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KARDIOLOGI (3) Dian Paramita, dr., Sp.JP

Kardiologi (3)

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Page 1: Kardiologi (3)

KARDIOLOGI (3) Dian Paramita, dr., Sp.JP

Page 2: Kardiologi (3)

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

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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.

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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

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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).

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3. AGENTS THAT PROMOTE NO SYNTHESIS OR ACTIVIT Y 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

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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.

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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

HR: 88 bpm

■ Physical examination

Lungs: Bibasilar crackles and decreased breath sounds at base

Cardiac: Regular rate and rhythm, JVP 15 cm, S3 present

Extremities: 2+ lower extremity pedal edema bilaterall

What is the most likely diagnosis given these findings?

a. Amyloid heart disease

b. HCM

c. Hypertensive heart disease

d. Severe mitral valve regurgitation

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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

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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

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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.

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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

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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.

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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 S TATE OF HEALTH LAS T WEEK, BUT RES TING BP TAKEN BY HER PRIMARY CARE PHYSICIAN WAS 175/50 MMHG. THE PRESENT ED EVALUATION REVEALED THE FOLLOWING:

■ Vital signs

BP: 210/55mmHg

HR:90 bpm, irregularly irregular

■ Laboratory

Creatinine: 2.4mg/dL (1.3mg/dL a week ago)

Chest radiograph: Bilateral pleural effusions.

In the ED, she was administered IV NTG, which lowered her

BP to 125/50mmHg and improved her symptoms. Which

answer best describes the arterial baroreflex response to the

abrupt drop in BP?

a. Stimulation of efferent parasympathetic activity

b. Inhibition of efferent sympathetic activity

c. Decreased HR

d. Decreased carotid sinus baroreceptor discharge rate

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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.

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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

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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.

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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

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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.

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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

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• 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.

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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 S TAIRS. THERE IS NO CHES T 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) SYS TOLIC PRESSURE OF 50 MMHG. WHAT IS THE MOS T PRODUCTIVE NEXT S TEP?

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

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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.

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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

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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.

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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

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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.

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14. THE MAJOR FRAMINGHAM CRITERIA FOR HF INCLUDE:

A. S3

B. Paroxysmal nocturnal dyspnea

C. Basal rales

D. All of the above

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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

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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

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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.

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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

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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.

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19 . AN INCREASE IN LV END-SYSTOLIC SIZE WOULD INCREASE WHICH OF THE FOLLOWING?

A. LV preload

B. LV afterload

C. None

D. Both

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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).

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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

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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.

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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

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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.

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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

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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.

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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.

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24. A 49-YEAR-OLD MALE COMES TO YOUR OFFICE FOR AN EVALUATION AS PART OF HIS EXECUTIVE CHECK-UP. HE REPORTS FEELING WELL. HE DENIES PREVIOUS HISTORY OF DIABETES OR CORONARY ARTERY DISEASE. PHYSICAL EXAMINATION IS UNREMARKABLE EXCEPT FOR HIS BP, WHICH WAS MEASURED AT 165/98 MMHG. HIS BP RECHECKED AFTER 5 MIN WAS 160/98 MMHG. WHAT WOULD YOUR RECOMMENDATION BE TO THIS PATIENT?

A. Reassurance

B. Initiate drug therapy

C. Come back for a follow up

in 3 months

D. Come back for a follow up

after 6 months

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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.

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25. A 40-YEAR-OLD FEMALE IS ADMITTED TO THE HOSPITAL. ON EXAMINATION SHE IS FOUND TO HAVE PULMONARY EDEMA. HER PAST HISTORY IS ONLY SIGNIFICANT FOR HYPERTENSION. SHE IS ON A MEDICAL REGIMEN CONSISTING OF A THIAZIDE DIURETIC, AMLODIPINE, LOSARTAN, AND CARVEDILOL. HER FAMILY ALSO GAVE A HISTORY OF RECENT UNCONTROLLED HIGH BP AND ONE OTHER EPISODE OF PULMONARY EDEMA 2 MONTHS AGO. HER BP WAS 220/110 MMHG. THE REST OF HER EXAMINATION IS UNREMARKABLE. WHAT IS THE INITIAL DIAGNOSIS?

A. Pseudohypertension

B. Primary

hyperaldosteronism

C. Reno-vascular hypertension

D. Coarctation of aorta

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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.