Flashcards in Cardio L3 ECG Deck (36):
Electrical Conducting system:
consists of and function
1. Consists of modified myocytes with few contractile filaments.
Function: Generates and conducts the electrical impulses that trigger contraction
Exhale against closed glottis therefore increase intrathoracic pressure and impeding return of blood to heart.
Sinoatrial node: (5)
1. Physiological pacemaker
2. Excitability (generates AP
3. Automaticity (spontaneous – separate from CNS)
4. Rhythmicity (regular)
5. Dominance over other potential pacemakers by overdrive suppression.
Electrophysiology of the SA Node:
1. Several currents are involved
2. No “fast” sodium channels (unlike neurone)
3. Unstable resting membrane potential or pacemaker potential – as membrane drifts towards threshold AP will occur.
Process: of SA node
a. During pacemaker potential slow Na influx (funny current)
b. Upstroke Calcium influx
c. Repolarisation K current.
Control of Heart rate:
1. Resting adult Human has a heart rate of 60-100 beats per minute
2. Autonomic control
Innervates large areas of heart and the artrioventricular and sinoatrial nodes.
Carried in vagus nerve predominatly innervates sinoatrial node and atrioventricular node.
Parasympathetic System and Acetylcholine: SLOW HR process
1. Fibres in the vagus (left and right) nerves
2. Release Ach
3. Ach binds to muscarinic receptors
4. Pacemaker cells become hyperpolarised
a. Decreases rate at which pacemaker potential reaches threshold (Negative chronotropism) -> decreases heart rate.
b. Block: atropine
Sympathetic: SPEEDDS HR
1. Postganglionic fibres originate T1 to T5 and synapse in the paravertebral ganglia
2. Postganglionic fibres release noradrenaline]Noradrenaline agonises Beta-1 adrenoceptors
3. Increases slope of pacemaker potential
4. Increases heart rate (Positive chronotropism)
Intrinsic Heart Rate:
1. At rest parasympathetic and sympathetic systems are tonically active.
2. Pharmacological blockade of both systems causes 50% increase in intrinsic heart rate, thus at rest the parasympathetic effects are dominant
a. Tachycardia >100/min
b. Bradycardia <60/min
1. Atria acts as a syncytium cells physically separate but electrically act together:
2. Myocytes are joined by intercalated dics containing gap junctions
3. Rapid propagation as myocytes have fast sodium channels.
Atrioventricular Node: Calcium current
1. Located in the right atrium
2. Lacks fast sodium channels
Atrioventricular Node: function
: A slow conduction velocity ensures that atria contract and fill the ventricles before the ventricles contract.
change in conduction velocity
a. Positive during exercise
b. Negative decrease in rate of conduction between two nodes.
His Bundle, bundle Branches and purkinje Fibres:
1. All are formed from Purkinje cells
2. The bundle of His is the only electrical connection between the atria and ventricles.
3. Pathological connections such as the Bundle of Kent may predispose to arrhythmias (WPW syndrome) extra pathological connection between atria and ventricles.
1. These are cells adapted for rapid conduction (200 cm//sec)
2. Wide diameter
3. Few myofibrils
4. Numerous gap junctions
SA node and atrioventricular node channel typr
shallow up stoke as they lack fast sodium channels and depend on calcium channels
Atrial mycocytes, ventricular myocytes and purkinje
fast upstroke as they have fast Na channels.
Chain of events:
1. SA Noda
3. AV Node
4. Purkinje Fibres
Ventricular myocyte AP: phase 0
Rapid depolarisation due to opening sodium channels (Na)
Ventricular myocyte AP: phase 1
Inactivation of sodium channels
Ventricular myocyte AP: phase 2
Slow inward calcium channels (L-type) (Ica). Also known as the Plateau phase – contraction of myocyte.
Ventricular myocyte AP: phase 3
Rapid repolarisation including IK via delayed rectifier potassium channels
Ventricular myocyte AP: phase 4
Resting membrane potential
ECG PR segment
Delay due to atrial-ventricular node
ECG P-R interval
0.12-0.2s Atrioventricular conduction
Clinically affected by diseases that affect conduction between atria and ventricle = heart block and increase in PR interval.
ECG QRS complex
Generated by depolarisation of ventricles.
ECG S-T segment
Period that the ventricles are depolarised. Clinically:
1. ST elevation = can be an indicated of MI
ST depression – indicator of myocardial ischemia in angina
ECG T wave
Repolarisation of ventricles – same as depolarisation as it occurs from the outer surface (epi) to endocardial.
Can be altered with electrolyte disturbance – hyperkalaemia = tall peak T waves. (arryhtmias causing)
ECG QT interval
<0.44s duration of ventricular activation
Varies with heart weight
Prolonged = major risk factor for arrhythmias.
Combination of antihistamines and grapefruit juice to causes prolonged QT intervals
ECG U wave
Not in every ECG (more common in younger) or a sign hypokaelaemia (U prominent and T wave flatten)
The heart rate is between 60-100 bpm.
Every P wave is followed by a QRS complex