Physiology of the heart Flashcards
What is the resting membrane potential of cardiac cells?
-70 mV
In what types of tissue is the pacemaker potential found?
Nodal and conducting tissue
What are the electrophysiological features of nodal tissue (SA node and AV node)?
Slower depolarisation due to slow Ca2+ influx
Gradual upsloping depolarisation (pacemaker activity)
What are the electrophysiological features of conducting tissue (Purkinje fibres)?
Rapid depolarisation due to fast Na+ current
Long plateau phase due to Ca2+ influx
What are the electrophysiological features of atria?
Rapid depolarisation due to fast Na+ current
What are the electrophysiological features of ventricles?
Rapid depolarisation due to fast Na+ current
Long plateau phase due to Ca2+ influx
Describe the process of triggered activity
Increased intracellular Ca2+ can trigger a large after-depolarisation which triggers a series of action potentials, resulting in tachyarrhythmias
Describe the process of increased automaticity
If the SA node fails, other cardiac tissues such as the AV node or Purkinje fibres can take over and fire at a lower rate as a safety mechanism.
Sometimes, the other pacemakers take over inappropriately, resulting in abnormal ectopic activity
Describe the process of re-entry
Under normal conditions, if an impulse has to go around an obstruction, the impulse splits and propagates in both directions and then joins up again when the two impulses meet. Leaves behind refractory tissue so impulses cannot go backwards.
In a damaged heart, a unidirectional conduction block is present. impulse can only go in one particular direction.. by the time the impulse comes around and reaches the damaged tissue, if damaged tissue can conduct retrogradely, it can conduct back up to tissues that are now repolarised. continuous circulation of the impulse can occur, this is a phenomenon known as circus movement. repetitively excites a region of the heart.
What is the length of the AV delay?
200ms
1st degree heart block
longer PR interval
impulses still reach the ventricles
2nd degree heart block
consecutive normal ECGs followed by P wave with no QRS complex
3rd degree heart block
atria contract independently of ventricles
ventricles fire at a slower rate
Normal heart rate? (normal sinus rhythm)
60-80bpm
What heart rate is classed as sinus bradycardia?
Less than 60bpm
Atrial tachycardia
Multiple P waves because atria contract quickly
ventricles do not contract at the same speed (because of AV delay)
Ventricular tachycardia
wide QRS complex - impulses activating the ventricles take longer as they come from a different part of the heart
Atrial fibrillation
no p waves
fibrillating waves in the atria hit the AV node and randomly fire the ventricles, resulting in an irregular ventricular response
results in blood clots e.g. atrial thrombus
Ventricular fibrillation
variable morphology
no clear ventricular rhythm
irregular ventricular response
What effect does sympathetic stimulation have on the heart?
- NA activates B1 adrenoceptors on the myocytes
- Activates cAMP
- Increases slope of pacemaker potential
- Depolarisation takes shorter amount of time to reach threshold so fires AP faster
- heart rate increases and automaticity increases
What effect does parasympathetic stimulation have on the heart?
- ACh acts on M2 receptors on the nodal and atrial tissue
- Decreases slope of pacemaker potential
- Depolarisation takes longer to reach threshold
- heart rate decreases and automaticity decreases
ACh released by the vagal nerve acts on M2 receptors on nodal tissue and slows conduction through AV node –> PR interval increases
What are the classes of the Vaughan Williams Classification of anti-arrhythmic drugs?
class I = sodium channel blockers class II - Beta adrenoceptor antagonists class III - drugs prolonging action potential class IV - Ca2+ channel blockers
What are the effects of digoxin on the heart?
Causes increase in intracellular Ca2+:
Increases vagal tone by accentuating vagus nerve, slowing heart rate
Slows conduction of AV node
Increases ectopic activity (because of increase in intracellular Ca2+)
Increases force of contraction (because of increase in intracellular Ca2+)
How is digoxin used in atrial fibrillation?
Blocks AV node to slow ventricular response
How is digoxin used in severe heart failure?
Slows the heart rate and increases the force of contraction
What is the danger of drugs which prolong AP?
Prolonging AP causes QT prolongation
triggers arrhythmias such as polymorphic ventricular tachycardia - can be lethal
What are the adverse effects of amiodarone?
- interstitial pneumonitis (in the lungs)
- abnormal liver function
- hyperthyroidism or hypothyroidism
- sun sensitivity
- slate grey skin discolouration
- corneal microdeposits
- optic neuropathy
What is the effect of amiodarone on warfarin?
Warfarin is an anticoagulant which is attached to proteins while it is carried around the bloodstream
The part of warfarin in the plasma is active and causes anti-coagulation
Amiodarone displaces warfarin from the proteins, causing the patient to become over-coagulated
What is the equation for cardiac output?
cardiac output = heart rate x stroke volume
Define stroke volume (ml)
Volume of blood ejected each time the heart contracts
Define ejection fraction
% volume of blood ejected with each cardiac contraction
What is preload?
Filling pressure
What is venous return?
Blood volume coming back to the heart
What is afterload?
Resistance to ejection in the circulation
Describe the role of calcium in the cardiac AP
As the AP is conducted, a small amount of Ca2+ moves into the cells through L type Ca2+ channels but this is not enough to trigger a contraction
Ca2+ binds to ryanodine receptors on the membrane of the SR to cause release of Ca2+ from SR into the cell
Ca2+ binds to troponin, causing contraction
Describe how calcium causes cardiac muscle contraction
- myosin binding sites on actin are covered by troponin and tropomyosin so there is no interaction between actin and myosin
- Ca2+ attaches to troponin and reveals myosin binding sites. ATP is hydrolysed when myosin head is unattached.
- ADP and phosphate are bound to myosin as myosin head attaches to actin
- ADP and phosphate release causes head to change position and actin filament to move - contraction
- binding of ATP causes myosin head to return to resting position
Describe the structure of cardiac muscle and why it is important
cross-branching between muscle cells are important for:
fast electrical impulse transmission across the heart
mechanical contraction - muscle cells contract together so heart contracts as one functional unit
How do changes in venous return affect how the heart contracts?
increased venous return results in an increase in end-diastolic pressure which increases stroke volume/cardiac output
What changes in contractility and afterload result in heart failure?
Decrease in contractility - a large increase in pre-load is needed to increase cardiac output
Increase in afterload - heart ejects blood into high pressure + high resistance circulation. Will need to fill heart more to obtain required cardiac output.
Describe an experiment showing the effect of sympathetic NS on heart contraction
Infusion with a vehicle fluid - end diastolic pressure increases with an increase in stroke volume/cardiac output/stroke work
Infusion with a NA infused fluid - for a smaller change in end diastolic pressure there is a larger change in stroke volume/cardiac output
What are the features of heart failure patients?
Decreased contractility
Increased afterload
Operate on higher LVEDP to obtain more cardiac output
How can digoxin and diuretics be used to treat heart failure?
Digoxin is positively ionotropic, causing an increase in intrinsic contractility, increasing cardiac output
Then diuretics can lower pre-load without resulting in low cardiac output to treat pulmonary congestion
