TOPIC VI:

CONGESTIVE HEART FAILURE

PT 139

Jaecelle Marie G. Gamiao, PTRP

CHF
• Inability of the patient to maintain adequate cardiac output at
rest. This means a cardiac output at rest of less than 4 L per
minute. (Irwin, Scot 2004)
• Failure of the heart which causes congestion in the chest.
Systolic or diastolic dysfunction of the left ventricle results in a
gradual or acute increase in end diastolic volumes and
pressures
• The interdependence and interrelationship between the cardiac
and pulmonary systems are demonstrated in the clinical
manifestations of heart failure. One of the most clinical
manifestation is pulmonary edema (Hillegas, 2017)
N Physiology of Cardiac Output
• The greater the oxygen demand, the greater the cardiac output demand
• Stroke volume not linear in response to increasing oxygen demand
• Stroke volume is critically dependent on:
• Preload (end-diastolic volume: Venous return); venous return is dependent
on gravity and body positions;
• Passive process (squeezing action of muscle); full-length stockings and
abdominal binders;
• Contractility (autonomic system input); force of ventricular contraction
(Frank Starling Mechanism: stretch response curve that is representative of
cardiac muscle responses to increase in end-diastolic volume)
• Single best clinical measure of contractility is EJECTION FRACTION
• Ejection fraction= SV/ EDV (cardiac catheterization/ echocardiography); 55% to 65% (60-70%)
• Afterload (Resistance to blood flow); Resistance that the heart works against
during ejection
Etiology of CHF
• HTN
• CAD
• Cardiac dysrhythmias
• Renal insufficiency
• Cardiomyopathy
• Heart valve abnormality
• Pericardial effusion
• Pulmonary embolism
• SCI
• Age-related changes
Left CHF
• Frequently the result of left ventricular insult which causes
fluid to accumulate behind the left ventricle, If left-sided failure
is severe, there is progressive accumulation beyond the lungs,
manifesting as right-sided heart failure
Right CHF
• Fluid backs up behind the right ventricle and produces the
accumulation of fluid in the liver, abdomen, and bilateral ankles
and hands
Left vs Right CHF
Left Right
• Inability of the LV to contract • Inability of the RV to contract
effectively effectively
• Pulmonary edema • Congestion in the periphery and
• Cough organs
• Dyspnea or SOB • Bipedal edema
• Orthopnea • Jugular vein distention
• Paroxysmal nocturnal dyspnea • Hepatomegaly
• Cerebral hypoxia • Ascites
• Fatigue • Cyanosis
Systolic heart failure
• Impaired contraction of the ventricles that produce an
inefficient expulsion of blood (low stroke volume)

Diastolic heart failure

• Associated with an inability of the ventricles to accept the
blood ejected from the atria during rest or diastole
Pathophysiology of CHF
• Based on the Frank-Starling mechanism
• “The relation between ventricular filling pressure (or end-
diastolic volume) and ventricular mechanical activity,”
expressed as the volume output of the heart, or the stroke
volume (cardiac output divided by heart rate because CO = HR ×
SV).
Compensatory and
pathophysiologic
interrelationships
among organs
Factors Affecting Myocardial Contractility
Biomechanical Markers: Natriuretic Peptide

• Group of related proteins, each with a slightly different

structure but all involved in regulating fluid balance in the body
• Atrial natriuretic peptide (ANP)
• From the heart’s atria
• Brain natriuretic peptide (BNP)
• Mostly produced in the heart’s ventricles but was first discovered in
the brain
• Dendroaspis natriuretic peptide (DNP)
• Can be measured in the blood and increases heart failure
• Helps relax blood vessels
• ANP and BNP are released
when the heart or blood
vessels stretch due to high
pressure or volume. Once
released, they help to:
• Relax blood vessels (making
them wider)
• Lower blood volume by helping
the kidneys get rid of extra salt
and water (natriuresis)
• Reduce the release of other
hormones like renin and
aldosterone, which usually
help the body hold onto salt
and water.
Mechanisms of CHF
• Decreased cardiac output occurs when
the heart is unable to pump blood
effectively
• RAAS stimulates the kidneys to retain salt
and water, which increases circulating
blood volume and preload (the amount of
blood returning to the heart)
• ADH promotes water retention by the
kidneys, contributing to the increase in
blood volume and preload
• All the compensatory mechanisms aim to
help maintain blood pressure and support
cardiac output
• As blood volume increases and the heart
struggles to pump effectively, fluid builds
up in the tissues
Physiologic effects of CHF
• Decreased cardiac output is the root cause
of heart failure decompensation.
• Reduced blood flow to the kidneys causes a
drop in the delivery of oxygen to kidney
tissues. This leads to hypoxia (low oxygen
levels in tissues) and acute kidney injury
(AKI).
• The activation of angiotensin II,
norepinephrine (NE), and vasopressin (AVP)
leads to the retention of sodium and water
by the kidneys.
• The kidneys, in response to decreased blood
flow and neurohormonal signaling,
reabsorb more sodium and water in an
attempt to maintain blood pressure. This
increases oxygen consumption (since the
kidneys work harder) and worsens hypoxia
Pulmonary Function: Pulmonary Edema
• Stage I is when extra fluid flow might
briefly help the lungs, but if it keeps
going, it can cause fluid buildup and
breathing problems.
• Stage II fluid buildup in the lungs makes
breathing less effective, leading to low
oxygen levels, rapid breathing, and a
direct connection between lung
pressure and oxygen problems.
• Repeated episodes of pulmonary edema
(which are common in CHF) can cause
significant damage to lung function,
leading to a global respiratory
impairment. This can result in both
obstructive and restrictive lung
conditions, further complicating
breathing and oxygen exchange.
Clinical Manifestations of CHF
• Dyspnea
• Tachypnea
• Paroxysmal nocturnal dyspnea (PND)
• Orthopnea
• Peripheral edema
• Cold, pale, and possibly cyanotic extremities
• Weight gain
• Hepatomegaly
• Jugular venous distention
• Rales (crackles)
• Tubular breath sounds and consolidation
• Presence of an S3 heart sound
• Sinus tachycardia
• Decreased Exercise tolerance or physical work capacity
 Primary
Auscultatory
Areas
Jugular Vein Distention
• Can result from fluid overload
• EJV is medial to the EJA and can be measured in a 45-degree
semirecumbent position for signs of distension
• Visible pulsation is determined by measuring the distance between
the highest point of pulsation and the sternal angle.
• Degree of elevation and magnitude of distension (mild, moderate,
severe) should be noted.
• N level: 3-5cm above the sternal angle of Louis
• A mean pulmonary artery pressure greater than 25 mm Hg
indicates pulmonary hypertension and is associated with hypoxia,
cardiac arrhythmias, and pulmonary abnormalities.
Pitting Edema Scale
Pulsus Alternans
• Alternating strong and weak pulses with a regular rhythm
• Ax: apply light pressure at the radial pulse with the patient
holding their breath during mid-expiration, avoiding
interference from respiratory variations.
• A 20 mm Hg or greater decrease in systolic blood pressure
during breath holding is typical in pulsus alternans, due to
increased resistance to left ventricular ejection.
Changes in the Extremities
• Cold and appear pale and cyanotic
• Abnormal sensation and appearance are a result of the
increased sympathetic nervous system activation of CHF, which
increases peripheral vascular vasoconstriction and decreases
peripheral blood flow
Weight Gain
• As fluid is retained, total body fluid volume increases, as does total body
weight.
• Fluctuations of a few pounds from day to day are usually considered
normal, but increases of several pounds per day (more than 3 lb) are
suggestive of CHF in a patient with CMD.
Sinus Tachycardia
• The body attempts (via increased heart rate) to increase the delivery of
fluid and oxygen to the peripheral tissues where it is needed.
• Unfortunately, this only compounds the problem and makes the heart
work even harder, which further impairs its ability to pump.
Quality of Life in CHF
• Minnesota Living with Heart
Failure Questionnaire
• This questionnaire consists of
21 questions that the patient
answers to the best of the
patient’s ability. This self
administered questionnaire
appears to be more accurate
and reliable with a modest
degree of supervision.
Laboratory Findings in CHF
Radiologic Findings in CHF
• Interstitial, perivascular, and alveolar edema form the radiologic hallmark
of CHF and generally occur when pulmonary capillary pressures (which
reflect the left ventricular end-diastolic pressure) exceed 20 to 25 mm
Hg. Pleural effusions (parenchymal fluid accumulations) and atelectasis
(collapsed lung segments) may also be present.
Laboratory Findings in CHF
• Proteinuria; elevated urine specific gravity, BUN, and creatinine levels;
• Decreased erythrocyte sedimentation rates (because of decreased fibrinogen
concentrations resulting from impaired fibrinogen synthesis) are associated with
CHF.
• PaO2 and oxygen saturation levels are reduced and PaCO2 levels elevated.
• Liver enzymes, such as AST and alkaline phosphatase, are often elevated, and
hyperbilirubinemia commonly occurs, resulting in subsequent jaundice.
• Serum electrolytes are generally normal, but individuals with chronic CHF may
demonstrate hyponatremia (decreased Na+) during rigid sodium restriction and
diuretic therapy or hypokalemia (decreased K+),
• Brain natriuretic peptide and its amino-terminal fragment NT-proBNP have an
established role in the diagnosis of patients presenting with dyspnea of
uncertain etiology and possibly in determining decompensation in CHF.
Medical Management
• Goal: improve the heart’s pumping ability
• Medications
• Diuretics to reduce fluid buildup
• Digitalis and positive inotropic agents to enhance heart contractility
• Vasodilators and venodilators to reduce heart’s workload
• ACE inhibitors to help relax BV and improve blood flow
• β-adrenergic blockers to reduce HR and workload
• Key measures:
• Sodium restriction to prevent fluid restriction
Diuretics
• Cornerstone of treatment for CHF, helping to reduce fluid
overload by increasing urine output
• Work by inhibiting solute (substances dissolved in a solution)
and water reabsorption in the kidneys
• Furosemide (Lasix): most commonly used diuretic, which
inhibits the cotransport of sodium, potassium, and chloride
Digoxin (Lanoxin) and other Positive Inotropic Agents

• Digoxin (Digitalis): one of the oldest drugs used in medicine,

derived from the leaves of the foxglove plant (Digitalis
purpurea)
Dopamine
• Dopamine hydrochloride is a chemical precursor of
norepinephrine, which stimulates dopaminergic, β2-adrenergic,
and α-adrenergic receptors, as well as the release of
norepinephrine. This results in increased cardiac output and, at
doses greater than 10 μg/kg/min, markedly increased systemic
vascular resistance and preload. For this reason, the primary
indication for dopamine is hemodynamically significant
hypotension in the absence of hypovolemia.
Amrinone/Milrinone
• Amrinone and milrinone are phosphodiesterase inhibitors that
lead to increased cAMP by preventing its breakdown, thereby
producing rapid inotropic and vasodilatory effects
Vasodilators and Venodilators
• Relax smooth muscle in peripheral arterioles, resulting in
peripheral vasodilation.
• Reduce filling pressures and decrease afterload.
• Decrease the work of the heart, alleviating symptoms of heart
failure.
• Examples: calcium-channel blockers and α-blockers
Angiotensin-Converting Enzyme
Inhibitor and α-Receptor Blockers
• The combined use of ACE inhibitors, vasodilators, and
venodilators has been demonstrated to be very effective in
reducing symptoms and improving exercise tolerance. The
primary mechanism of action of these inhibitors is probably via
the reduction of angiotensin II, a hormone that causes
vasoconstriction.
α-Adrenergic Antagonists and Partial
Agonists
• One of the many uses of β blockers is to lower blood pressure,
primarily via a reduction in cardiac output. This reduction in
cardiac output is the result of a decrease in heart rate and
stroke volume, which causes an increase in end-diastolic
volume and end-diastolic pressure (the slowing of the heart
rate allows more time for the ventricles to fill before the next
myocardial contraction with more time for the coronary
arteries to fill) but somewhat paradoxically reduces the
myocardial oxygen requirement.
Anticoagulation
• The patient hospitalized with heart failure is at increased risk
for thromboembolic complications and deep venous
thrombosis and should receive prophylactic anticoagulation
with either intravenous unfractionated heparin or
subcutaneous preparations of unfractionated or low-
molecular-weight heparin, unless contraindicated.
Mechanical Management
• Implantable Cardiac
Defibrillator Implantation
• Cardiac Resynchronization
Therapy
• Special Measures
• Dialysis and ultrafiltration
• Assisted circulation
• Ventricular Assist Devices
Surgical Management
• Reparative
• Correct cardiac malfunctions such as ventricular septal defect, atrial
septal defect, mitral stenosis to improve cardiac performance
• Reconstructive
• Coronary artery bypass graft surgery
• Excisional
• Myxomas (tumors) and large LVs
• • Ablative
• Used in patients with persistent and symptomatic Wolff-Parkinson-
White syndrome or intractable ventricular tachycardia
Cardiac Transplantation
• Cardiac transplantation is the last treatment effort for a patient
with CHF and CMD because “potential recipients of cardiac
transplants must have end-stage heart disease with severe
heart failure and a life expectancy of less than 1 year.”
Prognosis
• The most significant predictors of survival in individuals with CHF
have been identified and include:
• Decreasing LVEF
• Worsening NYHA functional status
• Degree of hyponatremia
• Decreasing peak exercise oxygen uptake
• Decreasing hematocrit,
• Widened QRS on 12-lead electrocardiogram
• Chronic hypotension
• Resting tachycardia
• Renal insufficiency
• Intolerance to conventional therapy
• Refractory volume overload
Interventions for CHF
Rehabilitation for CHF
Exercise Training Guideline for CHF
Functional Classifications of Cardiac Patients

Definition Degree of Limitation Max METs

Class Ordinary activities does not

No limitation of PA 6.5 METs
I cause cardiac sx
Class Ordinary activities cause
Slight limitation of PA 4.5 METs
II cardiac sx
Class Less than ordinary activities
Marked limitation of PA 3 METs
III cause cardic sx
Class Presence of cardiac sx at rest Inability to carry any
1.5 METs
IV which is aggravated by PA PA without discomfort
Self-Management Techniques