KARDIOLOGI (3)

Dian Paramita, dr., Sp.JP

1. A 62-YEAR-OLD MAN WITH ISCHEMIC CARDIOMYOPATHY (EF 25%) AND NYHA
CLASS III SYMPTOMS PRESENTS TO THE ED WITH WORSENING DYSPNEA.
DESPITE INCREASED VENTRICULAR FILLING PRESSURES, CARDIOPULMONARY
BARORECEPTOR REFLEXES ARE ATTENUATED IN THIS PATIENT, RESULTING IN
WHICH OF THE FOLLOWING?

a. Decreased adrenergic activity

b. Increased adrenergic activity
c. Systemic vasodilatation
d. Suppression of the renin–angiotensin–aldosterone system
Cardiopulmonary receptors are located within the atria, ventricles,
coronary vessels, and lungs and are important in neurohumoral control.
In normal conditions and in response to stretch (ie, pressure or volume
overload), these baroreceptors are activated, leading to inhibition of the
adrenergic nervous system.
heart failure  cardiopulmonary baroreceptors are attenuated, leading to
impaired inhibition of the adrenergic nervous system; thus, there is
vasoconstriction, adrenergic stimulation, and activation of the renin–
angiotensin–aldosterone system.
2. A 91-YEAR-OLD WOMAN PRESENTS TO THE ED
WITH SEVERE SHORTNESS OF BREATH AT REST.
SHE HAS A HISTORY OF HTN FOR 35 YEARS. A
RECENT ECHOCARDIOGRAM REVEALED AN EF OF
65%, LVH, AND A PSEUDONORMAL PATTERN OF
VENTRICULAR DIASTOLIC FILLING.

■Vital Signs
BP: 192/45mmHg
HR: 108 bpm, irregularly irregular
Respiration: 34 per min, labored
Oxygen saturation: 86%, room air
■ Laboratory
Creatinine: 1.4mg/dL
Troponin T: 0.01 ng/mL

What would be the next most

appropriate step in management?
a. Reduce BP
b. Control HR
c. Diuresis
d. TEE with electrical cardioversion
e. All of the above
The clinical presentation is consistent with hypertensive urgency
and AF (rapid ventricular response). However, this patient likely has
coexistent heart failure with normal EF.
Appropriate management goals include BP and HR control as well
as diuresis.
Given her advanced diastolic dysfunction, the tachycardia and
relative loss of “atrial kick” is also confounding the problem and
thus electrical cardioversion would likely be beneficial following TEE
(to exclude left atrial thrombi).
3. AGENTS THAT PROMOTE NO SYNTHESIS OR ACTIVITY HAVE RECENTLY
GAINED INTEREST IN THE TREATMENT OF HEART FAILURE. WHICH ONE
OF THE FOLLOWING BEST DESCRIBES THE ACTION OF NO?

a. Promotes vasodilatation
b. Promotes ventricular hypertrophy and fibrosis
c. Contributes to essential HTN
d. Contributes to atherosclerosis
e. Activates the renin–angiotensin–aldosterone system
NO is an endogenous endothelial cell-derived relaxing factor that
stimulates guanylate cyclase and activates cGMP. NO is a potent
vasodilator and its production is impaired in heart failure as well as
atherosclerosis. NO synthetase is the enzyme responsible for NO
production. Answers b–e are incorrect, as data suggest that NO
promotes the opposite effects.
4. A 42-YEAR-OLD MAN WITH SIGNIFICANT
DYSPNEA, FATIGUE, PERIPHERAL EDEMA, AND
ORTHOSTATIC HYPOTENSION PRESENTS TO THE
ED FOR EVALUATION.

■ Vital signs
BP: 96/60mmHg supine and 74/45mmHg standing
What is the most likely diagnosis given these findings?
HR: 88 bpm
a. Amyloid heart disease
■ Physical examination
Lungs: Bibasilar crackles and decreased breath b. HCM
sounds at base
c. Hypertensive heart disease
Cardiac: Regular rate and rhythm, JVP 15 cm, S3
present
d. Severe mitral valve regurgitation
Extremities: 2+ lower extremity pedal edema
bilaterall
This patient has evidence of progressive heart failure, orthostasis, and an
ECG that reveals low voltage. Thus, the most likely diagnosis from the
choices is amyloid heart disease.
This would need to be confirmed by echocardiography, serum, and/or urine
electrophoresis and biopsy (ie, fat aspirate, endomyocardial biopsy, or
bone marrow biopsy).
The clinical presentation, physical examination, and ECG do not support a
diagnosis of HCM, hypertensive heart disease, or mitral valve disease
5. YOU DISCUSS MEDICAL MANAGEMENT WITH A 52-YEAR-OLD MAN WITH
IDIOPATHIC CARDIOMYOPATHY (EF 35%) WHO DESCRIBES NYHA FUNCTION C LASS
III SYMPTOMS. YOU INFORM HIM THAT AN ACE INHIBITOR IS APPROPRIAT E SINCE
IT HAS BEEN SHOWN TO DO WHICH ONE OF THE FOLLOWING?

a. Increase LV end-systolic volume

b. Improve survival and hospitalization rate
c. Increase LV mass
d. Promote vasoconstriction
ACE inhibitors are beneficial in heart failure with reduced EF
because these agents have been demonstrated to reduce
vasoconstriction, ventricular hypertrophy, and dilatation, as well as
mortality and morbidity.
6. ENDOTHELIN PRODUCTION IS UP-REGULATED IN HEART
FAILURE. AN ENDOTHELIN-RECEPTOR ANTAGONIST MAY BE
EXPECTED TO DO WHICH ONE OF THE FOLLOWING?

a. Up-regulate the renin–angiotensin–aldosterone system

b. Improve survival in patients with left-sided heart failure and
severe pulmonary HTN
c. Promote vasoconstriction
d. Promote vasodilatation
Endothelin is a potent vasoconstrictor from direct and indirect
(activates angiotensin II) activity on the endothelium. Thus, an
endothelin-receptor antagonist would be expected to promote
vasodilatation. Thus far, there are no data to suggest a survival
benefit in heart failure (ie, LV dysfunction) with or without the
presence of pul- monary HTN.
7. AN 89-YEAR-OLD WOMAN WITH A 30-YEAR
HISTORY OF HTN PRESENTS TO THE ED WITH
WORSENING SHORTNESS OF BREATH AND 8 -POUND
WEIGHT GAIN. SHE WAS IN HER USUAL STATE OF
HEALTH LAST WEEK, BUT RESTING BP TAKEN BY
HER PRIMARY CARE PHYSICIAN WAS 175/50
MMHG. THE PRESENT ED EVALUATION REVEALED
THE FOLLOWING:

■ Vital signs
BP: 210/55mmHg In the ED, she was administered IV NTG, which lowered her
HR:90 bpm, irregularly irregular BP to 125/50mmHg and improved her symptoms. Which
answer best describes the arterial baroreflex response to the
■ Laboratory abrupt drop in BP?
Creatinine: 2.4mg/dL (1.3mg/dL a week ago)
a. Stimulation of efferent parasympathetic activity
Chest radiograph: Bilateral pleural effusions.
b. Inhibition of efferent sympathetic activity
c. Decreased HR
d. Decreased carotid sinus baroreceptor discharge rate
Arterial baroreceptors act as pressure (ie, mechanoreceptors) sensors and are located
at the carotid sinus and aortic arch. They respond to increased stretch (either from
higher distending pressure or widened pulse pressure) by increasing the discharge rate
of afferent nerve action potentials. The impulse travels from cranial nerves 9 and 10 to
the medulla oblongata in the brainstem. Then, efferent sympathetic or parasympa-
thetic nerves innervate the heart and blood vessels to regulate BP and HR accordingly.
In this particular case, an abrupt drop in BP decreased the discharge rate from arte- rial
baroreceptors (answer d), and thus the medulla responded by increasing sympa- thetic
and decreasing parasympathetic discharge from efferent neurons. To maintain
homeostasis, one would expect that BP and HR would increase due to sympathetic
discharge. Consider the opposite effect, such as occurs with carotid artery massage,
which is known to stretch the carotid baroreceptor. In that scenario, one would expect
that HR and BP would decline.
8. WHICH ONE OF THE FOLLOWING DOES NOT REPRESENT
ABNORMAL LV DIASTOLIC FUNCTION?

a. Restrictive filling pattern

b. Impaired LV relaxation filling pattern
c. Pseudonormal LV filling pattern
d. Diastolic predominant filling pattern
There are 3 abnormal filling patterns that can be observed echocardiographically and correlate
with filling pressures and diastolic abnormalities.
The most common pattern observed is impaired relaxation, which reflects reduced fill- ing in
early diastole and increased contribution of filling by atrial contraction. LV relax - ation and
compliance are abnormal, but filling pressures are normal at rest. A more advanced pattern of
diastolic dysfunction is termed pseudonormal as it resembles the normal filling pattern, although
diastolic abnormalities are clearly present. Patients with advanced diastolic dysfunction may
demonstrate a restrictive filling pattern, with vigorous filling in early diastole and little filling at
atrial contraction because of atrial failure. This can be either reversible or irreversible, but
clearly reflects elevated filling pressures.
A diastolic predominant pattern has little meaning because it does not spec- ify when diastolic
filling is occurring.
9. A 53-YEAR-OLD MAN WITH MULTIPLE ATHEROSCLEROTIC RISK FACTORS, INCLUDING
HTN, HYPERLIPIDEMIA, AND TOBACCO USE, PRESENTS WITH A 6 -MONTH HISTORY OF DOE
AND EXERTIONAL CHEST TIGHTNESS. HE HAS ORTHOPNEA AND PAROXYSMAL NOCTURNAL
DYSPNEA. ECHOCARDIOGRAPHY REVEALS A SEVERELY DILATED LV WITH AN EF OF 20%
AND GLOBAL VENTRICULAR HYPOKINESIS. THE ECG IS NORMAL.
THE NEXT STEP IN DIAGNOSTIC EVALUATION SHOULD BE:

a. Holter monitor
b. Stress test with measurement of maximal oxygen consumption
c. Coronary angiography
d. Heart transplant evaluation
This patient is at high risk for CAD since he has multiple CV risk
factors, cardiomyopathy, and apparent angina. Thus, coronary
angiography should be preferred and non- invasive stress bypassed.
A Holter monitor and transplant evaluation are not clinically
warranted at this time.
10. WHICH OF THE FOLLOWING BEST DESCRIBES THE
BIOLOGIC ACTIONS OF AN ACE?

a. Promotes degradation of angiotensin II

b. Directly stimulates the synthesis of aldosterone
c. Stimulates the production of norepinephrine
d. Converts angiotensin I to angiotensin II
e. All of the above
• Endothelial cells in the pulmonary vasculature (and systemic vascular
endothelium) produce ACE.
• This enzyme converts angiotensin I to the more potent and active
angiotensin II while also promoting the degradation of bradykinin.
• ACE inhibitor have proved useful in blocking the formation of
angiotensin II in heart failure and have demonstrated survival benefit
in those with LV systolic dysfunction or failure.
• Angiotensin II, not ACE, stimulates production of aldosterone and
norepinephrine; thus b and c are incorrect.

11. A 62-YEAR-OLD MAN WITH SMOKING,
HYPERTENSION, AND DIABETES MELLITUS COMPLAINS
OF SHORTNESS OF BREATH ON EXERTION. HE GETS
SHORT OF BREATH WALKING UP A FLIGHT OF STAIRS.
THERE IS NO CHEST PAIN. ON PHYSICAL EXAMINATION,
HEART RATE 72 BPM, REGULAR; BLOOD PRESSURE
148/90 MMHG, BODY MASS INDEX (BMI) 24. JUGULAR
VENOUS PRESSURE (JVP) AND HEART SOUNDS ARE
NORMAL. THE ELECTROCARDIOGRAM SHOWS NORMAL
SINUS RHY THM. THE ECHOCARDIOGRAM SHOWS MILD
LEFT VENTRICULAR (LV) HYPERTROPHY, NORMAL WALL
MOTION, NORMAL VALVULAR FUNCTION, MITRAL E/A
VELOCIT Y RATIO OF 0.7, E/E′ RATIO OF 7, PULMONARY
ARTERY (PA) SYSTOLIC PRESSURE OF 50 MMHG. WHAT
IS THE MOST PRODUCTIVE NEXT STEP?
A. Add calcium channel blocker
(CCB) as a lusiotropic agent as it
may reduce PA pressure
B. Computed tomography (CT)
pulmonary angiography to rule
out pulmonary embolism
C. Right heart catheterization
(RHC) to evaluate for pulmonary
vascular resistance and its
response to O2 and pulmonary
vasodilators
D. Diuresis to reduce left atrial
(LA) pressure as this may reduce
PA pressure
Right heart catheterization (RHC) to evaluate for pulmonary vascular
resistance and its response to O2 and pulmonary vasodilators.
Normal E/E′ ratio indicates normal LA pressure and pulmonary
hypertension (PH) being secondary to pulmonary vascular or parenchymal
disease. Diuresis would not help. Shortness of breath is unlikely to be due
to impaired LV relaxation as LA pressure is normal, and lusiotropic agents
do not help hemodynamics in clinical settings apart from in patients with
hypertrophic cardiomyopathy.
A CT pulmonary angiogram is a poor test for chronic pulmonary emboli –
a ventilation/perfusion (V/Q) scan would be better for this purpose.
12. A 45-YEAR-OLD MALE IS REFERRED TO YOU FOR TREATMENT OF UNCON TROLLED HYPERTENSION.
HE IS ON FOUR DIFFERENT ANTIHYPERTENSIVES AT MAXIMAL DOSES, INCL UDING A THIAZIDE-T YPE
DIURETIC. HE DENIES ANY OTHER MEDICAL HISTORY. HE IS ACTIVE. HIS BP IS 184/100 MMHG,
SITTING UPRIGHT IN A RELAXED POSTURE. HIS BLOOD CHEMISTRY IS UNR EMARKABLE EXCEPT FOR
SERUM POTASSIUM OF 2.9 MG/DL AND A PLASMA RENIN LEVEL OF <1 NG/( ML H). WHAT IS THE
CAUSE OF HYPERTENSION IN THIS PATIENT?

A. Reno-vascular hypertension
B. Primary aldosteronism
C. Pheochromocytoma
D. Renal parenchymal disease
In a patient with refractory hypertension, hypokalemia and
inappropriate kaliuresis (urine potassium >30 mEq/24 h), primary
aldosteronism should be con sidered. When serum potassium is
<3.5 mg/dL despite ACEI or ARB therapy or potassium
supplementation then one should suspect hyperaldosteronism.
WHAT IS THE BEST SCREENING TEST IN EVALUATING THE PATIENT IN QUE STION
13.8?

A. MRA of the renal arteries.

B. Ratio of PA to PRA
C. Urine metanephrine
D. Intravenous pyelogram
The best screening test for primary aldosteronism is the ratio between
PA/PRA.
All diuretics should be discontinued 1 week prior to obtaining the levels.
Then an elevated PA/PRA alone does not establish the diagnosis. It is
confirmed by demonstrating inappropriate aldosterone secretion. During
salt loading, a
nonsuppressed aldosterone excretion is diagnostic. A rate of >14 μg/24 h
fol- lowing a salt load (24 mL/kg physiologic saline in 4 h for 3 days or
home oral salt load) distinguishes most of the cases.
14. THE MAJOR FRAMINGHAM CRITERIA FOR HF INCLUDE:

A. S3
B. Paroxysmal nocturnal dyspnea
C. Basal rales
D. All of the above
15. THE MINOR FRAMINGHAM CRITERIA FOR HF INCLUDE WHICH OF THE
FOLLOWING?

A. Shortness of breath
B. Edema
C. Nocturnal cough
D. All of the above
16. WHICH OF THE FOLLOWING FACTORS AFFECT LV
DIASTOLIC FUNCTION?

A. LV relaxation process
B. Modulus of chamber stiffness
C. LV recoil
D. All of the above
The relaxation process affects the early LV filling, chamber stiffness,
the late filling, and recoil, which depends upon how well the left
ventricle squeezes and then recoils, which affects early filling. In
addition, LV filling is affected by pericardial restraint, intrathoracic
pressure, and interactions with the right ventricle.
17. WHICH OF THE FOLLOWING DOES
THE LV EF DEPEND UPON?
A. LV preload
B. LV afterload
C. LV contractility
D. All of the above
18. WHAT IS THE INCREASE IN MYOCARDIAL CONTRACTILE FORCE WITH
INCREASE IN PRELOAD CALLED?

A. Frank–Starling phenomenon
B. Anrep phenomenon
C. Bowditch phenomenon
D. None of the above.
19 . AN INCREASE IN LV END-SYSTOLIC SIZE WOULD INCREASE
WHICH OF THE FOLLOWING?

A. LV preload
B. LV afterload
C. None
D. Both
LV end-systolic wall stress is a measure of LV afterload and is
roughly proportional to blood pressure and LV end-systolic radius
and inversely proportional to LV wall thickness (Laplace equation).
20. IN WHICH PATIENTS WITH HFREF IS CORONARY
ANGIOGRAPHY MOST APPROPRIATE AND CLEARLY
INDICATED?

A. A 52-year-old patient with EF of 30%, diabetes, and angina on walking

one block
B. A 63-year-old man with prior ST elevation myocardial infarction,
scarred left anterior descending artery area on nuclear testing, no
reversible ischemia, EF of 30%, but short of breath on exertion
C. A 22-year-old patient with HF, EF of 10%, severely dilated left ventricle
D. None of the above
In this patient with angina and diabetes, there is a high likelihood of
having significant coronary artery disease (CAD) as the basis of LV
dysfunction and con- stitutes class I indication. In scenario B there is
no ischemia or chest pain and coronary angiogram would be
inappropriate. In C, the likelihood of CAD is very low.
21. SUBMASSIVE ACUTE PULMONARY EMBOLISM
MAY CAUSE ALL OF THE FOLLOWING EXCEPT WHICH
OPTION?

A. Increase in intrapericardial pressure

B. Increase in LV end-diastolic pressure
C. Reduced LV filling
D. Increase in stroke volume
Submassive pulmonary embolism may cause right ventricle
distention and invoke pericardial restraint (due to noncompliant
pericardium) through an acute increase in intrapericardial volume.
This will increase intrapericardial pressure, reduced transmural LV
diastolic pressure and hence a reduction in stroke volume in the
face of reduced LV preload due to reduced transmural LV diastolic
pressure.
22. YOU HAVE BEEN REFERRED A 52-YEAR-OLD MALE WITH REFRACTORY
HYPERTENSION BY A PRIMARY CARE PHYSICIAN. THE PATIENT GIVES A
HISTORY OF EPISODES OF HEADACHE, SWEATING,AND PALPITATIONS. ON
EXAMINATION HIS BP IS 198/112 MMHG. EXAMINATION IS OTHERWISE
UNREMARKABLE. WHAT IS THE BEST SCREENING TEST IN EVALUATING
THIS PATIENT
A. Serum cortisol
B. PA to PRA
C. Plasma catecholamines and urinary metanephrines
D. MRA of the abdomen
The combination of plasma catecholamines (>2000 pg/mL) and
urinary metanephrines (1.8 mg in 24 h) has a diagnostic accuracy
approaching 98% in diagnosing both sporadic and familial
pheochromocytomas.
23. WHICH IS THE MOST PREFERRED DRUG TO TREAT
HYPERTENSION IN PREGNANCY ACCORDING TO THE
JNC 8 GUIDELINES?

A. Labetalol
B. Nifedipine
C. Methyldopa
D. ACEI

Nifedipine and methyldopa are acceptable. An ACEI is

contraindicated.
24. A 49-YEAR-OLD MALE COMES TO YOUR A. Reassurance
OFFICE FOR AN EVALUATION AS PART OF HIS
EXECUTIVE CHECK-UP. HE REPORTS FEELING B. Initiate drug therapy
WELL. HE DENIES PREVIOUS HISTORY OF
DIABETES OR CORONARY ARTERY DISEASE. C. Come back for a follow up
PHYSICAL EXAMINATION IS UNREMARKABLE
EXCEPT FOR HIS BP, WHICH WAS MEASURED in 3 months
AT 165/98 MMHG. HIS BP RECHECKED
AFTER 5 MIN WAS 160/98 MMHG. WHAT D. Come back for a follow up
WOULD YOUR RECOMMENDATION BE TO THIS after 6 months
PATIENT?
The 2014 hypertension guidelines state that in the general population younger
than 60 years to initiate pharmacologic treatment to lower diastolic BP (DBP) of 90 mmHg or
higher to a goal of lower than 90 mmHg. For ages 30–59 years the recommendations are strong
and for ages 18–29 years the recommenda- tions are based on expert opinion. This
recommendation is based on data from five DBP trials (Hypertension Detection and Follow -up
Program, Hypertension– Stroke Cooperative Study, Medical Research Council trial, Australian
National Blood Pressure Study, and VA Cooperative Study), which showed improvements in
health outcomes in adults aged 30 through 59 with elevated BP. Initiating treatment at DBP 90
mmHg or higher and reducing the DBP to lower than 90 mmHg reduced cerebrovascular events,
HF, and overall mortality. There was no benefit in treating patients to a goal of 80 or 85 mmHg
based on the Hyper- tension Optimal Treatment trial. In patients younger than 30 years there are
no good or fair quality randomized control trails and hence is recommenda- tion is start
treatment when DBP is 90 mmHg or higher to a goal of less than 90 mmHg.
25. A 40-YEAR-OLD FEMALE IS ADMITTED TO
THE HOSPITAL. ON EXAMINATION SHE IS
FOUND TO HAVE PULMONARY EDEMA. HER A. Pseudohypertension
PAST HISTORY IS ONLY SIGNIFICANT FOR
HYPERTENSION. SHE IS ON A MEDICAL B. Primary
REGIMEN CONSISTING OF A THIAZIDE
DIURETIC, AMLODIPINE, LOSARTAN, AND hyperaldosteronism
CARVEDILOL. HER FAMILY ALSO GAVE A
HISTORY OF RECENT UNCONTROLLED HIGH C. Reno-vascular hypertension
BP AND ONE OTHER EPISODE OF PULMONARY
EDEMA 2 MONTHS AGO. HER BP WAS D. Coarctation of aorta
220/110 MMHG. THE REST OF HER
EXAMINATION IS UNREMARKABLE. WHAT IS
THE INITIAL DIAGNOSIS?
Clinical clues that point toward reno-vascular hypertension are: age
30– 55 years, accelerated or malignant hypertension, hypertension
refractory to triple drug therapy, epigastric bruit, recurrent flash
pulmonary edema, unexplained renal insufficiency, or ACEI-induced
renal insufficiency.