cardiac 1

Question 1

(ACE)

Answer 1

• Angiotensin Converting Enzyme (ACE) Inhibitors
  • They reduce the workload of the heart by lowering pulmonary and systemic resistance without affecting cardiac output.
  • ACE inhibitors work by blocking the conversion of Angiotensin I to
  Angiotensin II . This results in peripheral vasodilation

Question 2

adverse reactions with ACE

Answer 2

• Hypotension (which can be profound even after the first dose)
• Rash
• Taste Loss (within first 1-3 months but is usually self limiting)
• Cough – Occurs in up to 15% of patients. Persistent cough may require pt. to be taken off drug. Intal inhaler may be ordered to treat cough (often ineffective)
• Dizziness
• Headache
• GI upset
• Hyperkalaemia (due to increased potassium retention)
• Angio-oedema

Question 3

clinical considerations of ACE

Answer 3

• Stop diuretics at least 24 hours before starting ACE inhibitors
• Monitor BP after first dose
• Monitor renal function and electrolyte levels
• Monitor for hyperkalaemia: stop any potassium sparing
diuretics.
- Symptoms of hyperkalaemia include:
– Confusion
– Nervousness
– irregular heart beat
– numbness and tingling of limbs and lips
– muscle weakness
– Peaked T waves on ECG

Question 4

Angiotensin Receptor Blockers (ARB’s)

Answer 4

• ARBs are similar to ACE inhibitors. They are however better tolerated by patients who develop a cough with ACE inhibitors.
Clinical considerations are the same as ACE.
• ARB’s block the angiotensin II receptors. This results in:
– 1. vasodilation of vascular smooth muscle
– 2. decreased aldosterone secretion by the adrenal glands resulting in
less sodium and water reabsorption
• Preservation of renal function
• Decreased morbidity and mortality associated with heart failure

Question 5

how does digoxin work

Answer 5

inhibiting the enzyme involved in the sodium-potassium pump. This leads to the stores
of calcium within the heart muscle to be released,
elevating intracellular calcium levels. The elevated
calcium levels will result in a stronger contraction by
the heart > increased cardiac output.

Digoxin also enhances parasympathetic activity of
the heart. This alters the responsiveness of the SA
(sino-atrial) node decreasing impulse generation,
therefore decreasing pulse rate. This reduces the
workload of the heart.

Question 6

adverse effects of digoxin

Answer 6

Narrow margin of safety between the therapeutic dose and toxic dose.
• Incidence of Digoxin toxicity is high.
– GI disturbances (nausea, vomiting, anorexia,
diarrhoea)
– Cardiac arrhythmia’s including sinus bradycardia,
ectopic beats, bigeminy (coupled beats)
– Death often results from Ventricular Fibrillation
– Fatigue, headache, mental confusion
– Blurred vision, colour distortion, halos, and/or
flashing lights.

Question 7

beta blockers : Beta 1 adrenergic receptors:

Answer 7

Located in Heart and Kidneys.
Stimulation causes an increase in heart rate and force of
contraction. Kidneys release renin which causes an increase in blood pressure

Question 8

beta blockers : Beta 2 adrenergic receptors:

Answer 8

Located in Lungs, GI tract, Liver,
Uterus, Vascular smooth muscle, and Skeletal muscle.
Stimulation causes bronchodilation, vasodilation, relaxation of
the smooth muscle of the uterus, tremor of skeletal muscle,
glycogenolysis of liver and skeletal muscle

Question 9

method of actions of beta blocker

Answer 9

– Reduce cardiac workload by reducing heart rate and force
of contractions.
– Blocks sympathetic stimulation to the heart and reduces
the speed of impulse conduction from the atria to the
ventricles.
– Thus Beta Blockers have a negative inotropic, chronotropic
and dromotropic effect
– B1 receptor antagonists are relatively cardioselective and
produce fewer side effects than non selective agents which
block both Beta 1 and 2 receptors.

Question 10

Calcium Channel Blockers

• Also known as Calcium Antagonists

Answer 10

• Work by inhibiting the movement of calcium ions
into the vascular and smooth muscle.
• Calcium ions are necessary for muscle contraction
• With reduced calcium, blood vessels dilate,
particularly coronary arteries in spasm and so the
force of contraction is reduced
• Work of the heart is decreased
• Decreased myocardial oxygen demand and an
increase in blood flow to the heart.

Question 11

class 1 calcium channel blockers

Answer 11

Class 1:
– Identified by the suffix “pine”.
– Selective for vascular smooth muscle
and therefore used to treat mild to
moderate hypertension.
– The exception is amlodipine which is
also used to treat chronic stable
angina and vasospastic angina
– Nifedipine (Adalat)
– Felodipine (Feldodur ER)
– Amlodipine (Norvasc)
– Nimodipine (Crosses blood brain
barrier. Therefore used to
treat/prevent cerebral ischaemia)

Question 12

Class 2: calcium channel blockers

Answer 12

 Selective to the myocardium. Used
to treat primary hypertension,
angina and to control
supraventricular dysrhythmias
 Verapamil (Isoptin)

Question 13

Class 3:calcium channel blockers

Answer 13

 Used to treat hypertension with less
cardiac side affects than Verapamil
 Diltiazem (Cardizem)

Question 14

Antidysrhythmic drugs

Answer 14

– Class I (Sodium channel blockers)
– Class II (Beta blockers)
– Class III
– Class IV (Calcium channel blockers)

Question 15

Antidysrhythmic drugs ; Class I (Sodium channel blockers)

Answer 15

• Work by inhibiting the movement of sodium
into the cell
– Class 1a: Procainamide, Quinidine
– Class 1b: Lignocaine
– Class 1c: Flecainide

Question 16

Antidysrhythmic drugs : Class 3

Answer 16

• Prolong the action potential and the
refractory period e.g.
– Amiodarone (Cordarone X) – more commonly
used
– Sotalol (Cardol)