Heart Failure Treatment Strategies Quiz

Loop diuretics (e.g. furosemide, bumetanide), ACE inhibitors (e.g. ramipril, Lisinopril), Angiotensin II receptor blockers (e.g. candesartan, losartan), Beta-blockers (e.g. bisoprolol, carvedilol), Aldosterone receptor antagonists (e.g. spironolactone), SGLT-2 inhibitors.

Step 1 = “DAB” (D = Diuretic if fluid retention) A = ACE Inhibitor or ARB B = Beta-Blocker

Electrolyte disturbances – low K, Na, Mg, Ca, Hypotension, Renal impairment, Hypovolaemia, Nocturia if taken too late in day, Acute gout common with high doses.

Beta-blockers allow the ventricle to fill more completely during diastole, and some (e.g. carvedilol) cause vasodilation, reduce afterload, and reduce renin release by the kidney.

The main points are understanding the strategies for treatment of chronic and acute heart failure, recognizing the paradoxical use of beta blockers, understanding the mechanism of action and uses of drugs which inhibit the renin-angiotensin-aldosterone system, and knowing the mechanism of action and uses of digoxin and inotropes.

Cardiac Resynchronisation Therapy (Biventricular Pacing) and Implantable Cardiac Defibrillators

Sacubitril-Valsartan; Sacubitril inhibits Neprilysin which degrades BNP and other vasoactive peptides

Sequential use of Beta Blocker, Calcium Antagonist or Nitrates, Coronary Angioplasty, New antianginals (Ivabradine, Ranolazine), Coronary artery surgery

Emergency Aspirin, Angioplasty (if near hospital), Thrombolysis (if far away), Low MW Heparin or Fondaparinux, Statin, ACE Inhibitor, Beta Blocker (SAAB)

ACE Inhibitors (Cough, Renal dysfunction, Angioneurotic oedema), Angiotensin Blockers (Renal dysfunction, Never in pregnancy), Beta Blockers (Bradycardia/Heart Block, Tired, Asthma), Calcium Antagonists (Ankle oedema, Heart Block), Diuretics (Hypokalaemia, Diabetes, Gout)

Balloon dilatation, with 85% of children not needing further intervention.

Critical intervention to address heart failure and shock.

It may be compromised, leading to low cardiac output and signs of shock.

It accurately evaluates valve morphology and estimates pressure gradients.

Balloon valvuloplasty for infants and surgical options for older patients.

Diabetes-associated metabolic disorders include hyperglycemia, hypertriglyceridemia, hypercholesterolemia, hypoalphalipoproteinemia, and increased levels of advanced glycation end products, glycated and oxidized lipoproteins.

Systemic conditions that affect the cardiovascular system include diabetes mellitus, hypertension, chronic obstructive pulmonary disease, amyloidosis, rheumatoid arthritis, vasculitides & SLE, thyroid disease, sarcoidosis, nutrition, and drugs.

Exposure to under-nutrition during postnatal periods of development, including adolescence, may affect cardiovascular health in adult life.

Known mechanisms that accelerate vascular damage include diabetes, familial disease, and hypertension.

People with Rheumatoid Arthritis have a 50% to 70% higher risk for cardiovascular disease than the general population. People with Osteoarthrosis face a 24% higher risk for cardiovascular disease than the general population.

Surfactant greatly reduces the surface tension of water, making it easier to inflate the lungs. It reduces pressure by 4.5 times and minimizes fluid accumulation in the alveoli. Surfactant helps keep alveoli size relatively uniform during the respiratory cycle, reducing atelectasis (alveolar collapse).

The law of Laplace states that the pressure within a fluid-lined alveolus is dependent on the surface tension of the fluid and the radius of the alveolus. The formula is P = (2 x T) / r, where P is pressure, T is surface tension, and r is the radius of the alveolus.

The primary elastic forces affecting lung compliance include the elastic forces of the lung tissue itself, mainly determined by elastin and collagen fibers, and the elastic forces caused by surface tension of the fluid that lines the alveoli.

Pulmonary fibrosis, a restrictive lung disease, causes deposition of fibrous tissue, making the lungs stiff and decreasing lung compliance. This results in smaller than normal changes in lung volume for small changes in transpulmonary pressure, leading to shallow and rapid breathing.

The main pulmonary volumes and capacities measured in spirometry include tidal volume, inspiratory reserve volume, expiratory reserve volume, and residual volume.

The ventilation-perfusion ratio is the ratio of the amount of air reaching the alveoli (ventilation) to the amount of blood reaching the alveoli (perfusion) in the lungs.

Alveolar dead space refers to the portion of the alveoli that is ventilated but not perfused, leading to ineffective gas exchange.

Lung perfusion can be actively altered through mechanisms such as vasoconstriction or vasodilation of the pulmonary arterioles, which regulate blood flow to different lung regions.

multiplying frequency by the difference between tidal volume and dead space volume

The alveolar air equation describes the relationship between O2 and CO2 in the alveoli and is affected by various factors such as barometric pressure and respiratory quotient

The overall ventilation-perfusion ratio is approximately 0.84, contributing to a normal gas exchange efficiency.

Hypoxia refers to insufficient oxygen to carry out normal metabolic functions, which is indicated by a PaO2 less than 60 mmHg. Arterial hypoxemia is an abnormal PaO2, with an adult at sea level having a PaO2 less than 80 mmHg.

The four major causes of hypoxemia are anatomical shunt (perfusion that bypasses the lung), physiological shunt (absent ventilation to areas being perfused), V/Q mismatching (low ventilation to areas being perfused), and hypoventilation (underventilation of lung units).

Anatomical shunts involve distribution of CO changed as some blood bypasses gas exchange units, leading to hypoxemia that cannot be abolished by giving 100% O2. Physiological shunts occur when alveoli supplied by a completely blocked airway receive no ventilation. V/Q mismatching results from respiratory diseases producing global changes in lungs, leading to low V/Q (V/Q < 1). Hypoventilation brings less fresh gas to alveoli, decreasing O2 levels and increasing CO2 levels.

References for further reading on the topic of ventilation-perfusion relationships and hypoxemia include medical physiology textbooks such as Boron & Boulpaep's 'Medical Physiology', Guyton & Hall's 'Textbook of Medical Physiology', and other resources like 'Lippincott’s Illustrated Reviews: Physiology', 'Medical Sciences', and 'Physiology at a Glance'.