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CVPR > CV Exam 1 Week 1 > Flashcards

CV Exam 1 Week 1 Flashcards

1
Q

Myosin chains and isoforms

A

Two HC and 4 LC
HC = alpha and beta isoforms
ß=slower ATPase activity

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2
Q

Cardiac ATPase speed

A

Faster than smooth

Slower than skeletal

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3
Q

Intercalated disks

A

Desmosomes = mechanical junction

Gap junctions = electrical junction

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4
Q

Types of troponin

A 
C = binds calcium, 1 binding site
I = inhibitory, 2 PKA phos sites, conformation change
T = binds tropomyosin
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5
Q

Titin characteristics and two isoforms

A

Elastic spring, responsible for resting tension
N2B: more stiff
N2Ba: less stiff, longer

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6
Q

Ways to change stroke volume

A

Preload
Afterload (systemic resistance)
Contractility (inotropy)

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7
Q

Molecular basis for Starling’s Law

A
  1. Cardiac titin = stiff isoform (resists stretch past point)
  2. Calcium sensitivity increases at longer lengths
  3. Decreased lattice spacing
  4. Crossbridge overlap
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8
Q

SA intrinsic rate

A

100 bpm

Slowed to 60-80 by parasympathetic tone

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9
Q

Types of non-K cardiac Ion channels

A

Sodium: INa
Calcium: ICa-T, ICa-L (DHPR)
Na/Ca exchanger: INCX (NCX)
Cation: If (HCN)

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10
Q

5 K type cardiac ion channels

A 
Ito: voltage dependent
IKr (HERG): rapid delayed rectifier
IKs (GIRK): slow delayed rectifier
IK1: 
IKACh: increased by muscarinic receptors, slows pace
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11
Q

Cardiac refractory period

A

Absolute: R to mid T
Relative: mid T to end of T (avoid cardioversion)

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12
Q

Long QT progression to Vfib

A

Long QT increases time for afterdepolarizations to occur
Afterdepolarzations can trigger torsades
Torsades can lead to vfib

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13
Q

Na channel mutations

A

Prolong phase 2, preventing phase 3

Excess Na influx preventing repolarization

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14
Q

K channel mutations

A

Prolong phase 2, preventing phase 3

K+ channels are poorly folded, not expressed, and therefore repolarization is hindered

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15
Q

4 causes of arrhythmias

A 
Inappropriate impulse stimulation
1. Ectopic foci
2. Triggered afterdepolariations
Disturbed Impulse Conduction
3. Conduction block
4. Re-entry (circus rhythm)
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16
Q

Triggered AD’s causes and types

A

Both caused by calcium entry and increased chance with long QT
EAD: Ca-L activation
DAD: NCX dependent depolarization

17
Q

Factors increasing chance of AD’s

A

Long QT
HF (even w/out QT)
Increased sympathetic tone (ß-ad activity increases Ca2+ influx)
AD’s often trigger arrhythmias, but re-entry maintains

18
Q

Factors leading to re-entry

A

Initiated by EAD or DAD
MI
Drugs that block K+ channel
AD’s often trigger arrhythmias, but re-entry maintains

19
Q

Conditions for re-entry (circus rhythm)

A
  1. Unidirectional conduction block
  2. Conduction around circuit > refractory period
  3. Retrograde current has larger stimulus into blocked area
20
Q

Acute and chronic drug treatment of paroxysmal supraventricular tachycardia (PSVT)

A

Acute: Adenosine
Chronic: AV nodal blockers (II, III, IV)

21
Q

Acute and chronic drug treatment of atrial fibrillation (afib)

A

Acute: AV Block (II, III, IV)
Chronic: AV Block + Warfarin
Cardioversion

22
Q

Acute drug treatment of ventricular tachycardia/fibrillation (vtach/vfib)

A

Amiodarone, lidocaine

23
Q

Collagen type in cardiac muscle

A

Type I and III

24
Q

Systolic HF - cause and hallmarks

A

Dilated heart, loss of contractility

HErEF (LVSD, DCM)

25
Q

Systolic HF - 3 primary causes

A

Destruction of heart muscle
Overstressed heart muscle
Volume overloaded heart muscle

26
Q

Diastolic HF - mechanism and hallmarks

A

Hypertrophied heart, noncompliance problem

HFpEF (PSF, LVH)

27
Q

Diastolic HF - 3 primary causes

A

High afterload
Myocardial thickening/fibrosis
External compression

28
Q

ACC/AHA HF Stages

A
  1. Risk, no symptoms or disease
  2. Structural disease but no symptoms
  3. Structural disease with current/prior symptoms
  4. HF requiring specialized intervention
29
Q

NYHA Functional Classes

A

I: Asymptomatic
II: Symptomatic with moderate exertion
III: Symptomatic with mild/minimal exertion
IV: Symptomatic at rest

30
Q

S3 heart sound

A

After S1/S2 (Ken-tuc-ky)
Rapid expansion of ventricles relaxing (early in diastole)
Can be normal

31
Q

S4 heart sound

A

Before S1/S2 (Ten-ne-ssee)
Atria contracting against LV (louder = stiffer LV)
Abnormal
Absent in Afib

CVPR (5 decks)

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