porth end of chapter questions exam 1

Chapter 29: Why may coronary ischemia symptoms appear only after severe narrowing?

Coronary arterioles can initially dilate to preserve resting flow. With severe narrowing, the reduced radius causes resistance to rise dramatically according to Poiseuille's law, so flow cannot meet myocardial oxygen demand, especially during activity.

Chapter 29: How does Poiseuille's law relate vessel radius to resistance and flow?

Resistance varies inversely with the fourth power of radius. A small reduction in radius greatly increases resistance and decreases blood flow.

Chapter 29: Why does an arterial aneurysm tend to keep enlarging?

Laplace's law states that wall tension rises as pressure or radius rises. Expansion increases the aneurysm's radius and wall tension, promoting further dilation of the weakened wall.

Chapter 29: Why can a clot form inside a large aneurysm?

The widened area increases cross-sectional area and slows blood velocity. Slow, disturbed flow promotes stasis and thrombus formation.

Chapter 29: How does hypertension affect isovolumetric ventricular contraction?

High aortic pressure increases afterload. The left ventricle must generate more pressure and may spend longer contracting with all valves closed before the aortic valve opens.

Chapter 29: How does a faster heart rate affect diastole?

It shortens diastole more than systole, leaving less time for ventricular filling and coronary perfusion. If the rate is excessive, EDV and stroke volume may fall.

Chapter 29: How would prolonged isovolumetric relaxation affect ventricular filling?

The AV valves would open later, leaving less filling time. This can reduce EDV, preload, stroke volume, and cardiac output.

Chapter 29: What happens to right-heart output during forceful inspiration?

Lower intrathoracic pressure increases venous return, EDV, and preload. Frank-Starling then increases contraction strength and right-ventricular stroke volume.

Chapter 29: What happens to cardiac output during forceful expiration or straining?

Raised intrathoracic pressure compresses the great veins and reduces venous return. Preload, stroke volume, and cardiac output may fall.

Chapter 29: What important function does the Frank-Starling mechanism provide?

It matches ventricular output to venous return: more filling stretches myocardial fibers and produces a stronger contraction. It also helps balance right- and left-ventricular output.

Chapter 30: How does HDL help protect against atherosclerosis?

HDL supports reverse cholesterol transport by collecting cholesterol from peripheral tissues and plaques and carrying it toward the liver for reuse or elimination.

Chapter 30: Which findings increase the coronary risk of the man described in the textbook exercise?

His age, male sex, hypertension, low HDL, and total cholesterol contribute to risk. A formal risk estimate also requires the exact calculator assumptions, including smoking and diabetes status.

Chapter 30: How does an aortic dissection differ from an aortic aneurysm?

A dissection begins with an intimal tear that lets blood separate layers of the aortic wall. An aneurysm is an abnormal localized dilation caused by wall weakness.

Chapter 30: How can poorly controlled hypertension cause or worsen an aortic dissection?

High pressure and pulsatile force increase stress on the aortic wall, encouraging an intimal tear and continued separation of the wall layers.

Chapter 30: Why can arm pulses and blood pressure become unobtainable during an aortic dissection?

The dissection can obstruct branches supplying the arms, sharply reducing blood flow beyond the obstruction and weakening or eliminating the pulses.

Chapter 30: Why is aggressive blood-pressure control important in aortic dissection?

Lowering pressure and the force of ventricular ejection reduces stress on the damaged aortic wall and helps limit extension or rupture.

Chapter 30: A woman has cold-triggered episodes in which her fingers turn pale and numb, then red and painful. What disorder is likely?

Raynaud phenomenon, an episodic vasospasm of small arteries and arterioles in the fingers or toes.

Chapter 30: Why do cold exposure and emotional stress trigger Raynaud episodes?

They increase sympathetic vasoconstrictor activity, producing excessive digital arterial spasm and temporary ischemia. Rewarming then causes vasodilation and redness.

Chapter 30: How can Raynaud phenomenon be managed?

Avoid cold and emotional triggers, keep the extremities warm, avoid nicotine and other vasoconstrictors, and use vasodilators such as calcium-channel blockers when prescribed.

Chapter 33: An older patient has a heart rate of 121 and an irregular rhythm. Which arrhythmia is most likely, and what would the ECG show?

Atrial fibrillation is likely. The ECG would show no consistent P waves, a fibrillatory baseline, and irregularly irregular R-R intervals.

Chapter 33: What produces the irregular rhythm in atrial fibrillation?

Multiple chaotic atrial impulses and reentry circuits cause ineffective atrial contraction, while the AV node conducts a variable number of impulses to the ventricles.

Chapter 33: Why may a patient with atrial fibrillation feel tired?

Loss of effective atrial contraction and a rapid irregular ventricular response can reduce ventricular filling, stroke volume, and cardiac output.

Chapter 33: What are the major concerns associated with atrial fibrillation?

Atrial blood stasis can produce thrombi and embolic stroke. Rapid or poorly controlled AF can also worsen heart failure and reduce cardiac output.

Chapter 33: A premature beat has a QRS duration greater than 0.10 second. What type of beat is suspected?

A premature ventricular contraction is suspected because ventricular activation outside the normal conduction pathway produces an early, wide, abnormal QRS complex.

Chapter 33: What might the pulse feel like during frequent PVCs?

It may feel irregular, weak, or as though beats are missing because some early ventricular contractions eject too little blood to create a palpable peripheral pulse.

Chapter 33: What can cause PVCs during myocardial ischemia, and how are they managed?

Ischemia makes ventricular cells electrically irritable. Management focuses on the cause, including restoring oxygen supply, correcting electrolyte abnormalities, reducing stimulants, and treating persistent or dangerous ventricular arrhythmias.