarker test helps differentiate CHF from respiratory disease in cats? NAP NT-proBNP (normal = not CHF) What are radiographic features of pulmonary hypertension? Right heart enlargement (RA bulge, RV sternal contact, apex leftward), and often small pulmonary arteries/veins. Classic presenting sign of dogs with severe pulmonary hypertension? Exertional collapse What drug is used to manage pulmonary hypertension? Sildenafil Why might greyhounds have large hearts without disease? Normal athletic cardiomegaly Most common heart disease in Cavaliers? Myxomatous mitral valve disease (MMVD) Most common heart disease in cats? Hypertrophic cardiomyopathy (HCM) What finding suggests right-sided CHF on rads? Enlarged caudal vena cava ± hepatomegaly/ascites What does the P wave represent? Atrial depolarization

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VM 565 Exam 1: Learning Objectives

What is heart disease?
structural/functional abnormality

What is heart failure
inadequate output or needs high filling pressures.

Compliance definition?
ΔV/ΔP (distensibility); stiffness = 1/compliance.

What is passive compliance?
the inherent elasticity and distensibility of blood vessels or heart chambers, allowing
them to expand and store blood without active muscle contraction

what is active compliance?
the dynamic ability of arteries to expand and contract, which can be altered or regulated
by smooth muscles in their walls.

What determines pressure in a segment?
≈ Volume ÷ Compliance (or Volume × Stiffness).

Equation for flow?
≈ ΔPressure ÷ Resistance.

Where is resistance clinically meaningful?
Precapillary arterioles (small radii).

Biggest determinant of resistance?
Radius^−4.

Normal valves → resistance?
Essentially negligible.

Preload mainly reflects...
Ventricular end-diastolic volume (filling).

Afterload approximated by...
(Systolic pressure × Radius) ÷ Wall thickness.

↑ Afterload → ESV?
Increases.

↑ Contractility → ESV?

,Decreases.

Cardiac output equation?
SV × HR

SV equation?
EDV – ESV

Effect of ↑ HR on diastolic filling?
Decreases (less time).

A-fib effect on pulses?
Irregular rate with variable/weak pulses due to variable filling.

Where is most blood volume?
Systemic veins.

Why do veins hold the most blood?
High compliance + large capacity.

Venoconstriction effect on RA flow?
↑ Venous pressure → ↑ VR to RA.

Angiotensin II effect on venous system?
↓ Compliance (↑ stiffness) → ↑ venous pressures.

Why do high venous pressures cause edema?
↑ Capillary hydrostatic pressure → ↑ filtration.

Left-sided failure edema location?
Lungs (pulmonary edema).

Right-sided failure edema location?
Systemic (legs/abdomen—ascites).

Lymphatics prevent edema until...
Filtration > lymph drainage capacity.

Concentric hypertrophy stimulus?
Pressure overload (↑ afterload).

Eccentric hypertrophy stimulus?
Volume overload (↑ preload).

Concentric outcome?
Wall thickening, relatively normal chamber size; normalizes wall stress.

, Eccentric outcome?
Chamber dilation with proportional wall mass increase.

MMVD (dogs) primary lesion → sequence?
Mitral regurg → volume overload → eccentric LV hypertrophy.

DCM core defect?
Primary contractile weakness → dilation + low forward output.

HCM core defect?
Primary myocardial thickening → diastolic dysfunction.

How DCM breaks compensation?
Fails to generate pressure; dilation worsens MR/volume overload → neurohormonal
drive.

Major systems in chronic HF?
RAAS, SNS, vasopressin.

Short term effects of neuroendocrine activation?
maintains BP

Long term effects of neuroendocrine activation?
fibrosis, Na/H2O retention, vasoconstriction.

Hypovolemia (dehydration) hemodynamics?
↓ Preload → ↓ SV/CO → hypotension.

Rapid fluid bolus effect on pressures?
Increases venous/arterial pressures (if compliance unchanged).

Renal hypoperfusion: two causes?
↓ Arterial pressure gradient or ↑ renal arteriolar resistance.

High venous pressures risk?
Edema upstream of the failing side.

Diuretics main hemodynamic effect?
↓ Volume → ↓ venous pressures → relieve edema

ACE inhibitors key effects?
↓ Ang II → vasodilation, ↓ venous stiffness, ↓ remodeling

Arteriolar vasodilators lower BP by...
↓ Precapillary resistance → ↓ arterial volume/pressure.

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