General Flashcards
Brody Effect
Increase in QRS-wave amplitude induced by an increase in ventricular preload
Post-extrasystolic potentiation
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.
Branham Sign
A decrease in heart rate (HR) and an increase in blood pressure after the sudden occlusion of arteriovenous fistula (most commonly PDA)
Bainbridge Reflex
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
Bezold-Jarisch Effect
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”
Bernheim Syndrome
Severe left heart disease causes bulging of the IVS/compression of the RV lumen leading to elevated right-sided pressures and right-CHF
Reverse Bernheim Effect
Severe right-sided heart disease causes bulging of the IVS towards the LV lumen and causes left-CHF
R2A Anomaly
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.
Normal Coronary Anatomy
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.
Coanda Effect
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
Entrainment
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
Bix Rule
Whenever a P wave falls directly between two QRS complexes, SVT with 2:1 conduction should be suspected
Stokes-Adams Seizures
Syncope and seizures of cardiac origin
Acrocyanosis
Cyanosis to tips of extremities (ears, digits, etc.)
Kussmaul sign
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
Corrigan’s pulse
Similar to water hammer pulse, wide pulse pressure due to diastolic regurgitation; seen with severe AI
Myofiber
Group of myocytes held together by collagen
Myoctye
Functional cell of the cardiac muscle
Myofibril
The contractile elements of the myocytes, made up of actin and myosin strands
Afterload - definition and what is it determined by
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)
High-output CHF causes
Anemia, hyperthyroidism, pregnancy
How does B1 activation on the heart increase HR?
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
Determinants of CO?
Preload, afterload, HR, contractility, ventricular synchrony
Myocardial contractility- definition and what increases it
Intrinsic force of contraction of the moycardium independent of loading conditions
Increased by beta adrenergic stimulation, catecholamines, HR, and afterload
Chronic ill effects of beta stimulation?
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
Causes for renin release?
Decreased renal perfusion
Decreased sodium/chloride filtration at macula densa
Beta1 stimulation
What does ACE do?
Converts ATI to ATII, but also breaks down bradykinin
Other enzymes that convert ATI to ATII
Chymase (most important) Cathepsin G Elastase TPA CAGE
Functions of ATII
Potent vasoconstrictor
Promotes Na and H20 resorption via direct effects on distal tubules
Stimulates aldosterone release
Causes of beta sympathetic stimulation
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
ATII receptors - what happens when ATII binds to each
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
Causes of aldosterone release
ATII
Hyperkalemia
ACTH
Other messengers (catecholamines, ET1, AVP)
MOA of aldosterone
Acts on epithelial cells in distal collecting ducts to increase Na resorption and K secretion
Harmful effects of aldosterone
Provokes hypertrophy and fibrosis within vasculature and myocardium
Provoke endothelial cell dysfunction
Baroreceptor dysfunction
Inhibits NE reuptake
Sources for ROS in the heart
Mitchondria
Xanthine oxidase
NADPH oxidase
Antioxidants in the heart
Manganese superoxide dimutase (MnSOD)
Catalase and Glutathione peroxidase
Glutathione reductase (GR)
Stimulus for release of ADH/AVP
Increased plasma osmolality
Hypovolemia (decreased firing of stretch receptors in atria and large veins)
SNS
ADH receptors/function
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
What are the vaptan drugs? Which are specific for which receptors?
V1a - relcovaptan
V2 - tolvaptan, lixivaptan
V1a/V2 - conivaptan
Effects of ANP/BNP?
Induce natriuresis through binding to NPR-A receptors in collecting duct
Vasodilation of systemic/pulmonary circulation (NPR-B)
Direct inhibition of renin production
Function of Endothelin-1 when binding to ETA and ETB receptorts
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
Stimulus for ET-1 release
Hypoxia, stretch, low shear force, ATII, AVP, NE, bradykinin, transforming growth factor beta, TNF-a, IL-1
What is neuropeptide Y?
Vasoconstricting peptide, released with NE from sympathetic nerve endings, potentiates vasoconstriction of other agents (i.e. NE, ATII, etc.)
Nitric oxide effects on the vasculature and on cardiac tissue
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
What does bradykinin do?
Causes vasodilation
What is adrenomedullin?
Binds a number of G-protein coupled receptors, leads to vasodilation and opposes excessive vasoconstriction and vascular remodeling
What is apelin?
NO-mediated vasorelaxation, potent positive inotrope w/o causing significant hypertrophy
What are the important inflammatory cytokines released during CHF?
TNF-a, IL-1, IL-6
Law of Laplace?
Wall stress = pressure x radius / 2 x wall thickness
Three phases of pathologic hypertrophy?
- Hypertrophy develops in response to increased wall stress
- Wall stress normalized by hypertrophy (compensated state
- Exhaustion phase (death of myocytes, myocardial fibrosis, ventricular dilation, reduced CO)
PCWP generally required for pulmonary congestion to occur?
25 mmHg
CVP generally required for ascites to occur?
15 mmHg
Stimuli for expression of fetal genes in the heart?
Mechanical stretch of myocyte Neurohormones (NE, ATII) Cytokines (TNF-a, IL-6) Endothelin ROS
What is a left ventricular heave?
Movement of the thoracic wall due to heart motion
What causes physiologic splitting of S1
Inspiration leads to increased RV filling, RV ejection is longer so P2 is later than A2
Pathologic causes of delayed P2?
Left-to-right shunt PH (HWD) PS R-BBB VPC's (with R-BBB morphology) Dilated PA
Pathologic cause of early A2?
MR, MS, LA tumor
Pathologic cause of delayed A2 (paradoxical split S2)?
AS L-BBB PDA VPC's (L-BBB morphology) Hypertension
What determines loudness of S1?
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
What causes a split S1?
May be normal in some big dogs
BBB
MS/TS
What is an ejection click?
High-frequency, early systolic sound over PV/AoV, suggestive of SAS, PS, ToF, HWD
Not heard on auscultation, only seen on phono
What is a friction rub?
High-frequency sound, louder with inspiration, heard over left sternal border and highly specific for acute pericarditis
What are some causes of pulsus paradoxus?
Pericardial effusion, RCM, CP, pulmonary disease, PTE, shock
What causes a bifid pulse (pulsus bisferiens)?
HOCM, mixed AV disease, exercise, fever
What is Reynold’s number?
(Radius)(Velocity)(Density) / (Viscosity)
When number rises above threshold, turbulent flow occurs
What is a forme fruste?
Ductal remnant/ductus diverticulum
What is a Graham Steel murmur?
Soft, high frequency diastolic murmur from pulmonic insufficiency
What is the duct of Botalli?
Another name for ductus arteriosus
What is Chung’s effect?
The P wave following a premature atrial complex is wider and lower amplitude due to aberrant atrial conduction
What is Ashman’s phenomenon?
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
Normal P wave amplitude in a dog?
<0.4 mV
Normal P wave amplitude in a cat?
<0.2 mV
Normal P wave duration in a dog?
<40 mS
Normal P wave duration in a cat?
< 35 mS
Normal PQ interval in a dog?
60-130 mS
Normal PQ interval in a cat?
50-90 mS
Normal QRS duration in a dog?
<70 mS
Normal QRS duration in a cat?
<40 mS
Normal QT interval in a dog?
150-240 mS
Normal QT interval in a cat?
160-220 mS
What cardiac defect are Persians overrepresented for?
AVSD
What cardiac defects are Chartreux cats overrepresented for?
TVD, ASD
What cardiac defects are Siamese overrepresented for?
SVMS, endocardial fibroelastosis, AS
What defect can Griseofulvin cause?
AVSD
What is the name of the cardiac defect where the heart lies outside of the thoracic cavity?
Ectopia cordis
What is the name of an anomalous inwards deviation of the sternum?
Pectus excavatum
What is the name of an anomalous outwards deviation of the sternum?
Pectus carinatum
PPDH may result from incomplete closure of what structure?
Septum transversum
What are the 4 types of anomalous pulmonary venous return?
Type 1 - Supracardiac (PLVCV or CrVC)
Type 2 - Cardiac (RA or CS)
Type 3 - infracardiac (CaVC, portal vein)
Type 4 - Mixed
What forms the membrane for cor triatriatum sinister?
Membrane/out-pouching of the common pulmonary vein
What forms the membrane for cor triatriatum dexter?
Persistence of the right valve of the sinus venosus
What is Uhl’s anomaly?
Total lack of RV myocardium (direct apposition of endocardium to epicardium, paper thin RV)
Types of PA stenosis?
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
What is the Wendesky effect (Aka capture hysteresis)?
Voltage threshold is higher when measuring from low to high as opposed to high to low
What is the Hering-Breuer reflex?
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
What is the function of phospholambin?
Deactivates SERCA to prevent Ca uptake by SR; phosphorylated by PKA (secondary to Beta stimulation), results in increase in SERCA activity
What is the function of calsequestrin?
Binds Ca in SR
What is the function of calmodulin?
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
What is the function of β-agnoist receptor kinase (β-ARK)?
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
What is the MOA of glucagon for treating beta-blocker toxicity?
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
What is the Bowditch staircase effect of treppe?
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
What is coronary steal?
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
