• No results found

DESCRIPTION COMMON EXAMPLES

In document IM Platinum, 2nd Edition (1) (Page 53-56)

ATHEROSCLEROSIS AND DYSLIPIDEMIA

DESCRIPTION COMMON EXAMPLES

Systolic Heart Failure or HF with reduced EF (HfrEF)

Depressed HF

< 40%

Progressive disorder initiated by an index event (e.g., MI, volume overload, chronic anemia) that leads to a decline in the pumping capacity of the heart

 CAD (e.g., MI)

 Dilated cardiomyopathy

 Valvular heart disease

Diastolic Heart Failure or HF with preserved EF (HfpEF)

Preserved EF

> 40-50%

Proposed mechanisms include diastolic dysfunction and extra-cardiac mechanisms such as increased vascular stiffness and impaired renal function (still undefined and evolving)

 Pathologic hypertrophy (HOCM, HPN)

 Aging, fibrosis

 Restrictive cardiomyopathy

High-Output Heart Failure

Normal at first, then may decrease over

time

Occur when the body’s requirements for oxygen and nutrients are increased and the demand outstrips what the heart can provide

 Thyrotoxicosis

 Beriberi

 Chronic anemia

 Systemic arteriovenous shunting

B. American College of Cardiology / American Heart Association (ACC/AHA) Stages of Heart Failure

STAGE DESCRIPTION EXAMPLES

A

At high risk for HF but without structural heart disease or HF symptoms

Patients with HPN, CAD, DM or patients using cardiotoxins or with family history of cardiomyopathy

B

Structural heart disease but without signs or symptoms of HF

Patients with previous MI, LV systolic dysfunction, or asymptomatic valvular disease

C

Structural heart disease with previous or current symptoms of HF

Patients with known structural heart disease with shortness of breath, fatigue, reduced exercise tolerance

D

Refractory HF requiring specialized interventions

Patient who have marked symptoms at rest despite maximal therapy (e.g., patients with recurrent hospitalizations or cannot be safely discharged without special interventions)

C. New York Heart Association (NYHA) Functional Classification

NYHA DESCRIPTION COMMENTS

I

Symptoms occur with greater than ordinary physical activity

 No limitation of physical activity

 Can climb > 2 flights of stairs with ease

II

Symptoms occur with ordinary physical activity  Slight limitation of physical activity

 Can climb 2 flights of stairs but with difficulty

III

Symptoms occur with less than ordinary physical activity

 Marked limitation of physical activity

 Can climb <1 flight of stairs

IV

Symptoms may be present even at rest  Unable to carry on activity without symptoms

 Dyspnea at rest

54 III. CLINICAL MANIFESTATIONS

A. Symptoms

Fatigue and Shortness of Breath

 Cardinal symptoms

 Due to pulmonary congestion  juxtacapillary J-receptors are activated  cardiac dyspnea

Orthopnea/Nocturnal Cough  Redistribution of fluid from splanchnic and lower extremity into the central circulation on recumbency

Paroxysmal Nocturnal Dyspnea

 Severe dyspnea that awakens patient from sleep 1-3 hours after patient retires

 Increased pressure in the bronchial arteries

Cheyne-Stokes Respiration  In 40% of advanced HF: series of apnea  hyperventilation  hypocapnia

 Diminished sensitivity of the respiratory center to arterial PCO2

Others

 GI: anorexia, nausea, early satiety, abdominal fullness which may be due to congested liver and/or bowels

 CNS: confusion, disorientation, sleep and mood disturbance may be due to reduced cerebral perfusion

B. Signs

General Appearance and Vital Signs

 Uncomfortable when lying flat, labored breathing

 Normal or low BP

 Cardiac cachexia

Cardiovascular

Although essential, frequently does not provide information on the severity of HF

 JVP may be > 8 cm H2O

 Sinus tachycardia due to increased adrenergic activity

 Point of maximal impulse displaced due to cardiomegaly

S3 (protodiastolic gallop) at the apex: usually in volume overloaded patients

 S4: usually in diastolic dysfunction Pulmonary

 Crackles: transudation of fluid from intravascular space to alveoli

 Expiratory wheezes: cardiac wheezing caused by peribronchial cuffing from congestion

 Pleural effusions: often bilateral; if unilateral, more often on the right Abdomen

Hepatomegaly with pulsation (if with significant TR)

 Ascites: increased pressure in the hepatic veins

 Jaundice: impairment of hepatic function due to congestion Extremities

 Peripheral edema: ankles and pre-tibial region

 Indurated and pigmented skin: long standing edema

 Peripheral vasoconstriction: cool extremities IV. DIAGNOSIS OF HEART FAILURE

 The diagnosis of HF is straightforward when the patients presents with classic signs and symptoms

 Key to diagnosis is a high index of suspicion A. Framingham Criteria for Heart Failure

MAJOR CRITERIA MINOR CRITERIA

 Paroxysmal nocturnal dyspnea (PND) or orthopnea

 Neck vein distention

 Rales

 Cardiomegaly

 Acute pulmonary edema

 S3 gallop

 Increased venous pressure > 16 cm H2O

 Hepatojugular reflux

 Ankle edema

 Night cough

 Dyspnea on exertion

 Hepatomegaly

 Pleural effusion

 Vital capacity decreased by 1/3 from maximal capacity

 Tachycardia > 120 bpm

 Major or Minor Criteria: Weight loss > 4.5 kg in 5 days in response to treatment The diagnosis of HF requires simultaneous presence of at least:

 1 Major Criteria, or

 1 Major Criterion + 2 Minor Criterion

55

(use of minor criteria acceptable only if they cannot be attributed to another medical condition, such as pulmonary HPN, chronic lung disease, cirrhosis, ascites, nephrotic syndrome)

B. Diagnostics in HF

DIAGNOSTICS DESCRIPTION

2D Echocardiography with Doppler

 Most useful test, evaluation of ejection fraction (EF)

 Semi-quantitative assessment of LV size, function, wall motion abnormalities, valvular defects

12-L ECG  Assess cardiac rhythm, LV hypertrophy, prior MI

 A normal ECG virtually excludes LV systolic dysfunction

Chest Radiography  Assess the cardiac size and shape and state of pulmonary vasculature

 Identify non-cardiac causes of symptoms

Cardiac Biomarkers (BNP)  Relatively sensitive markers for the presence of HF

 Increase with age and renal impairment

Complete Blood Count  Look for anemia, signs of infection, and bleeding (may precipitate / worsen HF) Serum Electrolytes, BUN,

Crea, AST, ALT

 Assess for electrolyte disturbances, beginning cardiorenal syndrome, ischemic hepatitis or chronic passive congestion of the liver

FBS, OGTT  Assess for diabetes

Lipid Profile  Assess for dyslipidemia

FT4, TSH  Assess for thyroid hormone abnormalities V. MANAGEMENT OF HEART FAILURE

A. Non-Pharmacologic Management and Basic Principles

Sodium restriction: limit Na+ intake to 2-3 g/day in all patients with HF; and to less than 2 g/day in patients with moderate to severe HF

Fluid restriction: generally unnecessary unless with hyponatremia (< 130 mEq/L) and volume overload

Caloric supplement: for those with cardiac cachexia

B. Pharmacologic Management for Prevention and Treatment of Chronic Heart Failure

DRUG CLASS DESCRIPTION / MECHANISM DOSE

ACE-Inhibitors

 Cornerstone of modern HF treatment

 Interferes with RAAS by inhibiting the conversion of angiotensin I to angiotensin II

 Inhibits kininase which may lead to increase in bradykinin (ACE-I induced cough)

 Interferes with sustained activation of the adrenergic nervous system, particularly the deleterious effects of B1 activation

 Carvedilol 3.125-25 mg BID

 Bisoprolol 1.25-10 mg OD

 Metoprolol succinate 25-200 mg OD

Aldosterone Antagonist

 Inhibits action of aldosterone in collecting duct

 May also be used for fluid retention (diuretic)

 Spironolactone 25-50 mg OD

 Eplerenone 25-50 mg OD

Digoxin

 For symptomatic LV dysfunction + atrial fibrillation

 Add-on to standard therapy

 Digoxin 0.125-0.375 mg OD

56 stable angina

 May be used for HF with systolic dysfunction in patients with sinus rhythm and HR > 70 bpm

C. Management of Fluid Retention in Chronic HF

DRUG CLASS DESCRIPTION / MECHANISM DOSE

Loop Diuretics

 Act on the loop of Henle by reversibly inhibiting the reabsorption of Na+, K+, Cl in the thick ascending limb

 Furosemide 20-40 mg OD-BID

 Bumetanide 0.5-1.0 mg OD-BID

Thiazide and Thiazide-Like-Diuretics

 Reduce the reabsorption of Na+ and Cl in the first half of the distal convoluted tubule

 Tend to lose their efficiency with moderate to severe renal insufficiency (Crea > 2.5 mg/dL)

 Hydrochlorothiazide 25 OD-BID

 Indapamide 2.5 mg OD

 Metolazone 2.5-5.0 mg OD

Arginine Vasopressin Antagonists

 Interfere with action at the vasopressin receptors

 Primarily used for treatment of

hyponatremia by stimulating free-water excretion and improving plasma Na+concentration

 Tolvaptan 15 mg OD

 Satavaptan 25 mg OD

D. Indications for Use of Drugs in HF CLASS ASYMPTOMATIC LV

DYSFUNCTION (NYHA I)

Diuretic No Yes, if with fluid retention Yes Yes

B-Blocker Yes, if Post-MI Yes Yes Yes

Aldosterone Antagonist

Yes, if Recent MI Yes Yes Yes

Digoxin May be considered* May be considered* Yes Yes

*Digoxin may be considered for patients with NYHA-I for rate control in AF or when improved from more severe HF and in sinus rhythm E. Devices Used in HF

Cardiac resynchronization therapy (CRT) or biventricular pacing: device used to restore synchrony of the left ventricle in patients with HF and a widened QRS complex

Implantable cardioverter-defibrillator (ICD): device to treat tachyarrhythmias for primary / secondary prophylaxis against sudden cardiac death

VI. ACUTE DECOMPENSATED HEART FAILURE (ADHF) A. Distinctive Phenotypes

ACUTE DECOMPENSATION

PRESENTATION MANAGEMENT

Typical  Normo-hypertensive

 Usually not volume overloaded

 Vasodilators, diuretics

Pulmonary Edema  Severe pulmonary congestion with hypoxia  Vasodilators, diuretics, opiates

 O2 non-invasive ventilation Low Output

 Hypoperfusion with end-organ dysfunction

 Low pulse pressure, cool extremities

 Cardiorenal syndrome, hepatic congestion

 Inotropic therapy

 Vasodilators

 Hemodynamic monitoring Cardiogenic Shock

 Hypotension, low cardiac output, end-organ failure

 Extreme distress, pulmonary congestion, renal failure

 Inotropic therapy

 Mechanical circulatory support

In document IM Platinum, 2nd Edition (1) (Page 53-56)