Heart failure

1. HEART FAILURE
MUHAMMAD SALMAN
PharmD, MClinPharm, PhD

2.  Heart failure (HF) is a clinical syndrome caused by the inability of the heart to pump sufficient blood
to meet the metabolic needs of the body.
 HF can result from any disorder that reduces ventricular filling (diastolic dysfunction) and/or
myocardial contractility (systolic dysfunction)

4. PTHOPHYSIOLOGY
 Causes of systolic dysfunction (decreased contractility) are
 Reduction in muscle mass (e.g., myocardial infarction [MI]),
 Dilated cardiomyopathies, and
 Ventricular hypertrophy.
 Ventricular hypertrophy can be caused by pressure overload (e.g., systemic or pulmonary hypertension, aortic or
pulmonic valve stenosis) or volume overload (e.g., valvular regurgitation, shunts, high-output states)

5.  Causes of diastolic dysfunction (restriction in ventricular filling) are increased
 Ventricular stiffness,
 Ventricular hypertrophy,
 Infiltrative myocardial diseases,
 Myocardial ischemia and infarction,
 Mitral or tricuspid valve stenosis, and
 Pericardial disease (e.g., pericarditis, pericardial tamponade)

6.  The leading causes of HF are coronary artery disease and hypertension
 As cardiac function decreases after myocardial injury, the heart relies on the following compensatory mechanisms:
 tachycardia and increased contractility through sympathetic nervous system activation;
 the Frank-Starling mechanism, whereby increased preload increases stroke volume;
 Vasoconstriction; and
 Ventricular hypertrophy and remodeling.
 Although these compensatory mechanisms initially maintain cardiac function, they are responsible for the
symptoms of HF and contribute to disease progression

7.  The neurohormonal model of HF recognizes that an initiating event (e.g., acute MI) leads to decreased cardiac
output but that the HF state then becomes a systemic disease whose progression is mediated largely by
neurohormones and autocrine/paracrine factors.
 These substances include angiotensin II, norepinephrine, aldosterone, natriuretic peptides, arginine vasopressin,
proinflammatory cytokines (e.g., tumor necrosis factor ,
α interleukin-6 and interleukin-1 ),
β and endothelin-1
 Common precipitating factors that may cause a previously compensated patient to decompensate include
noncompliance with diet or drug therapy, coronary ischemia, inappropriate medication use, cardiac events (e.g.,
MI, atrial fibrillation), pulmonary infections, and anemia

8. Drugsmay precipitate or exacerbate HF because of their negative inotropic, cardiotoxic, or sodium- and
water-retaining properties

9. CLINICAL PRESENTATION
 The patient presentation may range from asymptomatic to cardiogenic shock.
 The primary symptoms are dyspnea (particularly on exertion) and fatigue, which lead to exercise intolerance.
Other pulmonary symptoms include orthopnea, paroxysmal nocturnal dyspnea, tachypnea, and cough
 Fluid overload can result in pulmonary congestion and peripheral edema

10.  Nonspecific symptoms
 Fatigue,
 Nocturia,
 Hemoptysis,
 Abdominal pain,
 Anorexia,
 Nausea,
 Bloating,
 Ascites,
 Poor appetite,
 Mental status changes, and
 Weight gain

11.  Physical examination findings may include
 Pulmonary crackles,
 An S3 gallop,
 Cool extremities,
 Cheyne-Stokes respiration - breathing disorder characterized by cyclical episodes of apnea and hyperventilation
 Tachycardia,
 Narrow pulse pressure,
 Cardiomegaly,
 Symptoms of pulmonary edema (extreme breathlessness, anxiety, sometimes with coughing pink, frothy sputum),
 Peripheral edema,
 Jugular venous distention,
 hepatomegaly

12. DIAGNOSIS
 A complete history and physical examination with appropriate laboratory testing are essential in the initial
evaluation of patients suspected of having HF
 Laboratory tests for identifying disorders that may cause or worsen HF include
 Compete blood count
 Serum electrolytes
 Renal function test
 Liver function test
 Thyroid function tests
 Urinalysis
 Lipid profile
 Hemoglobin A1C

13.  Chest X-ray
 ECG
 Echocardiogram is the single most useful evaluation procedure because it can identify abnormalities of the
pericardium, myocardium, or heart values and quantify the left ventricular ejection fraction (LVEF) to determine if
systolic or diastolic dysfunction is present
 In ambulatory patients with dyspnea, measurement of BNP or N-terminal pro-B-type natriuretic peptide
(NT-proBNP) is useful to support clinical decision making regarding the diagnosis of HF, especially in the setting
of clinical uncertainty
 Measurement of BNP or NT-proBNP is also useful for establishing prognosis or disease severity in chronic HF

14. CAUSES OF ELEVATED NATRIURETIC PEPTIDE CONC.
Cardiac Non-cardiac
Heart failure, including right ventricular syndrome Advancing age
Acute coronary syndrome Anemia
Heart muscle disease, including LVH Renal impairment
Valvular heart disease Pulmonary: obstructive sleep apnea, severe pneumonia,
pulmonary hypertension
Pericardial disease Critical illness
Atrial fibrillation Sepsis
Myocarditis Severe burns
Cardiac surgery Toxic-metabolic insults, including cancer chemotherapy
and envenomation
Cardioversion

15.  Both the ACCF/AHA stages of HF and the NewYork Heart Association (NYHA)
functional classification provide useful and complementary information about the presence and severity of
HF.
 The ACCF/AHA stages of HF emphasize the development and progression of disease and can be used to describe
individuals and populations, whereas
 The NYHA classes focus on exercise capacity and the symptomatic status of the disease

16. NEWYORK HEART ASSOCIATION FUNCTIONAL CLASSIFICATION
OF HF

17. AHA/ACC STAGING SYSTEM

18. DESIRED OUTCOMES
 The therapeutic goals for chronic HF are to
 Improve quality of life,
 Relieve or reduce symptoms,
 Prevent or minimize hospitalizations,
 Slow disease progression, and prolong survival.

19. TREATMENT
 Non-pharmacological treatment
 Patient education to facilitate HF self-care
 Cardiac rehabilitation
 Restriction of fluid intake (maximum 2 L/day from all sources) and dietary
 Sodium (approximately 2 to 3 g of sodium per day)
 Weight loss
 Smoking cessation

20. TREATMENT FOR STAGES A TO D (AHA/ACC GUIDELINES)
 Stage A: Recommendations
 Hypertension and lipid disorders should be controlled in accordance with contemporary guidelines to lower
the risk of HF
 Other conditions that may lead to or contribute to HF, such as obesity, diabetes mellitus, tobacco use, and
known cardiotoxic agents, should be controlled or avoided.

21.  Stage B: Recommendations
 Class I
 In all patients with a recent or remote history of MI or ACS and reduced EF, ACE inhibitors should
be used to prevent symptomatic HF and reduce mortality. In patients intolerant of ACE inhibitors, ARBs are
appropriate unless contraindicated (Level of Evidence: A)
 In all patients with a recent or remote history of MI or ACS and reduced EF, evidence-based beta
blockers should be used to reduce mortality (Level of Evidence: A)
 In all patients with a recent or remote history of MI or ACS, statins should be used to prevent
symptomatic HF and cardiovascular events (Level of Evidence: A)

22.  In patients with structural cardiac abnormalities, including LV hypertrophy, in the absence of a history of MI or
ACS, blood pressure should be controlled in accordance with clinical practice guidelines for hypertension to
prevent symptomatic HF
 ACE inhibitors should be used in all patients with a reduced EF to prevent symptomatic HF, even if they do
not have a history of MI
 Beta blockers should be used in all patients with a reduced EF to prevent symptomatic HF, even if they do not
have a history of MI (Level of Evidence: C)

23.  Class II a
 To prevent sudden death, placement of an implantable cardioverter-defibrillator (ICD) is
reasonable in patients with asymptomatic ischemic cardiomyopathy who are at least 40 days post-
MI, have an LVEF of 30% or less, are on appropriate medical therapy, and have reasonable
expectation of survival with a good functional status for more than 1 year (Level of Evidence: B)
 Class III: Harm
 Nondihydropyridine calcium channel blockers with negative inotropic effects may be harmful in
asymptomatic patients with low LVEF and no symptoms of HF after MI (Level of Evidence: C)

24. ACEI indicates angiotensin-converting enzyme inhibitor; ARB,
angiotensin receptor-blocker; ARNI, angiotensin receptor-
neprilysin inhibitor; BP, blood pressure; bpm, beats per
minute; C/I, contraindication; COR, Class of Recommendation;
CrCl, creatinine clearance; CRT-D, cardiac resynchronization
therapy–
device; Dx, diagnosis; GDMT, guideline-directed management
and therapy; HF, heart failure; HFrEF, heart failure with
reduced ejection fraction; ICD, implantable cardioverter-
defibrillator; ISDN/HYD, isosorbide dinitrate hydral-nitrates;
Kþ, potassium; LBBB, left bundle-branch block; LVAD, left
ventricular
assist device; LVEF, left ventricular ejection fraction; MI,

26. DRUGS COMMONLY USED FOR HFREF (STAGE C HF)

27. DRUGS COMMONLY USED FOR HFREF (STAGE C HF)
CONT’D