Physiology Flashcards
Bainbridge reflex
Increased blood volume (CVP) leads to increased HR
- Increased venous return stretches atria
- stimulation of stretch receptors increases firing of B fibers
- modulation of autonomics to SA node–>increased HR
Baroreceptor reflex
Increased BP leads to decreased HR
-
Bezold-Jarisch reflex
Cardioinhibitory, leads to bradycardia, peripheral vasodilation, and hypotension (inhibits sympa outflow)
Triggered by vigorous contraction of underfilled ventricle–>paradoxical increase in firing of LV inhibitory receptors
Shock
Inability of reflex sympathetic activation to sufficiently raise BP.
Tamponade
Clinical signs due to elevated RA pressure secondary to increased pericardial pressure
Eisenmengers physiology
L–>R shunt leading to overcirculation of lungs and remodeling of pulmonary arteries. Increased pressure (pulmonary hypertension) leads to shunt reversal (R–> L)
When are diastolic pressures the same in all chambers?
Tamponade
Constrictive pericarditis
What chromosome is associated with TVD?
Chromosome 9
pulses parvus et tarsus
Weak and slow pulses
Describe pacemaker syndrome
AV dyssychrony caused iatrogenically by VVI pacemaker.
Signs include decreased cardiac output, loss of atrial kick, loss of Total peripheral resistance
Change to VDD/DDD mode or add atrial lead.
When should you note possible RHF or LHF on the exam?
E/A restrictive filling pattern
E/e’ >10 (Oyama paper)
LA pressure >20 (pulmonary edema) (LVEDP equals mean LAP)
RA pressure >13
What is the definition of contractility?
Rate of sarcomere shortening at 0 load.
ESPVR is contractility
Systolic function is preload and afterload dependent
Phases of Valsalva maneuver
- Onset of straining with increased intrathoracic pressure.
- HR does not change but BP rises - Decreased venous return and reduction of SV and Pulse pressure as straining continues
- HR increases and BP drops - Release of straining.
- decreased intrathoracic pressure and normalization of pulmonary blood flow - BP overshoot with return of HR to baseline
Dynamic cardiac auscultation during Valsalva
- Phase 2: HOCM and MV prolapse murmurs increase due to decreased SV. Other murmurs decrease (even SAS).
- Phase 4: Right murmurs (PS) that decreased in Phase 2 will return to baseline intensity immediately. L murmurs like SAS may take 5-10 cardiac cycles to return to normal intensity.
Anrep effect
Autoregulation- contractility increases with afterload.
Sustained myocardial stretch activates Na/H exchangers, NCX gradient not as effective and Ca build up causes CICR- follows that pathway…
Carvallo sign
Patients with TR ; pansystolic murmur that becomes louder with inspiration
Carvallo sign pathophysiology
on inspiration, venous blood flow to RA. And RV are increased, increasing SV during systole. Therefore, leak of blood from RV to RA is larger during inspiration. MR murmur is opposite- gets louder on expiration due to increased venous return from pulmonary veins in left heart.
Corrigans pulse
Widened pulse pressure of AR. Water hammer pulse.
Cushing reflex
Increase in systolic and pulse pressure, bradycardia, irregular respiration secondary to increased ICP.
- first stage, sympa activation is greatest. Arterial constriction–> hypertension (trying to restore blood flow to brain), and Tachycardia.
- second stage, baroreceptors detect hypertension and trigger para response. Bradycardia ensues.
- Third stage, irregular respiratory pattern or apnea.
Flint murmur
Low-pitched rumbling mid diastolic or presystolic murmur
Associated with severe AI. Mitral leaf displacement and turbulent blood flow.
Graham Steel murmur
Associated with pulmonary regurgitation. High pitched diastolic murmur. Chronic cor pulmonale, mitral stenosis.
Kussmaul sign
Paradoxical rise in JVP during inspiration. Indicator of poor RV filling capacity
Typically, JVP decreases with inspiration because of reduced intrathoracic pressure and increased volume afforded to RV filling during diastole.
Pacemaker:
High voltage threshold
High-normal-low current threshold
High impedance
Wire fracture
Pacemaker:
Low voltage threshold
High current threshold
Low lead impedance
Insulation break
Pacemaker:
High voltage threshold
High current threshold
Normal lead impedance
Lead dislodgement
Pacemaker:
High voltage threshold
High current threshold
Normal lead impedance
Exit block
Normal mean RA pressures
2-6
With constriction or tamponade, RA pressures are—–, and approximate:
Elevated,
Approximate mean PAW and PA end diastolic pressures
Kussmauls sign
A paradoxical rise rather than a fall in RA pressures during inspiration with constrictive pericarditis.
Genetic basis- whippet MVD
Chromosome 15
Genetic correlation- CKCS DMVD
Chr 13 & 14
Genetic basis HCM Maine Coon
MyBPC3- A31P
Very common mutation with low penetrance
Homozygous has high entrance HCM and risk of SCD
Genetic basis HCM Ragdoll
MyBPC3- C820T
Name 4 quantitative methods to quantify MR
Color flow jet area
Vena contracts
PISA
Quant doppler volumetrics
What is quantitative doppler volumetric measurement
SV equals CSA x VTI
CSA is cross sectional area of annulus and VTI is velocity time interval of flow at annulus
Calculate MR regurgitate volume
Regurgitate volume equals SV mitral annulus- SV aortic annulus
Calculate MR regurgitate fraction
Regurgitant fraction equals Regurgitant volume/ SV mitral annulus
EROA
EROA equals regurgitant volume / VTI regurgitant jet
List 5 indirect (subjective) measurements of MR severity
- Dense signal approaching density of antegrade flow is severe
- Early peak of MR jet indicates high LA pressure
- Presence of PHT
- Dominant early filling mitral inflows (dominat A wave excludes severe MR)
- Pulmonary vein flow- normal means higher volume in systlole than diastole, severe MR when PV flow decreases/reverses
Inherited arrhythmia in English Springer Spaniels
KCNQ1 mutation in one family of dogs with sudden death. Thought to be LQT variant
B1 mutations affect on dogs (2015 Stern/Meurs paper)
Lower baseline heart rates in these dogs with and less response to atenolol
More sensitive method of predicting SAS in Goldens (Cote 2015)
Measure LVOT and effective orifice area indexed to BSA (EOAi)
EOAi< 1.46 indicates adult SAS
Best estimates to predict onset of CHF (Oyama 2012)
La size and NT-proBNP >1500
Brody effect
Phase 4 (bradycardia dep) aberrancy Filling of heart makes QRS taller--> blood conducts more than surrounding tissues
Overdrive suppression mechanism
Enhanced activity of Na/K exchanger that results from driving a pacemaker faster than its intrinsic rate.
Increased depolarization leads to increased intra Na, which stimulates Na/K exchanger (moves more Na out than K in).
Hyperpolarizes and slows phase 4 of AP. Prevent pacemaker currents from depolarizing cell.
When dominant PM stops, inhibition continues until Na/K normalizes cell again.
3 causes of AV dissociation
3AVB
VT with no retrograde VA conduction
Isorhythmic AV dissociation occurring at similar rates so that anterograde and retrograde conduction fall within the other’s refractory pd
Focal junctional tachycardia with isorhythmic dissociation
- Labradors
- Isorhythmic Type 1: AV gets longer and longer then dissociates
- Isorhythmic type II: AV is the same always.
Ventriculophasic sinus arrhythmia mechanisms
- Stim of arterial vagal baroreceptors
- Increased blood flow to SA node in ventricular systole
- Inhibition of Bainbridge reflex by decreased atrial pressure after ventricular contraction.
How does premature beat initiate re entry?
Usually induced by APC, which blocks antegrade conduction in bypass tract, travels to atrium, AV node, ventricle, and through Kent fiber.
Concertina effect?
- Sort of like sinus arrhythmia during preexcitation
2. PR intervals and QRS complexes show cyclic pattern, more prominent then less prominent…HR stays the same.
Dual physiology of AV node?
Concert of slow and fast pathways within AV node.
- fast pathway is normal for AP to travel
- slow pathway has shorter refractory pd than long
- dual pathways are substrate for AVNRT (not documented in dog)
3 requirements for re entry
- Presence of unidirectional block within a conducting pathway (excitable gap)
- Critical timing
- Length of the effective refractory pd of normal tissue
For example, tissue must be excitable when AP reaches it…not within the ERP
Rule of Bigeminy (3 mechanisms)
- Bidirectional conduction in reentrant pathway
- long RR–> unidirectional block–>PVC from other pathway
- Comp. pause facilitates block after sinus beat - Sinus rhythm with parasystolic rhythm
- EAD facilitated after long RR, then comp pause perpetuates.
Concealed conduction
Incomplete cardiac impulse conduction through specialized conduction tissue–> changes next complex.
Parasystole
Interaction between 2 fixed rate pacemakerswith different discharge rates.
Latent PM is protected from dominant rhythm (usually NSR) by entrance block.
Implanted pacemaker is example.
Dome and dart P waves
Indicate congenital heart disease and left atrial arrhythmias
Doxorubicin can also cause (along with RBBB)
Gap phenomenon
Short period in the cycle of AV or intraventricular conduction when a stimulus passes, even though just before or after it would be blocked.
Type of supernormal conduction
Paradoxical propagation of closely coupled stimuli wen stimuli at longer coupling interval are blocked
Rheobase
Lowest stimulus voltage that will electrically stimulate the myocardium at any pulse duration
Chronaxie
The threshold pulse duration at a stimulus (voltage) that is 2x the rheobase voltage
How does a VVI pacemaker set at 90bpm with a refractory pd of 320ms respond to a PVC occurring 250ms after the last beat.
The PVC is sensed but does not reset timing cycles
4 signs of lead perforation
- Pericardial effusion and pneumothorax
- Rising stimulation threshold (also with microdislodgement)
- change in ventricular depolarization pattern
- Diaphragmatic contraction with each output stimulus
VDD mode- how to avoid oversensing
Program atrial sensitivity to 33% of the measured atrial potential or extend the atrial refractory pd to avoid oversensing
Explain pacemaker mediated tachycardia
- Dual chamber pacemaker (DDD)
- PM forms anterograde (A–> V) conduction
- AV node is retrograde limb( V–> A)
- V–> A conduction has atrial activation time longer that programmed PVARP.
- Ventricular beat conducts retrograde, sensed by ventricle, which paces.
- Incessant reentrant arrhythmia bounded by upper rate limit.
Pacemaker blanking period
Period of refractory period when no sensing occurs
Equivalent to absolute refractory pd.
Noise reversion
Sensing of events within the refractory period leading to the pacemaker to switch to asynchronous pacing with repetitive refractory sensing
Programming methods to correct noise reversion
- Decrease refractory period
2. Decrease sensitivity (increase fence)
Methods for AAI pacemaker avoiding noise reversion
- Decreasing sensitivity may results in loss of capture, but high sensitivity results in far-field sensing.
- Blanking period can be adjusting to include ventricular depolarization.
What is TARP?
Total atrial refractory pd equals (AV delay) plus PVARP
AV delay is Time interval btwn an atrial paced/sensed event and delivery of the ventricular stimulus (like PR interval)
Upper rate tracking
Pacing characteristics in Dual chambered PM in atrial tracking mode.
Must limit the rate the ventricle is paced in the presence of high atrial rates (Max tracking rate (MTR)
Atrial rate > than MTR, pacemaker Wenkebach will occur.
PM will track atrium and prolong AV delay so that MRT not violated.
If P wave falls into PVARP, not tracked and cycle begins again.
How does pacemaker Wenckebach occur?
upper rate limit should be >TARP
If URI equals TARP or
Afterload
Peak systolic wall stress (peripheral resistance, arterial compliance, and peak intraventricular pressure)
OR- aortic impedance (another flash card)
Equation for aortic impedance
Aortic pressure divided by aortic flow at that instance
-a measure of instantaneous afterload
Bowditch/Treppe affect
Increased HR increases the force of ventricular contraction- NCX does not have time to extrude Na, Ca builds up within cell.
What is the vena contracta?
Smallest highest velocity region of jet flow downstream of regurgitant orifice.
Width <0.3mm= mild MR
>0.7mm= severe MR
Elasticity
Myocardium returns to normal shape after removal of systolic stress
Compliance
Relationship btwn change in stress and resultant strain
Percentage change in dimension or size
1. DV/dT (rate of volume change/rate of pressure change)
2. Restrictive CM=decreased compliance
3. Pseudonormalization occurs as LV loses compliance
Distensibility
Diastolic pressure required to fill ventricle to same volume
Starlings law of the heart
Increased ventricular filling (venous return) increases the ventricular fiber length–> this increases ventricular contraction and SV
1. Starling noted increased length to volume, Frank noted increased volume to pressure and rate
Fick principle (not formula)
Volume of oxygen taken up by blood in the lungs, divided by the arteriovenous O2 content difference, in equal to the CO.
Cardiac memory
T wave abnormalities manifested on resumption of normal ventricular activation pattern after a period of abnormal activation.
Reasons for high impedance
Lead fracture
Lead not seated within generator
Reasons for low impedance
Insulation break (current drain through break), also causes low resistance
B bump
Delayed closure of mitral valve on M mode due to decreased ventricular compliance
Pulse repetition frequency
Number of pulses per second. Decreases as death increases because transducer must receive sound wave before the next one is sent out. Or, this leads to range ambiguity
Range ambiguity
Occurs at high prf, when second pulse sent out before the first is received…displays correct structures in wrong location. If unexpected object in cardiac chamber- range ambiguity
Side lobe
main US beam is central but many other beams sent out as well. These beams are side lobes and can lead to images being paced int he wrong location.
In aorta, may look like false dissection
End systolic volume index
LVESV/BSA
Less dependent on afterload.
Measure of function
