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Cardiology > Cardiac cell/physiologypharmacolgy > Flashcards

Cardiac cell/physiologypharmacolgy Flashcards

1
Q

What cardiac cell types generate action potentials?

A

All

Atrial and Ventricular
Sinoatrial node cells

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2
Q

What are phases in Ventricular action potential?

A 
5 phases:
Phase 0: rapid depolarization I Na
Phase 1: repolarization
Phase 2: I Ca, sodium/k pump plateau
Phase 3: influx K repolarization 
Phase 4: resting Na / k pump resets baseline gradients
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3
Q

Voltage potential ventricular cells

A

-90 mV with threshold potential @ -65 mV

Depolarization to + 45 mV

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4
Q

Sino atrial action potential

Phase 0

A

Ca influx

Phase 4 spontaneously depolarizes with Na I(f)
Therefore Ca blockers (slow I Ca) and decrease automaticity

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5
Q

AAD classes

A 
Von Williams classification
Class 1 (Na channel)
A quinidine, C flecanide. Lengthen AP
B lidocaine, mex.    shorten AP
Class 2: b blocker.   Decrease automatic.
Class 3: k channel- lengthen AP (amio,soto,Ibutilide)
Class 4: Ca2+ block- L type- length AP, decrease automaticity
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6
Q

Digoxin

A

Na/K pump

Lengthens ap

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7
Q

Adenosine

A

K channel opens & shortens AP

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8
Q

Second messenger in electrical- contraction coupling

A

Calcium

Increasing intracelluar calcium increases contractility

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9
Q

Purposes of Action potential

A

When increases to - 60 mV ap initiates

1: propagates to other myocytes via I Na
2: mediates Ca influx into cell

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10
Q

Calcium induced Ca release

A

Ca into cell triggers Ca release from SR

Too much intracelluar Ca cytotoxic- must be taken up quickly
Force of contraction depends on rate/ amplitude of Ca influx
cAMP modulates SR Ca release/uptake

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11
Q

Sarcomere:

  1. Relation to HCM
  2. What does Ca do?
  3. What’sATP role?
A

Mutations of individual components cause HCM
Ca dislodges trop/tropomyosin complex allows myosin head to bind to actin
ATP needed for detaching myosin from actin
(Relaxation during diastole)

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12
Q

Drug Effects on Ca induced Ca release

Digoxin
CCB
B blockers
Phosphodiesterase inhibitors

A

Dig: increases Ca (Na/k pump less so more ic Na, so less ic Ca )
CCB: decreases ic Ca via L-type channel
BBlocker: decrease Ca via
adenylate cyclase by b1 adrenergic receptor
PD inh: inhibits cAMP

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13
Q

Cellular abnormalities in Heart Failure

A

SERCA dysfunction
Increased intracelluar Ca
B receptor down regulates

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14
Q

Ryanodine receptor?

A

Hyperphosphorylation causes Ca leak characteristic of HF

On sarcoplasmic reticulum

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15
Q

Angiotensin II
Vascular effects
Myocardial effects

A 
Vasoconstricts via G/PLC/IP3 increasing SR Ca
Na, h2o retention increases preload
Sympathetic activation
Endothelial activation
Atherosclerosis 
Myocardial- hypertrophy/fibrosis
Does not increase myo contraction
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16
Q

Cardiac remodeling

A

Response injury
Myocytes: lvh, fibrosis
Vascular: sm mm proliferation
Electrical: af begets af

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17
Q

Sympathetic system components:
Mediators
Receptors
Receptor coupled

A

Catecholamines: epi, norepinephrine
Alpha 1: vasoconstrictor Alpha 2: vasorelaxation (also inhibits NE release from axons)
B1: myocontraction, chrono B2: vasorelaxation B3 lipolysis- non cardiac

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18
Q

G Proteins

A

Protein that initiates signal transduction from coupled receptors (AT, alpha,beta, AR)
2 subunits: alpha and betay (not cardiac)
3 types of alpha: s ionotropy/chrono & vasorelaxation
i neg ionotropy/chrono
q peripheral vasoconstricton

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19
Q

Vascular signaling

A

B2 receptor: Coupled to Gs
activates ac to camp
Inhibits myosin light chain kinase (smooth mm)
Inhibits actin myosin binding causing vasodilation
Alpha1: coupled to Gq
Activates Plc to IP3, opens SR Ca channel causing vasoconstricton

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20
Q

Alpha2

A

Presynaptic alpha 2

Activation inhibits NE/ epi release so vasodilation occurs

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21
Q

Adrenergic signals: receptor specificity

A

Alpha 1, alpha 2, beta 2: vasculature

Beta 1 myocardium

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22
Q

Adrenergic agonists: 5

A 
Epi  alpha 1, beta 1, beta 2
Norepinephrine  alpha 1, beta 1
Dobutamine: beta 1, beta 2
Phenylepherine: alpha 1
Clonidine: alpha 2
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23
Q

Adrenergic antagonists (2)

A

Phentolamine: alpha 2- vasoconstricts

Propranolol: beta 1, beta 2

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24
Q

Parasympathetic mediators/receptors

A 
Acetylcholine mediated
Muscarinic receptors
M2 & M3 relevant
M2: heart- neg ionotropy /chrono
M3: vasc sm mm- constricts
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25
Q

Myocardial Parasympathetic Signaling

A

M2 receptor: Gi
Directly opposes beta 1 Gs stimulated contraction

Gi: neg ionotropy, neg chronotropy
Blocks adenylate cyclase so ATP conversion to cAMP inhibited

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26
Q

Parasympathetic Vascular SM signal

A

M3 receptor: coupled to Gq

Activates PLC/IP3 causing SR Ca release NO production causing vasodilation

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27
Q

Acetylcholine Vasculature Effects

A

Ach
Increases endothel. NO release causing vasodilation
Denuded endothelium ach access to myocyte causes constriction

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28
Q

Parasympathetic effects:
Cardiac
Vasculature

A

Cardiac: parasympathetic directly opposes beta 1 stimulation (M3 via Gq via PLC producing IP3 causing SR Ca release via IP 3 receptor)

Vascular: depends on endothelium - intact causes dilation via NO, denuded constricts via Gq/PLC/IP3

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29
Q

Coagulation

Pathways

A

Extrinsic: tissue factor + VIIa
Thrombin activates plts and intrinsic system, fibrin comprises clot

Intrinsic: amplifies signal

Pathways converge at factor X

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30
Q

Platelet activation:

potency of potential activators

A

Thrombin>collagen>ADP> epi

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31
Q

Platelet triggers binding to:

A

vWF (GP Ia/IIb)

Fibrinogen (GP IIB/IIIa)

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32
Q

Anti clotting Mechanisms:

A

Antithrombin: proteolyzed thrombin- Xa,IXa>Xa, Xia
Activated protein C, S
proteolyzed factors Va/VIIIa
Fibrinolysis: plasminogen mediated (plasmin cleaves fibrin)- activators tPA, urokinase
inactivators (plasminogen activator inhibitors) PAI 1, PAI 2

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33
Q

Aspirin

A

Target- platelets

COX 1- inhibits thromboxane a2 (txa2) synthesis

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34
Q

Abciximab

A

Repro
Platelets inhibit
GP IIb/IIIa

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35
Q

Clopidogrel

A

Plavix
Platelet
ADP receptor antagonist

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36
Q

Dibigatran

A

Hirudin
Clotting cascade
Thrombin

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37
Q

Heparin

A

Clotting cascade

Thrombin, Xa via anti thrombin

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38
Q

LMW heparin

A

Clotting cascade

Xa> thrombin

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39
Q

Fondaparinux

A

Arixtra
Clotting cascade

Xa

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40
Q

Warfarin

A

Clotting cascade

Thrombin
VII, VIII, IX, X protein C, protein S

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41
Q

Pure thrombin inhibitor

A

Dabigatran

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42
Q

Marfans
Characteristic
Gene/chromosome

A

Dilated aortic root, dissection Autosomal Dom
Fibrillin gene: FBN1
Chromosome 15

Less common: TGFb receptor gene chromosome 3 (less than 10% of cases)

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43
Q

Ehlers-danlos

A

Aorta not usually involved- large to med size arterial rupture

Auto Dom and Recessive

7 types: collagen defect

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44
Q

Marfans characteristics

A

MVP,ectopic lentis, dural ectasia, pectins exc.

45
Q

Marfan pregnancy

A

10% dissection risk if Ao> 4 cm

If dissect 3rd term, C section first, then Ao repair

46
Q

Marfan screening

A

If positive mutation then genetic screen-

Otherwise do chest imaging

47
Q

Channelopathies

A

Long QT:auto rec or dom:
Na channel: SCN5A, gain of function
K channel KCNQ1, KCNH2, loss of function

Brugada syndrome: ad
SCN5A loss of function

48
Q

Familial Hypercholesterolemia

A

LDL receptor defective/deficient
Auto dominant

Xanthomata , as,cad,pvd
Heterozygotes omset cad in 30’s

49
Q

Hypertrophic cardiomyopathy

A

Histologic
Myocardial disarray
75% sarcomere mutation-autodominant variable penetrance
14-26% with myosin binding protein C
13-25% beta myosin heavy chain
trop T 4-15%, trop I 2-7%, alpha tropom.<5%

50
Q

Muscular dystrophies

A

Duchenne: x linked dystrophin
death early adult
dilated fibrotic cm

Becker: dystrophin
mm dystrophies less severe, but CM worse

51
Q

Cardiac metabolism
fuel
sources

A

5kg ATP/d
70% Fatty Acids
Glucose 30%

FA passively diffuses into cell/ glu requires active xport- ATP/fa molecule> glu molecule

52
Q

Stressed cardiac metabolism

A

Substrate switch to glucose
less O2 used
May metabolize anaerobically

53
Q

Diabetes affecting cardiac metabolism

A

Increased insulin resistance decreases glu metabolism
Increases FA
Substrate switch to glucose not possible

54
Q

Starling Mechanism

A 
More x links at optimum length
Too long (over stretched) less force

Optimum actin- myosin cross linkage

55
Q

Afterload/wallstress

A

Wall stress: Laplace law

Pressure x radius/ 2 (wall thickness)

56
Q

v wave

A

Tricuspid regurg
Mitral regurg
size similar to degree

57
Q

Cannon a wave

A

Complete heart block

Vent tachy

58
Q

Square root sign

A

Diastolic pressure equalization

Restriction: concordant between lv and rv

Constriction: discordant lv/ rv

59
Q

Calculate cardiac output

Echo

A

CO= SV x HR

Pressure CO= P/R
Echo: CO=CSA x VTI x HR
= 3.14(dia/2) squared x (xcm) x beats/min

60
Q

Cardiac output
Thermo
Fick

A

Thermo: tr causes Underestimation
Low output overestimates

Fick: MVO2 80% high
Assumed O2 consumption

61
Q

Ohm’s Law

A

CO~ pressure / resistance

r= pressure/ co

svr=mean abp/ cardiac index

62
Q

Sodium channel drugs

A 
Von Williams class 1
A: lengthens ap- quinidine, flecainide

B: shortens ap- lidocaine, mexilitine

63
Q

AAD affecting calcium channel

A 
Von Williams class
2: b blockers- indirectly decreases automaticity

4: ca blockers- L type channel- lengthens ap and decreases automaticity

64
Q

AAD K channel

A

Von Williams class 3
Lengthens ap
Amiodarone, sotolol, ibutalide (Covert)

65
Q

Sarcoplasmic Reticulum Ca channels

A

Ryr- phosphorylated pumps Ca into cytoplasm

SERCA- PLB phosphorylated pumps Ca into SR

66
Q

What does Ca do to actin/myosin

A

Binds to troponin-tropomysin complex so actin/myosin can bind

67
Q

Milrinone

A

Phosphodiesterase inhibitor
Increases cAMP
Increases phos of Ryr and SERCA

68
Q

B blockers cellular action

A 
Decrease intracellular Ca
B adrenergic receptor blocked so
Less activation of G alpha s
Less Adyl cycl- less cAMP 
Less phor of Ryr and SERCA
69
Q

Digoxin

A

Blocks Na/K pump
Slowly increases Ca intracellular

Prob more effects via parasympathetic tone

70
Q

Laplace law

A

Pressure x radius/ 2x wall thickness

71
Q

Cellular CHF events

A

SERCA dysfunction
Increases Ca influx
B receptor down reg
Poor Ca flux

72
Q

Angiotensin 2
Vascular
Cardiac

A

Vasc: vaso const via G alpha q/Plc/ipb Ca Myo: hyper/fib/ not Myo
Na h2o retention Contractile
Increase sympath
Endothel dysfunction
Atherosclerosis

73
Q

B1 vs B2

A

B1 myocardium

B2 vasodilation. Also alpha 1,2

74
Q

Direct thrombin inhibitor

A

Dabigatran

75
Q

Prominent y descent

A

Look for constriction / restriction

76
Q

Large v waves

A

MR

Also diastolic dysfunction

77
Q

Mitral valve repair: loop effects on CO?

A

Decreases preload
Increases after load, so CO less
(Loop smaller)

78
Q

Mean pressure formula

A

1/3 pulse pressure + diastolic pressure

79
Q

CO and mixed venous sat

A

> 80% ? Shunting
65%-80% normal
<65% low output

80
Q

Pitfalls: Fick

A

Assume O2 consumption
Tech challenging
High output- lower denominator causes more error
CO=

81
Q

PVR Xplant issue

A

Threshold t tolerate more R

PVR= mean PAP -PCWP/CO (results in Woods units)

82
Q

Qp/Qs
Significant values
Why values may decrease

A

1.5-2 signif
May decrease in vsd in Eisenminger
In asd low likely not sig

83
Q

Qp/Qs calculation

A

mvO2= .6 svc+.3ivc
Assume 100% art sat=pv sat
Qp/Qs= 100-MVO2/100-PaO2

84
Q

renal and class 3 AA

A

sotalol and dofetilide renal excreted and contraindicated in renal dysfunction

85
Q

amiodarone

A

features of all 4 vaughn williams classes
every organ systems
drug interaction: warfarin, dig, statin

86
Q

drodarenone

A

avoid in CHF and liver dz
permanent afib has increased risk
monitor rhythm every 3 mths of paroxysmal in the case perm. afib occurs

87
Q

digoxin

mechanism

A

increase vagal tone (binds to Na pumps in neuronal membranes) inhibits sympathetic outflow, increases parasympathetic tone and decreases av nodal conduction
blocks na/k atpase- increases intracellular Ca- mild ionotrope
foxglove

88
Q

adenosine

mechanism

A

binds to adenosine receptor
1. Decreases conduction:
decreases cAMP- decreases Ca and Na into cells
2. Reduces automaticity: reduces automaticity by hyperpolarizing cell increases outward K flow

89
Q

adenosine in atrial fib

A

outward K current shortens atrial refractoriness and increases propensity for atrial fibrillation

90
Q

adenosine contraindications

A

flushing, chest pain, bronchospasm
CI in asthmatics
xplant patients denervated and may have prolonged pauses- decrease dose of adenosine

91
Q

atropine mechanism

A

blocks action of acetylcholine at parasympathetic sites

SE
tachy, urin retention, glaucoma, delerium

92
Q

atrial fibrillation etiologies:

A

altered atrial anatomy:
fibrosis, inflammation, enlarged size

altered refractoriness (shortened)
hyperthyroid, etoh, vagal tone
93
Q

CHADS 2

A

CHF (1), HTN (1), AGE (1), DM (1), CVA/TIA (2)
0= 1.9
1= 2.8
2= 4.0
3= 5.9 4= 8.5 5= 12.5 6= 18.2 (risk ~double chads #)

94
Q

anticoagulation guidelines chads2

A

1 asa 81-325mg

>= 2 asa or warf inr 2.5 or dabigatran/ rivaroxaban

95
Q

alternative anticoagulants

A

dabigatran- IIa bid dosing,
rivaroxaban- Xa 20/d
stops prothrombin conversion to thrombin

96
Q

wide complex tachycardia- irreg

A

consider atrial fib with bypass tract
may degenerate into vent fibrillation
if bypass tracts; avoid ca, b blockers, dig- conduction preferentially down bpt
rx dccv, procainamide, sotalol, amio, ibut. ablation

97
Q

effectiveness of AA in afib recurrance

A

SR for 1 yr
amio 69%
sotalol/propafenone 39%

98
Q

afib ablation success

A

ideal pt- 60-80%, >80% requires multiple procedures

higher risk pt- 50-70% multiple > 70%

99
Q

afib ablation complication

A 
major  2-12%
flutter 5%
vascular 1-5%
tampanode 0.5-3%
esophageal, infection, death, phrenic injury
100
Q

AA in ischemic CM with afib

A

dofetilide tikosyn

amiodarone

101
Q

fluoropyrimidine

A

5fu

May cause transient Myo ischemia

102
Q 
Over counter meds with warfarin:
St. John wart
Vick
Coq10
Melatonin     Primrose oil?
A

Primrose oil increases inr

Others lower inr

103
Q

B blockers and depressed EF

A

Metoprolol succinate
Coreg
Bisoprolol

104
Q

Elderly bp goals

A

> 80 140-145 sbp goal

105
Q

Friedwield calculation

A

LDL= TC-HDL-TG/5

106
Q

B blocker not metabolized by liver

A

Atenolol

Lipid insoluble

107
Q

Vardinafil med interactions

A

Levitra

Prolongs qt

108
Q

Quinidine

A

G6pd

Deficiency may cause hemolytic anemia

109
Q

Brugada

A

S5cna

Cardiology (15 decks)

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