Effects of Different Anti-Arrhythmic Drugs on QT Interval

The QT interval is an important measure of cardiac repolarization, and abnormalities in this interval can lead to life-threatening arrhythmias. Different anti-arrhythmic drugs have varying effects on the QT interval.

Cardiac glycosides such as digoxin and ouabain can shorten the QT interval, even at therapeutic doses. This is due to their ability to shorten the atrial and ventricular refractory periods.

Class Ia drugs like disopyramide, class Ic drugs like flecainide, and class III drugs like amiodarone and sotalol all prolong the QT interval. Disopyramide can result in a long PR interval, while flecainide can cause a broad QRS or prolonged QT interval. Amiodarone is a class III drug that prolongs the QT interval, and sotalol causes dose-related prolongation of the QT interval.

β-blockers like atenolol have a neutral effect on the QT interval in patients with a normal QT interval. However, they can act to stabilise the QT interval in patients with long QT syndrome.

In summary, different anti-arrhythmic drugs have varying effects on the QT interval, and it is important to monitor this interval when prescribing these medications.

Warfarin should be continued indefinitely due to the patient’s risk factors for stroke and history of atrial fibrillation. It is preferred over direct oral anticoagulants due to his valvular heart disease.

NICE recommends using the CHA2DS2-VASc score to determine the need for anticoagulation in patients with any history of AF. The ORBIT scoring system should be used to assess bleeding risk, but anticoagulation should not be withheld solely on the grounds of age or risk of falls. DOACs are now recommended as the first-line anticoagulant for patients with AF, with warfarin used second-line if a DOAC is contraindicated or not tolerated. Aspirin is not recommended for reducing stroke risk in patients with AF.

If the Wells score for a suspected deep vein thrombosis (DVT) is 2 or higher, a proximal leg vein ultrasound scan should be arranged within 4 hours. In this case, the patient’s Wells score is 2 due to recent major surgery within 12 weeks and a calf swelling at least 3 cm larger than the asymptomatic side. It is important to note that a CT angiogram of the leg is not appropriate for diagnosing DVT, and ultrasound is the preferred imaging modality. A CT pulmonary angiogram would only be necessary if the patient had symptoms suggestive of pulmonary embolism. A chest X-ray is not relevant in this scenario. If ultrasound is not possible within 4 hours, a D-dimer test could be performed and interim therapeutic anticoagulation given, but the initial choice is to perform an ultrasound scan as soon as possible.

NICE updated their guidelines on the investigation and management of venous thromboembolism (VTE) in 2020. The use of direct oral anticoagulants (DOACs) is recommended as first-line treatment for most people with VTE, including as interim anticoagulants before a definite diagnosis is made. Routine cancer screening is no longer recommended following a VTE diagnosis. The cornerstone of VTE management is anticoagulant therapy, with DOACs being the preferred choice. All patients should have anticoagulation for at least 3 months, with the length of anticoagulation being determined by whether the VTE was provoked or unprovoked.

Treatment Options for Deep Vein Thrombosis in Pregnancy

Start subcutaneous low molecular weight heparin (LMWH) throughout pregnancy and change to warfarin in the postpartum period: LMWH is recommended for the treatment of DVT during pregnancy. Treatment should be continued for at least three months and until six weeks postpartum. Warfarin can be used after day five of the postpartum period. Both LMWH and warfarin are safe to use while breastfeeding.

Elastic band compression of the affected leg, bedrest, and foot elevation: These measures have no benefit in treating DVT and may even increase the risk of developing a pulmonary embolism (PE) or another DVT.

Commence intravenous (IV) heparin: IV heparin can be used for the treatment of a shocked patient with PE if thrombolysis is not possible. It should not be used for DVT alone.

Oral anticoagulation with warfarin daily throughout pregnancy and the postpartum period: Warfarin is not recommended during pregnancy as it can cross the placenta and increase the risk of congenital malformations and bleeding.

Aspirin 300 mg daily throughout pregnancy and the postpartum period: Aspirin is not effective in treating DVT or PE as it is an antiplatelet drug, not an anticoagulant.

Treatment Options for Deep Vein Thrombosis in Pregnancy

Physiological Changes in Cardiovascular System During Pregnancy

During pregnancy, the cardiovascular system undergoes significant changes to accommodate the growing fetus. These changes include a drop in diastolic blood pressure by 10 mmHg during the second trimester, circulating blood volume increases by approximately 50%, leading to a dilutional ‘physiological anaemia’ and cardiac output increases most sharply throughout the first trimester.

During pregnancy, heart rate progressively increases until reaching a peak in the third trimester. The overall change in heart rate represents approximately a 20–25% increase from baseline. However, a grade 2/6 diastolic murmur at the mitral area and pulsus alternans are not typical findings in a healthy pregnancy. It is important for healthcare providers to be aware of these physiological changes to properly monitor and manage the health of pregnant individuals.

Acute coronary syndrome (ACS) is a term that covers various acute presentations of ischaemic heart disease, including ST elevation myocardial infarction (STEMI), non-ST elevation myocardial infarction (NSTEMI), and unstable angina. ACS develops in patients with ischaemic heart disease, which is the gradual build-up of fatty plaques in the coronary arteries. ACS can cause chest pain, dyspnoea, sweating, and nausea and vomiting. The two most important investigations for ACS are an ECG and cardiac markers. Treatment for ACS includes preventing worsening of presentation, revascularising the vessel is occluded, and treating pain. Patients who have had an ACS require lifelong drug therapy to reduce the risk of a further event.

An ST-elevated myocardial infarction affecting the inferior leads (II, III, aVF) can cause arrhythmias due to the involvement of the right coronary artery, which supplies blood to the AV node. This is evidenced by the patient’s presentation with 1st-degree heart block following the MI.

Anteroseptal changes in V1-V4 indicate involvement of the left anterior descending artery. Inferior changes in II, III, and aVF suggest the right coronary artery is affected. Anterolateral changes in V1-6, I, and aVL indicate the proximal left anterior descending artery is involved. Lateral changes in I, aVL, and possibly V5-6 suggest the left circumflex artery is affected. Posterior changes in V1-3 may indicate a posterior infarction, which is confirmed by ST elevation and Q waves in posterior leads (V7-9). This type of infarction is usually caused by the left circumflex artery, but can also be caused by the right coronary artery. Reciprocal changes of STEMI are typically seen as horizontal ST depression, tall and broad R waves, upright T waves, and a dominant R wave in V2. It is important to note that a new left bundle branch block (LBBB) may indicate acute coronary syndrome.

Overall, understanding the correlation between ECG changes and coronary artery territories is crucial in diagnosing acute coronary syndrome. By identifying the specific changes in the ECG, medical professionals can determine which artery is affected and provide appropriate treatment. Additionally, recognizing the reciprocal changes of STEMI and the significance of a new LBBB can aid in making an accurate diagnosis.

Verapamil is contraindicated in ventricular tachycardia, which is the most probable diagnosis.

Managing Ventricular Tachycardia

Ventricular tachycardia is a type of rapid heartbeat that originates in the ventricles of the heart. In a peri-arrest situation, it is assumed to be ventricular in origin. If the patient shows adverse signs such as low blood pressure, chest pain, heart failure, or syncope, immediate cardioversion is necessary. However, in the absence of such signs, antiarrhythmic drugs may be used. If drug therapy fails, electrical cardioversion may be needed with synchronised DC shocks.

There are several drugs that can be used to manage ventricular tachycardia, including amiodarone, lidocaine, and procainamide. Amiodarone is ideally administered through a central line, while lidocaine should be used with caution in severe left ventricular impairment. Verapamil should not be used in VT. If drug therapy fails, an electrophysiological study (EPS) may be conducted, or an implantable cardioverter-defibrillator (ICD) may be implanted. The ICD is particularly indicated in patients with significantly impaired LV function.

Management of Bradycardia in Peri-Arrest Rhythms

The 2015 Resuscitation Council (UK) guidelines highlight the importance of identifying adverse signs and potential risk of asystole in the management of bradycardia in peri-arrest rhythms. Adverse signs indicating haemodynamic compromise include shock, syncope, myocardial ischaemia, and heart failure. Atropine (500 mcg IV) is the first line treatment in this situation. If there is an unsatisfactory response, interventions such as atropine (up to a maximum of 3mg), transcutaneous pacing, and isoprenaline/adrenaline infusion titrated to response may be used. Specialist help should be sought for consideration of transvenous pacing if there is no response to the above measures.

Furthermore, the presence of risk factors for asystole such as complete heart block with broad complex QRS, recent asystole, Mobitz type II AV block, and ventricular pause > 3 seconds should be considered. Even if there is a satisfactory response to atropine, specialist help is indicated to consider the need for transvenous pacing. Effective management of bradycardia in peri-arrest rhythms is crucial in preventing further deterioration and improving patient outcomes.

Hyperkalaemia is caused by ACE inhibitor.

Angiotensin-converting enzyme (ACE) inhibitors are commonly used as the first-line treatment for hypertension and heart failure in younger patients. However, they may not be as effective in treating hypertensive Afro-Caribbean patients. These inhibitors are also used to treat diabetic nephropathy and for secondary prevention of ischaemic heart disease. The mechanism of action of ACE inhibitors is to inhibit the conversion of angiotensin I to angiotensin II. They are metabolized in the liver through phase 1 metabolism.

ACE inhibitors may cause side effects such as cough, which occurs in around 15% of patients and may occur up to a year after starting treatment. This is thought to be due to increased bradykinin levels. Angioedema may also occur up to a year after starting treatment. Hyperkalaemia and first-dose hypotension are other potential side effects, especially in patients taking diuretics. ACE inhibitors should be avoided during pregnancy and breastfeeding, and caution should be exercised in patients with renovascular disease, aortic stenosis, or hereditary or idiopathic angioedema.

Patients receiving high-dose diuretic therapy (more than 80 mg of furosemide a day) are at an increased risk of hypotension when taking ACE inhibitors. Before initiating treatment, urea and electrolytes should be checked, and after increasing the dose, a rise in creatinine and potassium may be expected. Acceptable changes include an increase in serum creatinine up to 30% from baseline and an increase in potassium up to 5.5 mmol/l. Patients with undiagnosed bilateral renal artery stenosis may experience significant renal impairment. The current NICE guidelines provide a flow chart for the management of hypertension.