Cardio 4 Flashcards

1
Q

What is acute pericarditis and what are its causes?

A

Acute pericarditis is inflammation of the pericardial sac, leading to chest pain and other systemic symptoms.

Causes:
β€’ Idiopathic (post-viral): Often follows a viral infection, such as coxsackievirus, echovirus, or adenovirus.
β€’ Infectious: Bacterial (e.g., tuberculosis), fungal, and parasitic.
β€’ Acute MI: Can occur within the first 24 hours after a myocardial infarction (post-MI pericarditis).
β€’ Uremia, collagen vascular diseases (SLE, RA), neoplasms, and radiation.

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2
Q

What are the clinical features of acute pericarditis?

A

Chest pain: Retrosternal, radiates to the neck and back, worsens with inspiration and coughing, and is relieved by sitting forward.

Fever and leukocytosis.

Pericardial friction rub: Best heard during expiration, a hallmark sign but not always present.

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3
Q

How is acute pericarditis diagnosed and treated?

A

Diagnosis:
β€’ ECG: Diffuse ST elevation in all leads and PR depression (more specific).
β€’ Echocardiography: May show pericardial effusion.

Treatment:
β€’ NSAIDs (e.g., aspirin or ibuprofen) for pain and inflammation.
β€’ Colchicine to reduce recurrence.
β€’ Glucocorticoids if there is no response to NSAIDs.
β€’ Bed rest during the acute phase.

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4
Q

What is constrictive pericarditis and its causes?

A

Constrictive pericarditis occurs when the pericardium becomes thickened and fibrotic, restricting the heart’s ability to fill during diastole.

Causes:
β€’ Any cause of pericarditis that leads to chronic inflammation and fibrosis (e.g., tuberculosis, post-viral infections).

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5
Q

What are the clinical features and signs of constrictive pericarditis?

A

Symptoms: Signs of right heart failure (RHF), including peripheral edema, distended JVP, ascites, and hepatomegaly.

Signs:
β€’ Kussmaul’s sign: JVP increases paradoxically on inspiration.
β€’ Pulsus paradoxus.
β€’ Pericardial knock: An extra heart sound during diastole from restricted filling.

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6
Q

How is constrictive pericarditis diagnosed and treated?

A

Diagnosis:
β€’ CXR: Normal heart size with pericardial calcifications.
β€’ CT/MRI: Shows pericardial thickening and calcification.

Treatment:
β€’ Diuretics for symptom control.
β€’ Surgical excision of the pericardium (pericardiectomy) for severe cases.

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7
Q

What is pericardial effusion and its causes?

A

Pericardial effusion refers to the accumulation of fluid in the pericardial sac.

Causes:
β€’ Acute pericarditis.
β€’ Salt and water retention in conditions like CHF, cirrhosis, nephrotic syndrome, or trauma.

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8
Q

What are the symptoms and signs of pericardial effusion?

A

Symptoms: Muffled heart sounds and chest discomfort.

Signs:
β€’ Dullness at the left lung base.
β€’ Pericardial friction rub may be heard if the fluid is minimal.

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9
Q

How is pericardial effusion diagnosed and treated?

A

Diagnosis:
β€’ Echocardiography: The procedure of choice.
β€’ CXR: Cardiomegaly with a flask-shaped appearance.

Treatment:
β€’ Most cases resolve spontaneously.
β€’ Pericardiocentesis may be required if the effusion does not resolve or is symptomatic.

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10
Q

What is cardiac tamponade and its clinical features?

A

Cardiac tamponade is a medical emergency where rapid accumulation of fluid in the pericardial space impairs the heart’s ability to fill, leading to decreased cardiac output.

Clinical features:
β€’ Pulsus paradoxus: A decrease in pulse strength during inspiration, with a >10 mmHg drop in systolic BP.
β€’ Tachypnea, tachycardia, hypotension, and elevated JVP.
β€’ Beck’s triad: Muffled heart sounds, jugular venous distention (JVD), and hypotension.

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11
Q

What are the causes of cardiac tamponade?

A

β€’ Trauma (e.g., penetrating injury).
β€’ Iatrogenic: During central line placement or pericardiocentesis.
β€’ Pericarditis: Inflammation or infection of the pericardium.
β€’ Post-myocardial infarction (post-MI) tamponade due to rupture of the free wall or septum.
β€’ Aortic dissection: Can lead to tamponade if the aorta ruptures into the pericardium.

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12
Q

How is cardiac tamponade diagnosed and treated?

A

Diagnosis:
β€’ Echocardiography: The most sensitive and specific test for diagnosing cardiac tamponade, showing diastolic collapse of the right atrium and right ventricle.
β€’ CXR: Enlargement of the cardiac silhouette.
β€’ ECG: Electrical alternans (alternating amplitudes of QRS complexes).
β€’ Catheterization: Shows equalization of pressures in all heart chambers during diastole.

Treatment:
β€’ If hemodynamically unstable: Immediate pericardiocentesis to remove the fluid and relieve pressure.
β€’ If hemorrhagic tamponade (e.g., trauma): Emergency surgery is required.
β€’ If stable and renal failure is present: Dialysis may help manage the tamponade.

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13
Q

What is myocarditis and its causes?

A

Myocarditis is inflammation of the myocardium, often leading to heart failure and arrhythmias.

Causes:
β€’ Viral: Most commonly caused by Coxsackievirus B, parvovirus B19, or human herpesvirus 6 (HHV6).
β€’ Bacterial: Group A beta-hemolytic streptococcus, Lyme disease, and Mycoplasma pneumonia.
β€’ Autoimmune diseases: Systemic lupus erythematosus (SLE).
β€’ Medications: Sulfonamides, adriamycin.

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14
Q

What are the symptoms of myocarditis?

A

β€’ Fatigue.
β€’ Chest pain: Similar to a heart attack.
β€’ Arrhythmias: Palpitations or irregular heartbeat.
β€’ Heart failure symptoms: Shortness of breath, swelling in the legs.
β€’ Some patients may be asymptomatic, especially in mild cases.

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15
Q

How is myocarditis diagnosed and treated?

A

Diagnosis:
β€’ ECG: Sinus tachycardia, low voltage, electrical alternans, or ST elevation.
β€’ Cardiac enzymes: Elevated levels of troponin.
β€’ Chest X-ray: May show cardiomegaly.
β€’ Echocardiography: May show decreased ejection fraction (EF).
β€’ Endomyocardial biopsy: The gold standard for diagnosis, but not routinely performed.

Treatment:
β€’ Bed rest and management of heart failure with beta-blockers and ACE inhibitors.
β€’ NSAIDs and steroids are generally contraindicated in viral myocarditis as they may worsen the condition.

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16
Q

What is coarctation of the aorta and its pathophysiology?

A

Coarctation of the aorta is a congenital narrowing of the aorta, typically just distal to the insertion of the ductus arteriosus.

The narrowing increases the resistance to blood flow, leading to hypertension in the upper body (e.g., arms and head), while the lower body (e.g., legs) receives less perfusion.

17
Q

What are the clinical features of coarctation of the aorta?

A

β€’ Hypertension in the upper extremities and low blood pressure in the lower extremities.
β€’ Radio-femoral delay: A delay in the pulse when comparing the arms and legs.
β€’ Chest pain and murmur, typically systolic.
β€’ CXR: Shows rib notching due to collateral vessels eroding the ribs.

18
Q

How is coarctation of the aorta diagnosed and treated?

A

Diagnosis:
β€’ Echocardiogram: Can confirm the narrowing of the aorta.
β€’ CXR: Shows rib notching and post-stenotic dilation.

Treatment:
β€’ Surgical repair: In infants or young children with severe coarctation.
β€’ Balloon angioplasty: An alternative for older patients or those with recurrent stenosis.
β€’ Beta-blockers or ACE inhibitors may be used to control blood pressure.

19
Q

What is pulmonary heart disease (cor pulmonale) and its causes?

A

Pulmonary heart disease (cor pulmonale) refers to right-sided heart failure due to pulmonary hypertension, which results from diseases affecting the lungs or pulmonary vessels.

Causes:
β€’ Chronic obstructive pulmonary disease (COPD).
β€’ Pulmonary hypertension due to left heart failure, lung diseases, or recurrent pulmonary emboli.
β€’ Pulmonary stenosis or other pulmonary vessel abnormalities.

20
Q

What are the clinical features of pulmonary heart disease?

A

β€’ Exertional dyspnea.
β€’ Fatigue and lethargy due to decreased cardiac output.
β€’ Right-sided heart failure (RHF): Edema, hepatomegaly, and JVP elevation.
β€’ Loud P2: Increased intensity of the second heart sound due to pulmonary hypertension.

21
Q

How is pulmonary heart disease diagnosed and treated?

A

Diagnosis:
β€’ Right heart catheterization: To measure pulmonary artery pressure (PAP).
β€’ CXR: Shows right heart enlargement.
β€’ ECG: May show right ventricular hypertrophy (RVH) or right atrial enlargement.

Treatment:
β€’ Oxygen therapy: To improve oxygenation and reduce pulmonary hypertension.
β€’ Diuretics: To relieve fluid retention.
β€’ Anticoagulation: If there is a history of pulmonary embolism.
β€’ Treat underlying lung disease: COPD management, pulmonary embolism treatment.

22
Q

What is hypertension and its causes?

A

Hypertension is defined as a systolic blood pressure (SBP) β‰₯140 mmHg or diastolic blood pressure (DBP) β‰₯90 mmHg based on two separate readings.

Causes:
β€’ Primary (essential) hypertension: No known cause, but often linked to genetics, obesity, and lifestyle factors.
β€’ Secondary hypertension: Caused by other conditions such as renal parenchymal disease, renovascular disease, pheochromocytoma, or Cushing’s syndrome.

23
Q

What are the risk factors for hypertension?

A

β€’ Modifiable: Obesity, high salt intake, excessive alcohol use, lack of exercise, smoking, and stress.
β€’ Non-modifiable: Age (older age increases risk), family history, and gender (men are at higher risk before age 55, women after menopause).

24
Q

What is the treatment approach for hypertension?

A

β€’ Lifestyle changes: Weight loss, increased physical activity, reduced salt intake, alcohol reduction, and smoking cessation.
β€’ Medications:
β€’ First-line: ACE inhibitors, angiotensin receptor blockers (ARBs), or calcium channel blockers (CCBs) for patients under 55; CCBs or thiazide-like diuretics for those above 55 or of African descent.
β€’ Combination therapy: If monotherapy fails, combinations of ACE inhibitors, ARBs, CCBs, or diuretics are often used.

25
26
What is the difference between hypertensive urgency and hypertensive emergency?
Hypertensive urgency: Blood pressure β‰₯180/120 mmHg without end-organ damage. Patients are usually asymptomatic or have mild symptoms. Treatment is initiated with oral antihypertensive agents to gradually lower BP. Hypertensive emergency: Blood pressure β‰₯180/120 mmHg with end-organ damage (e.g., myocardial ischemia, acute heart failure, stroke, aortic dissection, renal failure). Treatment requires immediate hospitalization and the use of IV antihypertensive agents to rapidly lower BP.
27
What are the common causes of hypertensive crisis?
Hypertensive urgency: Nonadherence to antihypertensive medications, secondary hypertension (e.g., pheochromocytoma, renovascular disease). Hypertensive emergency: Severe hypertensive heart disease, acute aortic dissection, acute myocardial infarction, eclampsia, or acute kidney failure.
28
What is the treatment approach for hypertensive urgency?
Oral antihypertensive agents: Clonidine (Ξ±2 agonist), nifedipine (calcium channel blocker), captopril (ACE inhibitor), or labetalol (beta-blocker). Goal: Gradual reduction of BP to <160/100 mmHg within 2-6 hours, followed by further adjustment over a few days.
29
What is the treatment approach for hypertensive emergency?
Immediate IV antihypertensive medications: Nitroprusside, nitroglycerin, nicardipine, or labetalol. Goal: Lower mean arterial pressure by 10-20% in the first hour and by 25% over the next 2-3 hours. In cases like acute ischemic stroke or aortic dissection, more aggressive lowering may be required. Monitoring: Patients must be closely monitored in an ICU setting.
30
What are the different types of shock and their characteristics?
Distributive shock: Characterized by peripheral vasodilation and low systemic vascular resistance. Causes: Sepsis, neurogenic shock. Clinical features: Warm extremities, low BP, high heart rate, low central venous pressure (CVP), and low pulmonary capillary wedge pressure (PCWP). Cardiogenic shock: Occurs due to pump failure, such as from acute myocardial infarction or valve failure. Clinical features: Cold extremities, low BP, high heart rate, high CVP, increased systemic vascular resistance (SVR), and high PCWP. Hypovolemic shock: Caused by a decrease in circulating volume (e.g., GI bleed). Clinical features: Low BP, high heart rate, low CVP, and high SVR (cold extremities). Obstructive shock: Caused by obstruction to blood flow (e.g., cardiac tamponade, tension pneumothorax, pulmonary embolism). Clinical features: Low BP, high heart rate, normal or high CVP, and normal or increased SVR.
31
What are the general treatment principles for shock?
ABCs: Ensure airway, breathing, and circulation are stabilized. Oxygen therapy: Administer oxygen to support tissue oxygenation. IV fluids: Aggressive fluid resuscitation, particularly in hypovolemic shock. Inotropic agents: For cardiogenic shock, medications like epinephrine or dopamine may be used to support cardiac output. Treatment of underlying cause: Sepsis: Broad-spectrum antibiotics. Pulmonary embolism: Thrombolysis or anticoagulation. Cardiac tamponade: Pericardiocentesis.
32
What are the key steps in managing hypovolemic shock?
IV fluid resuscitation: Use crystalloids (e.g., normal saline, Ringer’s lactate) to restore circulating volume. Blood transfusion: In cases of significant blood loss. Hemodynamic monitoring: To ensure effective resuscitation and avoid fluid overload.
33
What is the treatment for cardiogenic shock?
Inotropic support: Use medications like dobutamine or dopamine to improve cardiac output. Mechanical support: Consider intra-aortic balloon pump (IABP) or left ventricular assist device (LVAD) for patients with severe LV failure. Revascularization: If the cause is an acute myocardial infarction, urgent PCI or thrombolysis may be needed.