Heart Failure Clinical Presentation by Maen Karadsheh

1. Introduction to Clinical Medicine
Maen Karadsheh
Presentation: 3/22/2010

2. Heart Failure: Outline
1) Definition
2) Epidemiology
3) Classification
4) Etiology
5) Pathophysiology
6) CLINICAL PRESENTATION
7) Dx/DDx
8) Treatment

3. 1) DEFINITION: HEART FAILURE
Commonly called “Congestive” Heart Failure
Congestive = Ventricle pumping action is reduced
to the point that circulatory manifestation occur in
the form of edema
Cardiac output ≠ tissue perfusion demand

4. “Congestive” Heart Failure
Chest X-ray showing THE TWO MAIN MANIFESTATIONS OF HF:
1. Enlarged Cardiac Silhoutte
2. Edema at base of lung

5. 2) HEART FAILURE: EPIDEMIOLOGY
 PREVALENCE: Affects approximately 6 Million Americans
 INCIDENCE: 670,000 New Cases per year
 Leading cause of hospitalization in people older than age 65
 Prevalence on a rise
1. Improved survival of patients that suffer MI
2. Aging population in the U.S

6. 3) HEART FAILURE: CLASSIFICATION
 Right versus Left-sided Heart Failure
 The New York Heart Association (NYHA) based on physical activity
limitations/Functional Statues:
 Class I: No limitation
 Class II: Slight limitation
 Class III: Marked limitation
 Class IV: Symptoms occur even during rest
• The American College of Cardiology/American Heart Association (ACC/AHA)
based on stages and progression of the disease
 Stage A: Patient at high risk for developing HF
 Stage B: Structural heart disorder currently present but no symptoms HF
 Stage C: Previous or current symptoms of HF with an underlying structural heart problem
(managed with medical treatment)
 Stage D: Advanced disease requiring hospital-based support (End-Stage Disease)

7. 4) HEART FAILURE: ETIOLOGY
Causes of HF divided into pathological result:
1) PRESSURE OVERLOAD
 Hypertension (increased afterload)
 Diabetes
 Aortic Stenosis
2) VOLUME OVERLOAD
 CAD/Ischemic Myocytes/MI
 Mitral Insufficiency (Mitral Regurgitation)
 Aortic Insufficiency (Aortic Regurgitation)

8. 5) HEART FAILURE: PATHOPHYSIOLOGY
Heart Failure is a CHRONIC DISEASE
Compensatory Mechanism dominant for a
while (BEFORE WE SEE OVERT SYMPTOMS
ASSOCIATED WITH DECREASED CO):
 To compensate for decreased CO, ↑SV
(in Pressure Overload Etiology etc. HT) ➔
Cardiac Function Curve Shifts to the Left
(for a given Pre-load ⇒ increased SV)
 Mechanism: Simple Starling’s Law Reflex =
↓CO → ↑ESV → ↑EDV (Next cycle) ↑Stretch
→ ↑Contractility

9. HEART FAILURE: PATHOPHYSIOLOGY
 Other Compensatory Mechanisms:
1) INCREASED SYMPATHETIC DRIVE➔ Increased Contractility (and
HR); Shift LV functional curve up
2) Increased RAAS activation: ↑ MAP/↑BV → maintain tissue perfusion

10. HEART FAILURE: PATHOPHYSIOLOGY
 WHEN DOES THE REAL PROBLEMS START??
DIASTOLIC HEART FAILURE
i. We talked about the pressure overlaod etiology of HF and the adaptations the heart
undergoes….BUT these mechanisms ACTUALLY Percepitate HF
ii. In Pressure overload problems, the heart is facing a constant increased afterload...
What do muscles do to become more powerful?? ➜ HYPERTROPHY
iii. The constant wall tension felt in the LV due to pressure overload and the chronic
increase in contractility ➜ CONCENTRIC HYPERTROPHY = INCREASED WALL
THICKNESS/DECREASED LV CHAMBER = ↓COMPLIANCE AND DIASTOLIC
DYSFUNCTION (Muscle is in a chronic tense state, unable to relax, which is needed for
proper diastole)

11. HEART FAILURE: PATHOPHYSIOLOGY
 WHEN DOES THE REAL PROBLEMS START??
SYSTOLIC HEART FAILURE
 On the other hand, in Volume Overload Etiology, we have a
state of CHRONIC STRETCH (versus pressure overload, state of
chronic tension)
 LV undergoes ECCENTRIC HYPERTROPHY = LENGHTENING
WITHOUT MUCH THICKENING = LV chamber radius actually
increases…
 Do you remember Law of Laplace? ➜ P = T/r ➜ with this
increase in LV chamber, the heart must creates greater tension
to drive blood at the same systolic pressure AND THUS
SYSTOLIC FAILURE OCCURS DUE TO THE HEART’S INABILITY TO
MAINTAIN THIS INCREASED TENSION

12. HEART FAILURE: PATHOPHYSIOLOGY
 OTHER DAMAGING “COMPENSATORY” MECHANISMS THAT PERCIPITATE HF SYMPTOMS:
 Chronic activation of RAAS ➔ Increased hydrostatic pressure in capillaries (2º to ↑ BP and BV) ➔
EDEMA

13. 6. HEART FAILURE: CLINICAL
PRESENTATION
A. ASK ABOUT:
1) History of CAD? Previous MI
2) Hypertension?
3) Diabetes?
4) Dyslipidemia (Lipid Profile)?
5) Valvular Heart Disease assessment?
6) Apnea? Sleep Disorders?
7) PHEOCHROMOCYTOMA?
8) Alcohol, Tobacco, Substance Abuse?

14. HEART FAILURE: CLINICAL
PRESENTATION
B. ASK ABOUT:
1. DYSPNEA (Sign for pulmonary edema and decreased perfusion of lungs)
 Dyspnea at Rest
 Exertional Dyspnea (how much activity before onset?)
 Orthopnea: SOB upon lying in recumbent position/relieved with head elevation (how many
pillows needed?)
 Nocturnal Dyspnea: Sudden awakening due to SOB
2. Chest Pain/Pressure and Palpitation
 1∘ (coronary) versus 2∘ (↓ CO)
3. Fatigue and Weakness (secondary to reduced perfusion, especially in skeletal muscles)

15. HEART FAILURE: CLINICAL
PRESENTATION
C. PHYSICAL EXAMINATION FOR LEFT-HEART HF:
1. Appearance/Inspection: Dyspneic, malnourished,
exophthalmos (↑ systemic venous pressure), severe
tricuspid regurgitation (visible pulsation of eyes and
neck veins), central cyanosis, diminished pulse
pressure, and dusky discoloration of skin
2. Depending on stage of disease:
 Stage of compensation (with increases adrenergic
activity) = tachycardia, diaphoresis, pallor, peripheral
cyanosis,
 Late, Sever, noncompensated HF = depressed
systolic pressure, weak, rapid pulse, extremely
decreased pulse pressure

16. HEART FAILURE: CLINICAL
PRESENTATION
3. EDEMA...EDEMA
 Strong diagnostic value in patients with combined symptoms of
DYSPNEA
 Left-Sided HF is mostly associated with Pulmonary Edema
 Respiratory manifestation with edema: fatigue and cyanosis (2º
to hypoxia), ↑ RR, labored breathing
 Lung Auscultation: Rales heard over lung base, whizzing (in the
presence of pulmonary edema), cough with frothy, blood-tinged
sputum
4. Cardiac Findings:
a) S3 Sound: Rapid ventricle filling during diastole/ sound is
exaggerated in LV ventricle abnormal structure
(cardiomyopathy) or/and function
 Heard after S1 and S2 as low pitch sound (use bell of
stethoscope) at cardiac apex (left midclavicular 5th intercostal)
b) Apex Beat: Palpate 5th intercostal space / midclavicular line;
Suggests cardiomegaly (heart enlargement)

17. HEART FAILURE: CLINICAL
PRESENTATION
D. PHYSICAL EXAMINATION for Right-HEART HF
1. Jugular Venous Distention: manifestation of systemic venous hypertension
 In HF: venous pressure increases with respiration = Kussmaul Sign (normally,
inspiration causes decreased R. Atrial pressure and increased VR; RHF →
patients have high R. Atrial pressure due to R.Vent dysfunction → thus
increased VR with inspiration on a overloaded R. Atrium cause increased
pressure in venous system (internal jugular vein)
 Inclined position (45º), determine IJV filling/pulsation along SCM muscle when
patient turn head to opposite right side (pen-light can help to locate), first
ruler placed vertically at sternal angle and second ruler is placed horizontally
from top of vein to first ruler (normal is < 3cm)
2. EDEMA…EDEMA
 Peripheral Edema: Distinguish between pitting versus non-pitting
a. Pitting Edema (Found in CHF): pressure is applied to lower liimb ➔
indentation persists after release of pressure (WATER RETENTION)
b. Non-pitting Edema: (NOT found in CHF): indentation does not persist
(associated with lymphatic problems)
 Ascites and Hepatomegaly (elevated pressure in R. Atrium ➔ retrograde
blood movement into portal vein)

18. 7. HEART FAILURE: DIAGNOSTIC CRITERIA

19. 7. HEART FAILURE: DIFFERENTIAL
DIAGNOSIS
1. Many Diseases can DECREASE CO or INCREASED CO DEMAND
 Heart Disease:
 Arrhythmias (Bradycardia = ↓ Demand; Tachycardia = ↑
Demand)
 Structural Heart Disease
 Systemic Disease:
 Anemia (↑Demand)
 Sepsis (↑ Demand)
 Pulmonary Disease

20. 7. HEART FAILURE: TREATMENT
1. Nonpharmacological Therapy:
 Dietary Sodium and Fluid Restriction (decrease
edema)
 Physical Activity (as appropriate)
 Monitoring Weigh Gain (sign of edema)
2. Pharmacological
 Diuretics
 Vasodilators (ACE inhibitors)
 Inotropic Agents
 Anticoagulants
 Beta-Blockers (Decreased HR/ Decreased Renin)

21. HEART FAILURE: TREATMENT
 THE SIGNIFICANCE OF EXERCISE AND EFFICIENCY OF CARDIAC WORK IN HF:
 Total Energy used by heart in one cardiac cycle:
E = P×V + 0.5 mv2 + k×T×∆t
External work needed
to eject blood (isotonic contraction)
Area under curve
 HF patients want to increase
cardiac efficiency and decrease
isovolumetric contraction (loss
of ATP to heat)
 k×T×∆t
T = Tension (afterload/BP)
∆t = time in isometric contraction
(decrease time in systole by
decreasing HR)
EXERCISE REGIME that maintains
decreased HR and BP