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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
Myocardial Parasympathetic Signaling
M2 receptor: Gi Directly opposes beta 1 Gs stimulated contraction Gi: neg ionotropy, neg chronotropy Blocks adenylate cyclase so ATP conversion to cAMP inhibited
26
Parasympathetic Vascular SM signal
M3 receptor: coupled to Gq | Activates PLC/IP3 causing SR Ca release NO production causing vasodilation
27
Acetylcholine Vasculature Effects
Ach Increases endothel. NO release causing vasodilation Denuded endothelium ach access to myocyte causes constriction
28
Parasympathetic effects: Cardiac Vasculature
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
29
Coagulation | Pathways
Extrinsic: tissue factor + VIIa Thrombin activates plts and intrinsic system, fibrin comprises clot Intrinsic: amplifies signal Pathways converge at factor X
30
Platelet activation: | potency of potential activators
Thrombin>collagen>ADP> epi
31
Platelet triggers binding to:
vWF (GP Ia/IIb) | Fibrinogen (GP IIB/IIIa)
32
Anti clotting Mechanisms:
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
33
Aspirin
Target- platelets COX 1- inhibits thromboxane a2 (txa2) synthesis
34
Abciximab
Repro Platelets inhibit GP IIb/IIIa
35
Clopidogrel
Plavix Platelet ADP receptor antagonist
36
Dibigatran
Hirudin Clotting cascade Thrombin
37
Heparin
Clotting cascade | Thrombin, Xa via anti thrombin
38
LMW heparin
Clotting cascade | Xa> thrombin
39
Fondaparinux
Arixtra Clotting cascade Xa
40
Warfarin
Clotting cascade Thrombin VII, VIII, IX, X protein C, protein S
41
Pure thrombin inhibitor
Dabigatran
42
Marfans Characteristic Gene/chromosome
Dilated aortic root, dissection Autosomal Dom Fibrillin gene: FBN1 Chromosome 15 Less common: TGFb receptor gene chromosome 3 (less than 10% of cases)
43
Ehlers-danlos
Aorta not usually involved- large to med size arterial rupture Auto Dom and Recessive 7 types: collagen defect
44
Marfans characteristics
MVP,ectopic lentis, dural ectasia, pectins exc.
45
Marfan pregnancy
10% dissection risk if Ao> 4 cm If dissect 3rd term, C section first, then Ao repair
46
Marfan screening
If positive mutation then genetic screen- | Otherwise do chest imaging
47
Channelopathies
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
Familial Hypercholesterolemia
LDL receptor defective/deficient Auto dominant Xanthomata , as,cad,pvd Heterozygotes omset cad in 30's
49
Hypertrophic cardiomyopathy
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
Muscular dystrophies
Duchenne: x linked dystrophin death early adult dilated fibrotic cm Becker: dystrophin mm dystrophies less severe, but CM worse
51
Cardiac metabolism fuel sources
5kg ATP/d 70% Fatty Acids Glucose 30% FA passively diffuses into cell/ glu requires active xport- ATP/fa molecule> glu molecule
52
Stressed cardiac metabolism
Substrate switch to glucose less O2 used May metabolize anaerobically
53
Diabetes affecting cardiac metabolism
Increased insulin resistance decreases glu metabolism Increases FA Substrate switch to glucose not possible
54
Starling Mechanism
``` More x links at optimum length Too long (over stretched) less force ``` Optimum actin- myosin cross linkage
55
Afterload/wallstress
Wall stress: Laplace law | Pressure x radius/ 2 (wall thickness)
56
v wave
Tricuspid regurg Mitral regurg size similar to degree
57
Cannon a wave
Complete heart block | Vent tachy
58
Square root sign
Diastolic pressure equalization Restriction: concordant between lv and rv Constriction: discordant lv/ rv
59
Calculate cardiac output | Echo
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
Cardiac output Thermo Fick
Thermo: tr causes Underestimation Low output overestimates Fick: MVO2 80% high Assumed O2 consumption
61
Ohm's Law
CO~ pressure / resistance r= pressure/ co svr=mean abp/ cardiac index
62
Sodium channel drugs
``` Von Williams class 1 A: lengthens ap- quinidine, flecainide ``` B: shortens ap- lidocaine, mexilitine
63
AAD affecting calcium channel
``` Von Williams class 2: b blockers- indirectly decreases automaticity ``` 4: ca blockers- L type channel- lengthens ap and decreases automaticity
64
AAD K channel
Von Williams class 3 Lengthens ap Amiodarone, sotolol, ibutalide (Covert)
65
Sarcoplasmic Reticulum Ca channels
Ryr- phosphorylated pumps Ca into cytoplasm SERCA- PLB phosphorylated pumps Ca into SR
66
What does Ca do to actin/myosin
Binds to troponin-tropomysin complex so actin/myosin can bind
67
Milrinone
Phosphodiesterase inhibitor Increases cAMP Increases phos of Ryr and SERCA
68
B blockers cellular action
``` 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
Digoxin
Blocks Na/K pump Slowly increases Ca intracellular Prob more effects via parasympathetic tone
70
Laplace law
Pressure x radius/ 2x wall thickness
71
Cellular CHF events
SERCA dysfunction Increases Ca influx B receptor down reg Poor Ca flux
72
Angiotensin 2 Vascular Cardiac
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
B1 vs B2
B1 myocardium | B2 vasodilation. Also alpha 1,2
74
Direct thrombin inhibitor
Dabigatran
75
Prominent y descent
Look for constriction / restriction
76
Large v waves
MR | Also diastolic dysfunction
77
Mitral valve repair: loop effects on CO?
Decreases preload Increases after load, so CO less (Loop smaller)
78
Mean pressure formula
1/3 pulse pressure + diastolic pressure
79
CO and mixed venous sat
>80% ? Shunting 65%-80% normal <65% low output
80
Pitfalls: Fick
Assume O2 consumption Tech challenging High output- lower denominator causes more error CO=
81
PVR Xplant issue
Threshold t tolerate more R | PVR= mean PAP -PCWP/CO (results in Woods units)
82
Qp/Qs Significant values Why values may decrease
1.5-2 signif May decrease in vsd in Eisenminger In asd low likely not sig
83
Qp/Qs calculation
mvO2= .6 svc+.3ivc Assume 100% art sat=pv sat Qp/Qs= 100-MVO2/100-PaO2
84
renal and class 3 AA
sotalol and dofetilide renal excreted and contraindicated in renal dysfunction
85
amiodarone
features of all 4 vaughn williams classes every organ systems drug interaction: warfarin, dig, statin
86
drodarenone
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
digoxin | mechanism
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
adenosine | mechanism
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
adenosine in atrial fib
outward K current shortens atrial refractoriness and increases propensity for atrial fibrillation
90
adenosine contraindications
flushing, chest pain, bronchospasm CI in asthmatics xplant patients denervated and may have prolonged pauses- decrease dose of adenosine
91
atropine mechanism
blocks action of acetylcholine at parasympathetic sites SE tachy, urin retention, glaucoma, delerium
92
atrial fibrillation etiologies:
altered atrial anatomy: fibrosis, inflammation, enlarged size ``` altered refractoriness (shortened) hyperthyroid, etoh, vagal tone ```
93
CHADS 2
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
anticoagulation guidelines chads2
1 asa 81-325mg | >= 2 asa or warf inr 2.5 or dabigatran/ rivaroxaban
95
alternative anticoagulants
dabigatran- IIa bid dosing, rivaroxaban- Xa 20/d stops prothrombin conversion to thrombin
96
wide complex tachycardia- irreg
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
effectiveness of AA in afib recurrance
SR for 1 yr amio 69% sotalol/propafenone 39%
98
afib ablation success
ideal pt- 60-80%, >80% requires multiple procedures | higher risk pt- 50-70% multiple > 70%
99
afib ablation complication
``` major 2-12% flutter 5% vascular 1-5% tampanode 0.5-3% esophageal, infection, death, phrenic injury ```
100
AA in ischemic CM with afib
dofetilide tikosyn | amiodarone
101
fluoropyrimidine
5fu | May cause transient Myo ischemia
102
``` Over counter meds with warfarin: St. John wart Vick Coq10 Melatonin Primrose oil? ```
Primrose oil increases inr | Others lower inr
103
B blockers and depressed EF
Metoprolol succinate Coreg Bisoprolol
104
Elderly bp goals
> 80 140-145 sbp goal
105
Friedwield calculation
LDL= TC-HDL-TG/5
106
B blocker not metabolized by liver
Atenolol Lipid insoluble
107
Vardinafil med interactions
Levitra | Prolongs qt
108
Quinidine
G6pd | Deficiency may cause hemolytic anemia
109
Brugada
S5cna

Cardiology (15 decks)

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