Sample Question

A 45-year-old obese woman developed dyspnea and shortness of breathing after chest trauma due to
road traffic accidents. Initial assessment shows blood pressure 132/90 mmHg, heart rate 92/min, and O2
saturation 94% on room air. Suddenly her pulse increases from 92 to 140/min; systolic Blood Pressure
drops from 132 to 90 mm Hg; jugular vein congested. On chest examination, breath sounds are absent
on the left side. What is the most likely physiological explanation that can occur with this woman?

A. Decrease right ventricular filling

B. Increase cardiac preload
C. Decrease central venous pressure
D. Increase oxygen partial pressure
E) Increase diastolic blood pressure

A. Decrease right ventricular filling

Tension pneumothorax is a possible complication of chest trauma due to RTA. The rapid collapse of the
lung and compression of the mediastinum can lead to impaired right ventricular filling.

B. Increase cardiac preload

Increase cardiac preload incorrect option due to mediastinal shifting away from the pressure. This
results in compression of the vena cava leading to decreased venous return and decreased cardiac
preload.

C. Decrease central venous pressure

Decrease central venous pressure incorrect and can increase result in distended neck veins, and
hypotension.

D. Increase oxygen partial pressure

Lungs have a tendency to collapse due to elastic recoil. Pneumothorax enlarges, and the lung gets
smaller due to this vital capacity and leads to oxygen partial pressure decreases.

E) Increase diastolic blood pressure

Increase diastolic blood pressure is not occur and can lead to a decrease in diastolic blood pressure due
to decreased venous return and decreased cardiac preload.

A 44-year-old woman comes to the emergency department with exertional dyspnea and dry cough. She
Also has occasional attacks of continuous dry cough at night that is only relieved by sitting up. She has a
significant history of myocardial infarction 8 months ago. Current medications include metoprolol and
baby aspirin. Her father died of an ischemic CVA. On examination: her blood pressure is 146/100 mm Hg
and her pulse are 60/min. The chest examination shows crackles in the base of both lungs. The cardiac
apex is palpated in the left sixth intercostal space. Bilateral pitting leg edema is present. Which of the
following physiology is most likely to be associated with this patient's condition?

A. Decrease sodium resorption in the proximal tubules

 B. Decrease renal vascular resistance
C. Increased renal perfusion
D. Decreased plasma colloid pressure
E. Increase in intracellular fluid volume

A. Decrease sodium resorption in the proximal tubules

Direct stimulation of sodium resorption in the proximal tubules and increased secretion of aldosterone
from the adrenal glands, which in turn promotes further sodium resorption in the cortical collecting
tubule. These actions lead to decreased sodium delivery to the distal tubule and an increase in
extracellular fluid volume.

B. Decrease renal vascular resistance

Patients with systolic CHF and reduced cardiac output have an increase in renal vascular resistance due
to activation of the sympathetic nervous system and the renin-angiotensin-aldosterone system

C. Increased renal perfusion

Decreased renal perfusion can occur in a patient with CHF and activation of the renin-angiotensin-
aldosterone system leads to increased angiotensin II levels. Angiotensin II causes effects including
Vasoconstriction of the afferent and efferent glomerular arterioles

D. Decreased plasma colloid pressure

Decreased plasma colloid pressure is the mechanism responsible for peripheral or generalized edema in
patients with severe proteinuria and hypoalbuminemia.

E. Increase in intracellular fluid volume

such this case leads to neurohumoral adaptations, including increased sympathetic nervous system
tone, activation of the renin-angiotensin-aldosterone system, and increased secretion of antidiuretic
hormone. These compensatory mechanisms attempt to maintain cardiac output and systemic pressure
by increasing myocardial contractility, peripheral vasoconstriction, and expansion of extracellular fluid
volume.