T4 Acute HF

• What is the most common reason for adult hospital admission?

  Heart failure.
• What cardiovascular diseases are associated with HF?

  Coronary artery disease, hypertension, and myocardial infarction.
• What are the primary risk factors for HF?

  Hypertension and Coronary artery disease.
• What is cardiomyopathy?

  Genetic heart muscle disease that weakens the heart leading to HF.
• Can cardiomyopathy be acquired instead of inherited?

  Yes.
• Inherited forms of cardiomyopathy are autosomal dominant with variable genetic expression.
• How does cardiomyopathy cause heart failure?

  Weakens ventricular structure and stability of the heart.
• What is post viral myocarditis?

  Interaction between a virus and genetic disposition.
• What is Paget's disease?

  Bone disease that causes bones to be larger, weaker, and deformed.
• What is the difference between primary and secondary causes of heart failure?

  Primary: Conditions that directly damage the heart. Secondary: Conditions that strain the heart or increase the heart's workload.
• Where does blood back up with left sided heart failure?

  Lungs and left atrium.
• What does left sided heart failure cause?

  Pulmonary congestion and edema.
• What EF is considered systolic failure?

  40% where the heart cannot pump blood effectively.
• What is considered diastolic failure for left sided heart failure?

  Primarily caused by hypertension that leads to the ventricles unable to relax and fill properly leading to lower stroke volume and cardiac output.
• What is the most common cause of right sided heart failure?

  Left-sided heart failure.
• When does compensated heart failure occur?

  When compensatory mechanisms are able to have a high enough cardiac output to perfuse tissue.
• When does decompensated heart failure occur?

  When the compensatory mechanisms can't maintain a high enough cardiac output anymore leading to tissue not being perfused enough.
• What mechanisms compensate for heart failure?

  • RAAS
  • Sympathetic nervous system
  • Ventricular remodeling - dilation and hypertrophy
• How does RAAS increase cardiac output?

  Angiotensin I converts to Angiotensin II which vasoconstricts, aldosterone retains sodium and water while excreting potassium, pituitary gland releases ADH to reabsorb water.
• How does the SNS increase cardiac output?

  Baroreceptors feel a low arterial pressure, catecholamines are released which stimulated beta receptors to increase HR (chronotropy) and contractility (inotropy).
• How does dilation increase CO?

  Enlargement of the left ventricle elevates over time which is only effective for a little bit (Frank-Starling Law).
• How does hypertrophy increase CO?

  Muscle and heart wall thickness increases which is initially effective but then leads to poor contractility, increase oxygen needs, poor coronary artery circulation which causes a risk for dysrhythmias.
• What are counterregulatory mechanisms in regards to HF?

  Natriuretic peptides, nitric oxide and prostaglandin.
• What are the natriuretic peptides and what do they do?

  ANP (from atria) and BNP (from ventricles) release in response to high blood volume and heart wall stretching to cause diuresis, vasodilation, and decreased BP.
• What do nitric oxide and prostaglandin do?

  They are released from endothelium in response to compensatory mechanisms to relax smooth arterial muscle which causes vasodilation and decreased afterload.
• What is a normal BNP level?

  Anything less than 100 pg/mL.
• How do natriuretic peptides work on the kidneys?

  Increase the GFR rate and lead to more urine output and sodium excretion.
• What is ADHF?

  Acute decompensated heart failure that are usually sudden.
• What are early signs of ADHF?

  Increased pulmonary venous pressure, mild increase in respiratory rate, decrease in PaO2.
• What are late signs of ADHF?

  Tachypnea, dyspnea, alveolar edema, respiratory acidosis.
• When does ADHF become life threatening?

  When alveoli fill with fluid.
• What are signs of pulmonary edema?

  Shortness of breath, coughing, wheezing, pink frothy sputum, crackles with wheezing, tachycardia, abnormal S3 or S4 sounds, use of accessory muscles, orthopnea.
• What is dry and warm for HF?

  • PAWP is normal, CO is normal, no signs of HF.
• What is Wet and Warm for HF?

  • PAWP is increased
  • CO is normal
  • Dyspnea, edema, orthopnea
• What is Dry and Cold for HF?

  • PAWP is decreased or normal
  • CO is decreased
  • Edema, hypotension, cool extremities
• What is wet and cold for HF?

  • PAWP is increased
  • CO is decreased
  • Altered mental status, decreased O2 saturation, reduced urine output, shock
• What makes a patient with HF "wet"?

  Fluid overload.
• What makes a patient with HF "warm"?

  Adequate perfusion.
• If a HF patient is cold, what goes down?

  Cardiac output.
• If a HF patient is wet, what increases?

  PAWP.