Congestive heart failure
Presentation and Diagnosis
The most common reason for hospitalization in
adults >65 years old
Dr Shahid Abbas
Consultant Interventional Cardiologist
Road Map
– Definition
– Causes and pathophysiology
– Types of heart failure
– Compensatory mechanism of heart failure
– Clinical manifestations
– Classification of heart failure
– Diagnostic evaluation
– Management
Definition
A clinical syndrome that develops when
the heart cannot maintain an adequate
cardiac output
The heart pumps blood inadequately,
leading to reduced blood flow, back-up
(congestion) of blood in the veins and
lungs Leading to
Other changes that may further weaken
the heart
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Etiology
• A syndrome of Pulmonary and/ or Systemic
congestion due to C.O
• Heart is unable to pump enough blood to
meet tissues O2 requirements
Pulmonary pressure fluid in alveoli
(PULMONARY EDEMA)
Systemic pressure fluid in tissues
(PERIPHERAL EDEMA)
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Etiology
• Heart failure is caused by systemic
hypertension in 75% of cases
• About one third of clients experiencing
myocardial infarction also develop heart
failure
• Structural heart changes, such as valvular
dysfunction, cause pressure or volume
overload on the heart
Cardiac Physiology
(remember this?)
• CO = SV x HR
• HR: parasympathetic and sympathetic tone
• SV: preload, afterload, contractility
Preload
• Passive stretch of muscle prior to contraction
• Measurement: Swan-Ganz
– LVEDP
• Really a function of LVEDV
• Affected by compliance
– Low compliance = higher LVEDP @ lower LVEDV
– False high estimate of preload
• Frank-Starling right?
Afterload
• Force opposing/stretching muscle after
contraction begins
• Measurement: SVR
• Really a function of:
– SVR
– Chamber radius (dilated cardiomyopathies)
– Wall thickness (hypertrophy)
Contractility
• Normal ability of the muscle to contract at a
given force for a given stretch, independent of
preload or afterload forces
• In other words:
– How healthy is your heart muscle?
• Ischemia, Hypertrophy (?), Muscle loss
CHF: the heart muscle sarcomere
March 2013 ghennersdorf DGK ESC SES
Pathophysiology
Renin + Angiotensinogen
Angiotensin I
Angiotensin II
Peripheral
Vasoconstriction
Afterload
Cardiac Output
Heart Failure
Salt & Water Retention
Plasma Volume
Preload
Cardiac Workload
Edema
Aldosterone Secretion
Renin-angiotensin system
Heart Failure
• Pathophysiology
• A. Cardiac compensatory mechanisms
– 1.tachycardia
– 2.ventricular dilation-Starling’s law
– 3.myocardial hypertrophy
• Hypoxia leads to dec. contractility
Acute decompensated heart failure
Pulmonary edema, often life-threatening
• Early
–Increase in the respiratory rate
–Decrease in PaO2
• Later
–Tachypnea
–Respiratory acidemia
Acute Decompensated Heart Failure
(ADHF) Pulmonary Edema
Pulmonary edema begins with an increased
filtration through the loose junctions of the
pulmonary capillaries.
As the intracapillary pressure increases, normally
impermeable (tight) junctions between the alveolar cells
open, permitting alveolar flooding to occur.
END RESULT
FLUID OVERLOAD > Acute Decompensated Heart Failure
(ADHF)/Pulmonary Edema
Medical Emergency!
MMildild
Heart Failure
(progression)
Drugs
Diet
Fluid
Restriction
Cardiogenic shock
Cardiomyopathy
CDHF(Pulmonary Edema) Severe End Stage
Irreversible
Needs new ventricle
VAD
IABP
VAD
IABP
Heart Transplant
Control With
Emergency-Upright, O2, morphine, etc
Classifying Heart Failure
• Anatomically
– Left versus Right
• Physiologically
– Systolic versus Diastolic
• Functionally
– How symptomatic is your patient?
Congestive heart failure
Types
• Left-sided heart failure
There are two types of left-sided heart failure
Systolic dysfunction
Diastolic dysfunction
• Right-sided heart failure
Left versus Right Failure
Left Heart Failure
- Dyspnea
- Dec. exercise tolerance
- Cough
- Orthopnea
- Pink, frothy sputum
Right Heart Failure
- Dec. exercise tolerance
- Edema
- HJR / JVD
- Hepatomegaly
- Ascites
Classification of heart failure
New York Heart Association (NYHA) Functional Classification
Class % of patients Symptoms
No symptoms or limitations in ordinary
physical activity
I 35%
Mild symptoms and slight limitation
during ordinary activity
II 35%
Marked limitation in activity even
during minimal activity. Comfortable
only at rest
III 25%
Severe limitation. Experiences
symptoms even at rest
IV 5%
Heart Failure
Clinical Manifestations
• Acute decompensated heart
failure (ADHF)
• Physical findings
• Orthopnea
• Dyspnea, tachypnea
• Use of accessory muscles
• Cyanosis
• Cool and clammy skin
•Physical findings
•*Cough with frothy,
blood-tinged sputum
•Breath sounds: Crackles,
wheezes, rhonchi
•Tachycardia
•Hypotension or
hypertension
ADHF/Pulmonary Edema
(advanced L side HF)
When PA WEDGE pressure is approx 30mmHg
– Signs and symptoms
• wheezing
• pallor, cyanosis
• Inc. HR and BP
• S3 gallop
• Rales,copious pink, frothy sputum
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PULMONARY EDEMA
Rapid fluid accumulation in lung spaces that
has leaked from engorged pulmonary
capillaries
Etiology – most common cause is sudden
deterioration of LV function
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Cardiogenic Shock
Significant reduction in SV & CO causes drop in
pressure & poor tissue perfusion a/r/o LV MI
• Clinical signs:
– BP, pulse, peripheral pulses
– confusion/ agitation (cerebral hypoxia)
– cold/ clammy skin
– urine output
– Resp distress
– Chest pain
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(R) SIDED HF
Blood “BACKS UP” into venous circulation. High
oncotic pressure pushes fluids into tissues.
CLINICAL SIGNS:
CVP SUDDEN WT. GAIN
JVD DEPENDENT EDEMA
FATIGUE LIVER CONGESTION
LETHARGY ASCITES
ORTHOPNEA ANOREXIA
Heart Failure
Complications
• Pleural effusion
• Atrial fibrillation (most common
dysrhythmia)
– Loss of atrial contraction (kick) -reduce CO by
10% to 20%
– Promotes thrombus/embolus formation inc.
risk for stroke
– Treatment may include cardioversion,
antidysrhythmics, and/or anticoagulants
Heart Failure
Complications
• **High risk of fatal dysrhythmias (e.g., sudden
cardiac death, ventricular tachycardia) with HF and
an EF <35%
– HF lead to severe hepatomegaly, especially with
RV failure
• Fibrosis and cirrhosis - develop over time
– Renal insufficiency or failure
Heart Failure
Diagnostic Studies
• Primary goal- determine underlying cause
– History and physical examination( dyspnea)
– Chest x-ray
– ECG
– Lab studies (e.g., cardiac enzymes, BNP- (beta
natriuretic peptide- normal value less than 100)
electrolytes
– EF
Clinical Data
• CXR
– Kerley’s lines : A and B
– Pulmonary Edema
– Cephalization
– Pleural Effusions (bilateral)
• EKG
– Left atrial enlargement
– Arrhythmias
– Hypertrophy (left or right)
Cardiomegaly/ventricular remodeling occurs as heart overworked> changes in size, shape, and function
of heart after injury to left ventricle. Injury due to acute myocardial infarction or due to causes that inc.
pressure or volume overload as in Heart failure
Clinical Data
• Laboratory Data
• Chemistry
– Renal Function: Be Wary
• BNP
– Used in ER departments the world over
– Good negative correlation
– Need baseline for positivity
– Pulmonary versus cardiac dyspnea