Cardio physiology

Question 1

What is the role of the sarcoplasmic reticulum in muscle cells?

Answer 1

dd

Question 2

What are the steps in pacemaker cell contraction?

Answer 2

ATP binds to myosin head
Myosin releases Actin
ATP -> ADP + P
Tropomysoin and Troponin 
Ca binds to troponin

Question 3

Steps in muscle contraction (skeletal and cardiac)?

Answer 3

Muscle contraction involves actin filaments, myosin head and troponin and tropomyosin.

Myosin heads at attaching to actin filament causes muscle contraction.
Tropomyosin blocks myosin head from attaching to actin filament
Troponin keeps the tropomysoin in place to block myosin head
When there is a high Ca concentration, Ca attaches to troponin, allowing the tropomyosin to move.
This enables myosin head to attach the actin filament causing muscle contraction.

Question 4

Describe the cardiac myocyte contraction ?

Answer 4

Dependent on extracellular Ca which enters through the cells during plateau of action potential and stimulates calcium release through from the cardiac muscle through Type 2 Ryanodine channels on the sarcoplasmic reticulum (Ca induced Ca release)

Question 5

In contrast to skeletal muscle, cardiac muscle..?

Answer 5

1. Cardiac muscle action potenital has a plateu which is due to Ca influx
2. cardiac nodal cells spontaneously depolarise resulting in automatcity
3. Cardiac myocytes are electrically coupled to each other by gap junctions

Question 6

Steps in skeletal muscle contraction?

Answer 6

Na influx activated in Terminal axon on nerve which activates Ca.
Ca causes ACh release from nerve ending.
ACh causes Na to enter muscle cell.
Na activates Ca release from SR through Type 1 Ryanodine channels (Physically coupled to the SR) which then causes the release of Ca from the SR involved in muscle contraction.

Question 7

Steps in ventricular action potential?

Answer 7

Cardiac action potential resting membrane is - 90 mV.
Phase 0 = Na influx into cell through voltage gated Na channels, making the cell +ve

Phase 1 = initial repolarisation - inactivation of Na channels. Voltage gated K channels open and K exit cell.

Phase 2 = Plateau. Ca influx through Voltgae gated Ca channels blances K+ efflux.
Ca triggers Ca release from SR and mycocyte contraction

Phase 3 = rapid repolarisation. Efflux of K+ through voltage gated slow K channels and closure of V- Ca channels

Phase 4 = resting potenital - high K+ permeability through K channels

Question 8

Describe the step in the pacemaker action potential.

Answer 8

Pacemaker AP occurs in SA and AV nodes.

Phase 0 = upstroke - opening of V-gated Ca channels.
These cells lack Na channels in comparison to Ventricular AP.
Results in a slow conduction that is used by AV node to prolong transmission from atria to ventricles.

Phase 2 = does not occur

Phase 3 = Ca channels inactivated.
K channels activated and efflux of K -> -ve resting membrane.

Phase 4 = slow diastolic depolarisation
Membrane potenital spontaneously depolarises as Na conductance increases
Accounts for automaticity of SA and AV nodes
SLope of phase 4 determines HR.
ACh decreases the rate of diastolic depolarisation and heart rate
Catecholamines increase depolarization and increase HR.

Question 9

MOA Digoxin?

Signs of Dig toxicity?

Answer 9

Binds to N/K ATPase. Na influx into cardiac myocyte. No calcium is exchanged via the Na/Ca channel due to increased Na in cell therefore there is an accumulation of Ca in the cell and SR.
Contraction is therefore more forceful.

Phase 4 and O lengthened due to Na influx in cell caused by inhibition of Na/K ATPase by dig therefore maintaining a positive charge on the cell.

Dig toxicity:
HyperK
Arrhythmias
AV node blockade
GIT symptoms

Tx:
Digifab/Digibind is the Tx

Question 10

MOA of amiodarone?

Answer 10

Class III
Main effect is blocking Ca efflux in phase 3 of cardiac cycle
Prolongs the whole action potential as also block Na influx (Phase 0) and Phase 1 (K efflux)

Question 11

List the 5 classes of anti-arrhythmics and MOA

Answer 11

Class I: act via Na channels
Flecainide
Phenytoin
Procainide
Quinidine
Lidocaine

Class II: block sympathetic activity
BB - metoprolol and bisoprolol

Class III (K channel blockers):
Amiodarone
Sotalol (as well as class II)

Class IV: CBB
Verapmil
Diltiazem

Class V: Miscellaneous
Adenosine
Dig
Mg

Question 12

What is the O2 saturation of the coronary sinus?

Answer 12

30%
Myocardial tissue extracts 65% of O2.
Normal tissue extracts 25%.
(Normal tissue can compensate to reduced blood flow and extract more O2 however cardiac cannot)

Heart muscle relies on blood flow for more O2.
Other muscles cannot extract more O2.

Question 13

Hypoalphalipoproteinaemia. Genetic defect?

Answer 13

mutations in gene for pa AL resulting in isolated low HDL.

Question 14

What is Cholesteryl ester transfer protein (CETP) deficiency associated with?

Answer 14

Increased CAD

High HDL - proinflammatory afect

Question 15

What is the most common cause of cardiac disease in SLE?

Answer 15

Coronary at 25-50x risk

Can also have vasculitis, pericarditis