Examkin

Soru

Zorluk: ZorCardiovascular System

A 62-year-old man presents to the clinic with a three-week history of a nonproductive cough and progressively worsening shortness of breath. He reports that his breathing becomes particularly difficult when he lies down to sleep at night, forcing him to prop himself up with three pillows. His medical history includes hypertension, osteoarthritis of the knees, and a 25-pack-year smoking history. Three weeks ago, he was evaluated for worsening knee pain and elevated blood pressure, at which time naproxen and amlodipine were added to his daily regimen. Temperature is 37.0°C (98.6°F), blood pressure is 152/92 mm Hg, pulse is 92/min, and respirations are 20/min. BMI is 31 kg/m². Lung auscultation reveals diffuse expiratory wheezing with no crackles. Cardiac examination shows a regular rhythm with normal S1 and S2; a faint, low-frequency sound is heard just after S2 at the cardiac apex. Trace bilateral pitting edema is present at the ankles. Which of the following is the most likely pathophysiologic mechanism underlying this patient's current respiratory symptoms?

  1. Elevated left ventricular end-diastolic pressureCevap
  2. B
    Inflammatory narrowing of the bronchial airways
  3. C
    Accumulation of bradykinin in the respiratory tract
  4. D
    Precapillary pulmonary arterial hypertension
  5. E
    Preferential precapillary arteriolar vasodilation

Cevap

Elevated left ventricular end-diastolic pressure
The correct answer is elevated left ventricular end-diastolic pressure. This patient presents with classic signs of acute decompensated heart failure (ADHF), including orthopnea (requiring three pillows to sleep), a nonproductive cough, and an S3 gallop (a low-frequency sound heard just after S2 at the apex). His wheezing represents 'cardiac asthma,' which occurs when fluid transudation into the peribronchial interstitium causes airway narrowing. The precipitating factor is the recent initiation of naproxen, a nonsteroidal anti-inflammatory drug (NSAID). NSAIDs inhibit prostaglandin synthesis, leading to afferent arteriolar vasoconstriction, reduced glomerular filtration rate, and subsequent renal sodium and water retention. In a patient with underlying cardiovascular disease (e.g., chronic hypertension causing diastolic dysfunction), this sudden intravascular volume expansion elevates left ventricular end-diastolic pressure (LVEDP), causing backward failure and pulmonary venous congestion.

Adım Adım Çözüm

1
Identify the patient's primary syndrome based on the physical exam and history.
The patient has orthopnea, nocturnal cough, wheezing, and an S3 gallop at the apex.
These findings are highly specific for left-sided volume overload and pulmonary venous congestion (acute decompensated heart failure), presenting atypically with wheezing ('cardiac asthma').
2
Identify the likely precipitating trigger for the acute decompensation.
The patient was recently started on naproxen (an NSAID) and amlodipine.
NSAIDs promote renal sodium and water retention, which expands intravascular volume and can precipitate heart failure in patients with underlying susceptible cardiac disease (such as hypertensive heart disease).
3
Connect the clinical syndrome and trigger to the underlying pathophysiology.
The volume expansion from the NSAID led to an increase in left ventricular end-diastolic pressure (LVEDP).
Elevated LVEDP causes backward transmission of pressure into the pulmonary veins and capillaries, resulting in fluid transudation into the peribronchial space and the observed symptoms.

Anahtar Kavram

Acute decompensated heart failure can present with wheezing (cardiac asthma) and can be precipitated by medications that cause fluid retention, such as NSAIDs, which elevate left ventricular end-diastolic pressure.
Tahmini Süre:1m 30s
Bu soruyu puanla

Konular

Cardiovascular System

Bu konudan daha fazla soru