Cardiac muscle Flashcards

1
Q

Cardiac muscle implicated in which diseases

A

Hypertension (can be from higher CO)
Ischaemic heart disease (due to reduced blood flow to the cardiac muscles)
Chronic heart failure (due to reduced cardiac muscle-mediated CO)

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2
Q

Initiation of cardiac contraction and duration

A

SA and then AV nodes fire, and Ca influxes from EC space through VGCCs and is released from the sarcoplasmic reticulum (SR). The cardiac APs are long (approx 250ms) followed by a refractory period to ensure the heart does not contract too soon: lets the heart refill.

Frequency and force of contraction regulated by autonomic nervous system, e.g., B1-AR reduces phase 4 depolarisation - faster HR.

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3
Q

Phases of cardiac contraction

A

Phase 0: rapid depolarisation mediated by Na (initiated by AP)

Phase 1: partial repolarisation due to Na+ channels closing

Phase 2: plateau from Ca influx

phase 3: repolarisation from VGCC closing and VGPC opening

Phase 4 (only in pacemaker cells): pacemaker potential, gradual depolarisation until next AP occurs

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4
Q

Characteristics of atrial contraction and atrial fibrillation

A

During relaxation of heart, blood flows into atria. Upon contraction blood sent to ventricle. The 0.1s delay between SA and AV node firing allows complete filing of ventricle before next contraction.

Atrial fibrillation is when the atria is not fully emptied upon contraction, some blood remains.

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5
Q

Characteristics of ventricular contraction and ventricular fibrillation

A

AP travels down the bundle of His and then through the purkinje fibres of the ventricles. They then contract.

Ventricular fibrilation is from uncoordinated contraction, leading to incomplete pumping of the blood out the heart.

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6
Q

Mechanism of electricak defibrillation

A

Electrical current is applied and simultaneously depolarises the cardiac muscles. Triggers sycnhronised contraction of the heart.

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7
Q

Parasympathetic innervation of which regions of heart, and effect

A

vagus nerve innervates SA, AV nodes, and atrium. M2 (Gai) isoform predominant

ACh on the SA node reduces K+ channel closure, increasing repolarisation, thus increasing the time before the node depolarises to next AP - lower HR

ACh on the AV node reduces the conduction of AP and delays the contraction of ventricles.

Atrial innervation decreases contraction

mAChR antagonists seen to increase HR.

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8
Q

Sympathetic innervation of the heart

A

Innervates the SA, AV node, and the cardiac muscles (more in ventricles).

NA on the SA node increaess K+ closing, decreasing the K+ mediated hyperpolarisation. Requires less time for the SA to depolarise to initiate AP. Increases HR.

AV node innervation increases AP conduction.

Increases the Ca influx into the cardiac muscles, increasing contractile force.

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9
Q

Beta-blockers uses and mechanism

A

Blocks cardiac B1-ARs to treat angina and hypertension.

Decreases HR (by blocking NA effect on SA and AV node).

Decreases cardiac contractile force (primarily of ventricles)

Increases the diastolic period, increasing the time of blood being able to enter the cardiac muscles to treat angina.

Ultimately decrease HR and CO.

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