Paroxysmal supraventricular tachycardia is an intermittent tachycardia (HR > 100 bpm) and has the following characteristics:
1. Sudden onset/offset (Contrast with sinus tachycardia)
2. Electrical activity originates above the ventricle (Contrast with ventricular tachycardia)
3. Produces narrow QRS complex (<120ms) The most common cause of PSVT is Atrioventricular nodal re-entrant tachycardia (AVNRT), most common in young women with a mean age onset of 32 years old. There are recurrent episodes of palpitations, and most of the episodes spontaneously. Sometimes, some vagal manoeuvres are required:
1. Valsalva manoeuvre
2. immersing the face in ice-cold water
3. carotid sinus massage.

If PSVT keeps persisting or is causing severe symptoms, the treatment of choice is intravenous adenosine. The patient’s ECG should be continuously monitored throughout the treatment.

The recommended doses in adults are as follows:
– Initial dose of adenosine is 6 mg by rapid IV bolus
– If unsuccessful, give another dose of adenosine 12 mg by rapid IV bolus
– If unsuccessful, give a further dose of adenosine 12 mg by rapid IV bolus
The latest ALS guidelines advocate 18 mg for the third dose, whereas the BNF/NICE guidelines advocate 12 mg.

If adenosine fails or is contraindicated, intravenous verapamil can be used as an alternative, but it should be avoided in patients recently treated with beta-blockers.

Synchronized electrical cardioversion will be necessary with signs of hemodynamic instability or if drug treatment has failed to restore sinus rhythm.
Recurrent episodes of paroxysmal supraventricular tachycardia can be treated by catheter ablation or prevented with drugs such as flecainide, sotalol, diltiazem, or verapamil.

Heparin is a polymer of glycosaminoglycan. It occurs naturally and is found in mast cells. Clinically, it is used in two forms:
1. Unfractionated: widely varying polymer chain lengths
2. Low molecular weight: Smaller polymers only

Heparin works by binding to and activating the enzyme inhibitor antithrombin III. Antithrombin III inactivates thrombin (factor IIa) by forming a 1:1 complex with thrombin. The heparin-antithrombin III complex also inhibits factor Xa and some other proteases involved with clotting. The heparin-ATIII complex can also inactivate IX, XI, XII, and plasmin.

Heparin is not thrombolytic or fibrinolytic. It prevents the progression of existing clots by inhibiting further clotting. The lysis of existing clots relies on endogenous thrombolytics.

Heparin is used for:
1. Prevention and treatment of venous thromboembolism
2. Treatment of disseminated intravascular coagulation
3. Treatment of fat embolism
4. Priming of haemodialysis and cardiopulmonary bypass machines

There is no evidence that heparin is superior to low-molecular-weight heparins in preventing mortality from thrombosis.

Vitamin K is used to reverse the effects of warfarin but not heparin. For heparin, protamine sulphate is used to counteract its effects.

Dopamine is a catecholamine that occurs naturally and is used to treat low cardiac output, septic shock, and renal failure. It is both adrenaline and noradrenaline’s immediate precursor.

Dopamine acts on D1 and D2 dopamine receptors in the renal, mesenteric, and coronary beds at low doses (1-5 g/kg/min). Dopamine causes a significant decrease in renal vascular resistance and an increase in renal blood flow at these doses. Within this dose range, it is also involved in central modulation of behaviour and movement.

Dopamine stimulates beta- and alpha-adrenergic receptors directly and indirectly at higher doses. Beta-stimulation predominates at a rate of 5-10 g/kg/min, resulting in a positive inotropic effect that increases cardiac output and coronary blood flow. Alpha-stimulation predominates at infusion rates greater than 15 g/kg/min, resulting in peripheral vasoconstriction and an increase in venous return and systolic blood pressure.

Below is a summary of the mechanisms and effects of various inotropic agents:
Inotrope
Mechanism
Effects
Adrenaline (epinephrine)
Beta-1 and -2 agonist at increasing doses;
Alpha-agonist at high doses
Increased cardiac output;
Vasoconstriction at higher doses
Noradrenaline (norepinephrine)
Mainly alpha-agonist;
Beta-1 and -2 agonist at increasing doses
Vasoconstriction;
Some increased cardiac output
Dopamine
Dopamine agonist at low doses;
Beta-1 and -2 agonist at increasing doses;
Alpha-agonist at high doses
Increased cardiac output;
Vasoconstriction at higher doses
Dobutamine
Mainly beta-1 agonist
Increased cardiac output

End-organ damage (e.g. encephalopathy, intracranial haemorrhage, acute myocardial infarction or ischaemia, dissection, pulmonary oedema, nephropathy, eclampsia, papilledema, and/or angiopathic haemolytic anaemia) characterises a hypertensive emergency (also known as ‘accelerated hypertension’ or malignant hypertension’ It’s a life-threatening condition that necessitates rapid blood pressure reduction to avoid end-organ damage and a negative outcome.

Hypertensive encephalopathy is a syndrome that includes headaches, seizures, visual changes, and other neurologic symptoms in people who have high blood pressure. It is reversible if treated quickly, but it can progress to coma and death if not treated properly.

Any patient with suspected hypertensive encephalopathy should have an urgent CT scan to rule out an intracranial haemorrhage, as rapid blood pressure reduction could be dangerous in these circumstances.

The drug of choice is labetalol, which reduces blood pressure steadily and consistently without compromising cerebral blood flow.
An initial reduction of approximately 25% in mean arterial pressure (MAP) over an hour should be aimed for, followed by a further controlled MAP reduction over the next 24 hours. In patients who are unable to take beta-blockers, nicardipine can be used as a substitute.

Amiodarone is an anti-arrhythmic medication that can be used to treat both ventricular and atrial arrhythmias.

The use of amiodarone is contraindicated in the following situations:
Conduction disturbances that are severe (unless pacemaker fitted)
Sinus node disease is a condition that affects the lymph nodes in (unless pacemaker fitted)
Sensitivity to iodine
Blockage of the Sino-atrial heart valve (except in cardiac arrest)
Bradycardia in the sinuses (except in cardiac arrest)
Thyroid disorders

Hypoperfusion, renal failure, and the oligohydramnios sequence are all linked to ACE inhibitor use in the second and third trimesters.

The oligohydramnios sequence refers to a foetus’ or neonate’s atypical physical appearance as a result of oligohydramnios in the uterus. It’s also linked to aortic arch obstructive malformations and patent ductus arteriosus.

The inhibitory effects on the renin-angiotensin-aldosterone system appear to be the cause of these defects. To avoid these risks, ACE inhibitors should be stopped before the second trimester.

Loop diuretics are drugs used to manage and treat fluid overload associated with CHF, liver cirrhosis, and renal disease. The drugs commonly used are:

• Furosemide
• Bumetanide
• Torsemide
• Ethacrynic Acid

Loop diuretics inhibit the Na-K-Cl pump in the ascending loop of Henle, resulting in salt-water excretion. This relieves congestion and reduces oedema.

The contra-indications to the use of loop diuretics are:
1. Anuria
2. Comatose and precomatose states associated with liver cirrhosis
3. Renal failure due to nephrotoxic or hepatotoxic drugs
4. Severe hypokalaemia
5. Severe hyponatremia
6. History of hypersensitivity to furosemide, bumetanide, or torsemide (or sulphonamides)

The following conditions or states are not contraindications, but loop diuretics needs to be used cautiously in these conditions:
1. Diabetes (but hyperglycaemia less likely than with thiazides)
2. Gout
3. Hypotension (correct before initiation of treatment)
4. Hypovolaemia (Correct before initiation of treatment)

Overdosing on calcium-channel blockers should always be taken seriously and regarded as potentially fatal. Verapamil and diltiazem are the two most lethal calcium-channel blockers in overdose. These work by binding the alpha-1 subunit of L-type calcium channels, preventing calcium from entering the cell. In cardiac myocytes, vascular smooth muscle cells, and islet beta-cells, these channels play an important role.

The following summarises the toxicity of calcium-channel blockers:
Cardiac effects
Vascular smooth muscle tone affects
Metabolic effects
Excessive negative inotropy: myocardial depression
Negative chronotropy: sinus bradycardia
Negative dromotropy: atrioventricular node blockade
Decreased afterload
Systemic hypotension
Coronary vasodilation
Hypoinsulinaemia
Calcium channel blocker-induced insulin resistance

Propranolol, like other non-selective beta-blockers, is contraindicated in patients with asthma. These drugs can cause acute bronchospasm, therefore worsening symptoms, especially in high doses. However, there has been some recent evidence that long-term use of selective beta-blockers in mild or moderate asthma patients can be safe.

Lidocaine is a tertiary amide local anaesthetic and also a class IV antiarrhythmic.

Like other local anaesthetics, lidocaine works on the voltage-gated sodium ion channel on the nerve cell membranes. It works in the following steps:
1. diffuses through neural sheaths and the axonal membrane into the axoplasm
2. binds fast voltage-gated Na+ channels in the neuronal cell membrane and inactivates them
3. With sufficient blockage, the membrane of the postsynaptic neuron will not depolarise and will be unable to transmit an action potential, thereby preventing the transmission of pain signals

The same principle applies to Lidocaine’s actions in the heart as it blocks the sodium channels in the conduction system and the myocardium. This raises the threshold for depolarizing, making it less likely for the heart to initiate or conduct any action potential that can cause arrhythmia.