Hypertension, heart failure and shock

Less baroreceptor input means pressure has fallen. The cardiovascular center raises sympathetic output and lowers vagal output, which raises heart rate, contractility and TPR.

• Raises vagal output and lowers sympathetic output:
• Correct: Raises sympathetic output and lowers vagal output:
• Stops all output to the heart until pressure recovers:

A rise in venous pressure passes back into the capillaries and raises capillary hydrostatic pressure, so more fluid filters out. More albumin or constricted arterioles would reduce filtration.

• Correct: A rise in venous pressure:
• A rise in plasma albumin:
• Constriction of the arterioles feeding the bed:

Angiotensin II makes the kidneys keep sodium directly and releases aldosterone, which increases sodium reabsorption further. Water follows the sodium.

• Makes them excrete more, through ANP:
• Has no effect on the kidneys:
• Correct: Makes them keep more, directly and through aldosterone:

Immediately, the loss of whole blood lowers volume without changing blood's makeup. Within minutes the reflex speeds the heart and constricts arterioles. Over hours, fluid moves into the plasma and dilutes it, and the kidneys keep salt and water. Over weeks, EPO rebuilds the red cells.

• Hematocrit, first minutes: no change. Whole blood was lost, cells and plasma together, so the fraction made of red cells has not changed yet.
• Heart rate, ten minutes later: up. Lower MAP reduces baroreceptor firing, so sympathetic output to the SA node rises and vagal output falls.
• Pulse pressure, ten minutes later: down. Stroke volume is smaller, which lowers systolic pressure, while arteriole constriction holds diastolic pressure up.
• Hematocrit, eight hours later: down. Low capillary pressure first drew interstitial fluid into the plasma. Then filtration stayed below the drainage returning fluid, so cell-free fluid kept being added, diluting the remaining red cells.
• Urine output, first day: down. Aldosterone makes the kidneys keep sodium and the high ADH makes them keep water.
• Red blood cell count, three weeks later compared with the first day: up. Lower oxygen delivery to the kidneys raised EPO, which drives red blood cell production in the red bone marrow.

A large infarct leaves the left ventricle too weak to pump out what the lungs deliver. Cardiac output falls, which is cardiogenic shock. Pressure rises in the left atrium and lung capillaries, and fluid filters into the lung tissue and air spaces, causing the crackles.

• Correct: Cardiogenic; blood backs up behind the weak left ventricle: Correct. A failing pump with high filling pressure behind it is cardiogenic shock.
• Hypovolemic; blood lost into the damaged heart muscle wall: An infarct does not bleed away enough blood to cause hypovolemic shock, and low volume would leave the lungs dry, not wet.
• Distributive; dilated lung vessels leak plasma proteins: His cool, clammy skin shows reflex vasoconstriction, not widespread vasodilation. The lung fluid comes from high capillary pressure.
• Obstructive; a large clot blocks the pulmonary trunk: A clot in the pulmonary trunk would cause obstructive shock but would not back fluid up into the lungs, which lie beyond the right ventricle's outflow.

A left ventricle damaged by the infarct cannot pump out all that the lungs deliver. Pressure backs up into the left atrium, pulmonary veins and lung capillaries, and fluid filters into the lungs. Lying flat returns more blood from the legs to the chest and worsens it.

• Right-sided heart failure, raising systemic venous pressure: Right-sided failure backs blood up into the systemic veins and causes ankle swelling and bulging neck veins, not wet lungs. Her ankles are normal.
• Correct: Left-sided heart failure, raising lung capillary pressure: Correct. Breathlessness when lying flat and crackles in the lungs point to left-sided failure.
• Hypovolemic shock, from blood lost into the lungs: She shows no signs of shock or blood loss. The fluid in her lungs is filtered plasma, not lost blood.
• Distributive shock, from dilation of the lungs' vessels: Distributive shock lowers pressure throughout the body. Her problem is a backlog of blood behind a weak left ventricle.

Resistance varies with 1 / radius⁴. The ratio of new to old resistance is (3 ÷ 2)⁴ = 1.5⁴ = 1.5 × 1.5 × 1.5 × 1.5 ≈ 5.06. A one-third cut in radius makes resistance about 5 times higher.

• About 1.5 times: This uses the radius ratio, 1.5, without raising it to the fourth power.
• About 2.3 times: This squares the ratio (1.5² ≈ 2.25). Resistance depends on the fourth power, not the second.
• Correct: About 5 times: Correct. 1.5⁴ ≈ 5.
• About 81 times: This raises 3 to the fourth power instead of the ratio 3 ÷ 2.

The kidneys keep salt and water as if pressure were low. A failing ventricle sits on the flat part of its Frank–Starling curve, so more filling adds little stroke volume. The extra volume mostly raises venous and capillary pressures, worsening fluid in the lungs and tissues.

• Correct: Extra volume raises filling pressures and congestion without adding much stroke volume: Correct. More filling brings more congestion and little extra output.
• Extra volume dilutes the blood so much that it can no longer carry enough oxygen: Retained fluid dilutes the blood only mildly. The main harm is higher pressure behind the failing pump.
• Extra volume switches off the baroreceptor reflex, so heart rate falls to dangerous levels: Heart failure raises sympathetic output and heart rate. The baroreceptor reflex is not switched off by extra volume.
• Extra volume lowers TPR so much that the patient develops distributive shock: In heart failure TPR rises, from sympathetic stimulation and angiotensin II. It does not fall.

A young, elastic aorta stretches as the ventricle ejects, absorbing part of each surge. With age the aorta stiffens, so the same stroke volume raises pressure more during systole, and there is less stored recoil to hold pressure up in diastole. Systolic pressure rises and pulse pressure widens.

• Her heart rate is too slow, so diastole is too short: A slow heart rate lengthens diastole, not shortens it, and would not explain a high systolic value.
• Correct: Her stiff aorta stretches less when blood is ejected: Correct. Arterial stiffening raises systolic pressure and widens pulse pressure.
• Her blood volume is too low to fill the arteries: Low volume would lower pressures, not raise systolic pressure to 168.
• Her arterioles have dilated with age, lowering TPR: Lower TPR would lower pressure, especially diastolic, and would not raise systolic pressure.

Blood loss has lowered his stroke volume, but the baroreceptor reflex is holding MAP up with a fast heart and strong arteriole constriction. The narrow pulse pressure (22 mm Hg) and cool, clammy skin show how hard the reflex is working. This is compensated hypovolemic shock, and it can progress quickly if bleeding continues.

• He is not in shock: his systolic pressure is above 90 mm Hg: Shock is defined by oxygen delivery, not a pressure number. His fast heart, narrow pulse pressure and cool skin are early signs of shock.
• He is in distributive shock from widespread vasodilation: Widespread vasodilation would make his skin warm and his diastolic pressure low. His cool skin and high diastolic pressure show constriction.
• Correct: He is in compensated shock, with pressure held up by the reflex: Correct. His reflexes are compensating for the lost volume.
• He is in irreversible shock, shown by his narrow pulse pressure: A narrow pulse pressure is an early sign of compensation, not a sign of irreversible damage. He is alert enough to talk and still compensating.