Unit 3 Flashcards
How does cardiac muscle differ from skeletal?
Cardiac muscle is a syncytium - muscle fibres separated by intercalated discs
What are 2 differences in action potentials in cardiac/skeletal muscle?
1 - cardiac muscle action potential caused by opening of fast sodium and slow calcium channels (vs fast sodium only)
2 - in cardiac muscle, after onset of action potential membrane potassium permeability decreases until calcium channels close
Both cause plateau in action potential
Describe the stages of cardiac muscle action potential
0 - fast sodium channels open
1 - fast sodium channels close
2 - slow calcium channels open. K+ channels close
3 - calcium channels close, k+ channels open
What is a difference in excitation-contraction coupling between cardiac and skeletal muscle?
In cardiac muscle calcium diffuse into the sarcoplasm from the T tubules, as well as the sarcoplasmic reticulum
Where is the sinus node located?
In the right atrium
How much of ventricular filling is active/passive?
80% passive
20% active
What are the pressure changes in the atria known as?
a wave - atrial contraction
c wave - ventricular contraction
w wave - flow of blood from veins
What is preload?
End diastolic pressure
What is afterload?
Pressure in aorta
Where does the energy for cardiac contraction come from?
70-90% fat metabolism
10-30% glucose/lactate
What is the Bainbridge reflex?
Stretch of the right atrial wall increases HR by 40-60%
What are the effects of vagal stimulation on the heart?
Mostly decrease in HR, slight reduction in contractility (vagus innervates atria not ventricles)
What are the effects of sympathetic stimulation on the heart?
Increase in HR and contractility
What are the effects of excess potassium ions on the heart?
Dilated, flaccid, reduced HR
High extracellular potassium decreases membrane potential - less negative, reduced intensity of action potential
What are the effects of excess calcium ions on the heart?
Spastic contraction - direct effect of ions to initiate contraction
What are the effects of deficiency of calcium ions on the heart?
Cardiac weakness
What is the effect of increased body temperature on the heart?
Increased HR - increased permeability of cardiac membrane
What are the effects of increased arterial blood pressure on cardiac output?
Minimal up to 160mmHg - cardiac output determined by venous return
How is the tissue of the sinus node different to other heart muscle fibre?
Resting potential -55-60mV (vs -85-90mV)
Due to cell membrane being leaky to sodium and calcium
At less negative resting potential fast sodium channels blocked - only slow sodium channels open
How does the sinus node self excite?
Sodium ions leak through membrane - funny currents
Resting potential slowly rises until L-type calcium channels activate
L-type channels inactivate and potassium channels open - repolarisation
Which parts of the heart can exhibit intrinsic rhythmical activity?
Sinus node, AV node, Purkinje fibres
What is the mechanism of vagal effects on the heart?
ACh increases permeability to potassium => hyperpolarisation
Where is the majority of energy needed for heart contraction derived from?
Oxidative metabolism of fatty acids
How does high atrial stretch increase heart rate?
Directly increased by 10-20%
Bainbridge reflex (vagus) - increases an additional 40-60%
What causes respiratory sinus arrhythmia?
Spillover of signals from the medullary respiratory centre into the adjacent vasomotor centre
What are the possible causes of a SA block?
Myocardial ischaemia, myocarditis, medication, fitness
What are the possible causes of a SA block?
Ischaemia of the AV node/bundle
Compression of the AV bundle with scar tissue
Inflammation of the AV node/bundle
Extreme vagus stimulation
Degeneration of the AV conduction system
Medication (digitalis, beta blockers)
What are the types of second degree AV block?
What causes them
Mobitz type I (Wenckeback periodicity) - progressive prolongation of PR until ventricular beat dropped. Usually abnormal AV node, normally benign
Mobitz type II - fixed number of non-conducted P-waves. Usually associated with issue with His-Purkinje system, may require pacing
What is electrical alternans and what causes it?
Partial intraventricular block every other heartbeat
Tachycardia, ischaemia, myocarditis, digitalis toxicity
What are the causes of premature contractions?
Ischaemia
Calcified plaques
Toxic irritation of AV node, purkinje system or myocardium
What are the classical features of VPCs?
Prolonged QRS
High voltage QRS
T wave has opposite electrical potential polarity opposite to QRS
What is long QT syndrome and why are they of potential concern?
Delayed depolarisation of ventricles
Increased susceptibility to torsades de pointes
What are the possible causes of long QT?
Congenital - mutations of Na or K channels
Acquired - hypomagnesaemia, hypokalaemia, hypocalcaemia, drugs (quinidine, fluoroquinolone, erythromycin)
What causes ventricular tachycardia?
Usually considerable damage to ventricles
Digitalis
How can ventricular tachycardia be treated?
Lidocaine
Amiodarone
What is the MOA of lidocaine?
Reduced sodium permeability of cardiac muscle membrane
What is the MOA of amiodarone?
Prolongs action potential and refractory period in cardiac muscle
Slows AV conduction
What factors can predispose to circus movements?
Cardiac dilation
Delayed velocity of contraction - blockage of Purkinje, ischaemia, hyperkalaemia
Short refractory period - epinephrine, repeated stimulation
