CV Exam 1 Week 1 Flashcards
Myosin chains and isoforms
Two HC and 4 LC
HC = alpha and beta isoforms
ß=slower ATPase activity
Cardiac ATPase speed
Faster than smooth
Slower than skeletal
Intercalated disks
Desmosomes = mechanical junction
Gap junctions = electrical junction
Types of troponin
C = binds calcium, 1 binding site I = inhibitory, 2 PKA phos sites, conformation change T = binds tropomyosin
Titin characteristics and two isoforms
Elastic spring, responsible for resting tension
N2B: more stiff
N2Ba: less stiff, longer
Ways to change stroke volume
Preload
Afterload (systemic resistance)
Contractility (inotropy)
Molecular basis for Starling’s Law
- Cardiac titin = stiff isoform (resists stretch past point)
- Calcium sensitivity increases at longer lengths
- Decreased lattice spacing
- Crossbridge overlap
SA intrinsic rate
100 bpm
Slowed to 60-80 by parasympathetic tone
Types of non-K cardiac Ion channels
Sodium: INa
Calcium: ICa-T, ICa-L (DHPR)
Na/Ca exchanger: INCX (NCX)
Cation: If (HCN)
5 K type cardiac ion channels
Ito: voltage dependent IKr (HERG): rapid delayed rectifier IKs (GIRK): slow delayed rectifier IK1: IKACh: increased by muscarinic receptors, slows pace
Cardiac refractory period
Absolute: R to mid T
Relative: mid T to end of T (avoid cardioversion)
Long QT progression to Vfib
Long QT increases time for afterdepolarizations to occur
Afterdepolarzations can trigger torsades
Torsades can lead to vfib
Na channel mutations
Prolong phase 2, preventing phase 3
Excess Na influx preventing repolarization
K channel mutations
Prolong phase 2, preventing phase 3
K+ channels are poorly folded, not expressed, and therefore repolarization is hindered
4 causes of arrhythmias
Inappropriate impulse stimulation 1. Ectopic foci 2. Triggered afterdepolariations Disturbed Impulse Conduction 3. Conduction block 4. Re-entry (circus rhythm)
Triggered AD’s causes and types
Both caused by calcium entry and increased chance with long QT
EAD: Ca-L activation
DAD: NCX dependent depolarization
Factors increasing chance of AD’s
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
Factors leading to re-entry
Initiated by EAD or DAD
MI
Drugs that block K+ channel
AD’s often trigger arrhythmias, but re-entry maintains
Conditions for re-entry (circus rhythm)
- Unidirectional conduction block
- Conduction around circuit > refractory period
- Retrograde current has larger stimulus into blocked area
Acute and chronic drug treatment of paroxysmal supraventricular tachycardia (PSVT)
Acute: Adenosine
Chronic: AV nodal blockers (II, III, IV)
Acute and chronic drug treatment of atrial fibrillation (afib)
Acute: AV Block (II, III, IV)
Chronic: AV Block + Warfarin
Cardioversion
Acute drug treatment of ventricular tachycardia/fibrillation (vtach/vfib)
Amiodarone, lidocaine
Collagen type in cardiac muscle
Type I and III
Systolic HF - cause and hallmarks
Dilated heart, loss of contractility
HErEF (LVSD, DCM)
Systolic HF - 3 primary causes
Destruction of heart muscle
Overstressed heart muscle
Volume overloaded heart muscle
Diastolic HF - mechanism and hallmarks
Hypertrophied heart, noncompliance problem
HFpEF (PSF, LVH)
Diastolic HF - 3 primary causes
High afterload
Myocardial thickening/fibrosis
External compression
ACC/AHA HF Stages
- Risk, no symptoms or disease
- Structural disease but no symptoms
- Structural disease with current/prior symptoms
- HF requiring specialized intervention
NYHA Functional Classes
I: Asymptomatic
II: Symptomatic with moderate exertion
III: Symptomatic with mild/minimal exertion
IV: Symptomatic at rest
S3 heart sound
After S1/S2 (Ken-tuc-ky)
Rapid expansion of ventricles relaxing (early in diastole)
Can be normal
S4 heart sound
Before S1/S2 (Ten-ne-ssee)
Atria contracting against LV (louder = stiffer LV)
Abnormal
Absent in Afib
