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A1 > Cardiac APEX > Flashcards

Cardiac APEX Flashcards

1
Q

K vs Ca TP/ RMP

A

K-RMP
Ca- TP

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2
Q

Na K ATPase in the heart

A

3 Na out (Na was in from depolarization)
2 K in (K was out from repolarization)
Always on

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3
Q

How does Hyper K effect the cells?

A

Doesnt allow repolarization, which traps Na channel in their closed state

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4
Q

O2 consumption at rest of the heart

A

8-10 ml O2/100g/in
Higher than all others

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5
Q

Do all muscles have gap junctions?

A

No only heart

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6
Q

RMP of cardiac nueron cells (not myoctye/ ventricular AP)

A

RMP -70
TP -55
Peak +30

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7
Q

Ventricular action potential stages main conductance

A

0- na in
1- cl in, k out
2- ca out, k out
3- k out
4- rmp- NA K ATPase 3na out, 2k in, but also K is still leaking out

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8
Q

RMP/ TP/ peak of myoctye/ ventricular ap

A

-90
-70
+10

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9
Q

Absolute vs relative refractory period on ventricular AP

A

Absolute- 0-1st half of phase 3,qrs to middle of t wave
Relative- can fire with high stimulus, second half of phase 3 and t wave

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10
Q

Phases of SA node AP

A

403
4- sodium (via funny channels) and calcium (via t type tubules) enter- spontaneous depolarization
0-depolarization, ca in (L type)
3- repolarization, k out

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11
Q

Real name for sa node

A

Keith flack node

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12
Q

What nerve innervates the SA and AV node?

A

R vagus SA node
L vagus AV node

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13
Q

How does norepi effect electrolytes

A

B1 receptor lets ca in na in

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14
Q

What receptor does ACH bind to in the heart?

A

M2 increases K conductance (out)

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15
Q

DO2 vs VO2 in adult

A

1L/min
250ml/min or 3.5ml/kg/min

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16
Q

CaO2 vs Cvo2 range

A

20ml/o2/dl
15ml/dl

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17
Q

DO2 formula

A

CAO2 x 10 x CO
CaO2- (1.34 x hgb x sao2) + (pao2 x .003)

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18
Q

Map formula

A

[(CO x SVR) / 80] + CVP

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19
Q

Ohm vs poiselle

A

Ohm- flow= pressure gradient/ resistance
Poiselle is an extension of ohms law that incorporates diameter, viscosity, and tube length
Poiselles- (Pi x R^4 x AV pressure gradient) / (8 x n x L) where n= viscosity, l= length

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20
Q

Reynold number

A

<2000- laminar
2000-4000- transitional
>4000- turbulent

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21
Q

What can turbulent flow cause?

A

Bruit (carotid stenosis) or Murmur (valvular heart disease)

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22
Q

What can reduce myocardial compliance

A

Aging
Hypertrophy
Diastolic dysfunction
Fibrosis

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22
Q

Things that increase contractility

A

Calcium
SNS/ catecholamines
Dig
PDE inhibitors

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23
Q

Things that decrease contractility

A

Hypoxia
Hyperarbia
Acidosis
Kyperkalemia (arrests heart)
Hypocalcemia
Prop
BB
CCB
Volatile anesthetics (besides N2O which increases and des if started rapidly, and this decrease in CO is usually masked by vasodilation)
Ischemia

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24
Q

Intercalated discs

A

Gap junctions and desmosomes that hold cells together in skeletal muscle

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25
Q

How B1 increases contractility

A

B1 activates adenylate cyclase
AC converts to ATP to cAMP
cAMP increases PKA
PKA will;
1. activate more L type Ca channels
2. Stimulate ryr2 receptors to release more Ca
3. Stimulate SERCA2 to increase ca uptake, which will allow for a sooner ca release (both positive inotropy and lusitrophy)

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26
Q

Law of laplace

A

wall stress=pressure x radius / (ventricular thickness)

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27
Q

L vs R dominant

A

R- RCA feeds PDA (80%)
L- CXA feeds PDA (10-20%)

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28
Q

Which branches feed the nodes, bundle, and branches

A

RCA SA
RCA AV
LCA Bundle of his
LCA BB

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29
Q

Cardiac veins

A

Great cardiac vein (LAD)
Anterior Cardiac vein (RCA)
Middle cardiac vein (PDA)

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30
Q

Thesbian veins

A

RL shunt
Drain in all four chambers

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31
Q

TEE best view for LV ischemia

A

Short axis- midpapillary muscle level

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32
Q

Extraction ratio of oxygen in the heart

A

70%
Cant extract more, needs to increase blood flow

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33
Q

What percent of CO goes to the heart?

A

5%

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34
Q

3 things that make up autoregulation

A

Local metabolism- most important, adenosine vasodilates, NO, PG, CO2, flushes out products
Myogenic response- vessels innate ability to resist change in size
ANS- less important

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35
Q

Alpha 1 and histamine 1 effects on blood flow in heart

A

Constrict!

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36
Q

Beta 2 and H2 and Muscarinic blood flow in heart

A

Vasodilate!

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37
Q

PLC pathway and activators

A

Constriction
Phenyl, levo, epi, AT2
IP3
increased Ca influx

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38
Q

Where to listen for aortic stenosis

A

r sternal border 2 ics

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39
Q

S1 valves

A

mitral and tricuspid
Marks onset of systole

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40
Q

S2 valves

A

Aortic and pulmonary
Marks onset of diastole

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41
Q

S3 and S4 causes

A

s3- HF, during middle 1/3 of diastole
s4- atrial kick

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42
Q

Where to listen for pulmonic

A

L sternal 2 ICS

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43
Q

Where to listen for tricuspid

A

L sternal 4 ICS

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44
Q

Where to listen for mitral

A

L mid clavicular 5ICS

45
Q

Concentric vs eccentric regurg or stenosis

A

Eccentric- regurg- they gag
Concentric- stenosis- harder to push

45
Q

concentric/ eccentric sarcomeres

A

Concentric- parrallel
Eccentric- series

46
Q

Normal vs stenotic aortic valve size

A

Normal- 3cm
Stenotic- <0.8 cm

47
Q

Etiologies of aortic stenosis

A

Bicuspid valve/ calcification
Rheumatic fever
Infective endocarditis

48
Q

Classic presentation of aortic stenosis

A

Its SAD
Syncope
Angina
Dyspnea
Although asymptomatic until ventricular dysfunction occures, thats why we have to listen for murmur in elderly

49
Q

When can spinals cause cardiovascular collapse?

A

Severe AS

50
Q

Anesthetic management for Aortic stenosis

A

Full slow and constricted

51
Q

A waveform in AS

A

Pulsus tardus slow systolic upstroke
Pulses parvus narrow pulse pressure

52
Q

Anesthetic considerations for Aortic Regurg

A

Fast full forward

53
Q

Aortic regurg A line

A

Biphasic- bisferiens pulse

54
Q

Causes of Aortic regurd, acute and chronic

A

Endocarditis common
Aortic root dissection
—
Calcifications, marfan, ehler danlos, ankylosing spond

55
Q

Anesthetic considerations for Mitral stenosis

A

Slow, full, forward

56
Q

N2o effect on pvr

A

Increases

57
Q

Mitral valve size normal vs stenose

A

normal- 4-6cm
Severe- <0.8cm

58
Q

Most common cause mitral stenosis

A

Rheumatic fever
Endocarditis
Calcifications/ atherosclerosis

59
Q

Anesthetic considerations for mitral regurg

A

Full fast forward

59
Q

Etiologies of Mitral insufficiency

A

Rheumatic fever
Ischemic heart disease
Endocarditis

60
Q

TAVR

A

Minimally invasive Aortic valve replacement

61
Q

3 surgical approaches of TAVR

A

Transfemoral
Transaortic
Transapical (antegrade)

62
Q

Most common TAVR valves

A

SAPIAN- balloon plasty, RVR 200bpm to produce cardiac standstill, HOTN,
Corevalve-No need for plasty or RVPacing bc it is self expanding

63
Q

How do u assess new valve after tavr

A

TEE and fluoroscopy

64
Q

Most feared complication and result of TAVR surgery

A

Malpositioned valve
Aortic regurg
Surgery tx

65
Q

Which valve disease is associated with genetic conditions?

A

Aortic regurg
Marfans, ehler danlos, ankylosing spondlytis

66
Q

SAM

A

MV repair complication
Induced by nitrog, dobutamine

67
Q

What are the highest risk procedures for Cardiovascular M/M with CAD?

A

Emergency surgery
Open aortic surgery
Long procedures with alot of blood loss/ fluid shift
Peripheral vascular surgery

68
Q

Risk of MI

A

General population- 0.3%
Previous MI patients
>6 months- 6%
3-6 months- 15%
<3 months- 30%
<30 days- highest

69
Q

General risk factors for cardiac surgery

A

Surgery type- emergent, aortic, peripheral vasculr, long
CHF, CVA, DM, CKD

70
Q

How long to wait for surgery after MI

A

4-6 weeks (30%)

71
Q

NYHA

A

4 categories that assess HF
1- no symptoms with physical activity
2- symptoms during normal activity
3- symptoms with less than normal activity
4- symptoms at rest
Symptoms= fatigue, angina, palpitations, dyspnea, syncope

72
Q

When to consult cardio for NYHA

A

3-4 under GA for high or intermediate risk surgery
MAC is ok if stable heart

73
Q

Which lead to detect dysrhytmias and LV ischemia

A

ii
v3,v4,v5

74
Q

Biomarkers of myocardial ischemia

A

Troponin I- 3 hours
Troponin T- 3 hours
CKMD- 3 hours- least sensitive

75
Q

What decreases heart compliance? (decreased diastolic function)

A

Old age
Ischemia
HTN/stenosis
HOC

76
Q

What can decrease heart compliance?

A

Age >60
Ischemia
Presure overload- aortic stenosis, HTN
Hypertophic obstructive cardiomyopathy
Pericardial pressure

77
Q

Anesthetic considerations for decreased compliance

A

U need to keep NSP bc atrial kick is important
Risk for pulmonary edema- increased pressures
Reduced compliance- CVP and PCWP will OVERESTIMATE LDEDV- its actually pressure not volume but cvp and pcwp dont know that

78
Q

What conditions increase compliance

A

Dilated cardiomyopthy
Chronic aortic insufficiency

79
Q

How and why to give propofol to a CHF patient

A

Why- they rely on SNS tone for blood pressure and prop will decrease sns tone

80
Q

Systolic failure vs diastolic failure etiologies

A

Systolic- ischemia, valve regrug, dilated cardiomyopathy
Diastolic- stenosis, ischemia, htn, obesity gives u a fat thick septum, cor pulmonale, hypertrophic CMP

81
Q

Compensatory mechanisms of HFrEF

A

Increased SNS, increased RAAS, increased preload

82
Q

How do compensatory mechanisms eventually cause more damage for the heart?

A

SNS- increased myocardial work, down regulation of B receptors
Vasoconstriction- decreased CO
Fluid retention- heart dilations and increased wall stress
remodeling- decreased performance- can be reversed with ACE I and aldosterone antagonists- spironalactone

83
Q

What does bnp do?

A

improve sodium and fluid balance via diuresis, vasodilation
Counteracts RAAS?

84
Q

What conditions increase PVR?

A

Hpoxia, hyperarbia, acidosis, PEEP, N2O, hypothermia

85
Q

Treatment of RV failure

A

Inotropes, vasodilators like NO or viagra, reversing the cause

86
Q

N2o vs No in PVR

A

N2O increased
NO decreased

87
Q

BP diagnostic criteria

A

normal- 120/80
Elevated- 120-129/80
HTN 1 130-139/80-89
HTN 2 >140/>90
HTN 3 (htn crisis) >180/ 120

88
Q

Primary vs secondary htn

A

1- no identifiable cause 95%
2- has identifiable cause 5%

89
Q

Possible causes of primary htn

A

SNS overreactivity
chronic vasoconstriction
deceased vasodilatory effects of pg and no
diet (too much salt and too little k/ca)

90
Q

Anesthetic considerations for hypertensive pt

A

Exaggerated HOTN on induction, exaggerated HTN on emergence
Adequate fluid intake helps promote stability

91
Q

BB considerations for htn pt

A

Continue if already prescribed, but NOT AS A FIRST DOSE

92
Q

ACEI/ARBs under GA

A

Can cause vasoplegia- hotn refractory to conventional pressors
Need vasopressing, meth blue, or terlipressin

93
Q

When to delay a case based off bp

A

180/110

94
Q

What MAP for BP patients

A

20% of preop

95
Q

What is the most common cause of intra-op HTN?

A

Surgical stimulation

96
Q

HTN crisis vs emergency and when to delay a case

A

Crisis 180/120
Emergency - end organ damage (CNS- encephalopathy, stroke, papilledema CARDIAC- chf, ischemia/agina RENAL- htn induced AKI)
Delay 180/110

97
Q

Tx of htn crisis

A

BB
CCB
SNP

98
Q

Complications of HTN

A

Stroke
LV hypertrophy
Ischemia
CHF
AA
ESRD

99
Q

Etiologies of secondary htn

A

renal artery stenosis (atherosclerosis, fibromuscular dysplasia) causes less blood flow to the kidneys, and then kidneys activate RAAS to improve BP
pheocromocytoma
Coarction of aorta

100
Q

Definitive Tx of renal artery stenosis

A

Renal artery endarectomy
Nephrectomy
NO ACEI bc they will drop bp and cause renal failure

101
Q

Mixed A and B blockers

A

Coreg
Labetalol
Bucindolol

102
Q

NDCCB vs DCBB

A

NDCCB-dilt and verapimil- target heart to decrease contractility, chronotropy, dromotropy, svr
DCBB- dipine targets vasculature to decrease SVR and vasodilate

103
Q

Arteriodilators vs neodilators

A

A- Hydralazine, SNP (50/50)- NO decreases SVR
V- NTG, SNP is 50/50, NO decreases preload

104
Q

ACEI effects

A

Inhibits AT2 vasoconstriction and aldosterone release

105
Q

Loop diuretics effects/moa

A

Lasix, Bumex
Inhibits Na-K-2Cl transporter in ascending loop of henle
Decreases preload via diuresis

106
Q

Thiazide diuretics

A

HCTZ, metolazone
Inhibits Na-Cl transporter in the distal convoluted tubules

107
Q

Aldosterone antagonists

A

Spirnolactone
Inhibits K excretion and Na reabsorption in collecting ducts
Blocks aldosterone at mineralcorticoid receptors

108
Q

K sparing diuretics

A

Spironalactone (actually an aldosterone antagonist_
Triamterene, amiloride- Inhibits K excretion and Na reabsorption by principle cells in the collecting ducts
ACTS independently of aldosterone

109
Q
A

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