CC: “I’ve been short of breath off and on for a few months.”
VS: R: 18 breaths/minute; BP: 142/92 mm Hg; P: 78 beats/minute; T: 97°F
HPI: A 54-year-old man with a history of hypertension for the last 5 years presents to the ambulatory care center with intermittent episodes of dyspnea. These episodes are worse with exertion, particularly walking up stairs.
ROS:
No chest pain
No palpitation
No syncope
Occasional orthopnea and paroxysmal nocturnal dyspnea
PE:
Cardiovascular: no JVD, 2/6 murmur at the apex radiating to the axilla, S4 gallop
Extremities: 2+ pitting edema
What is the mechanism of the S4 gallop on examination?
a. Rapid ventricular filling in diastole
b. Calcification of the mitral valve
c. Atrial systole into the noncompliant ventricle
d. Shunt from left to right
Answer c. Atrial systole into the noncompliant ventricle
Normally, the atrium should contract and the blood will easily enter the ventricle without a sound. This is because the ventricle should relax to receive the blood. Hypertension causes thickening of the LV. Compliance = volume change/pressure change. A noncompliant ventricle exhibits a large change in pressure with only a small change in volume.
Calcification of the mitral valve (choice b) is from mitral stenosis. Mitral stenosis gives a diastolic murmur. Shunt from left to right (choice d) is a ventricular septal defect, which gives a continuous “machinery murmur.”
Initial Orders:
ECG
Chest x-ray
Transthoracic echocardiogram
On a CCS case, as you move the clock forward, results of tests will automatically be sent to your screen. You will see the notice “report available.” In a relatively stable office or ambulatory case, you do not have to see the patient each time a result comes back. You can let the test results accumulate and see the patient in 1 to 2 weeks for a case such as this.
Test Results:
ECG: left ventricular hypertrophy, SV1 and RV5 >35 mm
Chest x-ray: left ventricular hypertrophy
Echocardiogram: dilated left ventricle; 32% ejection fraction (EF); modest mitral regurgitation (MR)
Some segmental wall motion abnormalities present
Because of dilated cardiomyopathy, you start an ACE inhibitor, such as lisinopril or enalapril. CCS does not allow you to test doses, and you cannot order medications by class name. You must enter “lisinopril” on a CCS case, and are not allowed to order just “ACE inhibitor.” In a single-best-answer question, never order a cardiology consultation in a CHF case. You are expected to manage CHF without consultation. The only way to know if this person had systolic or diastolic dysfunction is with echocardiogram. Hypertension initially gives hypertrophic cardiomyopathy, but over time, the heart tires and begins to dilate. This can eventually lead to a dilated cardiomyopathy.
What is the main difference between ACE inhibitors?
a. Efficacy in lowering mortality in CHF
b. Usefulness in hypertension
c. Dosing
d. Propensity to cause cough
e. Propensity to cause hyperkalemia
Answer c. Dosing
The only major difference between ACE inhibitors is dosing. All lower mortality in systolic dysfunction and all cause cough and hyperkalemia.
ACE increases bradykinin, which causes cough.
ACE inhibitors increase potassium by blocking aldosterone release.
Which of the following is most likely to lower this patient’s mortality?
a. Metoprolol
b. Digoxin
c. Furosemide
d. Spironolactone
e. Hydrochlorothiazide
Answer a. Metoprolol
Beta-blockers lower mortality in systolic dysfunction. The effect of beta-blockers is not ubiquitous to the entire class of medications. Beta-blockers useful for CHF are:
• Metoprolol
• Carvedilol
• Bisoprolol
Digoxin does not lower mortality in CHF. Spironolactone is most useful in severe class III and IV CHF in which there is dyspnea with minimal exertion or at rest. Loop diuretics such as furosemide are frequently used to decrease fluid overload, but they do not lower mortality. Thiazide diuretics are used for hypertension, but the effect in CHF is not beneficial beyond just controlling BP.
The patient returns a week after starting the ACE inhibitor and beta-blocker. He denies having a cough, but his dyspnea is not improved. You increase the dose, and on follow-up a week later, he is still symptomatic. Spironolactone is added orally. Although spironolactone was invented as a potassium-sparing diuretic, the dose used in CHF is well below the diuretic dose. Like most medications in CHF that lower mortality, it is used to inhibit the rennin-angiotensin-aldosterone system. Loop diuretics such as furosemide are used to control symptoms of fluid overload such as edema. Two weeks later, the patient’s symptoms of dyspnea are well controlled.
Which should you test for?
a. Potassium level
b. Sodium level
c. Repeat echocardiogram
d. Holter (24-hour) ambulatory ECG monitor
e. Urine electrolytes
Answer a. Potassium level
All the medications the patient is on can alter the potassium level. ACE inhibitors, beta-blockers, and mineralocorticoid-receptor blockers such as spironolactone can increase potassium levels, and furosemide can lower potassium levels. Although CHF and a number of the medications used can alter sodium levels, there is no point in routinely monitoring the blood or urine sodium level because there is nothing you will do different therapeutically. In the absence of symptoms, neither the Holter monitor nor echocardiogram are useful. To assess intermittent arrhythmia, such as nonsustained VT or AFib, 24-hour ambulatory ECG or Holter monitoring is useful. If there is severe hyperkalemia with the use of ACE inhibitors or ARBs, the solution is to switch to hydralazine and nitrates. This combination both dilates arterioles directly with hydralazine and dilates coronary arteries so blood is not “stolen” away from the coronary arteries.
Furosemide inhibits potassium reabsorption at the thick ascending limb of the loop of Henle.
If there are persistent symptoms despite the use of ACE inhibitors, beta-blockers, spironolactone, and loop diuretics, the next medication to add is digoxin. Digoxin does not lower mortality. This is the most commonly tested point about digoxin. It decreases symptoms and decreases rates of hospitalization, but does not lower mortality.
Which of these is most likely to inhibit androgens?
a. Enalapril
b. Losartan
c. Carvedilol
d. Spironolactone
e. Digoxin
f. Furosemide
g. Indapamide
h. Hydrochlorothiazide
Answer d. Spironolactone
Spironolactone is a direct antagonist of the androgens (dehydroepiandrosterone [DHEA] and androstenedione) that originate from the adrenal gland as well as an inhibitor of the gonadal androgen testosterone. It inhibits both the receptor as well as androgen production. When this occurs, switch spironolactone to eplerenone. Eplerenone has a proven mortality benefit without the antiandrogenic adverse effects. Spironolactone is so antiandrogenic that it is used with the specific therapeutic intent of inhibiting androgens in women with acne, hirsutism, and male pattern hair loss.
The vast majority of cases of CHF are controlled with ACE inhibitors, beta-blockers, spironolactone, diuretics, and digoxin. If the patient is still short of breath, and the QRS interval is wide, resynchronization with a biventricular pacemaker is very useful in getting both ventricles to contract together. An implantable defibrillator will decrease mortality, but because its only function is to restart the heart if the person actually has sudden death, it will not decrease symptoms.
Ultimately, cardiac transplantation is sometimes needed if there are persistent symptoms despite maximum medical therapy.
Do not combine ACE with ARB medication. Combining will not improve morbidity or lower mortality.
Which decreases mortality in diastolic dysfunction?
a. Metoprolol
b. Digoxin
c. Furosemide
d. Enalapril
e. Eplerenone
f. Valsartan
g. Nothing is proven to lower mortality in diastolic dysfunction.
Answer g. Nothing is proven to lower mortality in diastolic dysfunction.
Diastolic dysfunction is also called “heart failure with preserved EF” because there is a normal EF. There is no medication that is clearly proven to lower mortality in this diastolic dysfunction. We use beta-blockers, diuretics, and sometimes calcium channel blockers (CCBs), but that does not mean they are proven to lower mortality.
The most accurate method for assessing EF is nuclear ventriculogram or multigated angiogram (MUGA). Nucleotide angiography surpasses echocardiogram for accuracy of EF measurement.