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Cardiovascular > Cardiovascular - physio, heart failure > Flashcards

Cardiovascular - physio, heart failure Flashcards

1
Q

CO equation

A

SV X HR

SV = end-diastolic volume - end-systolic volume

CO left heart = CO right heart

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2
Q

MAP equation

A

1/3 SBP + 2/3 DBP or (SBP + 2 DBP)/3 or DBP + (SBP-DBP)/3

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3
Q

4 humoral vasoconstrictor agents and 4 humoral agents causing vasodilation of arterioles

A
  • Norepinephrine, epinephrine, angiotensin II, vasopressin, serotonin, thromboxane A2
  • Bradykinin, histamine, prostaglandins (prostacyclin and E-series prostaglandins)
    (bradykinin and histamine cause VENOUS vasoCONSTRICTION)
  • histamine also increases capillary permeability
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4
Q

Blood flow equation

A

Q = (MAP - right atrial pressure) / total peripheral resistance

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5
Q

Poiseuille’s law

A

R = (8 * n * l)/ (pi * r^4)

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6
Q

Phases of ventricular action potential and ion currents

A

Phase 0 = depolarization = inward Na+
Phase 1 = early repolarization = outward K+
Phase 2 = plateau = inward Ca2+ and outward K+
Phase 3 = repolarization = outward K+
Phase 4 = resting membrane potential

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7
Q

Phases of SA node action potential and ion currents

A

Phase 0 = upstroke (depolarization) = inward Ca2+
Phase 3 = repolarization = outward K+
Phase 4 = slow depolarization = inward Na+ (funny current If)
No phase 1 and phase 2
Similar for AV node

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8
Q

Name the sympathetic and parasympathetic neurotransmitters and receptors on the heart

A

Sympathetic: catecholamines (norepinephrine) on beta1-receptors (Gs receptors)
- increases Ca2+ inward current during the plateau of the action potential –> increase contractility

Parasympathetic: acetylcholine on muscarinic receptors (Gi receptors)
- Decreases the inward Ca2+ current during the plateau

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9
Q

What are the parasympathetic receptors on the vessels and what is their action

A

Muscarinic M2 receptors located on the endothelial cells -> lead to NO release and vasodilation (mostly venous)

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10
Q

Describe phases of a normal ECG

A
  • P wave = atrial depolarization
  • PR interval = conduction velocity through AV node
  • QRS = ventricular depolarization
  • ST interval = period when ventricles are depolarized
  • T wave = ventricular repolarization

Atrial depolarization is buried in the QRS complex

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11
Q

Draw the left ventricle pressure-volume loop with phases of the cardiac cycle and closing / opening of valves. Show the effects of increased preload, increased afterload, increased contractility

A

Increased preload -> increased end-diastolic volume
Increased after load -> increased pressure at beginning of and during ejection + increased end-systolic volume (decreased stroke volume)
Increased contractility -> increased pressure during ejection with decreased end-systolic volume (increased SV)

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12
Q

Draw the cardiac function curve and systemic vascular function curve. Describe the parameters influencing each curve.

A

Parameters affecting cardiac function: preload, afterload, contractility
Parameters affecting systemic vascular function: systemic vascular resistance, blood volume, venus compliance

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13
Q

Which compartment contains stressed vs unstressed volume?

A

Stressed volume = blood volume contained in the arteries

Unstressed volume = blood volume contained in the veins

  • the veins contain the highest proportion of the blood in the CV system
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14
Q

Where is the highest resistance in the vascular system?

A

Arterioles

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15
Q

Describe each component of the vasculature with one term

A
  • Arteries = conduit vessels
  • Arterioles = resistance vessels
  • Capillaries = exchange vessels
  • Veins & venules = capacitance vessels
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16
Q

What are the 4 determining factors of transcapillary diffusion rate?

A
  • Concentration difference
  • Surface area for exchange
  • Diffusion distance
  • Capillary permeability
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17
Q

How is arteriolar resistance regulated?

A

By the autonomic nervous system

  • α1-Adrenergic receptors are found on the arterioles of the skin,
    splanchnic, and renal circulations.
    -> vasoconstriction
  • also found in the veins
  • β2-Adrenergic receptors are found on arterioles of skeletal muscle and coronaries.
    ->vasodilation
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18
Q

Velocity equation

A

V = blood flow / cross sectional area

Higher in the aorta than the sum of all capillaries (optimizing conditions for substance exchange)

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19
Q

When considering Poiseuilles’s law, which factors influence resistance and how do they do it?

A
  1. Viscosity - Resistance is directly proportional to viscosity
  2. Length of blood vessel - Resistance is directly proportional to length
  3. Radius of blood vessel - Resistance is inversely proportional to radius (to the power of 4! Huge influence on resistance)
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20
Q

Name the 2 main mechanisms of BP regulation and give their respective timing

A
  1. Baroreceptor reflex (very acute, min to min) - neurally mediated
  2. Renin-angiotensin-aldosterone system (slow, long-term) - hormonally regulated
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21
Q

Label Wiggers diagram

A

See picture

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22
Q

Label CVP curve (or right atrial pressure curve)

A

See picture

  • normal CVP is 0-8 cm H2O
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23
Q

What are the normal pressures within each compartment of the heart?

A
  • Aorta: 120/80
  • LV: 120/0
  • LA: 5/0
  • RA: 5/0
  • RV: 30/0
  • PA: 30/10
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24
Q

Where are the baroreceptors located

A

Carotid sinus (mostly) + some additional in aortic arch (responding to increases in BP only)

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25
Q

4 effects of baroreceptor reflex

A
  • Increased HR
  • Increased contractility (-> increased SV)
  • Vasoconstriction of arterioles
  • Vasoconstriction of veins
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26
Q

Describe steps leading to production of angiotensin-II (say where it happens)

A
  • Decreased in renal perfusion pressure -> decreased Cl delivery to macula densa -> renin secretion by juxtaglomerular cells of the afferent arteriole
  • Renin converts angiotensinogen to angiotensin I in plasma
  • Angiotensin-converting enzyme (ACE) converts angiotensin I to angiotensin II in lungs
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27
Q

4 effects of angiotensin II

A
  1. Stimulates secretion of aldosterone by the adrenal cortex (-> Na reabsorption in distal tubule, increase in blood volume)
  2. Increases Na-H exchange in proximal tubule (-> more Na reabsorption + contraction alkalosis)
  3. Increases thirst
  4. Vasoconstriction of arterioles
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28
Q

2 effects of vasopressin and respective receptors

A
  • Vasoconstriction of arterioles (V1 receptor)
  • Water reabsorption by distal tubule and collecting duct (V2 receptor)
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29
Q

3 effects of ANP

A
  • Relaxation of vascular smooth muscle (vasodilation)
  • Renal excretion of Na and water
  • Inhibits renin secretion
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30
Q

How can pCO2 and pO2 influence BP

A
  • Increased pCO2 in brain detected by chemoreceptors in vasomotor center -> peripheral vasoconstriction -> increased BP
  • Decreased pO2 in circulation detected by aortic and carotid chemoreceptors -> peripheral vasoconstriction -> increased BP
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31
Q

Starling’s equation

A

Jv = K[(Pc-Pi) - s(pc-pi)]

Jv = fluid movement (mL/min)
Kf = constant (filtration coefficient) (mL/min⋅mm Hg)
Pc = capillary hydrostatic pressure (mmHg)
Pi = interstitial hydrostatic pressure (mmHg)
s = protein reflection coefficient
pc = capillary oncotic pressure (mmHg)
pi = interstitial oncotic pressure (mmHg)

*
Jv positive = filtration (net fluid movement out of the capillary)
Jv negative = absorption (net fluid movement into the capillary)

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32
Q

What is normally the hydrostatic pressure in the interstitium?

A

0 or subatmospheric

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33
Q

Which factors increase capillary filtration?

A
  • Increased capillary hydrostatic pressure
  • Decreased interstitial hydrostatic pressure
  • Increased interstitial oncotic pressure
    Decreased capillary oncotic pressure
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34
Q

Most important control mechanism (local metabolic vs sympathetic) of the circulation of:
- heart (coronary)
- brain (cerebral)
- muscle
- skin
- lungs (pulmonary)

A
  • local metabolic (hypoxia, adenosine)
  • local metabolic (CO2, H+)
  • sympathetic at rest, local metabolic during exercise (lactate, K, adenosine)
  • sympathetic
  • local metabolic (O2)
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35
Q

How does CO2 and O2 influence arteriolar constriction?

A
  • Decreased O2 –> decreased arteriolar tone –> vasodilation –> increases blood flow and O2 delivery
  • Increased O2 –> increases arterial tone –> vasoconstriction –> reducing blood flow and O2 delivery
  • Increased CO2 —> arteriolar vasodilation
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36
Q

What organs have auto-regulation of BP

A

Brain, kidneys, heart
–> blood flow remains constant over a wide range of perfusion pressures

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37
Q

5 vasodilator metabolites

A

CO2, H+, K+, lactate, adenosine

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38
Q

How does nitric oxide lead to vasodilation?

A

By increasing levels of cGMP (cyclic guanosine monophosphate) which activates MLCP (myosin light chain phosphatase) which relaxes the actin-myosin complex

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39
Q

Describe compensatory mechanisms at play during hemorrhage

A
  • Decreased blood volume -> decreased CO and decreased BP
  • Hypotension sensed by carotid sinus baroreceptors -> baroreflex -> increased sympathetic tone and decreased parasympathetic tone -> increased HR, increased contractility, arteriolar constriction (except coronary / cerebral perfusion), venous constriction –> response of the vasomotor center to increase MAP back to set point (100 mmHg)
  • Hypoxia sensed by carotid and aortic chemoreceptors -> increased sympathetic tone
  • Cerebral ischemia -> increased cerebral pCO2 sensed by chemoreceptors in vasomotor center -> increased sympathetic tone
  • Decreased Pc -> capillary reabsorption favored
  • Hypotension -> secretion of epinephrine and norepinephrine by adrenal medulla
  • Decreased renal perfusion -> activation of RAAS -> vasoconstriction (angiotensin II), Na reabsorption (angiotensin II + aldosterone)
  • Hypotension sensed by carotid sinus baroreceptors ->ADH secretion -> vasoconstriction + water reabsorption
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40
Q

How does vasopressin (ADH) increase blood pressure (2)?

A
  1. Activation of V1 receptors on the arterioles –> vasoconstriction
  2. Activation of V2 receptors –> increased water reabsorption by the renal distal tubule and collecting ducts
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41
Q

Name the nerves of the afferent pathway for the carotid sinus and aortic baroreceptors

A
  • Carotid: Hering’s nerves and glossopharyngeal nerves (cranial nerve IX)
  • Aortic: vagus nerve (CN X)
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42
Q

2 stimuli for ADH release (which one is the most sensitive)

A
  • Increased plasma osmolality (as little as 1% change)
  • Decreased effective circulating blood volume (10 times more sensitive and potent)
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43
Q

Where is the signal from arterial baroreceptors integrated

A

In the medullary vasomotor center (in medulla oblongata). Afferent information integrated in nucleus tractus solitarius)

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44
Q

Cite negative consequences of RAAS activation in heart failure

A
  • Sodium and water retention
  • Myocardial and vascular fibrosis
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45
Q

Cite negative consequences of sympathetic nervous system activation in heart failure

A
  • Persistent tachycardia
  • Increased myocardial oxygen demand
  • Myocyte necrosis
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46
Q

What neurohormonal systems are involved in heart failure

A
  • RAAS
  • SNS
  • Natriuretic peptide system
  • Endothelin and vasopressin systems
  • Amplified expression of proinflammatory cytokines (IL-1, IL-6, TNF-alpha)
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47
Q

Cite negative consequences of endothelin I in heart failure

A
  • Vasoconstriction
  • Toxicity to cardiomyocytes
  • Altered calcium cycling
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48
Q

Describe the mechanism of cardiomyocyte contraction in response to the action potential

A
  • Ca2+ influx into myocyte leads to secretion of more Ca2+ from sarcoplasmic reticulum (ryanodine receptor)
  • Ca2+ binds troponin C on the actin-myosin complex, which releases tropomyosin and allows myosin binding to actin leading to sarcomere contraction.
  • Then Ca2+ is sequestered back into the reticulum through the SERCA (sarcoplasmic endoplasmic reticulum Ca2+-ATPase) channel under the influence of phospholamban and there is muscle relaxation
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49
Q

What are the 4 clinical stages of heart failure? At what stage is treatment initiation indicated?

A
  • Stage A = healthy animals at risk
  • Stage B = animals with evidence of heart disease without clinical signs (B1 = little evidence of cardiac remodelling / B2 = significant evidence of remodelling, usually moderate to severe LA enlargement)
  • Stage C = current or historical clinical signs of heart failure
  • Stage D = severe signs of heart failure even at rest / refractory to treatment

Treatment should be initiated in stage B2

50
Q

What are the 3 stages of cardiac remodeling?

A

Initial stage: hypertrophy develops in response to increased wall stress

Compensated stage: wall stress is normalized by the hypertrophy

Exhaustion stage: death of cardiomyocytes, fibrosis, ventricular dilation, reduced CO

51
Q

Using Laplace’s law, explain cardiac remodeling.

A

The wall stress or wall tension is equal to the pressure generated by the contracting ventricle X the radius of the ventricle, divided by the wall thickness.

  • Pressure overloads are compensated by increased wall thickness in the aims to normalize wall stress
  • Volume overload, is characterized by an enlarged chamber and only a modest increase in wall thickness, sufficient to normalize wall stress.
  • Wall stress is increased in patients with heart failure due to dilated cardiomyopathy as the chamber dimensions increase disproportionately to wall thickness
52
Q

What is the primary predisposing factor of myocardial infarction in veterinary patients

A

Hypercoagulable state

53
Q

What is the best biomarker of myocardial injury? What is the timing of increase?

A

Troponin I

Increases 2-4h after injury, peaks 18-24h after, can be increased for up to 14 days

54
Q

What is the gene associated with HCM in cats? In what breeds?

A

MYBP3 in Maine Coons and Ragdolls

55
Q

5 phenotypes of cardiomyopathies in cats

A
  • Hypertrophic cardiomyopathy
  • Dilated cardiomyopathy
  • Restrictive cardiomyopathy (endomyocardial form and myocardial form)
  • Arrhythmogenic right ventricular cardiomyopathy
  • Nonspecific cardiomyopathy
56
Q

Cite underlying diseases predisposing to HCM (6) and DCM (2)

A
  • HCM: hypertension, neoplastic myocardial infiltration, transient myocardial thickening, inflammatory myocardial infiltration, acromegaly, hyperthyroidism (* can also predispose to RCM and nonspecific CM)
  • DCM: taurine deficiency, chronic tachycardia
57
Q

What is the prevalence of CHF in cats with HCM? Of ATE?

A

24% and 11%

58
Q

What are ATE risk factors in cats with heart disease that are an indication for thromboprophylaxis?

A
  • Moderate to severe LA dilation
  • Reduced LA function (FS%)
  • Reduces auricular appendage velocity
  • Spontaneous echo contrast within the LA
59
Q

True or false: dynamic left ventricular outflow tract obstruction (DLVOTO) is associated with a worse prognosis in cats with HCM

A

False

60
Q

What vertebral scores have been associated with CHF in cats?

A

Score > 9.3 highly suggestive of severe cardiomyopathy ; score < 8 unlikely to be associated with CHF

61
Q

What is the Se and Sp of POC NT-proBNP assay to identify CHF in cats with respiratory distress?

A

Se 94%, Sp 72%

62
Q

What could be indications and contra-indications of pimobendan use in cats with CHF?

A

Indications: hypotension, bradycardia, decreased contractility

Contra-indications: DLVOTO (suspected if murmur of grade IV or higher)

63
Q

What LV wall thickness is indicative of hypertrophy in cats?

A

> or = 6mm

< 5mm is considered normal

64
Q

Which 2 factors increase blood turbulence?

A
  1. Decreased blood viscosity (ex: anemia)
  2. Increased blood velocity (ex: narrowing of a vessel)
65
Q

What are the mean pressures in the different compartments of the systemic circulation?

A
  • Aorta: 100 mmHg
  • Arterioles: 50 mmHg
  • Capillaries: 20 mmHg
  • Vena cava: 4 mmHg
66
Q

What is the most important determinant of pulse pressure?

A

Stroke volume

As blood is ejected from the left ventricle into the arterial system, arterial pressure increases because of the relatively low capacitance of the arteries. Because diastolic pressure remains unchanged during ventricular systole, the pulse pressure increases to the same extent as the systolic pressure

67
Q

What is pulse pressure?

A

SBP - DBP

68
Q

What surrogate is used to measure left atrial pressure?

A

Pulmonary wedge pressure - A catheter, inserted into the smallest branches of the pulmonary artery,
makes almost direct contact with the pulmonary capillaries. The measured pulmonary capillary pressure is approximately equal to the left atrial pressure.

69
Q

Which 2 organs can withstand a decrease in blood flow?

A

Kidneys and lungs as they recondition blood condition, therefore the blood flow to these organs is increased to meet their metabolic needs and they can withstand a decrease in blood flow

*Other organs such as brain, myocardium and skeletal muscles receive blood flow solely to supply metabolic needs, therefore, do not tolerate blood flow interruptions

70
Q

Describe the Fick principle

A

X (rate of transport) = Q (blood flow) x (Xa (arterial concentration) - Xv (venous concentration))

Determines tissue consumption or production of a substance - rate of substance loss from blood within a tissue equals the rate of metabolism within that tissue.

71
Q

Name 5 requirements for effective operation of the heart

A
  1. No arrhythmia
  2. No stenosis
  3. No insufficiency or regurgitation
  4. No failure
  5. Adequate ventricular filling during diastole
72
Q

List causes of secondary DCM in the dog (6)

A
  • Nutritionally mediated (taurine deficiency, L-carnitine deficiency)
  • Myocarditis (infectious / non-infectious)
  • HypoT4
  • Hypoadrenocorticism
  • Tachycardia-induced cardiomyopathy
  • Doxorubicin
73
Q

Which medications can delay the occurrence of CHF in dogs with DCM?

A

Pimobendan (delays by 9 months) and ACE inhibitors (delays by 3 months).
Beta-blockers have no proven benefit.

74
Q

What are the 2 major dog breeds affected by DCM? (+ prevalence for each)

A
  • Doberman Pinschers (prevalence 45-63%)
  • Great Danes (prevalence 4-12%)

(- Others: Irish Wolfhounds, Newfoundlands, Golden Retrievers, etc)

75
Q

What breeds are more susceptible to nutritionally mediated DCM?

A

Golden Retriever, American Cocker Spaniel, Newfoundland

76
Q

What are the 3 types of ARVC?

A
  • Type I = subclinical ventricular arrhythmias
  • Type II = ventricular arrhythmias and syncope
  • Type III = structural cardiac changes and CHF (*usually left sided although arrhythmias originate from the the right)
77
Q

What is the diagnostic criteria for ARVC?

A

At least 300 VPCs on 24-h Holter

78
Q

List complications of MMVD

A
  • CHF
  • LA tear -> pericardial effusion with cardiac tamponnade or atrial septal defect with left-to-right shunting
  • Pulmonary hypertension (-> right heart failure)
  • Supraventricular and ventricular arrhythmias
79
Q

What vertebral heart score (VHS) and vertebral left atrial size (VLAS) are suggestive of significant cardiomegaly in a dog with MMVD?

A

VHS >/= 11.5 or VLAS >/= 3.0

(* counted from the cranial edged of the 4th vertebra)

80
Q

List vasodilator therapies that can be used in the management of CHF due to MMVD

A
  • Pimobendan (venodilator)
  • Sodium nitroprusside
  • Clevidipine (Ca-channel blocker)
  • Hydralazine
  • Amlodipine
81
Q

What is the life expectancy of a dog with MMVD following its first episode of HF?

A

6-18 months (one study reported 9 months median survival time)

82
Q

What are the 7 mechanisms of blunt cardiac trauma

A
  • Direct impact to the chest at end diastole (ventricles) or end systole (atria)
  • Sudden increase in preload due to impact to peripheral or abdominal vessels
  • Bidirectionnal forces compressing the heart within the thoracic cage
  • Forces of acceleration and deceleration causing the heart to move (damage to myocardium / large vessels / coronary arteries)
  • Blast forces leading to cardiac contusion or rupture
  • Concussive forces leading to arrhythmias
  • Cardiac penetration by displaced fractures
83
Q

List 6 types of blunt cardiac injury

A
  • Myocardial rupture
  • Septal injury
  • Pericardial laceration
  • Valve rupture
  • Myocardial contusion (hemorrhagic form, necrotized form, or mixed)
  • Commotio cordis
84
Q

What are the 3 forms of myocardial contusions?

A
  1. Hemorrhagic form - extravasation of blood without muscle fibre disruption
  2. Necrotized form - coagulation necrosis / contraction band necrosis of the muscle fibers
  3. Mixed form
85
Q

What is the mechanism of arrhythmia provocation in myocardial contusion?

A

Induction of an electrically silent region of myocardium leading to initiation of reentrant circuit around this silent region –> inciting development of tachyarrhythmias (most commonly ventricular)

86
Q

What is the mechanism of commotio cordis?

A

Blunt impact to precordium within 15-30 msec before peak T wave leading to R on T, Vfib, and cardiac death

  • absence of histopathologic change to the myocardium
87
Q

Describe the sequence of invents in contraction of smooth muscle

A
  1. Depolarization of the cell membrane opens voltage-gated Ca2+ channels and Ca2+ flows into the cell down its electrochemical gradient, increasing the intracellular [Ca2+]. Hormones and neurotransmitters may open ligand-gated Ca2+ channels in the cell membrane. Ca2+ entering the cell causes release of more Ca2+ from the SR in a process called Ca2+- induced Ca2+ release. Hormones and neurotransmitters also directly release Ca2+ from the SR (sarcoplasmic reticulum) through inositol 1,4,5-trisphosphate (IP3)–gated Ca2+ channels.
  2. Intracellular [Ca2+] increases.
  3. Ca2+ binds to calmodulin. The Ca2+–calmodulin complex binds to and activates myosin light chain kinase (MLCK). When activated, myosin light chain kinase phosphorylates myosin and allows it to bind to actin, thus initiating cross-bridge cycling. The amount of tension produced is proportional to the intracellular Ca2+ concentration.
  4. A decrease in intracellular [Ca2+] produces relaxation.
88
Q

Describe the types of pericardial effusion, their characteristics and name a few differentials

A
  • Hemorrhagic (PCV>7%, SG>1.015, TP>3g/dL) => hemangiosarcoma, heart base tumour, pericardial mesothelioma, metastatic carcinoma, malignant histiocytosis, idiopathic
  • Transudate (pure: <1000cells/uL, SG<1.012, TP<2.5g/dL / modified: 1000-8000cells/uL, SG 1.015-1.030, TP 2.5-5g/dL) => CHF, hypoalbuminemia, increased vascular permeability (inflammation, toxin), congenital
  • Exudate (»3000cells/uL, SG>1.015, TP»3g/dL) => infection from migrating FB, bite, mediastinitis, FIP, lepto, Distemper
89
Q

What infectious agents are involved in pericardial effusion

A

Actinomyces, coccidioidomyces, aspergillus, lepto, tuberculosis, FIP, Distemper

90
Q

Explain pulsus paradoxus

A
  • Spontaneous inspiration -> decreased intrathoracic pressure -> decreased RA pressure -> increased venous return to right heart -> increased pulmonary blood flow
  • This causes a decrease in left heart filling (blood held in pulmonary vasculature and inter ventricular septum shifted to the left) -> decrease in arterial pressure during inspiration
  • Opposite effects during expiration
  • Pulsus paradoxus = exaggeration of this phenomenon when cardiac tamponade is present due to impaired venous return to the right heart and inability for the left ventricle to expand
91
Q

What ECG findings are suggestive of cardiac tamponade

A
  • Sinus tachycardia
  • Reduced QRS amplitude and electrical alternans +/- ST segment elevation
  • Possible atrial and ventricular arrhythmias
92
Q

What biomarker can be used to help identify HSA in dogs with pericardial effusion

A
  • cTnI in blood or pericardial fluid
  • Se 81% and Sp 100% for HSA when >0.25 ng/nL
93
Q

What are the 5 determinants of stroke volume?

A
  • Heart rate
  • Preload
  • Afterload
  • Compliance
  • Contractility
94
Q

Ejection fraction formula

A

Ejection fraction = SV/EDV

Normally 55%

95
Q

Name 4 factors that increase cardiac O2 consumption

A
  1. Increased afterload
  2. Increased size of the heart
  3. Increased contractility
  4. Increased heart rate
96
Q

Which troponins are specific to the cardiac muscle? Which one is used as a biomarker

A

Cardiac troponin I (cTnI) and cardiac troponin T (cTnT).

cTnI is used as a biomarker

97
Q

How to interpret NT-proBNP concentrations in a context of respiratory distress? What about the NT-proBNP ELISA?

A
  • NT-proBNP < 900 pmol/L in dogs or < 270 pmol/L in cats -> CHF unlikely
  • NT-proBNP > 1800 pmol/L in dogs or > 270 pmol/L in cats -> CHF likely

ELISA: established for a cut-off of 100 pmol/L (designed to diagnose occult cardiac disease) -> CHF unlikely if negative but unsure if positive (Se 93-100%, Sp 72-87%)

98
Q

What are the main uses of cTnI as a biomarker

A
  • Diagnosis of myocarditis (increased 10-100-fold)
  • Prognostic value in dogs with MMVD and DCM and cats with HCM
99
Q

What are extra-cardiac causes of increase in NT-proBNP and cTnI

A

Renal disease, systemic hypertension, hyperT4, IV fluid administration, pulmonary hypertension for NT-proBNP

100
Q

What is the normal blood pressure for dogs and cats

A

Dogs: SBP 150 +/- 20 mmHg, MAP 105 +/- 10, DBP 85 +/- 10
Cats: SBP 125 +/- 10, MAP 105 +/- 10, DBP 90 +/- 10

101
Q

What are the determinants of blood pressure (6)

A
  • Blood volume
  • Venous compliance
  • Afterload
  • Inotropy
  • HR
  • Systemic vascular resistance
102
Q

Draw the Frank-Starling curve and how it is affected in disease state and exercise. Explain how diuretics, vasodilators (arterial vs venous) and positive inotropes affect the curve.

A

see picture

103
Q

Beyond what pulmonary and systemic venous pressure can signs of congestion be seen?

A
  • Pulmonary venous pressure > 25 mmHg
  • Systemic venous pressure > 20 mmHg
104
Q

Describe SAM

A

Systolic anterior motion of the mitral valve occurs when the valve moves and makes contact with the inter ventricular septum during systole, impeding blood flow to the LV outflow tract

105
Q

What are causes of low / high pulse pressure?

A

Low:
- Cardiac tamponnade
- Tension pneumothorax
- Heart failure
- Aortic stenosis
- Hypovolemia

High:
- Aortic regurgitation
- Anemia
- Hyper T4
- Intracranial hypertension
- Endurance

106
Q

What is the coronary perfusion pressure

A

Diastolic aortic pressure - left ventricular end-diastolic pressure

(During CPR, diastolic aortic pressure - right atrial end-diastolic pressure because ventricular pressure very low)

107
Q

What are the normal / abnormal heart sounds and what do they reflect

A

Normal:
- S1 = closure of atrioventricular valves
- S2 = closure of semilunar (aortic and pulmonic) valves

Abnormal:
- S3 (just after S2) = ventricular gallop (can indicate ventricular failure / DCM)
- S4 (just before S1) = atrial gallop (indicates diastolic resistance, possibly HCM)
- Splitting of S2 = non-synchronized closure of aortic and pulmonic valve (possibly pulmonary hypertension)
- Systolic clic = mitral valve prolapse

108
Q

What amino-acid are catecholamines derived from

A

Tyrosine (converted to DOPA via tyrosine hydroxylase)

109
Q

What are the different receptors and neurotransmitters of the sympathetic nervous system

A

Pre-ganglionic nerve is always acetylcholine on nicotinic receptor.

Post-ganglionic nerve can be:
- adrenergic -> norepinephrine on alpha or beta adrenergic receptor (heart, vessels)
- dopaminergic -> dopamine on D1 receptor (in kidneys mostly)
- cholinergic -> ACh on muscarinic receptor (sweat glands and some vessels)

Also triggers epi and norepi release from adrenals

110
Q

What is the difference between sympathetic and parasympathetic pre-ganglionic neurons

A

Parasympathetic pre-ganglionic neurons are long (short post-ganglionic). Opposite for sympathetic.
Both use Ach on nicotinic receptors.

111
Q

To what large family of receptors belong the adrenergic receptors and what are the 3 types

A

G-protein coupled receptors: inhibitory Gi (decrease cAMP concentration), stimulatory Gs (increase cAMP concentration), or Gq (activate phospholipase C -> IP3 pathway)

112
Q

What type of phosphodiesterase(s) is/are present in the vessels

A

Phosphodiesterase 3 in most vessels, phosphodiesterase 5 in pulmonary vessels (and corpus cavernosum)

113
Q

What is the effect of phosphodiesterases

A

Hydrolysis of cAMP and/or cGMP

114
Q

What amino-acid is NO made from

A

L-arginine

115
Q

What happens to the ejection fraction in systolic vs diastolic heart failure?

A

Systolic: low EF
Diastolic: normal EF

116
Q

What is the name of the sarcoplasmic iCa channel leading to iCa release / recapture

A
  • Release = ryanodine receptor
  • Recapture = SERCA (sarcoplasmic / endoplasmic reticulum Ca2+ ATPase)
117
Q

Explain beta-receptor down regulation

A

When beta-receptors are bound to an agonist, they become internalized and removed by beta-ARK -> when there is a prolonged / excessive sympathetic stimulation, beta receptors are down-regulated and myocardial function decreases

118
Q

What are criteria to initiate treatment in dogs with myxomatous mitral valve disease and what treatment should be initiated

A

Initiate in stage B2:
- Murmur grade ≥ 3/6
- LA:Ao ratio ≥ 1.6
- Left ventricular internal diameter in diastole (normalized to body weight) ≥ 1.7
- Breed adjusted radiographic VHS > 10.5
(Ideally all criteria should be met, echocardiographic criteria are most important)

  • Pimobendan 0.25-0.3 mg/kg PO q12
  • Mild dietary sodium restriction
    +/- ACE inhibitors (if severe cardiac changes)
    (Spironolactone not recommended in consensus)
119
Q

What therapeutic requirement defines stage D of MMVD

A

Need for furosemide > 8 mg/kg/day in the face of appropriate dosage of pimobendan, ACE inhibitor, and spironolactone

120
Q

What additional treatments can be considered for a patient with stage D MMVD

A
  • Increase furosemide / switch to torsemide
  • Add hydrochlorothiazide (risk of kidney injury)
  • Increase pimobendan to 0.3 mg/kg q8
  • Arterial vasodilators: sodium nitroprusside, hydralazine / amlodipine
  • Dobutamine
  • Sildenafil if evidence of clinical pulmonary hypertension (syncope, cough)
  • Diltiazem / digoxin if concurrent Afib

Cardiovascular (8 decks)

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