Cardiovascular Disorders II

An S3 is a ventricular gallop that is produced by passive filling of blood into a noncompliant left ventricle. It is heard early in diastole, 0.12 to 0.16 second after the S2, best with the bell of the stethoscope at the apex, it sounds like the word "Ken-tuc-ky," and it occurs with conditions such as HF and cardiomyopathy when fluid overload is present (King, 2021, p. 168). The S4 in choice a is an atrial gallop that occurs late in diastole, immediately before the S1, it sounds like the word "Ten-nes-see," and it is associated with myocardial infarction, hypertension, and ventricular hypertrophy rather than with the early diastolic filling sound of volume overload (King, 2021, p. 168). The midsystolic click in choice c occurs in mid or late systole and is associated with mitral valve prolapse, not with a diastolic filling sound (King, 2021, p. 171). A split S2 occurs on inspiration and disappears with expiration or breath-holding, so the persistent split described in choice d is not a physiologic finding (King, 2021, pp. 167-168).

A pacing spike without a QRS complex represents failure to capture. The first interventions are to position the patient on the left side and to obtain a chest radiograph to assess for lead displacement, after which the amplitude can be increased to maximum and the battery or generator changed; with a temporary epicardial pacemaker, the wires may also be switched (Melander & Bauman, 2021, pp. 240-241). Increasing the mV setting in choice b decreases sensitivity, which is the intervention for failure to pace rather than for failure to capture (Melander & Bauman, 2021, p. 240). Decreasing the mA output in choice c would further impair capture, because the output should be increased to maximum when capture fails (Melander & Bauman, 2021, p. 240). Turning the pacemaker off in choice d is reserved for failure to sense with competing spikes when the patient's cardiac output is stable (Melander & Bauman, 2021, p. 241).

This patient has a hypertensive emergency, defined as a severe blood pressure elevation with new target organ damage, and the blood pressure should be lowered to a systolic pressure of 160 to 180 mm Hg or a diastolic pressure below 105 mm Hg, by no more than 25% within minutes to 1 to 2 hours, and then gradually lowered over several days with oral therapy to prevent coronary, cerebral, or renal ischemia (Vandewaa & Fellin, 2021, p. 182). Reducing the blood pressure to normal immediately, as in choice a, can precipitate coronary, cerebral, or renal ischemia (Vandewaa & Fellin, 2021, p. 182). Choice c describes the management of a hypertensive urgency, an asymptomatic elevation without acute target organ damage, but this patient has encephalopathy and papilledema and therefore requires immediate intravenous reduction (Vandewaa & Fellin, 2021, pp. 181-182). The reduction in choice d is too slow, because the initial reduction should occur within minutes to 1 to 2 hours (Vandewaa & Fellin, 2021, p. 182).

For a patient with chronic symptomatic heart failure with a reduced ejection fraction and NYHA class II or III symptoms who tolerates an ACE inhibitor, replacement with an angiotensin receptor-neprilysin inhibitor (ARNI) such as sacubitril/valsartan is recommended. The ARNI cannot be given in combination with an ACE inhibitor or within 36 hours of an ACE inhibitor dose (King, 2021, p. 291), so the lisinopril must be stopped at least 36 hours before the sacubitril/valsartan is started (King, 2021, p. 297). Adding the two agents together, as in choice a, is contraindicated because of the risk of angioedema (King, 2021, p. 291). Diltiazem in choice c is a nondihydropyridine calcium channel blocker, a class that should be avoided in patients with heart failure (King, 2021, p. 303). Amlodipine in choice d may be added for blood pressure control or angina, but it does not replace an ACE inhibitor, which reduces mortality in heart failure with a reduced ejection fraction (King, 2021, pp. 291, 303).

Mitral regurgitation produces a holosystolic, high-pitched, blowing murmur that is heard best at the apex and radiates to the left axilla, and it is associated with rupture of the papillary muscles after an acute MI (King, 2021, p. 170). Acute mitral regurgitation produces acute pulmonary edema, which is consistent with the sudden dyspnea, crackles, and hypoxemia in this scenario. Mitral stenosis in choice b produces a low-pitched, rumbling, diastolic murmur at the apex that follows an opening snap and does not radiate (King, 2021, p. 169). Aortic regurgitation in choice c produces an early diastolic, decrescendo murmur that intensifies when the patient sits forward and holds the breath (King, 2021, p. 169). Tricuspid regurgitation in choice d is a soft, systolic, blowing murmur heard best at the left lower sternal border, it intensifies during inspiration, and it radiates to the right sternal border and xiphoid rather than to the left axilla (King, 2021, p. 170).

The internal jugular vein is assessed with the patient positioned at a 45-degree angle, and the distance is measured vertically in centimeters from the angle of Louis to the highest point of pulsation. Because the angle of Louis is approximately 5 cm above the right atrium, 5 cm is added to the measurement, which gives a total of 11 cm for this patient; 7 to 9 cm is normal, and a value higher than 9 cm indicates volume overload (King, 2021, p. 173). Choice a fails to add the 5 cm for the distance from the angle of Louis to the right atrium, so the value it reports is incorrect (King, 2021, p. 173). The value in choice c is obtained by subtracting rather than adding the 5 cm, and it is not consistent with the patient's presentation (King, 2021, p. 173). The assessment in choice d is performed with the patient at a 45-degree angle, not supine, so the measurement does not need to be repeated in that position (King, 2021, p. 173).

An ICD is indicated for primary prevention of sudden cardiac death in patients with a low EF, whether ischemic or nonischemic, and no acute reversible cause; coverage has included patients with coronary artery disease and an EF below 35%, as well as dilated and other cardiomyopathies with an EF below 35% (Melander & Bauman, 2021, pp. 241-242). A leadless pacemaker in choice a is approved for ventricular pacing only and does not provide protection from ventricular arrhythmias (Melander & Bauman, 2021, p. 238). The wearable defibrillator in choice b is a temporary bridge to permanent therapy or recovery of ventricular function rather than a long-term therapy (Melander & Bauman, 2021, p. 241). Choice d is incorrect because ICD therapy is also used for primary prevention in patients who have never had a ventricular arrhythmia (Melander & Bauman, 2021, pp. 241-242).

For isolated systolic hypertension in the elderly, dihydropyridine calcium channel blockers and thiazide diuretics are the preferred first-line agents, and beta-blockers should be avoided (Vandewaa & Fellin, 2021, p. 175). The beta-blocker in choice a is therefore the wrong class for this patient (Vandewaa & Fellin, 2021, p. 175). Nondihydropyridine calcium channel blockers such as diltiazem in choice b directly relax the heart and are contraindicated in heart failure with a reduced ejection fraction, and they are not the preferred agents for isolated systolic hypertension (Vandewaa & Fellin, 2021, pp. 175, 179). Peripheral alpha-1 antagonists in choice c should not be used as monotherapy, and they are adjunct agents rather than the drug of choice in older adults (Vandewaa & Fellin, 2021, pp. 179-180).

This patient has congestion together with evidence of hypoperfusion, and intravenous inotropes such as milrinone or dobutamine may be considered in advanced heart failure with diminished peripheral perfusion or hypotension; vasodilators are reserved for patients without hypotension (King, 2021, p. 302). Intravenous nitroglycerin and diuretics in choice a are recommended for rapid improvement of congestion in patients without hypotension, but they are not the initial approach for this hypotensive patient (King, 2021, p. 302). A fluid bolus in choice c would worsen the existing congestion and is never the initial therapy for acute decompensated heart failure (King, 2021, p. 301). Morphine in choice d causes vasodilation that could further reduce blood pressure, and it is not indicated before perfusion is supported (King, 2021, pp. 301-302).

Mitral stenosis produces a low-pitched, rumbling murmur that is heard best with the bell of the stethoscope at the apex, is better appreciated in the left lateral position, follows an opening snap, and does not radiate; it is associated with rheumatic heart disease (King, 2021, p. 169). Aortic regurgitation in choice a produces a high-pitched, early diastolic, decrescendo murmur that intensifies when the patient sits forward and holds the breath (King, 2021, p. 169). Aortic stenosis in choice b produces a harsh, midsystolic, crescendo-decrescendo murmur that is heard best with the diaphragm over the aortic area and radiates to the carotids (King, 2021, p. 170). Tricuspid stenosis in choice d produces a mid-diastolic murmur that is louder with inspiration and is heard best along the left sternal border (King, 2021, pp. 169-170).