Download Congestive Heart Failure

Congestive Heart Failure
Dory Roedel Ferraro, DNP, ANP-BC, CBN
Heart Failure

Complex syndrome resulting from any functional or structural disorder of
the heart that results in or increases the risk of developing manifestations of
low cardiac output and/or pulmonary or systemic congestion
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Can be prevented or progression slowed by early detection and intervention
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Conditions that reduce the pumping ability of the heart
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Coronary artery disease
Hypertension
Dilated cardiomyopathy
Valvular heart disease
Heart Failure
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Systolic dysfunction
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 in cardiac myocardial contractility
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Impaired ability to eject blood from the left ventricle
Diastolic dysfunction
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Abnormality in ventricular relaxation and filling
Cardiac Output = HR x SV
Heart Rate

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sympathetic nervous system 
Parasympathetic 
Stroke Volume
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Preload
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Afterload
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Myocardial contractility
Systolic vs Diastolic Dysfunction
Systolic Dysfunction
Diastolic Dysfunction
EF
< 40%
Normal (55-70%)
Preload


Afterload


CO
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Etiology
 contractility
Abnormal ventricular
relaxation and filling
Preload (Volume)
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Volume of the ventricle at the end of diastole
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Determined by venous return
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End diastolic volume
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Causes a lengthening of the muscle fibers
Afterload (Force)
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Force that the contracting heart muscle must generate to eject blood from
the filled heart
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Components of afterload
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Systemic vascular resistance
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Ventricular wall tension
Myocardial Contractility (Inotropy)
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Contractile performance of the heart
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The ability of the actin and myosin filaments of the heart muscle to interact
and shorten against a load
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Requires the use of energy supplied by the breakdown of ATP and the
presence of Ca++ ions
Manifestations of Right-sided and Left-sided
Heart Failure
Right-sided CHF
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Impairs the ability to move deoxygenated blood from the systemic
circulation to the pulmonary circulation
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Congestion of blood in the systemic venous system and the viscera
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 in RV end diastolic, RA and systemic venous pressure
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Peripheral edema, ascites and weight gain
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Caused by LVF, pulmonary HTN, valvular heart disease, RV infarct,
cardiomyopathy
Left-sided CHF
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Impairs the movement of blood from the pulmonary circulation into the
systemic circulation
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in cardiac output to the systemic circulation
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 pulmonary venous pressure
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Shift of intravascular fluid into the interstitium of the lung and development
of pulmonary edema
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Most common causes are HTN and acute MI
Pharmacological Management of CHF
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Diuretic
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ACE inhibitor
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An inhibitor of the renin-angiotensin-aldosterone system (RAAS) to lower
aldosterone and normalize Na+ and K+ levels
β-blocker
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To reduce pulmonary and systemic edema
To reduce heart rate
Digoxin
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Increase myocardial contractility
Compensatory Mechanisms
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Frank-Starling mechanism
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Activation of neurohumoral influences
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RAAS mechanism
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Cardiac natriuretic hormones
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Locally produced vasoactive substances
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Myocardial hypertrophy and remodeling
Frank-Starling Mechanism
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Serves to match the outputs of the two ventricles
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Operates through an increase in preload
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Increased stretching of the myocardial fibers with a resultant increase in
the force of the next contraction ventricular wall tension
myocardial oxygen consumptionischemia
Frank-Starling Curve
Sympathetic Nervous System Activity
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Cardiac sympathetic tone and catecholamine levels (epinephrine and
norepinephrine) are elevated in late stages of CHF
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Helps to maintain perfusion of various body organs
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Augments BP and cardiac output
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 sympathetic activity by stimulation of β-adrenergic receptors leads to
tachycardia, vasoconstriction and cardiac arrhythmias
RAAS
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CO reduction in renal blood flow and GFR sodium and water
retention
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reduction in renal blood flow Renin, angiotensin II aldosterone
production reabsorption of water and sodiumedema
Natriuretic Peptides (NPs)
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Peptide hormones produced and secreted by the cardiac muscle (four known NPs)
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Potent diuretic, natriuretic, and vascular smooth muscle effects
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Atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) are most
commonly associated with heart failure
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In response to increased chamber stretch and pressure they promote rapid and
transient natriuresis and diuresis through an increase in GFR and inhibition of
tubular sodium and water reabsorption
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Inhibit the SNS, RAAS, endothelin inflammatory cytokines, vasopressin
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Used clinically in the diagnosis of heart failure
Myocardial Hypertrophy and Remodeling
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Principle mechanism by which the heart compensates for an increase in
workload
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Series of complex events at both the molecular and cellular level
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Three types
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Symmetric hypertrophy (proportionate in length and width) “athletes”
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Concentric hypertrophy (in wall thickness)
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Eccentric hypertrophy (disproportionate  in muscle length) “cardiomyopathy”
Clinical Manifestations of Heart Failure
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Respiratory manifestations
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Fatigue, weakness and confusion
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Fluid retention and edema
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Cachexia and malnutrition
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Cyanosis
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Arrhythmias and sudden cardiac death
Treatment of Heart Failure
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Non-pharmacologic
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Oxygen therapy
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Resynchronization and AICDs
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Mechanical support and heart transplant
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Pharmacologic
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Diuretics
ACE inhibitors
β-Adrenergic receptor blockers
Digitalis
Vasodilators (preload)
Circulatory Failure (Shock)
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Acute failure of the circulatory system to supply the peripheral tissues and
organs of the body with adequate blood supply
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An imbalance between oxygen supply and demand
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Hypotension and hypoperfusion usually present
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Syndrome that occurs in the course of many life-threatening traumatic
conditions or disease states
Pathophysiology of Shock
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Cellular responses
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Cell metabolism becomes anaerobic because of decreased availability of oxygen
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Excess amounts of lactic acid accumulate
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Limited amounts of ATP are produced
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Intracellular accumulation of sodium and loss of potassium
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Cellular edema
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Increased cell permeability
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Cell death with release of intracellular contents into the extracellular space
Pathophysiology of Shock
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Compensatory mechanisms which maintain CO and BP
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Sympathetic nervous system
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Stimulation of α receptors causes constriction of blood vessels
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Stimulation of β1 receptors increases heart rate and force of myocardial
contraction
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Stimulation of β2 receptors causes vasodilation of the skeletal muscle beds and
relaxation of the bronchioles
Renin-angiotensin mechanism
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Augments vasoconstriction and leads to aldosterone mediated increase in
sodium and water retention by the kidneys
Hypovolemic Shock
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Occurs when there is an acute loss of 15% or more of the circulating blood
volume (loss of whole blood, plasma, extracellular fluid or excessive
dehydration)
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10% of the total blood volume can be lost without changing CO or arterial
pressure (blood donation)
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Compensatory mechanisms are triggered with >15% loss
Manifestations of Hypovolemic Shock
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Depend on its severity
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Thirst, tachycardia, cool and clammy skin, decreased BP and urine output,
changes in mentation
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Tachypnea, weak and thready pulse
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Restlessness, agitation and apprehension
Treatment of Hypovolemic Shock
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Directed toward correcting or controlling the underlying cause and
improving tissue perfusion
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Ongoing loss of blood must be corrected
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Replacing volume is the first priority
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Intravenous administration of fluids, blood and blood products
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Vasopressor and inotropic medications
Cardiogenic Shock
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When the heart fails to pump blood sufficiently to meet the body’s demands
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Decreased cardiac output, hypotension, hypoperfusion and indications of tissue
hypoxia despite an adequate intravascular volume
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Causes
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Acute MI
Myocardial contusion
Acute mitral valve regurgitation due to papillary muscle rupture
Sustained arrhythmias
Severe dilated cardiomyopathy
Cardiac surgery
Manifestations of Cardiogenic Shock
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Cyanotic lips, nailbeds and skin
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Decreased mean arterial and systolic BP
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Decreased urine output
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Alterations in cognition and poor cerebral perfusion
Treatment of Cardiogenic Shock
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Improving CO and reducing the workload and oxygen needs of the heart
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Regulation of fluid volume to optimize the filling pressure and stroke volume
and decrease oxygen demands of the heart
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Increase coronary artery perfusion and BP
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Decrease ventricular wall tension
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Pharmacotherapy: inotropic and vasopressor agents
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Mechanical support: intraaortic balloon pump
Other Types of Shock
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Obstructive shock: dissecting aortic aneurysm, cardiac tamponade,
pneumothorax, ruptured hemidiaphragm, pulmonary embolism
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Distributive shock (normovolemic shock)
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Neurogenic shock: decreased sympathetic control of blood vessel tone
(spinal cord injury)
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Anaphylactic shock: immunologically mediated systemic allergic reaction
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Septic shock: systemic immune response to severe infection
Complications of Shock
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Acute lung injury/ARDS
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Acute kidney injury
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GI
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Disseminated intravascular coagulation (DIC)
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Multiple organ dysfunction syndrome