Hypertension

Goals

Case-based approach
Epidemiology
Associated

morbidity and mortality

Diagnostic evaluation
Risk stratification
Treatment
Follow-up

HTN: epidemiology

50 million Americans > 140/90 (70% have stage I

HTN)
Prevalence increases with age
average age at onset: 32 y.o.
at age 65: 30% whites, 50% blacks affected
Increased risk of stroke, peripheral vascular disease
(PVD), coronary artery disease (CAD), congestive
heart failure (CHF), atrial fibrillation, and death
Risk increases linearly for BP > 120/80

Why treat HTN?

A little reduction goes a long way

A meta-analysis of 14 RCTs showed that decreasing

DBP by 5-6 points decreases mortality by 42% over 4-6
years

Treatment reduces the risk of stroke, ischemic

heart events, CHF, and renal failure

Only 59% of patients with HTN are under

treatment, and < 1/3 are controlled to 140/90
JNC 7, JAMA 2003. 289:2560-72

Definition of hypertension
Systolic (mm Hg) Diastolic (mm Hg)
Normal
<120
<80
Prehypertension
120-139
80-89
Stage 1 Htn
140-159 or
90-99
Stage 2 Htn
>110
160 or

Based on 3 visits, if systolic vs. diastolic readings are in different

categories, choose higher
2 major changes with JNC 7 compared with JNC 6:
1. Simplification of Categories (elimination of Stage 3 HTN)
2. Introduction of Prehypertension, as opposed to High Normal
JNC 7. JAMA 2003. 289:3560-72.

Diagnosis

3 visits, unless BP > 180/110

Proper cuff size, arm supported at the level of the heart
Use the higher of the two arms
Repeat after several minutes
False positives

Cigarettes, caffeine, pain, anxiety

Drugs-amphetamines, cocaine, cold remedies, NSAIDS, estrogen,
steroids, cyclosporine, licorice, ma huang, ephedra
Consider white coat hypertension in patients with office-home
mismatch (about 25% of patients with mild office HTN)
Ambulatory BP monitoring may be helpful

Risk stratification

Those at greatest risk derive greatest benefit from

treatment
Assess for other cardiovascular disease or risk
factors

Existing ischemic heart disease (IHD), TIA or stroke,

PVD, CHF, diabetes, LVH, renal insufficiency, cigarette
smoking, dyslipidemia, obesity, FH of premature IHD

Risk stratification influences (a) intensity of

intervention and (b) choice of drug

History

Symptoms (HTN is generally asymptomatic)

Other CV risks: cigarette use, lipids, diabetes,
obesity, FH of premature coronary disease
Lifestyle: sodium and fat intake, alcohol, drugs,
medications /herbal), exercise (inactivity increases
risk by 20-50%)
Evaluate for end-organ damage
CAD, LVH, CHF, TIA, CVA, PVD, CRI (Cr >
1.5), albuminuria, retinopathy

Physical Exam

Height, weight, appearance (e.g. cushingoid)

BMI 25-29 is overweight, >30 is obese

Fundi, thyroid exam

Cardiac exam (PMI, S4, S3)
Vascular exam (bruits, aneurysm, pulses)
Extremities (pulses, cyanosis, edema)
Neurological exam

Laboratory Evaluation

Na, K, BUN, Cr: renal disease, hyperaldosteronism

Urine: dysmorphic red cells, casts, proteinuria
Glucose: diabetes, Cushings
Cholesterol: risk factor
EKG: evaluate for hypertrophy, ischemia
Special tests for secondary hypertension:

renal artery duplex; renin/aldosterone ratio; 24-hour

urinary cortisol; plasma free metanephrine

Case 1

A 20 y.o. woman college student is referred to your clinic for

evaluation for hypertension detected during a sports physical
and confirmed at a second visit. Today, she reports
intermittent episodes of anxiety, palpitations, and dizziness
that she has attributed to stress. PE: BP = 170/102; P = 102
supine. BP = 154/98; P = 118 standing. Thyroid is normal.
A faint bruit is heard on auscultation of her abdomen. Labs:
Na is 138; K 3.4; BUN 29; Cr 0.7.

List possible causes for her hypertension?

A colleague suggests starting HCTZ and seeing the patient
back in two weeks. Do you agree?

Resistant/Secondary Hypertension

Consider evaluation if: sudden onset, malignant,

evidence of end-organ damage, physical findings ,
poor response ( 3 drugs, including a diuretic)

Only 2-10% of outpatients have secondary causes of

hypertension

Yaklovlevitch and Black. Arch Intern Med 1991. 141:1786.

Causes of resistant HTN

Undetermined
and Other
Causes
12%

Secondary
Causes
11%
Noncompliance
11%

Psychiatric
Causes
8%

Drug
Intolerance
14%

Suboptimal
Therapy
44%

Yaklovlevitch and Black. Arch Intern Med 1991. 141:1786.

Secondary Hypertension

Causes of secondary hypertension

Intrinsic renal disease is 0.5-3%

Sleep apnea
Drugs: recreational, OTC, and prescribed
Renovascular: atherosclerosis or fibromuscular dysplasia
Endocrine: Cushings syndrome, hyperaldosteronism,
thyroid disease, acromegaly, hyperparathyroidism
Pre-eclampsia
Coarctation of the aorta
Pheochromocytoma

Case 2

A 48 y.o. black man who smokes 1 pack of cigarettes per

day, drinks 3-4 beers each night, and has Type 2 diabetes
treated with metformin, is referred for hypertension. His
father had hypertension and died of an MI at 50. His BP
remains 192/104 despite atenolol 100 mg qd. Pulse 62.
BMI 29. He has an S4, and left carotid and right femoral
bruits. The patient reports difficulties paying for his
medications.

What are his cardiac risks?

Outline a treatment strategy.

Lifestyle Modification

Cigarette cessation!
Alcohol < 1 drink/day
Salt restriction (2.4 gm Na=6 gm salt)

Decrease of 2.9 + 1.6 mm Hg; decrease in CV events

50% of black patients are salt sensitive
Most elderly patients
Obesity
Renal insufficiency

Adequate calcium and potassium modestly lower BP

Lifestyle Treatment: Exercise

Exercise recommendation
40

minutes of moderate exercise 4-5 days/week

Walking >20 minutes to work reduced risk of
hypertension in Japanese men by 29%: NNT 26
Walking at work >10,000 steps reduces BP by 10/8

Hayashi, Tsumura, et al. Ann Intern Med 1999. 131:21.

Iwane, Arita, et al. Hypertens Res 2000. 23:573.
Stevens, Obaranek, et al. Ann Intern Med 2001. 134:1.

Lifestyle Treatment: Weight loss

Weight loss: patients who lost 4.5 kg for 3

years (13%)
A 5/7

mm Hg decrease in bp corresponds to a
relative risk for HTN of 0.35
1/1.4 mm Hg decrease per kg weight loss
63% lost weight in one trial- better if satisfied
with body image
Hayashi, Tsumura, et al. Ann Intern Med 1999. 131:21.
Iwane, Arita, et al. Hypertens Res 2000. 23:573.
Stevens, Obaranek, et al. Ann Intern Med 2001. 134:1.

Treatment Pearls
Start with a single agent
Diuretics and -blockers decrease mortality
Recent ALLHAT study supports use of diuretic
as 1st agent in patients 55 yoa and additional
CV risk factors

Less

CHF than CCB (amlodipine)

Less CV events, stroke, and CHF than ACE-I
(lisinopril)
ALLHAT. JAMA 2002. 288:2981.

Treatment Pearls

Other agents are acceptable; consider side-effects and

cost
short-acting dihydropyridines are associated with
increased risk of CV events
-blockers help with BPH but increase risk of CHF
If inadequate response, increase dose or add a drug
with a complementary mechanism
25-45% of patients >50 yoa needed at least 2 agents
~20% needed more than 2 agents

Treatment:
Special Considerations

Diabetes: ACE-Is > ARBs

Target < 130/85, ideal < 120/80

Thiazides and -blockers increase insulin resistance and
lipids, but they decrease mortality!
The recent UKPDS study in type II diabetes suggests that
ACE-Is and -blockers confer equivalent benefit

Thiazides:

Do not exceed 25mg (perhaps an increase in sudden death)

Use with caution in patients with gout
UKPDS 39. BMJ 1998. 317:713.

Treatment:
Special Considerations

-blockers:

Potential for increasing LDL and, particularly, triglycerides

Ideal choice in patients with angina, dysrhythmias, migraine
difficult with asthma (consider 1-selective)
OK with COPD, diabetes
Pregnancy: methyldopa, hydralazine, -blockers
no diuretics or ACE-Is

Race

Diuretics may be more effective, ACE-Is less effective in

African-Americans
Perioperative -blockers reduce mortality

Case 3

A 42 year old lawyer comes in for his annual

physical exam and his BP is 148/96. He has no
family history, does not smoke, total cholesterol
was 180 last year. His BMI is 27. He does not get
regular exercise.

Does he have hypertension?

Should he be treated and how?

Should you treat mild HTN?

Treatment of mild HTN study (TOMHS)

45-69 y.o. patients with DBP<100

placebo vs. -blockers, -blockers, CCBs, ACEIs, or
thiazides
5.1% decrease in CV events over 4 years
no difference in CV outcomes by drug
QOL marginally better with thiazides and -blockers

Start with lifestyle for 6-12 months if low risk

Stage 1 (< 160/100 mm Hg)

And no CVD or diabetes
Liebson, Grandits, et al. Circulation 1995. 91:698.

Case 4

A 75 year old woman returns to the clinic for

follow-up. Blood pressures were 160-170/70-80
at presentation and are now 140-150/60-70 on
amlodipine 5 mg/day. She asks if she can stop her
medication because she thinks its making her
tired and her feet are swelling, making it difficult
to wear her best shoes. BP 149/62. P 84.

What should you tell her?

Should you treat systolic HTN?

Systolic hypertension is common: 87% of patients > 50

The SHEP trial showed that treatment to <160/95 decreases CV

events (including MI and stroke) ~ 30%

Elderly patients with mild hypertension on a single agent

salt restriction and weight loss of 4-5 kg decrease risk

Na restriction 30%, weight loss 40%, combined 50%

80% who comply can get off medications for > 1 year
Probstfield, Applegate, et al. Clin Exp Hypertens 1989. 11:973
Whelton, Appel, et al. JAMA 1998. 279:839.
Espeland, Whelton, et al. Arch Fam Med 1999. 8:228.

Case 5

A 62 y.o. white man presents to the ER with HA, confusion, and

blurred vision for 3 days. He has hypertension treated with
atenolol, lisinopril, and HCTZ. He has not had fever, chills, and
says he takes all his pills (verified by his wife). He has no
history of chronic headaches. BP = 230/124; P = 96; T = 36.8 C.
You notice bilateral retinal flame hemorrhages, a laterally
displaced PMI, and an S4. His neck is supple. Labs: BUN 36,
Cr 2.4 (Baseline BUN 22, Cr 1.6). CXR is normal. EKG
shows LVH with strain.

What is your differential diagnosis?

What is your initial management plan?

Malignant Hypertension

Acute process with end-organ damage: ~1% of patients with HTN

chest pain, EKG changes
HA, encephalopathy, papilledema
elevated creatinine, proteinuria, red cells
Treatment
Hospitalize with arterial monitoring
Lower DBP by 25 % over 2-6 hours to ~ 100
nitroprusside, labetolol, diazoxide, enalaprilat
avoid nifedipine (short-acting), captopril

HTN take home points

25% of Americans have HTN but only a very few have

secondary HTN: dont work everyone up

Ideal BP is 120/80 and most patients blood pressures are

not well controlled

Lifestyle change is important!

Talk to patients about lifestyle. Use motivational strategies.

Diuretics and -blockers are the medications of choice,

except in diabetes (ACE-Is)

Heart Failure

Heart Failure: epidemiology

Abnormal cardiac function resulting in

inadequate blood supply to maintain normal
body functions (arterial underfilling)

CAD most common cause, HTN, valvular disease

More common as we age:

10% of people >75 yoa have HF

88% of new diagnoses are in patients 65 yoa
Leading cause of hospitalization in Medicare population

5-year survival: 60% men, 45% women

NY class IV 1 year mortality is 50%

Death is usually due to ischemic/arrhythmic sudden death or
refractory HF

Case 1

A 62 y.o. woman presents to your office concerned

about shortness of breath, while walking and when
trying to sleep, one month after a non Q-wave MI.
She is taking atenolol and isosorbide dinitrate.
She has not had chest pain or palpitations since
her MI.

What is your impression and what physical exam

findings would confirm it?

Heart Failure: Symptoms

Left-Sided

DOE (LR 1.3)

Orthopnea (LR 2.0)
PND
Nocturnal cough
Nocturnal awakening
Palpitations
Exertional fatigue
Nocturia
Hemoptysis

Right-sided

Abdominal bloating
Hiccups
Anorexia
Weight loss

NYHA Functional Class

Class I: No limitations of ordinary physical
activity; ordinary activity does not produce
fatigue, dyspnea, palpitations, or angina
Class II: Slight limitation of activity
Class III: Marked limitation; minimal activity
leads to symptoms
Class IV: Symptoms at rest; exacerbation of
symptoms with any activity

Heart Failure: Progression

High risk of HF but without heart disease

Structural Heart Disease without symptoms

Known eg Previous MI
Unknown Hypertensive LVH, undetected valve disease,
undetected cardiomyopathy

Symptomatic Heart Failure

Hypertension, CHD or risk++, DM, Family History,

Cardiotoxins

Mild
Moderate-Severe

Refractory Heart Failure

Heart Failure: Progression of Stages

NORMAL
Asymptomatic
LV Dysfunction
Compensated
CHF
Decompensated
CHF
Refractory
CHF

No symptoms
Normal exercise
Normal LV fxn
No symptoms
Normal exercise
Abnormal LV fxn
? No symptoms
Exercise
Abnormal LV fxn
Symptoms
Exercise
Abnormal LV fxn

Symptoms not controlled

with treatment

American Heart Association

Heart Failure: Signs

Left-sided

S3
Rales
Pleural effusion
Altered respiration
Displaced/enlarged PMI
Murmur
Cool extremities
Pulsus alternans

Right-sided

Elevated CVP
Sternal lift
Peripheral edema
Ascites
Hepatomegaly
Abdominal Jugular Reflux
(AJR)

Evidence-Based Physical Exam

CVP > 8 cm @ bedside LR 9.0
Abdominojugular reflux

Sensitivity

24%, specificity 96%, L.R. 8.0 (> 4 cm

fall in pressure with release LR 10.4)

PMI > 4 cm in LL position LR 4.7 for

LVEDV
PMI lateral to MCL L.R. 8.0 for LVEDV
S3 L.R. 3.8-4.1 for depressed EF (insensitive)

Post-op

prediction of depressed EF L.R. > 14

Badgett, Lucey, and Mulrow. JAMA 1997. 277:1712.

McGee S. Evidence-based Physical Diagnosis. Saunders 2001.

HF: Differential Diagnosis

Leading etiologies:

IHD
Idiopathic
HTN
Valvular disease
Atrial fibrillation
Other causes

36%
34%
14%
7%
5%
5%

Types of heart failure:

1.
2.
3.
4.

Dilated (low output vs.

high output)
Restrictive (infiltrative)
Hypertrophic
Constrictive
(pericardial)

Cowie, Wood, et al. Eur Heart J 1999. 20:421.

Diagnostic Evaluation
Basic

Chemistry panel, Ca, Mg,

Phos
Cardiac enzymes
Lipids
EKG
CXR
Echocardiogram
? BNP

Other

Thyroid functions
Liver function tests
Ferritin
ANA
HIV
SPEP, UPEP

Combinations of findings are most

helpful in diagnosing HF

For elevated filling pressure

elevated

JVP and radiographic redistribution

For systolic dysfunction

abnormal

apical impulse, radiographic

cardiomegaly, and Q waves or left bundle
branch block

Diastolic dysfunction
elevated

blood pressure in CHF

Badgett, Lucey, and Mulrow. JAMA 1997. 277:1712.

Case 2

A 60 year-old man with a history of chronic stable

angina develops ankle swelling and increasing
shortness of breath during his daily walks. PMH:
type 2 DM, hyperlipidemia, quit smoking 5 years
ago. He takes metformin, pravastatin, ASA, and
prn nitroglycerin. JVP is 10 cm, RRR S1, S2, +S3
without murmurs; AJR is positive; 2+ edema. His
EKG shows old Q waves in II, III, and aVF.

How will you treat him?

A History of HF:
treatment reflects theory

Dropsy: too much blood (sanguine) bleeding

Weakness: foxglove tonic (digitalis)
Volume overload: diuretics
Increased afterload/remodeling: ACE-Is
Catecholamine-mediated: -blockers and ACE-Is
Aldosterone-mediated volume retention:
aldosterone antagonists
The futureADH-mediated volume retention:
specific water channel blockers

HF: general care

Low salt diet
average American diet = 10 gm
no added salt = 4 gm
Exercise
Avoid alcohol
Self-monitoring: daily weights
Discuss compliance
Check for medication interactions

Treatment by Functional Class

Mild Heart Failure: NYHA Class I
ACE-Is
Moderate Heart Failure: NYHA Class II-III
ACE-Is
Diuretics
Consider -blockers
Consider Digoxin
Severe Heart Failure: NYHA Class IV
Refer

ACE Inhibitors in HF

Decrease morbidity and mortality, including

Patients with moderately symptomatic HF

Patients with severe HF
Asymptomatic patients with EF<40% and patients after MI

Titrate to maximum doses or SBP 90 mm Hg

Side effects include hypotension, renal insufficiency,

and cough
If patients get cough stop their ACE-I for 1 week, if
cough resolves change to ARB, if little or no change
restart ACE-I
Many trials! Summarized in
Garg & Yusuf. JAMA 1995. 273:1450.

Angiotensin II Receptor Blockers (ARBs)

ELITE I: 32% less mortality with ARBs (pilot study)

ELITE II: ARBs = ACE-I in terms of mortality (10%) or cardiac
death (8%)
RCT of added Valsartan to ACE-I in CHF: No difference in
mortality but increased mortality when used with -blockers

Decreased hospitalization NNT 23

Dont use ACE-I, -blocker, and ARB together

Conclusion- ACE-Is remain the 1st choice

ARBs are a reasonable 2nd choice

ARBs have same Cr increase (~10%); Dont cause cough

Pitt, Lancet, 1997;349:747.

Pitt, Lancet, 2000;355:1582.
Cohn, NEJM, 2001;345:1667.

-blockers in HF

Rationale: CHF is catecholamine mediated

-blockers

Improve LVEF, and decrease mortality (~60%), progression,

hospitalization, and need for other CHF meds

Add to ACE-I and diuretics in compensated CHF (no

edema or rales)
Carvedilol, bisoprolol, and metoprolol-XL have been
studied
Start low, go slow: double dose every 2 weeks as
tolerated

May need to increase diuretics temporarily

Packer et al, NEJM, 1996;334:1349.

Hjalmarson, JAMA, 2000;283:1295.

Carvedilol decreases mortality

and is well-tolerated in severe HF

RPCT: 2289 NYHA Class 2-3 patients EF<25%

Clinically euvolemic and stable

Few rales and little pretibial edema

Mean age 63; excluded if K, H, MI, CABG

3.12525 bid; more withdrew from placebo
Cumulative risk of death at 1 year

Total population: 11.4% vs 18.5%

High risk group: 14.6% vs 24%

NNT 14
NNT 11

Packer et al, NEJM 2001;344:1651-8.

Combination -blockers and

ACE-Is are effective in the elderly

Observation of 20,902 pts > 65 yoa admitted with

MI and EF<40%;

Pts LVEF > 30%; Cr < 2

Mort

LVEF< 30; Cr>2

Mort

at 1 year 22%: NNT A+BB 15; BB 32; A 50

at 1 year 53%: NNT A+BB 5; BB 4; A 7

Combination most effective

Shiplak et al. Am J Med. 2001;110:425-33.

Digoxin in HF

No difference in mortality: serum level 1.0-2.0

DIG trial

Digoxin decreases hospitalizations for CHF

Captopril-Digoxin Multicenter Research Trial; DIG trial

Digoxin withdrawal results in worsening

symptoms and exercise tolerance despite ACEIs
RADIANCE Trial; PROVED Trial

Estimated savings of continuing = $406

million/year
Assuming < 33% digoxin toxicity

Other HF Treatment Tips

Diuretics: use a loop diuretic in all patients with

volume overload

Patients who cant tolerate ACEIs/ARBs

Dose QD until high dose, e.g.> 160 mg furosemide

Hydralazine and isosorbide dinitrate

Anticoagulation:

All patients should be on ASA (or other antiplatelet agent)

Consider warfarin in patients with EF < 25% (poor data)

Cohn, Archibald, et al. NEJM 1986. 314:1547.

Treatment of arrhythmias

Sudden death is a major cause of death in patients

with CHF
In general, treat only if symptomatic antiarrhythmics
tend to be proarrhythmic
Amiodarone: conflicting trials

meta-analysis suggests ~ 3% absolute decrease in

arrhythmic/sudden death

MADIT II: post-MI with EF < 30% (severe HF)

randomized to ICD vs. usual medical therapy

5.6% absolute decrease in mortality at 20 months (NNT =

18)

Amiodarone Trials Meta-analysis. Lancet 1997;350:1417.

Moss, Zareba, et al. NEJM 2002. 346:877.

Spironolactone in HF

Aldosterone increases sodium and water retention

RALES trial: RPCT of 1663 patients, EF < 35% and

class IV (or class III) HF

Excluded patients with Cr > 2.5 or K > 5 mmol/L

Almost all patients were on diuretics and ACE-I, only

10% were on -blocker

12.5 - 25 mg spironolactone vs. placebo

Pitt, Zannad, et al. NEJM 1999. 341:709.

Spironolactone in HF

Discontinued early: 30% risk reduction for mortality

Absolute risk reduction for mortality at 24 months was 9% (NNT =

11)

Fewer hospitalizations, significant symptom relief

Side effects: gynecomastia in 10%, no difference in serious

hyperkalemia

Conclusion: consider use in patients with severe HF, once

ACE-I and diuretics are optimized.

What about -blockers??

Hyperkalemia and renal insufficiency have been greater

issues in clinical use than in the trial
Pitt, Zannad, et al. NEJM 1999. 341:709.

Heart Failure: Progression of Stages

NORMAL
Asymptomatic
LV Dysfunction
ACEI Symptomatic CHF
NYHA II
? B
Symptomatic CHF
ACEI
Blocker
NYHA III
Diuretics: mild
Refractory
ACEI
CHF
Blocker
Diuretics: Loop Specialized therapy
Secondary prevention
SpironolactoneTransplant
Modification of physical activity
?Nitrates
Reduced Salt intake
American Heart Association

Chronic Heart Failure: Medical Treatment

Evidence based Treatment
Improved
Symptoms

Reduced
Morbidity

Reduced
Mortality

Yes

Just

No

Yes

Probably

Nitrates(+Hydralazi
ne)

Yes

Yes

ACE Inhibitors

Yes

Yes

Yes

Angiotensin II
Antagonists

= to ACEI

= to ACEI

(AIIRA+ACEI > ACEI)

(AIIRA+ACEI = ACEI)

Variable

Yes

Yes

Yes

Yes

Yes

No

Digoxin
Diuretics
(excl spironolactone)

Vasodilator

Blockers
Spironolactone
(in Severe HF)

Warfarin

Case 3

An 80 y.o. man is rushed to the emergency room by

paramedics with acute respiratory distress. On exam, he
appears short of breath. R 34, BP 130/90, P 167 and
irregularly irregular. You listen to his lungs and there are
absent breath sounds at the bases with crackles to the
apices.

What is the problem and what would you do

immediately?
How will you manage him after his acute symptoms are
controlled?

Case 4

A 78 yo man presents to the hospital with dyspnea on

exertion. He is a former smoker and had a 3V CABG 8 years
ago. He has chronic stable angina. His meds include aspirin,
metoprolol, simvastatin, ipratropium bromide, and albuterol.
BP is 156/95; P = 118 & regular, T = 37, RR 35. He has
diffuse coarse crackles. His heart sounds are distant, but no
S3 is appreciated. You and your resident disagree over
whether the JVP is elevated. He has no peripheral edema.
What is your differential?
What tests would be helpful?

BNP and the diagnosis of HF

BNP is released from both ventricles in

response to volume or pressure overload
It

acts as a vasodilator

Breathing Not Properly study (BNP)

1538

pts who presented to ERs with dyspnea

Clinical estimate of probability of CHF
BNP assay
Gold standard = chart review by cardiologists

BNP and the diagnosis of HF

BNP > 100 pg/mL was more accurate for the diagnosis
of CHF than clinical judgment by ER attendings

Clinicians were very good at designating high clinical

probability of CHF
BNP was a useful adjunct to clinical diagnosis in
intermediate clinical probability of CHF

Levels of BNP higher than 150 pg/mL are more

specific for CHF
BNP should not supplant clinical evaluation (or
echocardiography)
McCullough, Nowak, et al. Circulation 2002. 106:416.
Morrison, Harrison, et al. JACC 2002. 39:202.

Case 5

A 60 y.o. man with a history of mild renal insufficiency, Cr 1.7,

comes to your office complaining he has to sleep in a chair
because of shortness of breath. For months he has had to get
up to go to the window several times a night. He also
complains of worsening low back pain. On exam: BP 150/70,
P 97 reg., RR 26, T 37.0. He has an S4 and an S3 with a JVP
of 10 cm and 2+ pitting edema. Labs are remarkable for a Cr =
3.6, and Ca 2+ of 10.5 with an albumin of 2.5. Urinalysis
shows no protein. LS spine films show collapse of T10 with
several punched out lesions in other vertebral bodies.

What is the diagnosis & can it explain his CHF?

Diastolic Dysfunction

About 30% of patients with HF

Suspect in patients with chronic HTN, elderly
(women), diabetes, + S4, LVH on ECG, HTN with
CHF exacerbation, symptoms in excess of cardiac
silhouette on CXR

Causes: hypertension, diabetes, HOCM, or infiltration

Common in the elderly (women > men)

Diagnosis:

Echocardiogram
BNP may be helpful
No true gold standard for diagnosis
Dauterman, Massie, et al. Am Heart J 1998. 135:S310.

Diastolic Dysfunction

Treatment:
Lower BP & slow rate (improved diastolic filling)
Treat ischemia when possible
-Blockers (1st choice), verapamil or diltiazem
(no evidence for increased survival), ACE-I/ARB
Exercise training
Beware overdiuresis decrease LV filling

Dauterman, Massie, et al. Am Heart J 1998. 135:S310.

Case 6

A 55 y.o. man comes to your office with shortness of breath with

exertion. Previously, he could walk 3-4 miles without difficulty,
but he recently returned from Las Vegas where he had trouble
finishing 4 holes of golf. He has new 3-pillow orthopnea but no
history of chest pain. His ROS is positive for mild arthritis in his
hands and knees. He has no cardiac risk factors. He is quite tan.
JVP = 9 cm. Heart: RRR S1, S2, S4. Chest: Bibasilar
crackles. Abd: Liver is firm, 12 cm to percussion. Ext: 1+
edema, slightly boggy 2nd and 3rd MCP joints. Labs: Glu 220,
Cr 1.0, ALT 130, AST 150.

Aside from the usual suspects, what would you include in your
differential diagnosis?

Case 7

A 50 y.o. man comes to your office with his wife who says
that his snoring keeps her awake. She worries because stops
breathing for several seconds at a time while he is asleep. He
feels he sleeps fine but he feels sleepy in the afternoon and
cant seem to stay awake. He also has morning headaches.
PE reveals an obese man with BP 150/90, BMI 32. HEENT
is normal. CV: RRR S1,S2, S3. Chest: clear. Ext: 3+
pitting edema to the knees. EKG shows RVH and frequent
PVCs. CXR shows an enlarged heart and no lung edema.

What kind of heart failure is this?

Case 8

Your grandmother calls to ask your advice. She

has CHF and has recently been having diarrhea
and nausea. She also complains that all her
laundry has been turning yellow and she wonders
if you could come over and check her plumbing
and water supply. She is on several heart
medicines, but only sees her doctor infrequently.

What do you think is going on?

HF Take Home Message

Use your history and physical examination

DOE, orthopnea, JVP, S3, PMI > 3 cm, AJR

CXR and Echocardiogram are confirmatory
Classify by NYHA

Systolic versus diastolic

Consider other etiologies if cause is not obvious
Treat all patients with systolic dysfunction with ACE-Is
Add -blockers if possible
Use diuretics for volume overload

Thanks