Chronic heart failure is a condition that requires proper diagnosis and management. In 2018, NICE updated their guidelines on the diagnosis and management of this condition. Previously, the first-line investigation was determined by whether the patient had previously had a myocardial infarction or not. However, this is no longer the case. All patients should now have an N-terminal pro-B-type natriuretic peptide (NT‑proBNP) blood test as the first-line investigation.

Interpreting the NT-proBNP blood test is crucial in determining the severity of the condition. If the levels are high, specialist assessment, including transthoracic echocardiography, should be arranged within two weeks. If the levels are raised, specialist assessment, including echocardiogram, should be arranged within six weeks. B-type natriuretic peptide (BNP) is a hormone produced mainly by the left ventricular myocardium in response to strain. Very high levels of BNP are associated with a poor prognosis.

There are different levels of BNP, and each level indicates a different severity of the condition. High levels of BNP are greater than 400 pg/ml (116 pmol/litre) for BNP and greater than 2000 pg/ml (236 pmol/litre) for NTproBNP. Raised levels of BNP are between 100-400 pg/ml (29-116 pmol/litre) for BNP and between 400-2000 pg/ml (47-236 pmol/litre) for NTproBNP. Normal levels of BNP are less than 100 pg/ml (29 pmol/litre) for BNP and less than 400 pg/ml (47 pmol/litre) for NTproBNP.

It is important to note that several factors can alter the BNP level. Factors that increase BNP levels include left ventricular hypertrophy, ischaemia, tachycardia, right ventricular overload, hypoxaemia (including pulmonary embolism), GFR < 60 ml/min, sepsis, COPD, diabetes, and age > 70. On the other hand, factors that decrease BNP levels include diuretics, ACE inhibitors, beta-blockers, angiotensin 2 receptor blockers, and aldosterone antagonists.

Medications for Post-Myocardial Infarction (MI) Care

After a myocardial infarction (MI), certain medications are recommended to reduce mortality and manage symptoms. Nitrates, such as isosorbide mononitrate, offer no mortality benefit but can be used for angina symptoms. β-blockers, like timolol, provide both mortality and anti-anginal benefits and should be continued for at least 12 months post-MI. Statins, specifically atorvastatin 80 mg, are recommended for secondary prevention to reduce mortality. Angiotensin-converting enzyme (ACE) inhibitors, such as ramipril, offer good mortality benefit, but angiotensin receptor blockers (ARBs) can be used if the patient cannot tolerate ACE inhibitors. Aspirin, in combination with another antiplatelet therapy, is recommended for 12 months post-MI. Studies have shown that tirofiban, timolol, and ramipril reduce mortality after an MI, while isosorbide mononitrate showed no benefit. The MIRACL study found that atorvastatin reduced cardiovascular events by 17% when given for 3 months post-MI.

According to the 2011 NICE guidelines, the treatment for isolated systolic hypertension should be the same as that for standard hypertension, with calcium channel blockers being the preferred first-line medication for this age group.

Understanding Isolated Systolic Hypertension

Isolated systolic hypertension (ISH) is a common condition among the elderly, affecting approximately 50% of individuals over the age of 70. The Systolic Hypertension in the Elderly Program (SHEP) conducted in 1991 found that treating ISH can reduce the risk of strokes and ischaemic heart disease. The first line of treatment for ISH was thiazides. However, the 2011 NICE guidelines recommend treating ISH in the same stepwise manner as standard hypertension, which contradicts the previous approach.

It is important to understand ISH as it is a prevalent condition among the elderly population. The SHEP study showed that treating ISH can significantly reduce the risk of serious health complications. However, the recommended approach to treating ISH has changed over time, with the 2011 NICE guidelines suggesting a different method than the previous recommendation of using thiazides as the first line of treatment. It is crucial for healthcare professionals to stay up-to-date with the latest guidelines to provide the best possible care for patients with ISH.

To confirm posterior infarction, a posterior ECG should be recorded when ST elevation and Q waves are present in posterior leads (V7-9). In this case, the patient presented with symptoms suggestive of myocardial infarction and the ECG showed changes that indicated the need for a posterior ECG. This involves placing leads V4-V6 on the patient’s back to make leads V7-V9. ST-elevation and Q waves in these leads confirm posterior infarction, and the patient should be transferred for primary percutaneous coronary intervention as soon as possible. It is important to have a high index of suspicion for posterior MIs and a low threshold for getting a posterior ECG.

Giving IV potassium replacement or calcium gluconate IV would be incorrect in this case. These treatments are used for hypokalaemia and severe hyperkalaemia, respectively, and are not the most likely diagnoses. Ibuprofen and colchicine would be appropriate for pericarditis, which presents with chest pain that is worse on lying flat and has characteristic ECG changes. However, the clinical picture and ECG changes in this case are more consistent with ACS.

A CT aortogram is used to investigate for aortic dissection, which can present with severe chest pain, breathlessness, and sweating. However, it would be best to record a posterior ECG to investigate for posterior MI prior to investigating for an aortic dissection due to the classic features of ACS in the history.

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.

Medications for Post-Myocardial Infarction Patients

Post-myocardial infarction (MI) patients require specific medications to prevent further cardiovascular disease and improve their overall health. One of the most important drugs to offer is a beta-blocker, such as bisoprolol, as soon as the patient is stable. This medication should be continued for at least 12 months after an MI in patients without left ventricular systolic dysfunction or heart failure, and indefinitely in those with left ventricular systolic dysfunction. While beta-blockers can reduce mortality and morbidity for up to a year after an MI, recent studies suggest that continuing treatment beyond a year may not provide any additional benefits. Other medications, such as amiodarone, isosorbide mononitrate, and nicorandil, offer symptom relief but do not reduce mortality or morbidity. Calcium-channel blockers, like diltiazem, may be considered for secondary prevention in patients without pulmonary congestion or left ventricular systolic dysfunction if beta-blockers are contraindicated or discontinued. However, current guidelines recommend offering all post-MI patients an ACE inhibitor, dual antiplatelet therapy, beta-blocker, and statin to improve their long-term health outcomes.

The preferred initial diagnostic test for individuals with stable chest pain suspected to be caused by coronary artery disease is a CT coronary angiogram with contrast enhancement.

Assessment of Patients with Suspected Cardiac Chest Pain

When it comes to assessing patients with suspected cardiac chest pain, NICE has updated its guidelines in 2016. For patients presenting with acute chest pain, immediate management of suspected acute coronary syndrome (ACS) is crucial. This includes administering glyceryl trinitrate and aspirin 300 mg, but not other antiplatelet agents like Clopidogrel outside of the hospital. Oxygen therapy should not be routinely given, but only if sats are less than 94%. Referral depends on the timing of chest pain and ECG results. For patients presenting with stable chest pain, NICE defines anginal pain as constricting discomfort in the front of the chest, neck, shoulders, jaw, or arms, precipitated by physical exertion, and relieved by rest or GTN in about 5 minutes. Non-invasive functional imaging is recommended for patients in whom stable angina cannot be excluded by clinical assessment alone. Examples of non-invasive functional imaging include myocardial perfusion scintigraphy with single photon emission computed tomography (MPS with SPECT), stress echocardiography, first-pass contrast-enhanced magnetic resonance (MR) perfusion, or MR imaging for stress-induced wall motion abnormalities.

In summary, assessing patients with suspected cardiac chest pain requires immediate management for acute chest pain and referral based on timing and ECG results. For stable chest pain, NICE defines anginal pain and recommends non-invasive functional imaging for patients in whom stable angina cannot be excluded by clinical assessment alone.

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.

Individuals with heart failure and an ejection fraction of 40% or lower should be prescribed an ACE inhibitor, unless there are contraindications or intolerance. This is supported by numerous clinical trials that have shown their efficacy in reducing hospital admissions and mortality rates. The dosage should be started low and gradually increased until the target dose or the highest tolerated dose is achieved, with regular monitoring of renal function and serum electrolytes.

Loop Diuretics: Mechanism of Action and Indications

Loop diuretics, such as furosemide and bumetanide, are medications that inhibit the Na-K-Cl cotransporter (NKCC) in the thick ascending limb of the loop of Henle. This reduces the absorption of NaCl and increases the excretion of water and electrolytes, making them effective in treating conditions such as heart failure and resistant hypertension. Loop diuretics act on NKCC2, which is more prevalent in the kidneys.

As loop diuretics work on the apical membrane, they must first be filtered into the tubules by the glomerulus before they can have an effect. This means that patients with poor renal function may require higher doses to achieve a sufficient concentration within the tubules.

Loop diuretics are commonly used in the treatment of heart failure, both acutely (usually intravenously) and chronically (usually orally). They are also effective in treating resistant hypertension, particularly in patients with renal impairment.

However, loop diuretics can have adverse effects, including hypotension, hyponatremia, hypokalemia, hypomagnesemia, hypochloremic alkalosis, ototoxicity, hypocalcemia, renal impairment (from dehydration and direct toxic effect), hyperglycemia (less common than with thiazides), and gout.

In summary, loop diuretics are effective medications for treating heart failure and resistant hypertension, but their use should be carefully monitored due to potential adverse effects. Patients with poor renal function may require higher doses to achieve therapeutic effects.

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.

In cases of haemodynamically stable patients with SVT who do not respond to vagal manoeuvres, the recommended course of action is to administer adenosine.

Understanding Supraventricular Tachycardia

Supraventricular tachycardia (SVT) is a type of tachycardia that originates above the ventricles. It is commonly associated with paroxysmal SVT, which is characterized by sudden onset of a narrow complex tachycardia, usually an atrioventricular nodal re-entry tachycardia (AVNRT). Other causes include atrioventricular re-entry tachycardias (AVRT) and junctional tachycardias.

When it comes to acute management, vagal maneuvers such as the Valsalva maneuver or carotid sinus massage can be used. Intravenous adenosine is also an option, with a rapid IV bolus of 6mg given initially, followed by 12mg and then 18mg if necessary. However, adenosine is contraindicated in asthmatics, and verapamil may be a better option for them. Electrical cardioversion is another option.

To prevent episodes of SVT, beta-blockers can be used. Radio-frequency ablation is also an option. It is important to work with a healthcare provider to determine the best course of treatment for each individual case.

Overall, understanding SVT and its management options can help individuals with this condition better manage their symptoms and improve their quality of life.