Treatment Options for a Patient with Narrow-Complex Tachycardia and Low Blood Pressure

When a patient with a history of ischaemic heart disease presents with a narrow-complex tachycardia and low blood pressure, it is likely that they have gone into fast atrial fibrillation. In this case, the first step in resuscitation should be a synchronised direct current (DC) cardioversion with a 150-J biphasic shock. Administering 100% oxygen, a 500 ml Hartmann bolus, and 0.5 mg metaraminol may help increase the patient’s blood pressure, but it does not address the underlying cause of their haemodynamic instability.

Amiodarone 300 mg stat is recommended for patients with narrow-complex tachycardia and haemodynamic instability. However, administering 10 mmol magnesium sulphate is not the first-line treatment for tachycardia unless the patient has torsades de pointes.

Lastly, administering Intralipid® as per guideline for local anaesthetic toxicity is unlikely to be the main source of the patient’s hypotension and does not address their narrow-complex tachycardia. Therefore, it is important to prioritize the synchronised cardioversion and amiodarone administration in this patient’s treatment plan.

Hypokalaemia and Hyperkalaemia

Hypokalaemia is a condition characterized by low levels of potassium in the blood. This can be caused by excess loss of potassium from the gastrointestinal or renal tract, decreased oral intake of potassium, alkalosis, or insulin excess. Additionally, hypokalaemia can be seen if blood is taken from an arm in which IV fluid is being run. The characteristic ECG changes associated with hypokalaemia include S-T segment depression, U-waves, inverted T waves, and prolonged P-R interval.

On the other hand, hyperkalaemia is a condition characterized by high levels of potassium in the blood. This can be caused by kidney failure, medications, or other medical conditions. The changes that may be seen with hyperkalaemia include tall, tented T-waves, wide QRS complexes, and small P waves.

It is important to understand the causes and symptoms of both hypokalaemia and hyperkalaemia in order to properly diagnose and treat these conditions. Regular monitoring of potassium levels and ECG changes can help in the management of these conditions.

This patient exhibits features of mixed mitral valve disease, which can be challenging to diagnose due to contradictory signs. She has a mid-diastolic rumble, low-volume pulse, and atrial fibrillation, indicating mitral stenosis. However, she also has a displaced apex beat and a pan-systolic murmur, indicating mitral regurgitation. Mixed aortic valve disease is also common in these patients. Aortic stenosis and mixed aortic valve disease are unlikely diagnoses based on the clinical findings, while mitral stenosis and mitral regurgitation alone do not fully explain the examination results.

Differentiating Heart Murmurs and Symptoms

Tricuspid regurgitation is characterized by signs of right heart failure, such as dyspnea and peripheral edema, and a classical murmur. The backflow of blood to the right atrium leads to right heart dilation, weakness, and eventually failure, resulting in ascites and poor ejection fraction causing edema.

Mitral regurgitation has a similar murmur to tricuspid regurgitation but is heard best at the apex.

Aortic regurgitation is identified by an early diastolic decrescendo murmur at the left sternal edge.

Aortic stenosis does not typically result in ascites, and its murmur is ejection systolic.

Pulmonary stenosis is characterized by a mid-systolic crescendo-decrescendo murmur best heard over the pulmonary post and not a holosystolic murmur at the left sternal edge.

Understanding Heart Murmurs and Symptoms

Common Heart Conditions and Their Characteristics

Aortic stenosis is a condition where the aortic valve does not open completely, resulting in dyspnea, chest pain, and syncope. It produces a narrow pulse pressure, a low volume pulse, and an ejection systolic murmur that radiates to the carotids. An enlarged right ascending aorta is a common finding in aortic stenosis. Calcification of the valve is diagnostic and can be observed using CT or fluoroscopy. Aortic stenosis is commonly caused by calcification of the aortic valve due to a congenitally bicuspid valve, connective tissue disease, or rheumatic heart disease. Echocardiography confirms the diagnosis, and valve replacement or intervention is indicated with critical stenosis <0.5 cm or when symptomatic. Aortic regurgitation is characterized by a widened pulse pressure, collapsing pulse, and an early diastolic murmur heard loudest in the left lower sternal edge with the patient upright. Patients can be asymptomatic until heart failure manifests. Causes include calcification and previous rheumatic fever. Ventricular septal defect (VSD) is a congenital or acquired condition characterized by a pansystolic murmur heard loudest at the left sternal edge. Acquired VSD is mainly a result of previous myocardial infarction. VSD can be asymptomatic or cause heart failure secondary to pulmonary hypertension. Mitral regurgitation is characterized by a pansystolic murmur heard best at the apex that radiates towards the axilla. A third heart sound may also be heard. Patients can remain asymptomatic until dilated cardiac failure occurs, upon which dyspnea and peripheral edema are among the most common symptoms. Mitral stenosis causes a mid-diastolic rumble heard best at the apex with the patient in the left lateral decubitus position. Auscultation of the precordium may also reveal an opening snap. Patients are at increased risk of atrial fibrillation due to left atrial enlargement. The most common cause of mitral stenosis is a previous history of rheumatic fever.

Complications of Myocardial Infarction

Myocardial infarction (MI) is a serious medical condition that can lead to various complications. Among these complications, ventricular arrhythmia is the most common cause of death. Malignant ventricular arrhythmias require immediate direct current (DC) electrical therapy to terminate the arrhythmias. Mural thrombosis, although it may cause systemic emboli, is not a common cause of death. Myocardial wall rupture and muscular rupture typically occur 4-7 days post-infarction, while papillary muscle rupture is also a possibility. Pulmonary edema, which can be life-threatening, is accompanied by symptoms of breathlessness and orthopnea. However, it can be treated effectively with oxygen, positive pressure therapy, and vasodilators.

Understanding the Complications of Myocardial Infarction

Systolic Valvular Murmurs

A systolic valvular murmur can be caused by aortic/pulmonary stenosis or mitral/tricuspid regurgitation. It is important to note that the location where the murmur is heard loudest can be misleading. For instance, if it is aortic stenosis, the murmur is expected to radiate to the carotids. However, the significant factor to consider is that the murmur is heard loudest on inspiration. During inspiration, venous return to the heart increases, which exacerbates right-sided murmurs. Conversely, expiration reduces venous return and exacerbates left-sided murmurs. To remember this useful fact, the mnemonic RILE (Right on Inspiration, Left on Expiration) can be used.

If a systolic murmur is enhanced on inspiration, it must be a right-sided murmur, which could be pulmonary stenosis or tricuspid regurgitation. However, in this case, only pulmonary stenosis is an option. systolic valvular murmurs and their characteristics is crucial in making an accurate diagnosis and providing appropriate treatment.

Differential diagnosis of a patient with chest trauma

When evaluating a patient with chest trauma, it is important to consider various potential diagnoses based on the clinical presentation and mechanism of injury. Here are some possible explanations for different symptoms:

– Cardiac tamponade: If a projectile penetrates the fibrous pericardium, blood can accumulate in the pericardial cavity and compress the heart, leading to decreased cardiac output and potential death.
– Deep vein thrombosis: This condition involves the formation of a blood clot in a deep vein, often in the leg. However, it does not typically cause the symptoms described in this case.
– Stroke: A stroke occurs when blood flow to the brain is disrupted, usually due to a blockage or rupture of an artery. This is not likely to be the cause of the patient’s symptoms.
– Pulmonary embolism: If a clot from a deep vein thrombosis travels to the lungs and obstructs blood flow, it can cause sudden death. However, given the history of trauma, other possibilities should be considered first.
– Haemothorax: This refers to the accumulation of blood in the pleural cavity around a lung. While it can cause respiratory distress and chest pain, it does not typically affect jugular veins or heart sounds.

Cardiac Signs and Their Associated Conditions

Corrigan’s Sign: This sign is characterized by an abrupt distension and collapse of the carotid arteries, indicating aortic incompetence. It is often seen in patients with a collapsing pulse and an early diastolic murmur, which are suggestive of aortic regurgitation. A wide pulse pressure may also be found.

Malar Flush: Mitral stenosis is associated with malar flush, a mid-diastolic murmur, loudest at the apex when the patient is in the left lateral position, and a tapping apex. A small-volume pulse is also typical.

Tapping Apex: A tapping apex is a classical sign of mitral stenosis.

Pulsatile Hepatomegaly: Severe tricuspid regurgitation can cause reverse blood flow to the liver during systole, resulting in pulsatile hepatomegaly.

Clubbing: Clubbing is more commonly seen in lung pathology and is unlikely to present in aortic regurgitation. It is seen in congenital cyanotic heart disease.

Verapamil and Beta Blockers: A Dangerous Combination

Verapamil is a type of medication that blocks calcium channels in the heart, leading to a decrease in cardiac output and a slower heart rate. However, it also has negative effects on the heart’s ability to contract, making it a highly negatively inotropic drug. Additionally, it may impair the conduction of electrical signals between the atria and ventricles of the heart.

According to the British National Formulary (BNF), verapamil should not be given to patients who are already taking beta blockers. This is because the combination of these two drugs can lead to dangerously low blood pressure and even asystole, a condition where the heart stops beating altogether.

Therefore, it is important for healthcare professionals to carefully consider a patient’s medication history before prescribing verapamil. If a patient is already taking beta blockers, alternative treatments should be considered to avoid the potentially life-threatening consequences of combining these two drugs.