Common Endocrine Disorders and their Cardiac Manifestations

Endocrine disorders can have significant effects on the cardiovascular system, including the development of arrhythmias. Atrial fibrillation is a common arrhythmia that can be caused by hyperthyroidism, which should be tested for in patients presenting with this condition. Other signs of thyrotoxicosis include sinus tachycardia, physiological tremor, lid lag, and lid retraction. Graves’ disease, a common cause of hyperthyroidism, can also present with pretibial myxoedema, proptosis, chemosis, and thyroid complex ophthalmoplegia.

Hyperparathyroidism can cause hypercalcemia, which may present with non-specific symptoms such as aches and pains, dehydration, fatigue, mood disturbance, and constipation. It can also cause renal stones. Hypothyroidism, on the other hand, may cause bradycardia and can be caused by Hashimoto’s thyroiditis, subacute thyroiditis, iodine deficiency, or iatrogenic factors such as post-carbimazole treatment, radio-iodine, and thyroidectomy. Drugs such as lithium and amiodarone can also cause hypothyroidism.

Cushing syndrome, a disorder caused by excess cortisol production, is not typically associated with arrhythmias. Type 1 diabetes mellitus, another endocrine disorder, also does not typically present with arrhythmias.

In summary, it is important to consider endocrine disorders as potential causes of cardiac manifestations, including arrhythmias. Proper diagnosis and management of these conditions can help prevent serious cardiovascular complications.

When a patient presents with symptoms of thoracic aortic dissection and is stable, CT angiography is the preferred diagnostic test. This imaging technique provides a clear view of the aorta and helps plan surgical intervention if necessary. In cases of proximal aortic dissection, inter-arm blood pressure measurements may reveal a difference of over 20 mmHg, with the right arm showing higher pressure due to its proximity to the heart. The absence or reduction of femoral pulses on one or both sides is also a common finding. While a chest x-ray may show signs associated with aortic dissection, it is not specific enough for diagnosis. Transesophageal echocardiography (TOE) is used to confirm the diagnosis if CT angiography is inconclusive or if the patient is unstable. Transthoracic echocardiography (TTE) is less sensitive and specific than TOE for detecting aortic dissection.

Understanding Aortic Dissection: Classification, Investigation, and Management

Aortic dissection is a serious medical condition that requires prompt diagnosis and management. It is classified according to the location of the tear in the aorta, with type A affecting the ascending aorta in two-thirds of cases, and type B affecting the descending aorta distal to the left subclavian origin in one-third of cases. The DeBakey classification further divides aortic dissection into type I, which originates in the ascending aorta and propagates to at least the aortic arch, and type II, which is confined to the ascending aorta. Type III originates in the descending aorta and rarely extends proximally but will extend distally.

To diagnose aortic dissection, imaging studies such as chest x-ray and CT angiography of the chest, abdomen, and pelvis are essential. Transoesophageal echocardiography (TOE) may be more suitable for unstable patients who cannot undergo CT scanning. Management of type A aortic dissection requires surgical intervention, but blood pressure should be controlled to a target systolic of 100-120 mmHg while awaiting surgery. Type B aortic dissection can be managed conservatively with bed rest and IV labetalol to reduce blood pressure and prevent progression.

Complications of aortic dissection depend on the location of the tear. Backward tears can lead to aortic incompetence/regurgitation and myocardial infarction, while forward tears can cause unequal arm pulses and blood pressure, stroke, and renal failure. Endovascular repair of type B aortic dissection may have a role in the future. It is important to remember that patients may present acutely and be clinically unstable, so the choice of investigations and management should take this into account.

When treating heart failure patients, it is recommended to initiate therapy with either an angiotensin-converting enzyme (ACE) inhibitor or a beta-blocker licensed for heart failure treatment, but not both simultaneously. If the patient exhibits signs of fluid overload or has diabetes mellitus, an ACE inhibitor like ramipril is preferred. On the other hand, if the patient has angina, a beta-blocker such as bisoprolol, carvedilol, or nebivolol is preferred.

Drug Management for Chronic Heart Failure: NICE Guidelines

Chronic heart failure is a serious condition that requires proper management to improve patient outcomes. In 2018, the National Institute for Health and Care Excellence (NICE) updated their guidelines on drug management for chronic heart failure. The guidelines recommend first-line therapy with both an ACE-inhibitor and a beta-blocker, with clinical judgement used to determine which one to start first. Second-line therapy involves the use of aldosterone antagonists, which should be monitored for hyperkalaemia. SGLT-2 inhibitors are also increasingly being used to manage heart failure with a reduced ejection fraction. Third-line therapy should be initiated by a specialist and may include ivabradine, sacubitril-valsartan, hydralazine in combination with nitrate, digoxin, or cardiac resynchronisation therapy. Other treatments such as annual influenza and one-off pneumococcal vaccines are also recommended.

Overall, the NICE guidelines provide a comprehensive approach to drug management for chronic heart failure. It is important to note that loop diuretics have not been shown to reduce mortality in the long-term, and that ACE-inhibitors and beta-blockers have no effect on mortality in heart failure with preserved ejection fraction. Healthcare professionals should carefully consider the patient’s individual needs and circumstances when determining the appropriate drug therapy for chronic heart failure.

If a patient experiences cardiac arrest in VF/pulseless VT and is monitored, such as in a coronary care unit, critical care unit, or catheter laboratory, they should receive a maximum of three successive shocks instead of one shock followed by two minutes of CPR. After the shocks, chest compressions should be administered for two minutes. Once compressions restart, adrenaline 1mg IV and amiodarone 300 mg IV should be given for shockable rhythms (VT/pulseless VF). Adrenaline 1mg IV should be given after alternate shocks (every 3-5 minutes). For non-shockable rhythms (pulseless electrical activity/asystole), adrenaline 1mg IV should be given as soon as venous access is achieved and administered alongside CPR. Pulseless electrical activity is a type of cardiac arrest where there is electrical activity (other than ventricular tachycardia) that would normally have an associated pulse. Asystole is a complete cessation of any electrical and mechanical heart activity.

The 2015 Resus Council guidelines for adult advanced life support outline the steps to be taken when dealing with patients with shockable and non-shockable rhythms. For both types of patients, chest compressions are a crucial part of the process, with a ratio of 30 compressions to 2 ventilations. Defibrillation is recommended for shockable rhythms, with a single shock for VF/pulseless VT followed by 2 minutes of CPR. Adrenaline and amiodarone are the drugs of choice for non-shockable rhythms, with adrenaline given as soon as possible and amiodarone administered after 3 shocks for VF/pulseless VT. Thrombolytic drugs should be considered if a pulmonary embolus is suspected. Atropine is no longer recommended for routine use in asystole or PEA. Oxygen should be titrated to achieve saturations of 94-98% following successful resuscitation. The Hs and Ts should be considered as potential reversible causes of cardiac arrest.

Drug Management for Chronic Heart Failure: NICE Guidelines

Chronic heart failure is a serious condition that requires proper management to improve patient outcomes. In 2018, the National Institute for Health and Care Excellence (NICE) updated their guidelines on drug management for chronic heart failure. The guidelines recommend first-line therapy with both an ACE-inhibitor and a beta-blocker, with clinical judgement used to determine which one to start first. Second-line therapy involves the use of aldosterone antagonists, which should be monitored for hyperkalaemia. SGLT-2 inhibitors are also increasingly being used to manage heart failure with a reduced ejection fraction. Third-line therapy should be initiated by a specialist and may include ivabradine, sacubitril-valsartan, hydralazine in combination with nitrate, digoxin, or cardiac resynchronisation therapy. Other treatments such as annual influenza and one-off pneumococcal vaccines are also recommended.

Overall, the NICE guidelines provide a comprehensive approach to drug management for chronic heart failure. It is important to note that loop diuretics have not been shown to reduce mortality in the long-term, and that ACE-inhibitors and beta-blockers have no effect on mortality in heart failure with preserved ejection fraction. Healthcare professionals should carefully consider the patient’s individual needs and circumstances when determining the appropriate drug therapy for chronic heart failure.

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.

Treatment Options for Atrial Fibrillation: A Comprehensive Guide

Atrial fibrillation (AF) is a common cardiac arrhythmia that requires prompt and appropriate management to prevent complications. Here are some treatment options for AF:

Rate Control: This is recommended for patients who have had AF for more than 48 hours. Beta-blockers are the first-line treatment unless there is a contraindication such as asthma. Calcium channel blockers can also be used.

Digoxin: This drug can be used as rate control if the patient cannot have beta-blockers or calcium channel blockers. However, it should only be used as a third-line treatment or as an adjunct because it has been shown to increase mortality. It is also only effective in sedentary patients.

DC Cardioversion: This can be used to treat new-onset AF if the patient has had it for less than 48 hours. It can also be considered in patients who have had it for longer than that, once they have been on stable anticoagulation for at least 3 weeks.

Flecainide: This is a class Ic antiarrhythmic drug that can be used as chemical cardioversion in new AF (<48 hours) or if a patient has been anticoagulated for >3 weeks.

Rhythm Control: Nice guidelines advise that rhythm control can be used if AF onset was <48 hours ago, but should be avoided if longer ago because it can increase the risk of stroke from an atrial thrombus. In longer cases, rate control should be used, which is with beta-blockers or rate-limiting calcium channel blockers. Digoxin can be used third line or as an adjunct. In conclusion, the appropriate treatment for AF depends on the duration of the arrhythmia, the patient’s comorbidities, and other factors. It is important to consult with a healthcare professional to determine the best course of action.

Regardless of age, ACE inhibitors/A2RBs are the first-line treatment for hypertension in diabetics.

Blood Pressure Management in Diabetes Mellitus

Patients with diabetes mellitus have traditionally been managed with lower blood pressure targets to reduce their overall cardiovascular risk. However, a 2013 Cochrane review found that there was little difference in outcomes between patients who had tight blood pressure control (targets < 130/85 mmHg) and those with more relaxed control (< 140-160/90-100 mmHg), except for a slightly reduced rate of stroke in the former group. As a result, NICE recommends a blood pressure target of < 140/90 mmHg for type 2 diabetics, the same as for patients without diabetes. For patients with type 1 diabetes, NICE recommends a blood pressure target of 135/85 mmHg unless they have albuminuria or two or more features of metabolic syndrome, in which case the target should be 130/80 mmHg. ACE inhibitors or angiotensin-II receptor antagonists (A2RBs) are the first-line antihypertensive regardless of age, as they have a renoprotective effect in diabetes. A2RBs are preferred for black African or African-Caribbean diabetic patients. Further management then follows that of non-diabetic patients. It is important to note that autonomic neuropathy may result in more postural symptoms in patients taking antihypertensive therapy. Therefore, the routine use of beta-blockers in uncomplicated hypertension should be avoided, particularly when given in combination with thiazides, as they may cause insulin resistance, impair insulin secretion, and alter the autonomic response to hypoglycemia.

If a patient with extremity ischaemia is diagnosed with Raynaud’s phenomenon, Buerger’s disease should be considered as a possible underlying condition. Buerger’s disease is a condition where the small and medium arteries in the hands and feet become inflamed and thrombosed, leading to acute or chronic progressive ischaemic changes and potentially gangrene. It is strongly associated with smoking. Osteoarthritis, on the other hand, presents with joint pain and swelling, typically in the wrist, knee, hip, or thumb base, and is more common with age. Radial artery dissection is unlikely in the given scenario as there is no history of traumatic injury. Raynaud’s phenomenon, which is characterised by transient vasospasm of the digits triggered by cold, is usually treated conservatively with warmth and sometimes calcium channel blockers in severe cases. It is mostly idiopathic but can be associated with underlying connective tissue disease.

Understanding Buerger’s Disease

Buerger’s disease, also known as thromboangiitis obliterans, is a type of vasculitis that affects the small and medium-sized blood vessels. This condition is strongly linked to smoking and can cause a range of symptoms, including extremity ischemia, intermittent claudication, ischaemic ulcers, superficial thrombophlebitis, and Raynaud’s phenomenon.

Individuals with Buerger’s disease may experience reduced blood flow to their limbs, which can lead to pain, numbness, and tingling sensations. This can make it difficult to walk or perform other activities, and may even result in the development of ulcers or sores on the skin.

Superficial thrombophlebitis, or inflammation of the veins close to the surface of the skin, is another common symptom of Buerger’s disease. This can cause redness, swelling, and tenderness in the affected area.

Raynaud’s phenomenon, which is characterized by the narrowing of blood vessels in the fingers and toes, is also associated with Buerger’s disease. This can cause the affected areas to turn white or blue and feel cold and numb.

Marfan Syndrome: A Connective Tissue Disorder with Cardiovascular Manifestations

Marfan syndrome is an autosomal dominant connective tissue disorder that presents with a wide range of clinical manifestations. The ocular, skeletal, and cardiovascular systems are characteristically involved. Aortic root dilatation, occurring in 70-80% of cases, is the most common cardiovascular manifestation, followed by mitral valve prolapse at 60-70%. Mitral annular calcification is less common, occurring in 8-15% of cases. Aortic dissection, accounting for around 5% of all cases, is more likely in patients with Marfan syndrome, especially those with severe aortic root dilatation.

The weakening of the aortic media leads to a fusiform ascending aortic aneurysm, which may be complicated by aortic regurgitation and aortic dissection. Mitral regurgitation can result from mitral valve prolapse, dilatation of a mitral valve annulus, or mitral annular calcification. Pregnancy is particularly hazardous for patients with Marfan syndrome. Treatment with β blockers can reduce the rate of aortic dilatation and the risk of rupture.