CVS Week 3 Flashcards

Question

🩻 TLO 3.5.3: Relevant CXR Pathological Findings

Answer 1

CXR Feature Interpretation Alveolar oedema “Batwing” perihilar pattern – indicates pulmonary oedema Upper lobe diversion Redistribution of blood flow to upper lobes (CHF sign) Cardiomegaly Cardiothoracic ratio >50% Pleural effusions Usually bilateral, more on the right Kerley B lines Short horizontal lines at lung bases – indicate interstitial oedema

Answer 2

Acute Complications * Acute pulmonary oedema * Cardiogenic shock * Arrhythmias (e.g., AF, VT/VF) * Renal dysfunction Chronic Complications * Progressive decline in EF * Thromboembolism * Liver congestion → cardiac cirrhosis * Cachexia and muscle wasting * Anemia and hyponatraemia

Answer 3

Initial Management of ADHF: 1. Oxygen Therapy: o Administer oxygen if hypoxemia is present. o Non-invasive ventilation (NIV), such as CPAP (Continuous Positive Airway Pressure) or BiPAP (Bilevel Positive Airway Pressure), is often used in acute pulmonary oedema to improve oxygenation and reduce preload. 2. Diuretics: o Frusemide (Furosemide) – Loop diuretic:  Mechanism: Inhibits sodium and chloride reabsorption in the loop of Henle, leading to increased urine output.  Indication: Relieves pulmonary congestion and peripheral oedema.  Dose: Initial bolus, followed by continuous infusion or repeated bolus, depending on severity.  Monitor: Electrolytes, renal function, and fluid status. 3. Vasodilators: o Nitrates (e.g., nitroglycerin):  Mechanism: Venodilation (reduces preload) and arterial dilation (reduces afterload), leading to reduced myocardial oxygen demand.  Indication: Severe pulmonary oedema and when BP allows for vasodilation.  Administration: Sublingual or IV. 4. Inotropic Support (if necessary): o Dobutamine (Beta-1 agonist):  Mechanism: Increases myocardial contractility and cardiac output.  Indication: Used in cases of cardiogenic shock with severe hypotension. o Milrinone (Phosphodiesterase inhibitor):  Mechanism: Increases cardiac contractility and vasodilation.  Indication: Often used when dobutamine is ineffective or contraindicated. 5. Monitoring: o Regular assessment: Monitor vital signs, oxygenation, urine output, electrolytes, and acid-base status.

Answer 4

Pharmacologic Management of Chronic Heart Failure: 1. ACE Inhibitors (e.g., Enalapril, Lisinopril): o Mechanism: Inhibits conversion of angiotensin I to angiotensin II → vasodilation, reduced preload/afterload, and improved renal perfusion. o Indication: Standard treatment for systolic heart failure to reduce symptoms and mortality. o Monitor: Renal function, potassium levels (risk of hyperkalemia), blood pressure. 2. Angiotensin Receptor Blockers (ARBs) (e.g., Losartan, Valsartan): o Mechanism: Block angiotensin II receptors, providing similar benefits as ACE inhibitors with less risk of cough. o Indication: For patients intolerant to ACE inhibitors. 3. Angiotensin Receptor-Neprilysin Inhibitors (ARNI) (e.g., Sacubitril/Valsartan): o Mechanism: Combines ARB (Valsartan) with neprilysin inhibitor (Sacubitril) to reduce vasoconstriction, sodium retention, and myocardial fibrosis. o Indication: Standard therapy for patients with HFrEF (Heart Failure with Reduced Ejection Fraction). 4. Beta-blockers (e.g., Metoprolol, Carvedilol, Bisoprolol): o Mechanism: Reduce sympathetic nervous system activation, decreasing heart rate, blood pressure, and myocardial oxygen demand. o Indication: First-line for chronic heart failure to improve symptoms, prevent hospitalization, and prolong survival. o Monitor: Heart rate, blood pressure, and signs of fluid retention. 5. Mineralocorticoid Receptor Antagonists (MRAs) (e.g., Spironolactone, Eplerenone): o Mechanism: Block aldosterone effects → reduces sodium and water retention, and prevents myocardial fibrosis. o Indication: Beneficial in HFrEF, improves survival, and reduces hospitalizations. o Monitor: Renal function, potassium levels (risk of hyperkalemia). 6. SGLT2 Inhibitors (e.g., Dapagliflozin, Empagliflozin): o Mechanism: Inhibit sodium-glucose co-transporter 2, reducing glucose reabsorption in the kidneys and promoting natriuresis. o Indication: Shown to improve outcomes in both diabetic and non-diabetic patients with heart failure. o Monitor: Renal function, electrolytes, and risk of dehydration. 7. Digoxin: o Mechanism: Increases myocardial contractility and decreases heart rate through inhibition of Na+/K+ ATPase. o Indication: Used for rate control in atrial fibrillation and in severe heart failure for symptom relief. o Monitor: Serum digoxin levels, renal function, and electrolytes (especially potassium).

Answer 5

* Lifestyle modification: Weight management, low-sodium diet, fluid restriction. * Exercise: Regular, moderate activity as tolerated. * Device therapy: o Implantable cardioverter-defibrillator (ICD) for prevention of sudden cardiac death in high-risk patients. o Cardiac resynchronization therapy (CRT) for patients with intraventricular conduction delay (e.g., wide QRS).

Answer 6

Shock is a syndrome characterized by impaired tissue perfusion, resulting in cellular hypoxia and potential organ failure. It is usually classified based on its etiology:

Answer 7

Types of Shock: 1. Hypovolemic Shock: o Caused by decreased blood volume (e.g., hemorrhage, dehydration, fluid loss). 2. Cardiogenic Shock: o Caused by impaired cardiac function leading to inadequate cardiac output (e.g., acute myocardial infarction, heart failure). 3. Distributive Shock (e.g., septic shock, neurogenic shock, anaphylactic shock): o Caused by vasodilation and abnormal distribution of blood flow. 4. Obstructive Shock: o Caused by physical obstruction of blood flow (e.g., massive pulmonary embolism, cardiac tamponade, tension pneumothorax).

Answer 8

There are typically four stages of shock based on severity and clinical progression: 1. Compensated Shock (Non-progressive stage): * Body compensates for reduced perfusion using mechanisms like vasoconstriction, tachycardia, and fluid retention to maintain blood pressure and perfusion. * Clinical signs: Cold extremities, mild tachycardia, low-normal blood pressure, increased respiratory rate. 2. Progressive Shock: * The compensatory mechanisms begin to fail as the body is unable to maintain adequate perfusion. * Clinical signs: Hypotension, marked tachycardia, oliguria, altered mental status (confusion, lethargy). 3. Irreversible Shock: * Organ damage becomes irreversible; cells undergo necrosis, leading to multi-organ failure. * Clinical signs: Severe hypotension, bradycardia, severe metabolic acidosis, loss of consciousness, and multi-organ failure.

Answer 9

Pathophysiology: 1. Reduced Cardiac Output: o A fall in stroke volume (SV) and heart rate results in decreased cardiac output. 2. Compensatory Mechanisms: o Activation of sympathetic nervous system (SNS) and renin-angiotensin-aldosterone system (RAAS) to increase heart rate and vasoconstrict. 3. Increased Preload: o Venous congestion occurs due to backward failure (blood accumulates in the venous system), causing pulmonary edema or systemic edema. 4. Impaired Oxygen Delivery: o Decreased cardiac output leads to tissue hypoxia, organ dysfunction, and metabolic acidosis. 5. Metabolic Derangements: o Lactate accumulation and acidosis occur as cells switch to anaerobic metabolism.

Answer 10

1. Stage 1 (Initial Stage): o Clinical Manifestations: Mild hypotension, increased heart rate, mild tachypnea. o Compensatory Mechanisms: SNS and RAAS activation maintain blood pressure. 2. Stage 2 (Progressive Stage): o Clinical Manifestations: Severe hypotension (< 90 mmHg), rapid tachycardia, cold extremities, oliguria, restlessness. o Pathophysiology: Decreased perfusion to organs, worsening metabolic acidosis, and impaired oxygen delivery. 3. Stage 3 (Irreversible Stage): o Clinical Manifestations: Severe hypotension, bradycardia, altered consciousness, multi-organ failure. o Pathophysiology: Extensive tissue damage, irreversible cell death, and failure of compensatory mechanisms.

Answer 11

General Measures: * Oxygen therapy: To improve tissue oxygenation. * Monitoring: Continuous monitoring of vital signs, urine output, and central venous pressure (CVP). * Intensive care: Most patients require ICU admission. 2. Pharmacologic Treatment: * Inotropes (e.g., dobutamine, milrinone): o Mechanism: Increase myocardial contractility and cardiac output. * Vasopressors (e.g., norepinephrine, dopamine): o Mechanism: Vasoconstriction to improve systemic vascular resistance and raise blood pressure. * Diuretics (e.g., furosemide): o Mechanism: Reduce pulmonary edema and venous congestion by promoting fluid excretion. 3. Mechanical Support: * Intra-aortic balloon pump (IABP): o Mechanism: Increases coronary perfusion and reduces afterload by inflating during diastole and deflating during systole. * Left ventricular assist device (LVAD): o Used in refractory cases of cardiogenic shock when other treatments are ineffective. 4. Treatment of Underlying Cause: * Revascularization: Percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) in cases of acute myocardial infarction. * Valve repair/replacement: In cases of valvular heart disease. 5. Fluid Management: * Careful fluid resuscitation: Use judiciously to avoid fluid overload, which can worsen pulmonary congestion.

Answer 12

Summary of Key Management Points for Cardiogenic Shock: * Inotropes and vasopressors to maintain cardiac output and blood pressure. * Oxygen therapy to prevent tissue hypoxia. * Diuretics for fluid management, avoiding volume overload. * Mechanical support devices (IABP, LVAD) in refractory cases. * Revascularization or surgery to treat the underlying cardiac condition.