Cardiovascular diseases I (CVD I) – Arrhythmias, Heart failure, Angina
Learning objectives
• Discuss pathophysiology, causes and clinical manifestation in relation to treatments of the
following conditions:
• Arrhythmias
• Heart Failure
• Angina
Arrhythmias
• Arrhythmia: irregular heart beat or abnormal cardiac rhythm
Brady – Slow
Tachy – Fast
• Bradycardia = Heart beats v slowly. < 60 bpm
• Tachycardia = Heart beats v fast. > 100 bpm
• Both have similar symptoms, so you can’t use symptoms to diagnose the condition.
• Mechanisms:
• Disturbance in impulse formation
• Increase in pacemaker rate
• Causes: hypokalaemia, acidosis, cardiac injury, afterdepolarisations (EADs
and DADs)
- Impulse formation can be disturbed by an increase in the pacemaker rate/ rate at which
the SA node generates an impulse.
, - This often happens as a consequence of hypokalaemia, acidosis, cardiac injury,
afterdepolarisations (EADs, DADs)
- When the patient has a cardiac injury, mainly in the SA node. The heart can only send
out or form part of the impulse, there is partial depolarisation.
- When the patient’s heart is still in repolarisation, they experience afterdepolarisation.
- Early afterdepolarization (EAD) occurs during repolarisation of the action potential,
phase 2 and/or phase 3.
- Delayed afterdepolarization (DAD) occurs during phase 4, after full repolarisation.
• Disturbance in impulse conduction
• Heart block: damage to nodal tissue -> AV node
: results in ventricular premature beats
• Re-entry: results in A&V tachycardia, A&V fibrillation, atrial flutter and
Wolff-Parkinson-White syndrome
- Impulse has formed but can't be conducted properly. Involved with AV node.
- The impulse conduction will be disturbed when there is damage to the nodal tissue, mainly
the AV node.
- This results in ventricular premature beats.
- The other event that could disturb impulse conduction is the re-entry of impulse in the areas
of that heart which have already been excited by the previous set of impulses.
- Re-entry results in Atrial & Ventricular tachycardia, Atrial & Ventricular fibrillation, flutter +
Wolff-Parkinson-White syndrome.
• Disturbance in impulse formation and conduction
• Treatments: anti-arrhythmic drugs
Heart failure:
• Heart failure: a condition which occurs when cardiac output (CO) does CO - volume of blood
not meet metabolic demand of the body -> increased heart rate and ejected by heart in 1 min
ventricular hypertrophy*
- When this happens, our body responds by increasing the heart rate and strength of
contractility in the heart, so the heart can pump out more blood.
• Types:
• Systolic heart failure: reduced the contractile function of the ventricles
- The left ventricle loses its ability to contract normally. The heart can't pump with enough
force to push enough blood into circulation.
• Diastolic heart failure: reduced left ventricular filling
- The left ventricle loses its ability to relax normally (because the muscle has become stiff).
The ventricles can't fill properly during the resting period between each beat, reducing
the amount of blood pumped out to the body.
• High output cardiac heart failure: inability of the heart to maintain a high cardiac
output demand
Learning objectives
• Discuss pathophysiology, causes and clinical manifestation in relation to treatments of the
following conditions:
• Arrhythmias
• Heart Failure
• Angina
Arrhythmias
• Arrhythmia: irregular heart beat or abnormal cardiac rhythm
Brady – Slow
Tachy – Fast
• Bradycardia = Heart beats v slowly. < 60 bpm
• Tachycardia = Heart beats v fast. > 100 bpm
• Both have similar symptoms, so you can’t use symptoms to diagnose the condition.
• Mechanisms:
• Disturbance in impulse formation
• Increase in pacemaker rate
• Causes: hypokalaemia, acidosis, cardiac injury, afterdepolarisations (EADs
and DADs)
- Impulse formation can be disturbed by an increase in the pacemaker rate/ rate at which
the SA node generates an impulse.
, - This often happens as a consequence of hypokalaemia, acidosis, cardiac injury,
afterdepolarisations (EADs, DADs)
- When the patient has a cardiac injury, mainly in the SA node. The heart can only send
out or form part of the impulse, there is partial depolarisation.
- When the patient’s heart is still in repolarisation, they experience afterdepolarisation.
- Early afterdepolarization (EAD) occurs during repolarisation of the action potential,
phase 2 and/or phase 3.
- Delayed afterdepolarization (DAD) occurs during phase 4, after full repolarisation.
• Disturbance in impulse conduction
• Heart block: damage to nodal tissue -> AV node
: results in ventricular premature beats
• Re-entry: results in A&V tachycardia, A&V fibrillation, atrial flutter and
Wolff-Parkinson-White syndrome
- Impulse has formed but can't be conducted properly. Involved with AV node.
- The impulse conduction will be disturbed when there is damage to the nodal tissue, mainly
the AV node.
- This results in ventricular premature beats.
- The other event that could disturb impulse conduction is the re-entry of impulse in the areas
of that heart which have already been excited by the previous set of impulses.
- Re-entry results in Atrial & Ventricular tachycardia, Atrial & Ventricular fibrillation, flutter +
Wolff-Parkinson-White syndrome.
• Disturbance in impulse formation and conduction
• Treatments: anti-arrhythmic drugs
Heart failure:
• Heart failure: a condition which occurs when cardiac output (CO) does CO - volume of blood
not meet metabolic demand of the body -> increased heart rate and ejected by heart in 1 min
ventricular hypertrophy*
- When this happens, our body responds by increasing the heart rate and strength of
contractility in the heart, so the heart can pump out more blood.
• Types:
• Systolic heart failure: reduced the contractile function of the ventricles
- The left ventricle loses its ability to contract normally. The heart can't pump with enough
force to push enough blood into circulation.
• Diastolic heart failure: reduced left ventricular filling
- The left ventricle loses its ability to relax normally (because the muscle has become stiff).
The ventricles can't fill properly during the resting period between each beat, reducing
the amount of blood pumped out to the body.
• High output cardiac heart failure: inability of the heart to maintain a high cardiac
output demand
