Congestive Heart Failure - Free MCQ Practice Test with solutions, NEET

CVP is used to asses filling of the right heart with low values seen in hypovolemic shock and elevated in cardiogenic shock It cannot calculate cardiac output.
Thermodilution technique uses temperature deviation in pulmonary artery after injection of 10ml room temperature normal saline into the right atrium to calculate Cardiac output. Choices A and D are ruled out easily by English wording itself.

• The given patient with findings of heart failure has normal serum potassium and elevated creatinine.
• Spironolactone has been documented to reduce mortality in heart failure by 30% but is not to be given if eGFR is <30 ml/min, serum Creatinine is >2.5 mg% and K+ is >5.0meq/dl.
• For ACE inhibitors, CMDT 2018 on page 413 has clearly mentioned "Some patients may exhibit rise of serum creatinine and potassium but do not require discontinuation"
• Beta blockers are preferred agents from management of chronic compensated CHF,
• Digoxin has not been shown to reduce mortality in CHF but is not contraindicated in case of elevated Serum creatinine.

First Line of action In Management of Acute Pulmonary Oedema

• Furosemide
• Morphine
• Oxygen
• Nitroglycerin IV if SBP > 100 mm Hg
• Norepinephrine 0.5 - 30 μg/min IV if if SBP < 100 mm Hg and signs of shock are present.
• Dopamine 5 - 15 μg/kg per minute if SBP < 100 mm Hg and signs of shock are present.
• Dobutamine 2 - 20 μg/kg/minute IV if SBP 70 - 100 mm Hg and no Signs of shock are present.

• The findings of dyspnea, elevated JVP and pedal oedema are suggestive of right sided CHF
• Parasternal heave and palpable S2 indicates pulmonary artery hypertension
• This also explains why lungs are clear since pulmonary oedema is absent in PAH
• Reduced RV compliance in RVH leads to elevated JVP and oedema in feet
• The reason for dyspnea is less pulmonary flow due to PAH.

WHO classification of PAH

Etiologies of Heart Failure

For management of digoxin toxicity the following protocol is used:

1. Digoxin-specific antibody fragments for hemodynamically compromising dysrhythmias, Mobitz II or third-degree atrioventricular block, hyperkalemia {>5.5 meq/L; in acute poisoning only).
2. Temporizing measures include atropine, dopamine, epinephrine
3. External cardiac pacing for bradydysrhythmias
4. Magnesium, lidocaine, or phenytoin, for ventricular tachydysrhythmias.
5. Internal cardiac pacing and cardioversion can increase ventricular irritability.

• Both B-type natriuretic peptide (BNP) and N-termlnal pro-BNP, which are released from the failing heart, are relatively sensitive markers for the presence of HF with depressed EF; they also are elevated in HF patients with a preserved EF, albeit to a lesser degree. Levels can be falsely low in obese patients and may normalize in some patients after appropriate treatment. At present, serial measurements of BNP are not recommended as a guide to HF therapy.
• Other biomarkcrs, such as troponin T and I, C-reactive protein, TNF receptors, and uric acid, may be elevated in HF and provide important prognostic information.
• A family of histone deacetylases known as sirtuins. An important member of this family is SIRTI, homologues of which enhance the lifespans of model organisms. SIRTI is a putative target of resveratrol, which is thought to activate the enzyme and, therefore, might enhance lifespan and presumably health span as well.

• Beta-blocker therapy represents a major advance in the treatment of patients with a depressed Beta-blocker therapy represents a major advance in the treatment of patients with a depressed EF.
• These drugs interfere with the harmful effects of sustained activation of the adrenergic nervous system by competitively antagonizing one or more adrenergic receptors. Although there are a number of potential benefits to blocking all three receptors, most of the deleterious effects of adrenergic activation are mediated by the betal receptor.
• Therefore, beta blockers are indicated for patients with symptomatic or asymptomatic HF and a depressed EF <40%.Drugs that interfere with excessive activation of the RAA system and the adrenergic nervous system can relieve the symptoms of HF with a depressed EF by stabilizing and/ or reversing cardiac remodeling.
• In this regard, ACE inhibitors and beta blockers have emerged as the cornerstones of modern therapy for HF with a depressed EF.

This abnormal pattern of breathing, in which breathing is absent for a period and then rapid for a period, can be seen in patients with:

1. Heart failure
2. Stroke [Bihemispheric damage]
3. Traumatic brain injuries and brain tumors
4. Healthy people during sleep at high altitudes
5. Toxic metabolic encephalopathy like carbon monoxide poisoning.

• Morphine acts as a venodilator and anxiolytic.
• Frusemide reduces fluid overload and possible vasodilator.
• Positive pressure ventilation reduces alveolar, interstitial edema thus reducing venous return. CPAP or BiPAP can be used.
• Digoxin is used when pulmonary edema is associated with AF and fast ventricular rate; otherwise the use is limited.

Acute Pulmonary Edema
Administer

• Furosemide IV 0.5 to 1.0 mg/kg
• Morphine IV 2 to 4 mg
• Oxygen/intubation as needed
• Nitroglycerin 5L, then 10 to 20 mcg/min IV if SBP greater than 100 mm Hg
• Norepinephrine, 0.5 to 30 mcg/mln IV or Dopamine, 5 to 15 mcg/kg per minute IV if SBP < 100 mm Hg and signs/ symptoms of shock present
• Dobutamine 2 to 20 mcg/kg per minute IV if SBP 70 to 100 mm Hg and no signs/symptoms of shock