23
Heart Failure By:Dawit Ayele(MD,Internist)
Heart Failure
ByDawit Ayele(MDInternist)
ldquoHeart (or cardiac) failure is the pathophysiological state in which
the heart is unable to pump blood at a rate commensurate with the requirements of the metabolizing tissues or can do so only from an elevated filling pressurerdquo - Eugene Braunwald
ldquoCongestive heart failure (CHF) represents a complex clinical syndrome characterized by abnormalities of left ventricular function and neurohormonal regulation which are accompanied by effort intolerance fluid retention and reduced longevityrdquo - Milton Packer
Definition
Heart Failure Epidemiology
1048698 Burden of CHF is staggering1048698 5 million in US (15 of all adults)1048698 500000 cases annually1048698 In the elderly1048698 6-10 prevalence1048698 80 hospitalized with HF1048698 250000 deathyear attributable to CHF1048698 $38 billion (54 of healthcare cost)
Coronary artery disease-
HTN--both Valvular heart
disease (especially aorta and mitral disease)--chronic
Congenital
Alcohol-- Diabetesmdash Cardiomyopathies
Infection Arrhythmia PhysicalFluidDietaryEnvrsquotalEmotional excess MI Anemia Pulmonary embolism Worsening of HTN Thyrotoxicosis Infective endocarditis Rheumaticviral or other myocarditis
Precepitating factors
SYSTOLIC VERSUS DIASTOLIC FAILURE LOW-OUTPUT VERSUS HIGH-OUTPUT
HEART FAILURE ACUTE VERSUS CHRONIC HEART FAILURE RIGHT-SIDED VERSUS LEFT-SIDED HEART
FAILURE BACKWARD VERSUS FORWARD HEART
FAILURE
Forms of Heart Failure
1 Syndrome of decrease exercise tolerance 2 Syndrome of fluid retention 3 No symptoms but incidental discovery of
LV dysfunction
Typical presentations of heart failure
Major Criteria 1048698 OrthopneaPND 1048698 Venous distension 1048698 Rales 1048698 Cardiomegaly 1048698 Acute pulm edema 1048698 Elevated JVP 1048698 HJR 1048698 Circ time gt25s
1048698 Minor Criteria 1048698 Ankle edema 1048698 Night cough 1048698 Exertional dyspnea 1048698 Hepatomegaly 1048698 Pleural effusion 1048698 Tachycardia (gt120) 1048698 Decrease VC 1048698 Weight loss with CHF
tx Framingham Criteria
Heart Failure is a Clinical Diagnosis
Class I Symptoms with more than ordinary activity
Class II Symptoms with ordinary activity Class III Symptoms with minimal activity Class IIIa No dyspnea at rest Class IIIb Recent dyspnea at rest Class IV Symptoms at rest
NYHA Class1048698
Stages of Heart Failure
At Risk for Heart FailureSTAGE A High risk for developing
HF
STAGE B Asymptomatic LV dysfunction
Heart FailureSTAGE C Past or current
symptoms of HF
STAGE D End-stage HF
bull Designed to emphasize preventability of HF
bull Designed to recognize the progressive nature of LV dysfunction
Stages of Heart Failure
COMPLEMENT DO NOT REPLACE NYHA CLASSES
bull NYHA Classes - shift backforth in individual patient (in response to Rx andor progression of disease)
bull Stages - progress in one direction due to cardiac remodeling
Stages of Heart Failure
Occurs when the left ventricle fails as an effective forward pump
1048698back pressure of blood into the pulmonary circulation
1048698 pulmonary edema Cannot eject all of the
blood delivered from the right heart
Left atrial pressure rises 1048698 increased pressure in the pulmonary veins and capillaries
When pressure becomes too high the fluid portion of the blood is forced into the alveoli
1048698decreased oxygenation capacity of the lungs
AMI common with LVF suspect
Severe resp distressndash Evidenced by orthopnea
dyspnea Hx of paroxysmal
nocturnal dyspnea Severe apprehension
agitation confusionmdash Resulting from hypoxia Feels like heshe is
smothering Cyanosismdash
Diaphoresismdash Results from
sympathetic stimulation Pulmonary
congestion Often present Ralesmdashespecially at the
bases Rhonchimdashassociated
with fluid in the larger airways indicative of severe failure
Wheezesmdashresponse to airway spasm
Jugular Venous Distentionmdashnot directly related to LVF Comes from back pressure
building from right heart into venous circulation
Vital Signsmdash Significant increase in
sympathetic discharge to compensate
BPmdashelevated Pulse ratemdashelevated to
compensate for decreased stroke volume
Respirationsmdashrapid and labored
Neurohormonal system
Renin-angiotensin-aldosterone system
Ventricular hypertrophy
Neurohormonal Activation Contributes to the Progression of CHF
Myocardial Disease
LV Dysfunction
Impedance
Vasoconstriction
Neurohormonal Activation
LV RemodelingVascular Remodeling
PreloadRenal Blood Flow
Na Retention
Decreased renal blood flow secondary to low cardiac output triggers renin secretion by the kidneys
Aldosterone is released 1048698 increase in Na+ retention 1048698 water retention
Preload increases
Worsening failure
Long term compensatory mechanism
Increases in size due to increase in work load ie skeletal muscle
Principlesthorough Hx amp PE Supplemental investigations
especiallyBNPECGEchocardiographyCXR Management(1) general measures (2) correction of the underlying
cause (3) removal of the precipitating
cause (4) prevention of deterioration of
cardiac function and (5) control of the congestive HF state
Patient approach amp Mgt
Heart Failure Disease Management
Control Volume Slow Disease Progression
Diuretic RAAS Inhibition
Beta-Blockade
Treat residual symptoms
DIGOXIN
+
SPIRONOLACTONE
Am J Cardiol 199983(suppl 2A)9A-38A
ldquoHeart (or cardiac) failure is the pathophysiological state in which
the heart is unable to pump blood at a rate commensurate with the requirements of the metabolizing tissues or can do so only from an elevated filling pressurerdquo - Eugene Braunwald
ldquoCongestive heart failure (CHF) represents a complex clinical syndrome characterized by abnormalities of left ventricular function and neurohormonal regulation which are accompanied by effort intolerance fluid retention and reduced longevityrdquo - Milton Packer
Definition
Heart Failure Epidemiology
1048698 Burden of CHF is staggering1048698 5 million in US (15 of all adults)1048698 500000 cases annually1048698 In the elderly1048698 6-10 prevalence1048698 80 hospitalized with HF1048698 250000 deathyear attributable to CHF1048698 $38 billion (54 of healthcare cost)
Coronary artery disease-
HTN--both Valvular heart
disease (especially aorta and mitral disease)--chronic
Congenital
Alcohol-- Diabetesmdash Cardiomyopathies
Infection Arrhythmia PhysicalFluidDietaryEnvrsquotalEmotional excess MI Anemia Pulmonary embolism Worsening of HTN Thyrotoxicosis Infective endocarditis Rheumaticviral or other myocarditis
Precepitating factors
SYSTOLIC VERSUS DIASTOLIC FAILURE LOW-OUTPUT VERSUS HIGH-OUTPUT
HEART FAILURE ACUTE VERSUS CHRONIC HEART FAILURE RIGHT-SIDED VERSUS LEFT-SIDED HEART
FAILURE BACKWARD VERSUS FORWARD HEART
FAILURE
Forms of Heart Failure
1 Syndrome of decrease exercise tolerance 2 Syndrome of fluid retention 3 No symptoms but incidental discovery of
LV dysfunction
Typical presentations of heart failure
Major Criteria 1048698 OrthopneaPND 1048698 Venous distension 1048698 Rales 1048698 Cardiomegaly 1048698 Acute pulm edema 1048698 Elevated JVP 1048698 HJR 1048698 Circ time gt25s
1048698 Minor Criteria 1048698 Ankle edema 1048698 Night cough 1048698 Exertional dyspnea 1048698 Hepatomegaly 1048698 Pleural effusion 1048698 Tachycardia (gt120) 1048698 Decrease VC 1048698 Weight loss with CHF
tx Framingham Criteria
Heart Failure is a Clinical Diagnosis
Class I Symptoms with more than ordinary activity
Class II Symptoms with ordinary activity Class III Symptoms with minimal activity Class IIIa No dyspnea at rest Class IIIb Recent dyspnea at rest Class IV Symptoms at rest
NYHA Class1048698
Stages of Heart Failure
At Risk for Heart FailureSTAGE A High risk for developing
HF
STAGE B Asymptomatic LV dysfunction
Heart FailureSTAGE C Past or current
symptoms of HF
STAGE D End-stage HF
bull Designed to emphasize preventability of HF
bull Designed to recognize the progressive nature of LV dysfunction
Stages of Heart Failure
COMPLEMENT DO NOT REPLACE NYHA CLASSES
bull NYHA Classes - shift backforth in individual patient (in response to Rx andor progression of disease)
bull Stages - progress in one direction due to cardiac remodeling
Stages of Heart Failure
Occurs when the left ventricle fails as an effective forward pump
1048698back pressure of blood into the pulmonary circulation
1048698 pulmonary edema Cannot eject all of the
blood delivered from the right heart
Left atrial pressure rises 1048698 increased pressure in the pulmonary veins and capillaries
When pressure becomes too high the fluid portion of the blood is forced into the alveoli
1048698decreased oxygenation capacity of the lungs
AMI common with LVF suspect
Severe resp distressndash Evidenced by orthopnea
dyspnea Hx of paroxysmal
nocturnal dyspnea Severe apprehension
agitation confusionmdash Resulting from hypoxia Feels like heshe is
smothering Cyanosismdash
Diaphoresismdash Results from
sympathetic stimulation Pulmonary
congestion Often present Ralesmdashespecially at the
bases Rhonchimdashassociated
with fluid in the larger airways indicative of severe failure
Wheezesmdashresponse to airway spasm
Jugular Venous Distentionmdashnot directly related to LVF Comes from back pressure
building from right heart into venous circulation
Vital Signsmdash Significant increase in
sympathetic discharge to compensate
BPmdashelevated Pulse ratemdashelevated to
compensate for decreased stroke volume
Respirationsmdashrapid and labored
Neurohormonal system
Renin-angiotensin-aldosterone system
Ventricular hypertrophy
Neurohormonal Activation Contributes to the Progression of CHF
Myocardial Disease
LV Dysfunction
Impedance
Vasoconstriction
Neurohormonal Activation
LV RemodelingVascular Remodeling
PreloadRenal Blood Flow
Na Retention
Decreased renal blood flow secondary to low cardiac output triggers renin secretion by the kidneys
Aldosterone is released 1048698 increase in Na+ retention 1048698 water retention
Preload increases
Worsening failure
Long term compensatory mechanism
Increases in size due to increase in work load ie skeletal muscle
Principlesthorough Hx amp PE Supplemental investigations
especiallyBNPECGEchocardiographyCXR Management(1) general measures (2) correction of the underlying
cause (3) removal of the precipitating
cause (4) prevention of deterioration of
cardiac function and (5) control of the congestive HF state
Patient approach amp Mgt
Heart Failure Disease Management
Control Volume Slow Disease Progression
Diuretic RAAS Inhibition
Beta-Blockade
Treat residual symptoms
DIGOXIN
+
SPIRONOLACTONE
Am J Cardiol 199983(suppl 2A)9A-38A
Heart Failure Epidemiology
1048698 Burden of CHF is staggering1048698 5 million in US (15 of all adults)1048698 500000 cases annually1048698 In the elderly1048698 6-10 prevalence1048698 80 hospitalized with HF1048698 250000 deathyear attributable to CHF1048698 $38 billion (54 of healthcare cost)
Coronary artery disease-
HTN--both Valvular heart
disease (especially aorta and mitral disease)--chronic
Congenital
Alcohol-- Diabetesmdash Cardiomyopathies
Infection Arrhythmia PhysicalFluidDietaryEnvrsquotalEmotional excess MI Anemia Pulmonary embolism Worsening of HTN Thyrotoxicosis Infective endocarditis Rheumaticviral or other myocarditis
Precepitating factors
SYSTOLIC VERSUS DIASTOLIC FAILURE LOW-OUTPUT VERSUS HIGH-OUTPUT
HEART FAILURE ACUTE VERSUS CHRONIC HEART FAILURE RIGHT-SIDED VERSUS LEFT-SIDED HEART
FAILURE BACKWARD VERSUS FORWARD HEART
FAILURE
Forms of Heart Failure
1 Syndrome of decrease exercise tolerance 2 Syndrome of fluid retention 3 No symptoms but incidental discovery of
LV dysfunction
Typical presentations of heart failure
Major Criteria 1048698 OrthopneaPND 1048698 Venous distension 1048698 Rales 1048698 Cardiomegaly 1048698 Acute pulm edema 1048698 Elevated JVP 1048698 HJR 1048698 Circ time gt25s
1048698 Minor Criteria 1048698 Ankle edema 1048698 Night cough 1048698 Exertional dyspnea 1048698 Hepatomegaly 1048698 Pleural effusion 1048698 Tachycardia (gt120) 1048698 Decrease VC 1048698 Weight loss with CHF
tx Framingham Criteria
Heart Failure is a Clinical Diagnosis
Class I Symptoms with more than ordinary activity
Class II Symptoms with ordinary activity Class III Symptoms with minimal activity Class IIIa No dyspnea at rest Class IIIb Recent dyspnea at rest Class IV Symptoms at rest
NYHA Class1048698
Stages of Heart Failure
At Risk for Heart FailureSTAGE A High risk for developing
HF
STAGE B Asymptomatic LV dysfunction
Heart FailureSTAGE C Past or current
symptoms of HF
STAGE D End-stage HF
bull Designed to emphasize preventability of HF
bull Designed to recognize the progressive nature of LV dysfunction
Stages of Heart Failure
COMPLEMENT DO NOT REPLACE NYHA CLASSES
bull NYHA Classes - shift backforth in individual patient (in response to Rx andor progression of disease)
bull Stages - progress in one direction due to cardiac remodeling
Stages of Heart Failure
Occurs when the left ventricle fails as an effective forward pump
1048698back pressure of blood into the pulmonary circulation
1048698 pulmonary edema Cannot eject all of the
blood delivered from the right heart
Left atrial pressure rises 1048698 increased pressure in the pulmonary veins and capillaries
When pressure becomes too high the fluid portion of the blood is forced into the alveoli
1048698decreased oxygenation capacity of the lungs
AMI common with LVF suspect
Severe resp distressndash Evidenced by orthopnea
dyspnea Hx of paroxysmal
nocturnal dyspnea Severe apprehension
agitation confusionmdash Resulting from hypoxia Feels like heshe is
smothering Cyanosismdash
Diaphoresismdash Results from
sympathetic stimulation Pulmonary
congestion Often present Ralesmdashespecially at the
bases Rhonchimdashassociated
with fluid in the larger airways indicative of severe failure
Wheezesmdashresponse to airway spasm
Jugular Venous Distentionmdashnot directly related to LVF Comes from back pressure
building from right heart into venous circulation
Vital Signsmdash Significant increase in
sympathetic discharge to compensate
BPmdashelevated Pulse ratemdashelevated to
compensate for decreased stroke volume
Respirationsmdashrapid and labored
Neurohormonal system
Renin-angiotensin-aldosterone system
Ventricular hypertrophy
Neurohormonal Activation Contributes to the Progression of CHF
Myocardial Disease
LV Dysfunction
Impedance
Vasoconstriction
Neurohormonal Activation
LV RemodelingVascular Remodeling
PreloadRenal Blood Flow
Na Retention
Decreased renal blood flow secondary to low cardiac output triggers renin secretion by the kidneys
Aldosterone is released 1048698 increase in Na+ retention 1048698 water retention
Preload increases
Worsening failure
Long term compensatory mechanism
Increases in size due to increase in work load ie skeletal muscle
Principlesthorough Hx amp PE Supplemental investigations
especiallyBNPECGEchocardiographyCXR Management(1) general measures (2) correction of the underlying
cause (3) removal of the precipitating
cause (4) prevention of deterioration of
cardiac function and (5) control of the congestive HF state
Patient approach amp Mgt
Heart Failure Disease Management
Control Volume Slow Disease Progression
Diuretic RAAS Inhibition
Beta-Blockade
Treat residual symptoms
DIGOXIN
+
SPIRONOLACTONE
Am J Cardiol 199983(suppl 2A)9A-38A
Coronary artery disease-
HTN--both Valvular heart
disease (especially aorta and mitral disease)--chronic
Congenital
Alcohol-- Diabetesmdash Cardiomyopathies
Infection Arrhythmia PhysicalFluidDietaryEnvrsquotalEmotional excess MI Anemia Pulmonary embolism Worsening of HTN Thyrotoxicosis Infective endocarditis Rheumaticviral or other myocarditis
Precepitating factors
SYSTOLIC VERSUS DIASTOLIC FAILURE LOW-OUTPUT VERSUS HIGH-OUTPUT
HEART FAILURE ACUTE VERSUS CHRONIC HEART FAILURE RIGHT-SIDED VERSUS LEFT-SIDED HEART
FAILURE BACKWARD VERSUS FORWARD HEART
FAILURE
Forms of Heart Failure
1 Syndrome of decrease exercise tolerance 2 Syndrome of fluid retention 3 No symptoms but incidental discovery of
LV dysfunction
Typical presentations of heart failure
Major Criteria 1048698 OrthopneaPND 1048698 Venous distension 1048698 Rales 1048698 Cardiomegaly 1048698 Acute pulm edema 1048698 Elevated JVP 1048698 HJR 1048698 Circ time gt25s
1048698 Minor Criteria 1048698 Ankle edema 1048698 Night cough 1048698 Exertional dyspnea 1048698 Hepatomegaly 1048698 Pleural effusion 1048698 Tachycardia (gt120) 1048698 Decrease VC 1048698 Weight loss with CHF
tx Framingham Criteria
Heart Failure is a Clinical Diagnosis
Class I Symptoms with more than ordinary activity
Class II Symptoms with ordinary activity Class III Symptoms with minimal activity Class IIIa No dyspnea at rest Class IIIb Recent dyspnea at rest Class IV Symptoms at rest
NYHA Class1048698
Stages of Heart Failure
At Risk for Heart FailureSTAGE A High risk for developing
HF
STAGE B Asymptomatic LV dysfunction
Heart FailureSTAGE C Past or current
symptoms of HF
STAGE D End-stage HF
bull Designed to emphasize preventability of HF
bull Designed to recognize the progressive nature of LV dysfunction
Stages of Heart Failure
COMPLEMENT DO NOT REPLACE NYHA CLASSES
bull NYHA Classes - shift backforth in individual patient (in response to Rx andor progression of disease)
bull Stages - progress in one direction due to cardiac remodeling
Stages of Heart Failure
Occurs when the left ventricle fails as an effective forward pump
1048698back pressure of blood into the pulmonary circulation
1048698 pulmonary edema Cannot eject all of the
blood delivered from the right heart
Left atrial pressure rises 1048698 increased pressure in the pulmonary veins and capillaries
When pressure becomes too high the fluid portion of the blood is forced into the alveoli
1048698decreased oxygenation capacity of the lungs
AMI common with LVF suspect
Severe resp distressndash Evidenced by orthopnea
dyspnea Hx of paroxysmal
nocturnal dyspnea Severe apprehension
agitation confusionmdash Resulting from hypoxia Feels like heshe is
smothering Cyanosismdash
Diaphoresismdash Results from
sympathetic stimulation Pulmonary
congestion Often present Ralesmdashespecially at the
bases Rhonchimdashassociated
with fluid in the larger airways indicative of severe failure
Wheezesmdashresponse to airway spasm
Jugular Venous Distentionmdashnot directly related to LVF Comes from back pressure
building from right heart into venous circulation
Vital Signsmdash Significant increase in
sympathetic discharge to compensate
BPmdashelevated Pulse ratemdashelevated to
compensate for decreased stroke volume
Respirationsmdashrapid and labored
Neurohormonal system
Renin-angiotensin-aldosterone system
Ventricular hypertrophy
Neurohormonal Activation Contributes to the Progression of CHF
Myocardial Disease
LV Dysfunction
Impedance
Vasoconstriction
Neurohormonal Activation
LV RemodelingVascular Remodeling
PreloadRenal Blood Flow
Na Retention
Decreased renal blood flow secondary to low cardiac output triggers renin secretion by the kidneys
Aldosterone is released 1048698 increase in Na+ retention 1048698 water retention
Preload increases
Worsening failure
Long term compensatory mechanism
Increases in size due to increase in work load ie skeletal muscle
Principlesthorough Hx amp PE Supplemental investigations
especiallyBNPECGEchocardiographyCXR Management(1) general measures (2) correction of the underlying
cause (3) removal of the precipitating
cause (4) prevention of deterioration of
cardiac function and (5) control of the congestive HF state
Patient approach amp Mgt
Heart Failure Disease Management
Control Volume Slow Disease Progression
Diuretic RAAS Inhibition
Beta-Blockade
Treat residual symptoms
DIGOXIN
+
SPIRONOLACTONE
Am J Cardiol 199983(suppl 2A)9A-38A
Infection Arrhythmia PhysicalFluidDietaryEnvrsquotalEmotional excess MI Anemia Pulmonary embolism Worsening of HTN Thyrotoxicosis Infective endocarditis Rheumaticviral or other myocarditis
Precepitating factors
SYSTOLIC VERSUS DIASTOLIC FAILURE LOW-OUTPUT VERSUS HIGH-OUTPUT
HEART FAILURE ACUTE VERSUS CHRONIC HEART FAILURE RIGHT-SIDED VERSUS LEFT-SIDED HEART
FAILURE BACKWARD VERSUS FORWARD HEART
FAILURE
Forms of Heart Failure
1 Syndrome of decrease exercise tolerance 2 Syndrome of fluid retention 3 No symptoms but incidental discovery of
LV dysfunction
Typical presentations of heart failure
Major Criteria 1048698 OrthopneaPND 1048698 Venous distension 1048698 Rales 1048698 Cardiomegaly 1048698 Acute pulm edema 1048698 Elevated JVP 1048698 HJR 1048698 Circ time gt25s
1048698 Minor Criteria 1048698 Ankle edema 1048698 Night cough 1048698 Exertional dyspnea 1048698 Hepatomegaly 1048698 Pleural effusion 1048698 Tachycardia (gt120) 1048698 Decrease VC 1048698 Weight loss with CHF
tx Framingham Criteria
Heart Failure is a Clinical Diagnosis
Class I Symptoms with more than ordinary activity
Class II Symptoms with ordinary activity Class III Symptoms with minimal activity Class IIIa No dyspnea at rest Class IIIb Recent dyspnea at rest Class IV Symptoms at rest
NYHA Class1048698
Stages of Heart Failure
At Risk for Heart FailureSTAGE A High risk for developing
HF
STAGE B Asymptomatic LV dysfunction
Heart FailureSTAGE C Past or current
symptoms of HF
STAGE D End-stage HF
bull Designed to emphasize preventability of HF
bull Designed to recognize the progressive nature of LV dysfunction
Stages of Heart Failure
COMPLEMENT DO NOT REPLACE NYHA CLASSES
bull NYHA Classes - shift backforth in individual patient (in response to Rx andor progression of disease)
bull Stages - progress in one direction due to cardiac remodeling
Stages of Heart Failure
Occurs when the left ventricle fails as an effective forward pump
1048698back pressure of blood into the pulmonary circulation
1048698 pulmonary edema Cannot eject all of the
blood delivered from the right heart
Left atrial pressure rises 1048698 increased pressure in the pulmonary veins and capillaries
When pressure becomes too high the fluid portion of the blood is forced into the alveoli
1048698decreased oxygenation capacity of the lungs
AMI common with LVF suspect
Severe resp distressndash Evidenced by orthopnea
dyspnea Hx of paroxysmal
nocturnal dyspnea Severe apprehension
agitation confusionmdash Resulting from hypoxia Feels like heshe is
smothering Cyanosismdash
Diaphoresismdash Results from
sympathetic stimulation Pulmonary
congestion Often present Ralesmdashespecially at the
bases Rhonchimdashassociated
with fluid in the larger airways indicative of severe failure
Wheezesmdashresponse to airway spasm
Jugular Venous Distentionmdashnot directly related to LVF Comes from back pressure
building from right heart into venous circulation
Vital Signsmdash Significant increase in
sympathetic discharge to compensate
BPmdashelevated Pulse ratemdashelevated to
compensate for decreased stroke volume
Respirationsmdashrapid and labored
Neurohormonal system
Renin-angiotensin-aldosterone system
Ventricular hypertrophy
Neurohormonal Activation Contributes to the Progression of CHF
Myocardial Disease
LV Dysfunction
Impedance
Vasoconstriction
Neurohormonal Activation
LV RemodelingVascular Remodeling
PreloadRenal Blood Flow
Na Retention
Decreased renal blood flow secondary to low cardiac output triggers renin secretion by the kidneys
Aldosterone is released 1048698 increase in Na+ retention 1048698 water retention
Preload increases
Worsening failure
Long term compensatory mechanism
Increases in size due to increase in work load ie skeletal muscle
Principlesthorough Hx amp PE Supplemental investigations
especiallyBNPECGEchocardiographyCXR Management(1) general measures (2) correction of the underlying
cause (3) removal of the precipitating
cause (4) prevention of deterioration of
cardiac function and (5) control of the congestive HF state
Patient approach amp Mgt
Heart Failure Disease Management
Control Volume Slow Disease Progression
Diuretic RAAS Inhibition
Beta-Blockade
Treat residual symptoms
DIGOXIN
+
SPIRONOLACTONE
Am J Cardiol 199983(suppl 2A)9A-38A
SYSTOLIC VERSUS DIASTOLIC FAILURE LOW-OUTPUT VERSUS HIGH-OUTPUT
HEART FAILURE ACUTE VERSUS CHRONIC HEART FAILURE RIGHT-SIDED VERSUS LEFT-SIDED HEART
FAILURE BACKWARD VERSUS FORWARD HEART
FAILURE
Forms of Heart Failure
1 Syndrome of decrease exercise tolerance 2 Syndrome of fluid retention 3 No symptoms but incidental discovery of
LV dysfunction
Typical presentations of heart failure
Major Criteria 1048698 OrthopneaPND 1048698 Venous distension 1048698 Rales 1048698 Cardiomegaly 1048698 Acute pulm edema 1048698 Elevated JVP 1048698 HJR 1048698 Circ time gt25s
1048698 Minor Criteria 1048698 Ankle edema 1048698 Night cough 1048698 Exertional dyspnea 1048698 Hepatomegaly 1048698 Pleural effusion 1048698 Tachycardia (gt120) 1048698 Decrease VC 1048698 Weight loss with CHF
tx Framingham Criteria
Heart Failure is a Clinical Diagnosis
Class I Symptoms with more than ordinary activity
Class II Symptoms with ordinary activity Class III Symptoms with minimal activity Class IIIa No dyspnea at rest Class IIIb Recent dyspnea at rest Class IV Symptoms at rest
NYHA Class1048698
Stages of Heart Failure
At Risk for Heart FailureSTAGE A High risk for developing
HF
STAGE B Asymptomatic LV dysfunction
Heart FailureSTAGE C Past or current
symptoms of HF
STAGE D End-stage HF
bull Designed to emphasize preventability of HF
bull Designed to recognize the progressive nature of LV dysfunction
Stages of Heart Failure
COMPLEMENT DO NOT REPLACE NYHA CLASSES
bull NYHA Classes - shift backforth in individual patient (in response to Rx andor progression of disease)
bull Stages - progress in one direction due to cardiac remodeling
Stages of Heart Failure
Occurs when the left ventricle fails as an effective forward pump
1048698back pressure of blood into the pulmonary circulation
1048698 pulmonary edema Cannot eject all of the
blood delivered from the right heart
Left atrial pressure rises 1048698 increased pressure in the pulmonary veins and capillaries
When pressure becomes too high the fluid portion of the blood is forced into the alveoli
1048698decreased oxygenation capacity of the lungs
AMI common with LVF suspect
Severe resp distressndash Evidenced by orthopnea
dyspnea Hx of paroxysmal
nocturnal dyspnea Severe apprehension
agitation confusionmdash Resulting from hypoxia Feels like heshe is
smothering Cyanosismdash
Diaphoresismdash Results from
sympathetic stimulation Pulmonary
congestion Often present Ralesmdashespecially at the
bases Rhonchimdashassociated
with fluid in the larger airways indicative of severe failure
Wheezesmdashresponse to airway spasm
Jugular Venous Distentionmdashnot directly related to LVF Comes from back pressure
building from right heart into venous circulation
Vital Signsmdash Significant increase in
sympathetic discharge to compensate
BPmdashelevated Pulse ratemdashelevated to
compensate for decreased stroke volume
Respirationsmdashrapid and labored
Neurohormonal system
Renin-angiotensin-aldosterone system
Ventricular hypertrophy
Neurohormonal Activation Contributes to the Progression of CHF
Myocardial Disease
LV Dysfunction
Impedance
Vasoconstriction
Neurohormonal Activation
LV RemodelingVascular Remodeling
PreloadRenal Blood Flow
Na Retention
Decreased renal blood flow secondary to low cardiac output triggers renin secretion by the kidneys
Aldosterone is released 1048698 increase in Na+ retention 1048698 water retention
Preload increases
Worsening failure
Long term compensatory mechanism
Increases in size due to increase in work load ie skeletal muscle
Principlesthorough Hx amp PE Supplemental investigations
especiallyBNPECGEchocardiographyCXR Management(1) general measures (2) correction of the underlying
cause (3) removal of the precipitating
cause (4) prevention of deterioration of
cardiac function and (5) control of the congestive HF state
Patient approach amp Mgt
Heart Failure Disease Management
Control Volume Slow Disease Progression
Diuretic RAAS Inhibition
Beta-Blockade
Treat residual symptoms
DIGOXIN
+
SPIRONOLACTONE
Am J Cardiol 199983(suppl 2A)9A-38A
1 Syndrome of decrease exercise tolerance 2 Syndrome of fluid retention 3 No symptoms but incidental discovery of
LV dysfunction
Typical presentations of heart failure
Major Criteria 1048698 OrthopneaPND 1048698 Venous distension 1048698 Rales 1048698 Cardiomegaly 1048698 Acute pulm edema 1048698 Elevated JVP 1048698 HJR 1048698 Circ time gt25s
1048698 Minor Criteria 1048698 Ankle edema 1048698 Night cough 1048698 Exertional dyspnea 1048698 Hepatomegaly 1048698 Pleural effusion 1048698 Tachycardia (gt120) 1048698 Decrease VC 1048698 Weight loss with CHF
tx Framingham Criteria
Heart Failure is a Clinical Diagnosis
Class I Symptoms with more than ordinary activity
Class II Symptoms with ordinary activity Class III Symptoms with minimal activity Class IIIa No dyspnea at rest Class IIIb Recent dyspnea at rest Class IV Symptoms at rest
NYHA Class1048698
Stages of Heart Failure
At Risk for Heart FailureSTAGE A High risk for developing
HF
STAGE B Asymptomatic LV dysfunction
Heart FailureSTAGE C Past or current
symptoms of HF
STAGE D End-stage HF
bull Designed to emphasize preventability of HF
bull Designed to recognize the progressive nature of LV dysfunction
Stages of Heart Failure
COMPLEMENT DO NOT REPLACE NYHA CLASSES
bull NYHA Classes - shift backforth in individual patient (in response to Rx andor progression of disease)
bull Stages - progress in one direction due to cardiac remodeling
Stages of Heart Failure
Occurs when the left ventricle fails as an effective forward pump
1048698back pressure of blood into the pulmonary circulation
1048698 pulmonary edema Cannot eject all of the
blood delivered from the right heart
Left atrial pressure rises 1048698 increased pressure in the pulmonary veins and capillaries
When pressure becomes too high the fluid portion of the blood is forced into the alveoli
1048698decreased oxygenation capacity of the lungs
AMI common with LVF suspect
Severe resp distressndash Evidenced by orthopnea
dyspnea Hx of paroxysmal
nocturnal dyspnea Severe apprehension
agitation confusionmdash Resulting from hypoxia Feels like heshe is
smothering Cyanosismdash
Diaphoresismdash Results from
sympathetic stimulation Pulmonary
congestion Often present Ralesmdashespecially at the
bases Rhonchimdashassociated
with fluid in the larger airways indicative of severe failure
Wheezesmdashresponse to airway spasm
Jugular Venous Distentionmdashnot directly related to LVF Comes from back pressure
building from right heart into venous circulation
Vital Signsmdash Significant increase in
sympathetic discharge to compensate
BPmdashelevated Pulse ratemdashelevated to
compensate for decreased stroke volume
Respirationsmdashrapid and labored
Neurohormonal system
Renin-angiotensin-aldosterone system
Ventricular hypertrophy
Neurohormonal Activation Contributes to the Progression of CHF
Myocardial Disease
LV Dysfunction
Impedance
Vasoconstriction
Neurohormonal Activation
LV RemodelingVascular Remodeling
PreloadRenal Blood Flow
Na Retention
Decreased renal blood flow secondary to low cardiac output triggers renin secretion by the kidneys
Aldosterone is released 1048698 increase in Na+ retention 1048698 water retention
Preload increases
Worsening failure
Long term compensatory mechanism
Increases in size due to increase in work load ie skeletal muscle
Principlesthorough Hx amp PE Supplemental investigations
especiallyBNPECGEchocardiographyCXR Management(1) general measures (2) correction of the underlying
cause (3) removal of the precipitating
cause (4) prevention of deterioration of
cardiac function and (5) control of the congestive HF state
Patient approach amp Mgt
Heart Failure Disease Management
Control Volume Slow Disease Progression
Diuretic RAAS Inhibition
Beta-Blockade
Treat residual symptoms
DIGOXIN
+
SPIRONOLACTONE
Am J Cardiol 199983(suppl 2A)9A-38A
Major Criteria 1048698 OrthopneaPND 1048698 Venous distension 1048698 Rales 1048698 Cardiomegaly 1048698 Acute pulm edema 1048698 Elevated JVP 1048698 HJR 1048698 Circ time gt25s
1048698 Minor Criteria 1048698 Ankle edema 1048698 Night cough 1048698 Exertional dyspnea 1048698 Hepatomegaly 1048698 Pleural effusion 1048698 Tachycardia (gt120) 1048698 Decrease VC 1048698 Weight loss with CHF
tx Framingham Criteria
Heart Failure is a Clinical Diagnosis
Class I Symptoms with more than ordinary activity
Class II Symptoms with ordinary activity Class III Symptoms with minimal activity Class IIIa No dyspnea at rest Class IIIb Recent dyspnea at rest Class IV Symptoms at rest
NYHA Class1048698
Stages of Heart Failure
At Risk for Heart FailureSTAGE A High risk for developing
HF
STAGE B Asymptomatic LV dysfunction
Heart FailureSTAGE C Past or current
symptoms of HF
STAGE D End-stage HF
bull Designed to emphasize preventability of HF
bull Designed to recognize the progressive nature of LV dysfunction
Stages of Heart Failure
COMPLEMENT DO NOT REPLACE NYHA CLASSES
bull NYHA Classes - shift backforth in individual patient (in response to Rx andor progression of disease)
bull Stages - progress in one direction due to cardiac remodeling
Stages of Heart Failure
Occurs when the left ventricle fails as an effective forward pump
1048698back pressure of blood into the pulmonary circulation
1048698 pulmonary edema Cannot eject all of the
blood delivered from the right heart
Left atrial pressure rises 1048698 increased pressure in the pulmonary veins and capillaries
When pressure becomes too high the fluid portion of the blood is forced into the alveoli
1048698decreased oxygenation capacity of the lungs
AMI common with LVF suspect
Severe resp distressndash Evidenced by orthopnea
dyspnea Hx of paroxysmal
nocturnal dyspnea Severe apprehension
agitation confusionmdash Resulting from hypoxia Feels like heshe is
smothering Cyanosismdash
Diaphoresismdash Results from
sympathetic stimulation Pulmonary
congestion Often present Ralesmdashespecially at the
bases Rhonchimdashassociated
with fluid in the larger airways indicative of severe failure
Wheezesmdashresponse to airway spasm
Jugular Venous Distentionmdashnot directly related to LVF Comes from back pressure
building from right heart into venous circulation
Vital Signsmdash Significant increase in
sympathetic discharge to compensate
BPmdashelevated Pulse ratemdashelevated to
compensate for decreased stroke volume
Respirationsmdashrapid and labored
Neurohormonal system
Renin-angiotensin-aldosterone system
Ventricular hypertrophy
Neurohormonal Activation Contributes to the Progression of CHF
Myocardial Disease
LV Dysfunction
Impedance
Vasoconstriction
Neurohormonal Activation
LV RemodelingVascular Remodeling
PreloadRenal Blood Flow
Na Retention
Decreased renal blood flow secondary to low cardiac output triggers renin secretion by the kidneys
Aldosterone is released 1048698 increase in Na+ retention 1048698 water retention
Preload increases
Worsening failure
Long term compensatory mechanism
Increases in size due to increase in work load ie skeletal muscle
Principlesthorough Hx amp PE Supplemental investigations
especiallyBNPECGEchocardiographyCXR Management(1) general measures (2) correction of the underlying
cause (3) removal of the precipitating
cause (4) prevention of deterioration of
cardiac function and (5) control of the congestive HF state
Patient approach amp Mgt
Heart Failure Disease Management
Control Volume Slow Disease Progression
Diuretic RAAS Inhibition
Beta-Blockade
Treat residual symptoms
DIGOXIN
+
SPIRONOLACTONE
Am J Cardiol 199983(suppl 2A)9A-38A
Class I Symptoms with more than ordinary activity
Class II Symptoms with ordinary activity Class III Symptoms with minimal activity Class IIIa No dyspnea at rest Class IIIb Recent dyspnea at rest Class IV Symptoms at rest
NYHA Class1048698
Stages of Heart Failure
At Risk for Heart FailureSTAGE A High risk for developing
HF
STAGE B Asymptomatic LV dysfunction
Heart FailureSTAGE C Past or current
symptoms of HF
STAGE D End-stage HF
bull Designed to emphasize preventability of HF
bull Designed to recognize the progressive nature of LV dysfunction
Stages of Heart Failure
COMPLEMENT DO NOT REPLACE NYHA CLASSES
bull NYHA Classes - shift backforth in individual patient (in response to Rx andor progression of disease)
bull Stages - progress in one direction due to cardiac remodeling
Stages of Heart Failure
Occurs when the left ventricle fails as an effective forward pump
1048698back pressure of blood into the pulmonary circulation
1048698 pulmonary edema Cannot eject all of the
blood delivered from the right heart
Left atrial pressure rises 1048698 increased pressure in the pulmonary veins and capillaries
When pressure becomes too high the fluid portion of the blood is forced into the alveoli
1048698decreased oxygenation capacity of the lungs
AMI common with LVF suspect
Severe resp distressndash Evidenced by orthopnea
dyspnea Hx of paroxysmal
nocturnal dyspnea Severe apprehension
agitation confusionmdash Resulting from hypoxia Feels like heshe is
smothering Cyanosismdash
Diaphoresismdash Results from
sympathetic stimulation Pulmonary
congestion Often present Ralesmdashespecially at the
bases Rhonchimdashassociated
with fluid in the larger airways indicative of severe failure
Wheezesmdashresponse to airway spasm
Jugular Venous Distentionmdashnot directly related to LVF Comes from back pressure
building from right heart into venous circulation
Vital Signsmdash Significant increase in
sympathetic discharge to compensate
BPmdashelevated Pulse ratemdashelevated to
compensate for decreased stroke volume
Respirationsmdashrapid and labored
Neurohormonal system
Renin-angiotensin-aldosterone system
Ventricular hypertrophy
Neurohormonal Activation Contributes to the Progression of CHF
Myocardial Disease
LV Dysfunction
Impedance
Vasoconstriction
Neurohormonal Activation
LV RemodelingVascular Remodeling
PreloadRenal Blood Flow
Na Retention
Decreased renal blood flow secondary to low cardiac output triggers renin secretion by the kidneys
Aldosterone is released 1048698 increase in Na+ retention 1048698 water retention
Preload increases
Worsening failure
Long term compensatory mechanism
Increases in size due to increase in work load ie skeletal muscle
Principlesthorough Hx amp PE Supplemental investigations
especiallyBNPECGEchocardiographyCXR Management(1) general measures (2) correction of the underlying
cause (3) removal of the precipitating
cause (4) prevention of deterioration of
cardiac function and (5) control of the congestive HF state
Patient approach amp Mgt
Heart Failure Disease Management
Control Volume Slow Disease Progression
Diuretic RAAS Inhibition
Beta-Blockade
Treat residual symptoms
DIGOXIN
+
SPIRONOLACTONE
Am J Cardiol 199983(suppl 2A)9A-38A
Stages of Heart Failure
At Risk for Heart FailureSTAGE A High risk for developing
HF
STAGE B Asymptomatic LV dysfunction
Heart FailureSTAGE C Past or current
symptoms of HF
STAGE D End-stage HF
bull Designed to emphasize preventability of HF
bull Designed to recognize the progressive nature of LV dysfunction
Stages of Heart Failure
COMPLEMENT DO NOT REPLACE NYHA CLASSES
bull NYHA Classes - shift backforth in individual patient (in response to Rx andor progression of disease)
bull Stages - progress in one direction due to cardiac remodeling
Stages of Heart Failure
Occurs when the left ventricle fails as an effective forward pump
1048698back pressure of blood into the pulmonary circulation
1048698 pulmonary edema Cannot eject all of the
blood delivered from the right heart
Left atrial pressure rises 1048698 increased pressure in the pulmonary veins and capillaries
When pressure becomes too high the fluid portion of the blood is forced into the alveoli
1048698decreased oxygenation capacity of the lungs
AMI common with LVF suspect
Severe resp distressndash Evidenced by orthopnea
dyspnea Hx of paroxysmal
nocturnal dyspnea Severe apprehension
agitation confusionmdash Resulting from hypoxia Feels like heshe is
smothering Cyanosismdash
Diaphoresismdash Results from
sympathetic stimulation Pulmonary
congestion Often present Ralesmdashespecially at the
bases Rhonchimdashassociated
with fluid in the larger airways indicative of severe failure
Wheezesmdashresponse to airway spasm
Jugular Venous Distentionmdashnot directly related to LVF Comes from back pressure
building from right heart into venous circulation
Vital Signsmdash Significant increase in
sympathetic discharge to compensate
BPmdashelevated Pulse ratemdashelevated to
compensate for decreased stroke volume
Respirationsmdashrapid and labored
Neurohormonal system
Renin-angiotensin-aldosterone system
Ventricular hypertrophy
Neurohormonal Activation Contributes to the Progression of CHF
Myocardial Disease
LV Dysfunction
Impedance
Vasoconstriction
Neurohormonal Activation
LV RemodelingVascular Remodeling
PreloadRenal Blood Flow
Na Retention
Decreased renal blood flow secondary to low cardiac output triggers renin secretion by the kidneys
Aldosterone is released 1048698 increase in Na+ retention 1048698 water retention
Preload increases
Worsening failure
Long term compensatory mechanism
Increases in size due to increase in work load ie skeletal muscle
Principlesthorough Hx amp PE Supplemental investigations
especiallyBNPECGEchocardiographyCXR Management(1) general measures (2) correction of the underlying
cause (3) removal of the precipitating
cause (4) prevention of deterioration of
cardiac function and (5) control of the congestive HF state
Patient approach amp Mgt
Heart Failure Disease Management
Control Volume Slow Disease Progression
Diuretic RAAS Inhibition
Beta-Blockade
Treat residual symptoms
DIGOXIN
+
SPIRONOLACTONE
Am J Cardiol 199983(suppl 2A)9A-38A
bull Designed to emphasize preventability of HF
bull Designed to recognize the progressive nature of LV dysfunction
Stages of Heart Failure
COMPLEMENT DO NOT REPLACE NYHA CLASSES
bull NYHA Classes - shift backforth in individual patient (in response to Rx andor progression of disease)
bull Stages - progress in one direction due to cardiac remodeling
Stages of Heart Failure
Occurs when the left ventricle fails as an effective forward pump
1048698back pressure of blood into the pulmonary circulation
1048698 pulmonary edema Cannot eject all of the
blood delivered from the right heart
Left atrial pressure rises 1048698 increased pressure in the pulmonary veins and capillaries
When pressure becomes too high the fluid portion of the blood is forced into the alveoli
1048698decreased oxygenation capacity of the lungs
AMI common with LVF suspect
Severe resp distressndash Evidenced by orthopnea
dyspnea Hx of paroxysmal
nocturnal dyspnea Severe apprehension
agitation confusionmdash Resulting from hypoxia Feels like heshe is
smothering Cyanosismdash
Diaphoresismdash Results from
sympathetic stimulation Pulmonary
congestion Often present Ralesmdashespecially at the
bases Rhonchimdashassociated
with fluid in the larger airways indicative of severe failure
Wheezesmdashresponse to airway spasm
Jugular Venous Distentionmdashnot directly related to LVF Comes from back pressure
building from right heart into venous circulation
Vital Signsmdash Significant increase in
sympathetic discharge to compensate
BPmdashelevated Pulse ratemdashelevated to
compensate for decreased stroke volume
Respirationsmdashrapid and labored
Neurohormonal system
Renin-angiotensin-aldosterone system
Ventricular hypertrophy
Neurohormonal Activation Contributes to the Progression of CHF
Myocardial Disease
LV Dysfunction
Impedance
Vasoconstriction
Neurohormonal Activation
LV RemodelingVascular Remodeling
PreloadRenal Blood Flow
Na Retention
Decreased renal blood flow secondary to low cardiac output triggers renin secretion by the kidneys
Aldosterone is released 1048698 increase in Na+ retention 1048698 water retention
Preload increases
Worsening failure
Long term compensatory mechanism
Increases in size due to increase in work load ie skeletal muscle
Principlesthorough Hx amp PE Supplemental investigations
especiallyBNPECGEchocardiographyCXR Management(1) general measures (2) correction of the underlying
cause (3) removal of the precipitating
cause (4) prevention of deterioration of
cardiac function and (5) control of the congestive HF state
Patient approach amp Mgt
Heart Failure Disease Management
Control Volume Slow Disease Progression
Diuretic RAAS Inhibition
Beta-Blockade
Treat residual symptoms
DIGOXIN
+
SPIRONOLACTONE
Am J Cardiol 199983(suppl 2A)9A-38A
COMPLEMENT DO NOT REPLACE NYHA CLASSES
bull NYHA Classes - shift backforth in individual patient (in response to Rx andor progression of disease)
bull Stages - progress in one direction due to cardiac remodeling
Stages of Heart Failure
Occurs when the left ventricle fails as an effective forward pump
1048698back pressure of blood into the pulmonary circulation
1048698 pulmonary edema Cannot eject all of the
blood delivered from the right heart
Left atrial pressure rises 1048698 increased pressure in the pulmonary veins and capillaries
When pressure becomes too high the fluid portion of the blood is forced into the alveoli
1048698decreased oxygenation capacity of the lungs
AMI common with LVF suspect
Severe resp distressndash Evidenced by orthopnea
dyspnea Hx of paroxysmal
nocturnal dyspnea Severe apprehension
agitation confusionmdash Resulting from hypoxia Feels like heshe is
smothering Cyanosismdash
Diaphoresismdash Results from
sympathetic stimulation Pulmonary
congestion Often present Ralesmdashespecially at the
bases Rhonchimdashassociated
with fluid in the larger airways indicative of severe failure
Wheezesmdashresponse to airway spasm
Jugular Venous Distentionmdashnot directly related to LVF Comes from back pressure
building from right heart into venous circulation
Vital Signsmdash Significant increase in
sympathetic discharge to compensate
BPmdashelevated Pulse ratemdashelevated to
compensate for decreased stroke volume
Respirationsmdashrapid and labored
Neurohormonal system
Renin-angiotensin-aldosterone system
Ventricular hypertrophy
Neurohormonal Activation Contributes to the Progression of CHF
Myocardial Disease
LV Dysfunction
Impedance
Vasoconstriction
Neurohormonal Activation
LV RemodelingVascular Remodeling
PreloadRenal Blood Flow
Na Retention
Decreased renal blood flow secondary to low cardiac output triggers renin secretion by the kidneys
Aldosterone is released 1048698 increase in Na+ retention 1048698 water retention
Preload increases
Worsening failure
Long term compensatory mechanism
Increases in size due to increase in work load ie skeletal muscle
Principlesthorough Hx amp PE Supplemental investigations
especiallyBNPECGEchocardiographyCXR Management(1) general measures (2) correction of the underlying
cause (3) removal of the precipitating
cause (4) prevention of deterioration of
cardiac function and (5) control of the congestive HF state
Patient approach amp Mgt
Heart Failure Disease Management
Control Volume Slow Disease Progression
Diuretic RAAS Inhibition
Beta-Blockade
Treat residual symptoms
DIGOXIN
+
SPIRONOLACTONE
Am J Cardiol 199983(suppl 2A)9A-38A
Occurs when the left ventricle fails as an effective forward pump
1048698back pressure of blood into the pulmonary circulation
1048698 pulmonary edema Cannot eject all of the
blood delivered from the right heart
Left atrial pressure rises 1048698 increased pressure in the pulmonary veins and capillaries
When pressure becomes too high the fluid portion of the blood is forced into the alveoli
1048698decreased oxygenation capacity of the lungs
AMI common with LVF suspect
Severe resp distressndash Evidenced by orthopnea
dyspnea Hx of paroxysmal
nocturnal dyspnea Severe apprehension
agitation confusionmdash Resulting from hypoxia Feels like heshe is
smothering Cyanosismdash
Diaphoresismdash Results from
sympathetic stimulation Pulmonary
congestion Often present Ralesmdashespecially at the
bases Rhonchimdashassociated
with fluid in the larger airways indicative of severe failure
Wheezesmdashresponse to airway spasm
Jugular Venous Distentionmdashnot directly related to LVF Comes from back pressure
building from right heart into venous circulation
Vital Signsmdash Significant increase in
sympathetic discharge to compensate
BPmdashelevated Pulse ratemdashelevated to
compensate for decreased stroke volume
Respirationsmdashrapid and labored
Neurohormonal system
Renin-angiotensin-aldosterone system
Ventricular hypertrophy
Neurohormonal Activation Contributes to the Progression of CHF
Myocardial Disease
LV Dysfunction
Impedance
Vasoconstriction
Neurohormonal Activation
LV RemodelingVascular Remodeling
PreloadRenal Blood Flow
Na Retention
Decreased renal blood flow secondary to low cardiac output triggers renin secretion by the kidneys
Aldosterone is released 1048698 increase in Na+ retention 1048698 water retention
Preload increases
Worsening failure
Long term compensatory mechanism
Increases in size due to increase in work load ie skeletal muscle
Principlesthorough Hx amp PE Supplemental investigations
especiallyBNPECGEchocardiographyCXR Management(1) general measures (2) correction of the underlying
cause (3) removal of the precipitating
cause (4) prevention of deterioration of
cardiac function and (5) control of the congestive HF state
Patient approach amp Mgt
Heart Failure Disease Management
Control Volume Slow Disease Progression
Diuretic RAAS Inhibition
Beta-Blockade
Treat residual symptoms
DIGOXIN
+
SPIRONOLACTONE
Am J Cardiol 199983(suppl 2A)9A-38A
Severe resp distressndash Evidenced by orthopnea
dyspnea Hx of paroxysmal
nocturnal dyspnea Severe apprehension
agitation confusionmdash Resulting from hypoxia Feels like heshe is
smothering Cyanosismdash
Diaphoresismdash Results from
sympathetic stimulation Pulmonary
congestion Often present Ralesmdashespecially at the
bases Rhonchimdashassociated
with fluid in the larger airways indicative of severe failure
Wheezesmdashresponse to airway spasm
Jugular Venous Distentionmdashnot directly related to LVF Comes from back pressure
building from right heart into venous circulation
Vital Signsmdash Significant increase in
sympathetic discharge to compensate
BPmdashelevated Pulse ratemdashelevated to
compensate for decreased stroke volume
Respirationsmdashrapid and labored
Neurohormonal system
Renin-angiotensin-aldosterone system
Ventricular hypertrophy
Neurohormonal Activation Contributes to the Progression of CHF
Myocardial Disease
LV Dysfunction
Impedance
Vasoconstriction
Neurohormonal Activation
LV RemodelingVascular Remodeling
PreloadRenal Blood Flow
Na Retention
Decreased renal blood flow secondary to low cardiac output triggers renin secretion by the kidneys
Aldosterone is released 1048698 increase in Na+ retention 1048698 water retention
Preload increases
Worsening failure
Long term compensatory mechanism
Increases in size due to increase in work load ie skeletal muscle
Principlesthorough Hx amp PE Supplemental investigations
especiallyBNPECGEchocardiographyCXR Management(1) general measures (2) correction of the underlying
cause (3) removal of the precipitating
cause (4) prevention of deterioration of
cardiac function and (5) control of the congestive HF state
Patient approach amp Mgt
Heart Failure Disease Management
Control Volume Slow Disease Progression
Diuretic RAAS Inhibition
Beta-Blockade
Treat residual symptoms
DIGOXIN
+
SPIRONOLACTONE
Am J Cardiol 199983(suppl 2A)9A-38A
Jugular Venous Distentionmdashnot directly related to LVF Comes from back pressure
building from right heart into venous circulation
Vital Signsmdash Significant increase in
sympathetic discharge to compensate
BPmdashelevated Pulse ratemdashelevated to
compensate for decreased stroke volume
Respirationsmdashrapid and labored
Neurohormonal system
Renin-angiotensin-aldosterone system
Ventricular hypertrophy
Neurohormonal Activation Contributes to the Progression of CHF
Myocardial Disease
LV Dysfunction
Impedance
Vasoconstriction
Neurohormonal Activation
LV RemodelingVascular Remodeling
PreloadRenal Blood Flow
Na Retention
Decreased renal blood flow secondary to low cardiac output triggers renin secretion by the kidneys
Aldosterone is released 1048698 increase in Na+ retention 1048698 water retention
Preload increases
Worsening failure
Long term compensatory mechanism
Increases in size due to increase in work load ie skeletal muscle
Principlesthorough Hx amp PE Supplemental investigations
especiallyBNPECGEchocardiographyCXR Management(1) general measures (2) correction of the underlying
cause (3) removal of the precipitating
cause (4) prevention of deterioration of
cardiac function and (5) control of the congestive HF state
Patient approach amp Mgt
Heart Failure Disease Management
Control Volume Slow Disease Progression
Diuretic RAAS Inhibition
Beta-Blockade
Treat residual symptoms
DIGOXIN
+
SPIRONOLACTONE
Am J Cardiol 199983(suppl 2A)9A-38A
Neurohormonal system
Renin-angiotensin-aldosterone system
Ventricular hypertrophy
Neurohormonal Activation Contributes to the Progression of CHF
Myocardial Disease
LV Dysfunction
Impedance
Vasoconstriction
Neurohormonal Activation
LV RemodelingVascular Remodeling
PreloadRenal Blood Flow
Na Retention
Decreased renal blood flow secondary to low cardiac output triggers renin secretion by the kidneys
Aldosterone is released 1048698 increase in Na+ retention 1048698 water retention
Preload increases
Worsening failure
Long term compensatory mechanism
Increases in size due to increase in work load ie skeletal muscle
Principlesthorough Hx amp PE Supplemental investigations
especiallyBNPECGEchocardiographyCXR Management(1) general measures (2) correction of the underlying
cause (3) removal of the precipitating
cause (4) prevention of deterioration of
cardiac function and (5) control of the congestive HF state
Patient approach amp Mgt
Heart Failure Disease Management
Control Volume Slow Disease Progression
Diuretic RAAS Inhibition
Beta-Blockade
Treat residual symptoms
DIGOXIN
+
SPIRONOLACTONE
Am J Cardiol 199983(suppl 2A)9A-38A
Neurohormonal Activation Contributes to the Progression of CHF
Myocardial Disease
LV Dysfunction
Impedance
Vasoconstriction
Neurohormonal Activation
LV RemodelingVascular Remodeling
PreloadRenal Blood Flow
Na Retention
Decreased renal blood flow secondary to low cardiac output triggers renin secretion by the kidneys
Aldosterone is released 1048698 increase in Na+ retention 1048698 water retention
Preload increases
Worsening failure
Long term compensatory mechanism
Increases in size due to increase in work load ie skeletal muscle
Principlesthorough Hx amp PE Supplemental investigations
especiallyBNPECGEchocardiographyCXR Management(1) general measures (2) correction of the underlying
cause (3) removal of the precipitating
cause (4) prevention of deterioration of
cardiac function and (5) control of the congestive HF state
Patient approach amp Mgt
Heart Failure Disease Management
Control Volume Slow Disease Progression
Diuretic RAAS Inhibition
Beta-Blockade
Treat residual symptoms
DIGOXIN
+
SPIRONOLACTONE
Am J Cardiol 199983(suppl 2A)9A-38A
Decreased renal blood flow secondary to low cardiac output triggers renin secretion by the kidneys
Aldosterone is released 1048698 increase in Na+ retention 1048698 water retention
Preload increases
Worsening failure
Long term compensatory mechanism
Increases in size due to increase in work load ie skeletal muscle
Principlesthorough Hx amp PE Supplemental investigations
especiallyBNPECGEchocardiographyCXR Management(1) general measures (2) correction of the underlying
cause (3) removal of the precipitating
cause (4) prevention of deterioration of
cardiac function and (5) control of the congestive HF state
Patient approach amp Mgt
Heart Failure Disease Management
Control Volume Slow Disease Progression
Diuretic RAAS Inhibition
Beta-Blockade
Treat residual symptoms
DIGOXIN
+
SPIRONOLACTONE
Am J Cardiol 199983(suppl 2A)9A-38A
Long term compensatory mechanism
Increases in size due to increase in work load ie skeletal muscle
Principlesthorough Hx amp PE Supplemental investigations
especiallyBNPECGEchocardiographyCXR Management(1) general measures (2) correction of the underlying
cause (3) removal of the precipitating
cause (4) prevention of deterioration of
cardiac function and (5) control of the congestive HF state
Patient approach amp Mgt
Heart Failure Disease Management
Control Volume Slow Disease Progression
Diuretic RAAS Inhibition
Beta-Blockade
Treat residual symptoms
DIGOXIN
+
SPIRONOLACTONE
Am J Cardiol 199983(suppl 2A)9A-38A
Principlesthorough Hx amp PE Supplemental investigations
especiallyBNPECGEchocardiographyCXR Management(1) general measures (2) correction of the underlying
cause (3) removal of the precipitating
cause (4) prevention of deterioration of
cardiac function and (5) control of the congestive HF state
Patient approach amp Mgt
Heart Failure Disease Management
Control Volume Slow Disease Progression
Diuretic RAAS Inhibition
Beta-Blockade
Treat residual symptoms
DIGOXIN
+
SPIRONOLACTONE
Am J Cardiol 199983(suppl 2A)9A-38A
Heart Failure Disease Management
Control Volume Slow Disease Progression
Diuretic RAAS Inhibition
Beta-Blockade
Treat residual symptoms
DIGOXIN
+
SPIRONOLACTONE
Am J Cardiol 199983(suppl 2A)9A-38A
