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Veterinary Cardiology > General > Flashcards

General Flashcards

1
Q

Brody Effect

A

Increase in QRS-wave amplitude induced by an increase in ventricular preload

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2
Q

Post-extrasystolic potentiation

A

Increase in contractility in the beat that follows an extrasystole (PVC or PAC)

Compensatory pause follows an extrasystole due to failure to reset SA node which leads to a longer diastolic interval which augments ventricular filling and subsequently, contractility

May identify on Doppler, pressure tracings, etc.

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3
Q

Branham Sign

A

A decrease in heart rate (HR) and an increase in blood pressure after the sudden occlusion of arteriovenous fistula (most commonly PDA)

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4
Q

Bainbridge Reflex

A

Increase in CVP and atrial pressures stimulates stretch receptors in the atria at the venoatrial junction. Signal is carried to the brain via B-fibers (afferent limb), then returns via vagus and sympathetic fibers (efferent limb). Lowers PS tone and increase S tone to increase HR. Contributes to RSA in the dog

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5
Q

Bezold-Jarisch Effect

A

A triad of responses (bradycardia, hypotension, and apnea) which occurs via mechanical or pharmacological activation of non-myelinated vagus nerve fibers (C-fibers) that line the ventricles.

I.e. “empty ventricle syndrome”

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6
Q

Bernheim Syndrome

A

Severe left heart disease causes bulging of the IVS/compression of the RV lumen leading to elevated right-sided pressures and right-CHF

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7
Q

Reverse Bernheim Effect

A

Severe right-sided heart disease causes bulging of the IVS towards the LV lumen and causes left-CHF

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8
Q

R2A Anomaly

A

Since right coronary artery (RCA) branches off of the right sinus of Valsalva behind the right aortic valve cusp. The circumpulmonary segment of the left main CA in the R2A pattern in dogs branches shortly after the aorta and encircles the MPA, causing external compression of the pulmonary outflow tract and clinical signs of pulmonic stenosis at the subvalvular level.

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9
Q

Normal Coronary Anatomy

A

Coronary artery (CA) patterns in dogs and humans are similar. The left and right main CA originate from the left and right sinuses of Valsalva behind the respective leaflets of the aortic valve. The right CA extends around the right atrioventricular groove and supplies the posterior descending (subsinuosal) CA in over half of human patients. In dogs, the left main CA bifurcates 2-10 mm beyond its origin into the left circumflex artery (LCx) and the paraconal (left anterior descending) CA. Dogs almost always have a dominant left CA pattern; i.e. the LCx supplies the subsinuosal (posterior descending) artery. In addition, many dogs have a large ventricular septal artery that originates near the bifurcation of the left main CA and supplies a major portion of the interventricular septum.

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10
Q

Coanda Effect

A

The tendency of a fluid jet to stay attached to a convex surface. Results in underestimated Color flow jets when there is an eccentric/wall-hugging jet

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11
Q

Entrainment

A

Phenonenon where red blood cells adjacent to a regurgitant jet are incorporated into/swept along the flow, leading to impression of greater color Doppler jet area. Seen commonly with central MR jets or multiple jets

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12
Q

Bix Rule

A

Whenever a P wave falls directly between two QRS complexes, SVT with 2:1 conduction should be suspected

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13
Q

Stokes-Adams Seizures

A

Syncope and seizures of cardiac origin

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14
Q

Acrocyanosis

A

Cyanosis to tips of extremities (ears, digits, etc.)

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15
Q

Kussmaul sign

A

Rise in RA (CVC) pressure, or failure to decrease, with inspiration. Seen with constrictive pericarditis, restrictive cardiomyopathy, pulmonary embolism, RV infarction, and advanced systolic heart failure

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16
Q

Corrigan’s pulse

A

Similar to water hammer pulse, wide pulse pressure due to diastolic regurgitation; seen with severe AI

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17
Q

Myofiber

A

Group of myocytes held together by collagen

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18
Q

Myoctye

A

Functional cell of the cardiac muscle

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19
Q

Myofibril

A

The contractile elements of the myocytes, made up of actin and myosin strands

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20
Q

Afterload - definition and what is it determined by

A

Definition: The sum of all forces that oppose ejection of blood from the ventricles, i.e. the systolic tension or wall stress experienced by the ventricles during ejection

Determined by: SVR, compliance of the arterial tree, volume of blood in the ventricle at onset of systole, inertia of the blood column, resistance to flow through outflow tracts (i.e. PS, SAS, HOCM)

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21
Q

High-output CHF causes

A

Anemia, hyperthyroidism, pregnancy

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22
Q

How does B1 activation on the heart increase HR?

A

Increases slow inward calcium current (ICaL) to increase firing rate of SA node and shifts activation curve of the inward pacemaker current (If) to more positive voltages

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23
Q

Determinants of CO?

A

Preload, afterload, HR, contractility, ventricular synchrony

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24
Q

Myocardial contractility- definition and what increases it

A

Intrinsic force of contraction of the moycardium independent of loading conditions

Increased by beta adrenergic stimulation, catecholamines, HR, and afterload

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25
Q

Chronic ill effects of beta stimulation?

A

Depleted myocardial energy stores, increased afterload
Down-regulation of Beta receptors (reduced mRNA transcription)
Depletion of cardiac NE reserves
Increased myocardial expression of BARK, uncouples B1 and B2 receptors from G proteins
Circulating NE levels are high (poor prognostic indicator)
Myocyte hypertrophy
Myocyte necrosis, apoptosis, and fibrosis
Arrhythmias
Diastolic dysfunction
Increased tubular Na resorption
RAAS activation
Increased renal vascular resistance
Decreased response to natriuretic peptides
Increased renin release
Neurogenic vasoconstriction
Vascular hypertrophy

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26
Q

Causes for renin release?

A

Decreased renal perfusion
Decreased sodium/chloride filtration at macula densa
Beta1 stimulation

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27
Q

What does ACE do?

A

Converts ATI to ATII, but also breaks down bradykinin

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28
Q

Other enzymes that convert ATI to ATII

A 
Chymase (most important) 
Cathepsin G
Elastase
TPA
CAGE
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29
Q

Functions of ATII

A

Potent vasoconstrictor
Promotes Na and H20 resorption via direct effects on distal tubules
Stimulates aldosterone release

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30
Q

Causes of beta sympathetic stimulation

A

Loss of inhibitory signals from high-pressure carotid sinus (due to drop in BP) and low-pressure cardiopulmonary receptors (due to increase in cardiac/pulmonary pressures)

Increase in excitatory signals from nonbaroreflex peripheral chemoreceptors and miscle metaboreceptors

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31
Q

ATII receptors - what happens when ATII binds to each

A

ATI - predominant in vasculature and nerves of myocardium, leads to vasoconstriction, cell growth, aldosterone secretion, catecholamine release

ATII - leads to myocardial fibrosis, further release of NE

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32
Q

Causes of aldosterone release

A

ATII
Hyperkalemia
ACTH
Other messengers (catecholamines, ET1, AVP)

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33
Q

MOA of aldosterone

A

Acts on epithelial cells in distal collecting ducts to increase Na resorption and K secretion

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34
Q

Harmful effects of aldosterone

A

Provokes hypertrophy and fibrosis within vasculature and myocardium
Provoke endothelial cell dysfunction
Baroreceptor dysfunction
Inhibits NE reuptake

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35
Q

Sources for ROS in the heart

A

Mitchondria
Xanthine oxidase
NADPH oxidase

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36
Q

Antioxidants in the heart

A

Manganese superoxide dimutase (MnSOD)
Catalase and Glutathione peroxidase
Glutathione reductase (GR)

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37
Q

Stimulus for release of ADH/AVP

A

Increased plasma osmolality
Hypovolemia (decreased firing of stretch receptors in atria and large veins)
SNS

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38
Q

ADH receptors/function

A

V1a - found in vascular smooth mm/cardiac mm, leads to vasoconstriction, platelet aggregation, stim of myocardial GF, inotropic effects

V2 - epithelial cells of ascending limb and collecting duct, aquaporins inserted to retain free water

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39
Q

What are the vaptan drugs? Which are specific for which receptors?

A

V1a - relcovaptan
V2 - tolvaptan, lixivaptan
V1a/V2 - conivaptan

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40
Q

Effects of ANP/BNP?

A

Induce natriuresis through binding to NPR-A receptors in collecting duct
Vasodilation of systemic/pulmonary circulation (NPR-B)
Direct inhibition of renin production

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41
Q

Function of Endothelin-1 when binding to ETA and ETB receptorts

A

ETA - vasoconstriction, cell proliferation, increased contractility, aldosterone secretion, inhibits NO production

ETB - Increased NO production (vasodilation), aldosterone production

Leads to net decrease in BP, then increase, suppresses renin release, stimulates aldosterone

42
Q

Stimulus for ET-1 release

A

Hypoxia, stretch, low shear force, ATII, AVP, NE, bradykinin, transforming growth factor beta, TNF-a, IL-1

43
Q

What is neuropeptide Y?

A

Vasoconstricting peptide, released with NE from sympathetic nerve endings, potentiates vasoconstriction of other agents (i.e. NE, ATII, etc.)

44
Q

Nitric oxide effects on the vasculature and on cardiac tissue

A

NO activates guanylate cyclase, leads to production of cGMP which activates protein kinase G, which leads to smooth mm relaxation (vasodilation), modulates calcium channels involved in excitation-contraction coupling, alters mitochondrial respiratory complexes

45
Q

What does bradykinin do?

A

Causes vasodilation

46
Q

What is adrenomedullin?

A

Binds a number of G-protein coupled receptors, leads to vasodilation and opposes excessive vasoconstriction and vascular remodeling

47
Q

What is apelin?

A

NO-mediated vasorelaxation, potent positive inotrope w/o causing significant hypertrophy

48
Q

What are the important inflammatory cytokines released during CHF?

A

TNF-a, IL-1, IL-6

49
Q

Law of Laplace?

A

Wall stress = pressure x radius / 2 x wall thickness

50
Q

Three phases of pathologic hypertrophy?

A
  1. Hypertrophy develops in response to increased wall stress
  2. Wall stress normalized by hypertrophy (compensated state
  3. Exhaustion phase (death of myocytes, myocardial fibrosis, ventricular dilation, reduced CO)
51
Q

PCWP generally required for pulmonary congestion to occur?

A

25 mmHg

52
Q

CVP generally required for ascites to occur?

A

15 mmHg

53
Q

Stimuli for expression of fetal genes in the heart?

A 
Mechanical stretch of myocyte
Neurohormones (NE, ATII)
Cytokines (TNF-a, IL-6)
Endothelin
ROS
54
Q

What is a left ventricular heave?

A

Movement of the thoracic wall due to heart motion

55
Q

What causes physiologic splitting of S1

A

Inspiration leads to increased RV filling, RV ejection is longer so P2 is later than A2

56
Q

Pathologic causes of delayed P2?

A 
Left-to-right shunt
PH (HWD)
PS
R-BBB
VPC's (with R-BBB morphology)
Dilated PA
57
Q

Pathologic cause of early A2?

A

MR, MS, LA tumor

58
Q

Pathologic cause of delayed A2 (paradoxical split S2)?

A 
AS
L-BBB
PDA
VPC's (L-BBB morphology)
Hypertension
59
Q

What determines loudness of S1?

A

Body condition (loud in thin animals, soft in fat), HR (louder with tachycardia), sympathetic tone (louder with high tone), BP (accentuated with hypertension), accentuated with anemia/MR, attenuated with hernia, effusion, shock, myocardial depression

60
Q

What causes a split S1?

A

May be normal in some big dogs
BBB
MS/TS

61
Q

What is an ejection click?

A

High-frequency, early systolic sound over PV/AoV, suggestive of SAS, PS, ToF, HWD
Not heard on auscultation, only seen on phono

62
Q

What is a friction rub?

A

High-frequency sound, louder with inspiration, heard over left sternal border and highly specific for acute pericarditis

63
Q

What are some causes of pulsus paradoxus?

A

Pericardial effusion, RCM, CP, pulmonary disease, PTE, shock

64
Q

What causes a bifid pulse (pulsus bisferiens)?

A

HOCM, mixed AV disease, exercise, fever

65
Q

What is Reynold’s number?

A

(Radius)(Velocity)(Density) / (Viscosity)

When number rises above threshold, turbulent flow occurs

66
Q

What is a forme fruste?

A

Ductal remnant/ductus diverticulum

67
Q

What is a Graham Steel murmur?

A

Soft, high frequency diastolic murmur from pulmonic insufficiency

68
Q

What is the duct of Botalli?

A

Another name for ductus arteriosus

69
Q

What is Chung’s effect?

A

The P wave following a premature atrial complex is wider and lower amplitude due to aberrant atrial conduction

70
Q

What is Ashman’s phenomenon?

A

A long R-R interval causes a prolonged AP duration in the subsequent beat, making it susceptible to aberrant conduction. Long-short aberrancy, seen commonly with AF and sometimes other SVT’s

71
Q

Normal P wave amplitude in a dog?

A

<0.4 mV

72
Q

Normal P wave amplitude in a cat?

A

<0.2 mV

73
Q

Normal P wave duration in a dog?

A

<40 mS

74
Q

Normal P wave duration in a cat?

A

< 35 mS

75
Q

Normal PQ interval in a dog?

A

60-130 mS

76
Q

Normal PQ interval in a cat?

A

50-90 mS

77
Q

Normal QRS duration in a dog?

A

<70 mS

78
Q

Normal QRS duration in a cat?

A

<40 mS

79
Q

Normal QT interval in a dog?

A

150-240 mS

80
Q

Normal QT interval in a cat?

A

160-220 mS

81
Q

What cardiac defect are Persians overrepresented for?

A

AVSD

82
Q

What cardiac defects are Chartreux cats overrepresented for?

A

TVD, ASD

83
Q

What cardiac defects are Siamese overrepresented for?

A

SVMS, endocardial fibroelastosis, AS

84
Q

What defect can Griseofulvin cause?

A

AVSD

85
Q

What is the name of the cardiac defect where the heart lies outside of the thoracic cavity?

A

Ectopia cordis

86
Q

What is the name of an anomalous inwards deviation of the sternum?

A

Pectus excavatum

87
Q

What is the name of an anomalous outwards deviation of the sternum?

A

Pectus carinatum

88
Q

PPDH may result from incomplete closure of what structure?

A

Septum transversum

89
Q

What are the 4 types of anomalous pulmonary venous return?

A

Type 1 - Supracardiac (PLVCV or CrVC)
Type 2 - Cardiac (RA or CS)
Type 3 - infracardiac (CaVC, portal vein)
Type 4 - Mixed

90
Q

What forms the membrane for cor triatriatum sinister?

A

Membrane/out-pouching of the common pulmonary vein

91
Q

What forms the membrane for cor triatriatum dexter?

A

Persistence of the right valve of the sinus venosus

92
Q

What is Uhl’s anomaly?

A

Total lack of RV myocardium (direct apposition of endocardium to epicardium, paper thin RV)

93
Q

Types of PA stenosis?

A

Type I - single constriction at PA trunk or left or right PA
Type II - constriction begins at bifurcation and extends into branch PA’s
Type III - multiple segmental PA’s
Type IV - multiple stenoses at peripheral and central PA’s

94
Q

What is the Wendesky effect (Aka capture hysteresis)?

A

Voltage threshold is higher when measuring from low to high as opposed to high to low

95
Q

What is the Hering-Breuer reflex?

A

Causes an increase in HR (inhibits vagal activity, relative increase in SNS) during inspiration and is largely responsible for HR variability with respiratory sinus arrhythmia

96
Q

What is the function of phospholambin?

A

Deactivates SERCA to prevent Ca uptake by SR; phosphorylated by PKA (secondary to Beta stimulation), results in increase in SERCA activity

97
Q

What is the function of calsequestrin?

A

Binds Ca in SR

98
Q

What is the function of calmodulin?

A

Regulates Ca ions in cytosol; Can inactivate the inward calcium current; Can phosphorylate PL to cause more uptake of Ca into the SR (via calmodulin-kinase II). Also enhances activity of PDE, which breaks down cAMP

99
Q

What is the function of β-agnoist receptor kinase (β-ARK)?

A

 Phosphorylates the COOH tail of the receptor, which causes functional uncoupling from the G-protein
 Increases affinity of β receptors for a family of proteins called arrestins, which also decrease coupling to stimulatory G proteins

Ultimately leads to desensitization of β receptors and uncoupling from adenylyl cyclase

100
Q

What is the MOA of glucagon for treating beta-blocker toxicity?

A

 Stimulates formation of cAMP in liver cells to break down liver glycogen -> increased BG
 In the heart, glucagon receptors are coupled by Gs proteins to adenylyl cyclase and result in cAMP formation

Glucagon increases heart rate and contractile activity, and are able to do so while bypassing the beta receptors: used for treating beta blocker overdoses

101
Q

What is the Bowditch staircase effect of treppe?

A

HR progressively increases force of contraction - more Na and Ca ions enter the cell than can be handled by the sodium pump, so Ca builds up (via action of the Na/Ca exchanger

102
Q

What is coronary steal?

A

Vasodilation with some drugs (i.e. amlodipine) that act more distal in arterial tree can shunt blood away from an ischemic area in the heart

Veterinary Cardiology (1 decks)

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