Cardio Flashcards
CNS/NMJ vs ANS major differences
in the ANS:
- synapses are not as tight (en passant)
- metabotropic receptors, slower transmission
comparison between sympathetic and parasympathetic divisions of the ANS
Symp: thoracolumbar; more exist points; short pres (Ach- nicotinic), long posts (Ne/e- adrenergic)
PS: craniosacral; long pres (Ach- nicotinic), short post (Ach- muscarinic)
EC coupling in skeletal muscle
- electrically activated -
1. AP (Ach gated channels at NMJ) to t-tubule
2. depolarization activates DHPR
3. DHPR changes conformation and activates Ryr
4. Ca2+ released from SR
5. Ca2+ binds troponin
6. troponin moves tropomyosin to actin groove
7. myosin (thick) binds actin (thin)
8. crossbridge/power stroke
9. Ca2+ is sequestered by SRCA/relaxatio
EC coupling smooth muscle (vascular system) - NO t-tubules
- no electrical event -
1. increased in Ca2+ (hormones- IP3, pacemakers- voltage, NTs- ligand)
2. 4 Ca2+ binds calmodulin
3. activates myosin light chain kinase
4. phosphorylates light chain
5. P-myosin can bind actin (form cross bridge) with hydrolysis of ATP
6. inactivated by myosin light chain phosphatase
alpha- vasoconstriction
beta- vasodilation
how does calcium modulate sodium channel activity? what happens with hypercalcemia? hypokalemia?
- Ca binds to proteins surrounding Na channel, makes environment more positive, h-gate closes, less APs
- Na+ channels become inactive (less available), conduction slows
signs: weak reflexes - low K+ = prolonged QT
sequence of electical activity
SA atrial muscle AV His Bundle Purkinje
P-R interval
conduction time from atrial muscle-AV node-his-purkinje- 200 ms (most is AV nodal conduction)
QRS interval
conduction time from endocardial to epicardial surface in ventricular muscle- 100 ms
1st, 2nd, 3rd degree heart block
1st- abnormal prolongation in P-R interval
2nd- some atrial impulses fail to activate ventricles; not all P waves followed by QRS (e.g. 2:1 conduction)
3rd- complete AV block; no consistent P-R interval
what does digitalis inhibit and what can it cause
- inhibits Na/K ATPase (sodium out, potassium in), reverses Na/Ca2+ pump (sodium in, Ca out)
- DADs by abnormally increasing intracellular Ca2+
conduction of ventricular tachycardia
does not go through his-purkinje, goes through muscle in longitudinal way, conduction is slower, see slurred QRS
what does the QT interval represent? what does the ST wave of the EKG correspond to?
QT- AP duration/systole (not conduction parameter)
the plateau- normally records nothing
slow vs fast cardiac action potentials
slow- AV and SA node, long refractory (Ca2+)
fast- atrial & ventricular muscle, His-Purkinje, fast refractory (Na+)
In atrial fibrillation, what is determining the rate and rhythm of the ventricular activation? heart rate is slower during expiration/inspiration?
AV node refractory characteristics; expiration
electrical mechanisms responsible for dysrhythmias
altered automaticity, re-entry of excitation, triggered activity
Mechanism of EC coupling in the heart
- Ca2+ induced Ca2+ release*
1) AP goes down into T-tubules
2) Depolarization activates L-type Ca2+ currents on sarcolemma & t-tubule membrane (small Ca2+ influx)
3) Influx of Ca2+ binds to SR and opens Ryr channels
4) Released Ca2+ binds to troponin C
5) Relaxation occurs when Ca2+ is removed via Ca2+ ATPase
what does PKA phosphorylate in the catecholamine cascade? (Ne/E binds, activates cAMP, cAMP phosphorylates 3 things)
1- Ca2+ channels of sarcolemma- increases calcium influx
2- phospholamban- increases SRCA rate (relaxation- plb normally inhibits Ca2+ re-uptake)
3- troponin I- activate TI- reduces troponin C’s affinity for calcium
1&2 increase strength of contraction
2&3 decrease time course of relaxation
4 factors that determine cardiac output
heart rate, myocardial contractility, preload, after-load
what is after-load and what are 3 things that cause it
- any force that resists muscle shortening
1. higher arterial blood pressure
2. dilated heart
3. aortic stenosis
what is contractility
inherent ability of actin and myosin to form cross-bridges and generate tension based on Ca2+ ; give digitalis
- raises peak isometric tension
- enhances the rate of relaxation (sympathetics)
- increases the amount of muscle shortening
- increases the velocity of shortening
if you give someone a transfusion, how does it increase cardiac output?
increase end diastolic volume, increases max amount of force you can achieve by stretching the sarcomere, increases systolic pressure
3 requirements for re-entry of excitation ; 3 causes
1- geometry for conduction loop
2- slow or delayed conduction
3- unidirectional conduction block
causes:
ischemia
infarction
congenital bypass tracts (WPW)
systolic vs diastolic heart failure
systolic- decrease in contractility curve shifts out
diastolic- decrease in compliance curve shifts up (but same contractility)
difference between end systolic and end diastolic on PV curve
stroke volume
