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Cardiology > Physiology > Flashcards

Physiology Flashcards

1
Q

Bainbridge reflex

A

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
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2
Q

Baroreceptor reflex

A

Increased BP leads to decreased HR

-

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3
Q

Bezold-Jarisch reflex

A

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

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4
Q

Shock

A

Inability of reflex sympathetic activation to sufficiently raise BP.

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5
Q

Tamponade

A

Clinical signs due to elevated RA pressure secondary to increased pericardial pressure

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6
Q

Eisenmengers physiology

A

L–>R shunt leading to overcirculation of lungs and remodeling of pulmonary arteries. Increased pressure (pulmonary hypertension) leads to shunt reversal (R–> L)

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7
Q

When are diastolic pressures the same in all chambers?

A

Tamponade

Constrictive pericarditis

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8
Q

What chromosome is associated with TVD?

A

Chromosome 9

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9
Q

pulses parvus et tarsus

A

Weak and slow pulses

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10
Q

Describe pacemaker syndrome

A

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.

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11
Q

When should you note possible RHF or LHF on the exam?

A

E/A restrictive filling pattern
E/e’ >10 (Oyama paper)
LA pressure >20 (pulmonary edema) (LVEDP equals mean LAP)
RA pressure >13

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12
Q

What is the definition of contractility?

A

Rate of sarcomere shortening at 0 load.
ESPVR is contractility
Systolic function is preload and afterload dependent

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13
Q

Phases of Valsalva maneuver

A
  1. Onset of straining with increased intrathoracic pressure.
    - HR does not change but BP rises
  2. Decreased venous return and reduction of SV and Pulse pressure as straining continues
    - HR increases and BP drops
  3. Release of straining.
    - decreased intrathoracic pressure and normalization of pulmonary blood flow
  4. BP overshoot with return of HR to baseline
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14
Q

Dynamic cardiac auscultation during Valsalva

A
  1. Phase 2: HOCM and MV prolapse murmurs increase due to decreased SV. Other murmurs decrease (even SAS).
  2. 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.
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15
Q

Anrep effect

A

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…

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16
Q

Carvallo sign

A

Patients with TR ; pansystolic murmur that becomes louder with inspiration

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17
Q

Carvallo sign pathophysiology

A

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.

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18
Q

Corrigans pulse

A

Widened pulse pressure of AR. Water hammer pulse.

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19
Q

Cushing reflex

A

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.
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20
Q

Flint murmur

A

Low-pitched rumbling mid diastolic or presystolic murmur

Associated with severe AI. Mitral leaf displacement and turbulent blood flow.

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21
Q

Graham Steel murmur

A

Associated with pulmonary regurgitation. High pitched diastolic murmur. Chronic cor pulmonale, mitral stenosis.

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22
Q

Kussmaul sign

A

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.

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23
Q

Pacemaker:
High voltage threshold
High-normal-low current threshold
High impedance

A

Wire fracture

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24
Q

Pacemaker:
Low voltage threshold
High current threshold
Low lead impedance

A

Insulation break

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25
Q

Pacemaker:
High voltage threshold
High current threshold
Normal lead impedance

A

Lead dislodgement

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26
Q

Pacemaker:
High voltage threshold
High current threshold
Normal lead impedance

A

Exit block

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27
Q

Normal mean RA pressures

A

2-6

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28
Q

With constriction or tamponade, RA pressures are—–, and approximate:

A

Elevated,

Approximate mean PAW and PA end diastolic pressures

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29
Q

Kussmauls sign

A

A paradoxical rise rather than a fall in RA pressures during inspiration with constrictive pericarditis.

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30
Q

Genetic basis- whippet MVD

A

Chromosome 15

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31
Q

Genetic correlation- CKCS DMVD

A

Chr 13 & 14

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32
Q

Genetic basis HCM Maine Coon

A

MyBPC3- A31P
Very common mutation with low penetrance
Homozygous has high entrance HCM and risk of SCD

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33
Q

Genetic basis HCM Ragdoll

A

MyBPC3- C820T

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34
Q

Name 4 quantitative methods to quantify MR

A

Color flow jet area
Vena contracts
PISA
Quant doppler volumetrics

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35
Q

What is quantitative doppler volumetric measurement

A

SV equals CSA x VTI

CSA is cross sectional area of annulus and VTI is velocity time interval of flow at annulus

36
Q

Calculate MR regurgitate volume

A

Regurgitate volume equals SV mitral annulus- SV aortic annulus

37
Q

Calculate MR regurgitate fraction

A

Regurgitant fraction equals Regurgitant volume/ SV mitral annulus

38
Q

EROA

A

EROA equals regurgitant volume / VTI regurgitant jet

39
Q

List 5 indirect (subjective) measurements of MR severity

A
  1. Dense signal approaching density of antegrade flow is severe
  2. Early peak of MR jet indicates high LA pressure
  3. Presence of PHT
  4. Dominant early filling mitral inflows (dominat A wave excludes severe MR)
  5. Pulmonary vein flow- normal means higher volume in systlole than diastole, severe MR when PV flow decreases/reverses
40
Q

Inherited arrhythmia in English Springer Spaniels

A

KCNQ1 mutation in one family of dogs with sudden death. Thought to be LQT variant

41
Q

B1 mutations affect on dogs (2015 Stern/Meurs paper)

A

Lower baseline heart rates in these dogs with and less response to atenolol

42
Q

More sensitive method of predicting SAS in Goldens (Cote 2015)

A

Measure LVOT and effective orifice area indexed to BSA (EOAi)
EOAi< 1.46 indicates adult SAS

43
Q

Best estimates to predict onset of CHF (Oyama 2012)

A

La size and NT-proBNP >1500

44
Q

Brody effect

A 
Phase 4 (bradycardia dep) aberrancy 
Filling of heart makes QRS taller--> blood conducts more than surrounding tissues
45
Q

Overdrive suppression mechanism

A

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.

46
Q

3 causes of AV dissociation

A

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

47
Q

Focal junctional tachycardia with isorhythmic dissociation

A
  1. Labradors
  2. Isorhythmic Type 1: AV gets longer and longer then dissociates
  3. Isorhythmic type II: AV is the same always.
48
Q

Ventriculophasic sinus arrhythmia mechanisms

A
  1. Stim of arterial vagal baroreceptors
  2. Increased blood flow to SA node in ventricular systole
  3. Inhibition of Bainbridge reflex by decreased atrial pressure after ventricular contraction.
49
Q

How does premature beat initiate re entry?

A

Usually induced by APC, which blocks antegrade conduction in bypass tract, travels to atrium, AV node, ventricle, and through Kent fiber.

50
Q

Concertina effect?

A
  1. 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.

51
Q

Dual physiology of AV node?

A

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)
52
Q

3 requirements for re entry

A
  1. Presence of unidirectional block within a conducting pathway (excitable gap)
  2. Critical timing
  3. Length of the effective refractory pd of normal tissue

For example, tissue must be excitable when AP reaches it…not within the ERP

53
Q

Rule of Bigeminy (3 mechanisms)

A
  1. Bidirectional conduction in reentrant pathway
    - long RR–> unidirectional block–>PVC from other pathway
    - Comp. pause facilitates block after sinus beat
  2. Sinus rhythm with parasystolic rhythm
  3. EAD facilitated after long RR, then comp pause perpetuates.
54
Q

Concealed conduction

A

Incomplete cardiac impulse conduction through specialized conduction tissue–> changes next complex.

55
Q

Parasystole

A

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.

56
Q

Dome and dart P waves

A

Indicate congenital heart disease and left atrial arrhythmias
Doxorubicin can also cause (along with RBBB)

57
Q

Gap phenomenon

A

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

58
Q

Rheobase

A

Lowest stimulus voltage that will electrically stimulate the myocardium at any pulse duration

59
Q

Chronaxie

A

The threshold pulse duration at a stimulus (voltage) that is 2x the rheobase voltage

60
Q

How does a VVI pacemaker set at 90bpm with a refractory pd of 320ms respond to a PVC occurring 250ms after the last beat.

A

The PVC is sensed but does not reset timing cycles

61
Q

4 signs of lead perforation

A
  1. Pericardial effusion and pneumothorax
  2. Rising stimulation threshold (also with microdislodgement)
  3. change in ventricular depolarization pattern
  4. Diaphragmatic contraction with each output stimulus
62
Q

VDD mode- how to avoid oversensing

A

Program atrial sensitivity to 33% of the measured atrial potential or extend the atrial refractory pd to avoid oversensing

63
Q

Explain pacemaker mediated tachycardia

A
  1. Dual chamber pacemaker (DDD)
  2. PM forms anterograde (A–> V) conduction
  3. AV node is retrograde limb( V–> A)
  4. V–> A conduction has atrial activation time longer that programmed PVARP.
  5. Ventricular beat conducts retrograde, sensed by ventricle, which paces.
  6. Incessant reentrant arrhythmia bounded by upper rate limit.
64
Q

Pacemaker blanking period

A

Period of refractory period when no sensing occurs

Equivalent to absolute refractory pd.

65
Q

Noise reversion

A

Sensing of events within the refractory period leading to the pacemaker to switch to asynchronous pacing with repetitive refractory sensing

66
Q

Programming methods to correct noise reversion

A
  1. Decrease refractory period

2. Decrease sensitivity (increase fence)

67
Q

Methods for AAI pacemaker avoiding noise reversion

A
  1. Decreasing sensitivity may results in loss of capture, but high sensitivity results in far-field sensing.
  2. Blanking period can be adjusting to include ventricular depolarization.
68
Q

What is TARP?

A

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)

69
Q

Upper rate tracking

A

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.

70
Q

How does pacemaker Wenckebach occur?

A

upper rate limit should be >TARP

If URI equals TARP or

71
Q

Afterload

A

Peak systolic wall stress (peripheral resistance, arterial compliance, and peak intraventricular pressure)

OR- aortic impedance (another flash card)

72
Q

Equation for aortic impedance

A

Aortic pressure divided by aortic flow at that instance

-a measure of instantaneous afterload

73
Q

Bowditch/Treppe affect

A

Increased HR increases the force of ventricular contraction- NCX does not have time to extrude Na, Ca builds up within cell.

74
Q

What is the vena contracta?

A

Smallest highest velocity region of jet flow downstream of regurgitant orifice.
Width <0.3mm= mild MR
>0.7mm= severe MR

75
Q

Elasticity

A

Myocardium returns to normal shape after removal of systolic stress

76
Q

Compliance

A

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

77
Q

Distensibility

A

Diastolic pressure required to fill ventricle to same volume

78
Q

Starlings law of the heart

A

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

79
Q

Fick principle (not formula)

A

Volume of oxygen taken up by blood in the lungs, divided by the arteriovenous O2 content difference, in equal to the CO.

80
Q

Cardiac memory

A

T wave abnormalities manifested on resumption of normal ventricular activation pattern after a period of abnormal activation.

81
Q

Reasons for high impedance

A

Lead fracture

Lead not seated within generator

82
Q

Reasons for low impedance

A

Insulation break (current drain through break), also causes low resistance

83
Q

B bump

A

Delayed closure of mitral valve on M mode due to decreased ventricular compliance

84
Q

Pulse repetition frequency

A

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

85
Q

Range ambiguity

A

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

86
Q

Side lobe

A

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

87
Q

End systolic volume index

A

LVESV/BSA

Less dependent on afterload.
Measure of function

Cardiology (4 decks)

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