Heart Failure

Inability of the heart to pump an adequate amount of blood to meet the body’s metabolic needs (decreased CO) → body compensates → leads to volume overload (congestion) and fatigue

HF

3 primary cardiac problems of HF

• Muscular contraction problem

• Muscular relaxation problem

• Combination of contraction & relaxation

Muscular contraction problem =

Decreased ejection of blood

Muscular relaxation problem =

Preventing adequate filling with blood

Causes of HF

• Heart muscle disorders

• Pericardium disorders

• Problems with blood supply to the heart (perfusion)

• Heart valve disorders

• Abnormalities of blood vessels leading out of the heart

How does the body compensate for HF?

RAAS + SNS

BP =

CO * R (PVR)

CO =

SV * HR

What does RAAS regulate?

SV and R (PVR); pathway releases angiotensin II

Causes direct vasoconstriction and stimulate adrenal gland to release aldosterone (increase Na & H2O reabsorption in kidney)

Angiotensin II

What does SNS regulate?

R (PVR) through vasoconstriction; also increases contractility and HR

In HF, maintenance of

Maintenance of CO is necessary to preserve pressure gradient in CV system

Symptoms of HF

• Fatigue

• SOB

• Inability to exercise

• Swelling of extremities

Compensatory mechanisms for cardiac injury or impaired CO

• SNS to maintain CO

• RAAS to maintain CO

• Inflammatory mediators to repair and remodel heart muscle

• Compensation can be maladaptive over time

How does HF develop?

Initial cardiac injury damages the heart and impairs the contractility and pumping ability of the heart; leads to compensatory mechanism that activate due to reduced pumping capacity to maintain near-normal left ventricle function

Secondary damage from HF

• End-organ damage within ventricle (heart, brain, kidney, lungs, eyes)

• Left ventricular remodeling

• Cardiac compensation

Compensation leads to

Volume overload and fatigue in response to compensatory mechanisms triggered by decreased CO

• compensatory mechanisms cause fluid retention, vasoconstriction, and myocardial stimulation

New York Heart Association Staging for HF

The higher the class, the more severe the heart disease

Class I

Heart disease does not affect daily activities

Class II

Heart disease causes slight activity limitations but does not cause problems at rest

Class III

Heart disease causes marked activity limitations but does not cause problems at rest

Class IV

Heart disease causes symptoms with any level of activity and sometimes at rest

Staging and managing chronic HF

Describes physical condition at and treatment modalities for each stage

• Stage A, Stage B, Stage C

High risk for HF, no structural heart disease or symptoms

• Recommend lifestyle modifications

• Treatment of underlying disorder

What stage classification of chronic heart failure does this describe?

Stage A

Structural heart disease, no S&S of HF

• Treated by ACEIs, ARBs, BP control meds, and BBs

What stage classification of chronic heart failure does this describe?

Stage B

Structural heart disease with symptoms of HF

• Treated with diuretics and aldosterone blockers

What stage classification of chronic heart failure does this describe?

Stage C

How is Stage B chronic heart failure managed/treated?

Treated with ACEIs, ARBs, BP control meds/lifestyle modifications, and betablockers

How is Stage A chronic heart failure managed/treated?

Lifestyle modifications and treating the underlying disorder

How is Stage C chronic heart failure managed/treated?

Treated with diuretics and aldosterone blockers

Causes of left-sided HF

• Cardiomyopathy

• CAD

• Alcohol abuse

• Cocaine abuse

• HTN

Condition leads to volume overload and venous congestion of the lungs; sodium and water retention increases circulation blood volume → pulmonary venous congestion occurs and fatigue and SOB are the result

Left-sided HF

• Leads to volume overload and venous congestion in the lungs

• Sodium and water retention increase circulating blood volume

• Pulmonary venous congestion occurs

• Fatigue and shortness of breath are the result

Left-sided HF

Due to RAAS and SNS activity:

• Preload increases

  • Pulmonary venous pressure increases

  • SOB while sleeping (paroxysmal nocturnal dyspnea)

  • Cough, orthopnea, and rales (fine crackles) develop

• Extra heart sounds such as gallops and murmurs may occur

• Pulmonary edema → frothy blood-tinged sputum coughed up

• Decreased tissue perfusion and hypotension

• Afterload increases due to increased plasma volume and vasoconstriction (heart must work harder to pump blood)

What does this indicate?

Clinical manifestations of left-sided HF

Clinical manifestations of HF include PEPDA

• Preload increases

• Extra heart sounds such as gallops and murmurs may occur

• Pulmonary edema → frothy blood-tinged sputum

• Decreased tissue perfusion and hypotension

• Afterload increases

SOB while sleeping; can be caused by left-sided HF

Paroxysmal nocturnal dyspnea

PEPDA (manifestations of left-sided HF)

• Preload increases

• Extra heart sounds (murmurs & gallops)

• Pulmonary edema → frothy blood-tinged sputum

• Decreased tissue perfusion and hypotension occur

• Afterload increases due to increased plasma volume and vasoconstriction

Increased preload in left-sided HF causes

• Pulmonary venous pressure increases

• SOB while sleeping (paroxysmal nocturnal dyspnea)

• Cough, orthopnea, and rales (fine crackles) develop

Why does afterload increase in left-sided HF?

Increases due to increased plasma volume and vasoconstriction

Symptoms of left-sided HF 

• Paroxysmal nocturnal dyspnea

• Elevated pulmonary capillary wedge pressure

• Pulmonary congestion

  • cough

  • crackles

  • wheezes

  • blood-tinged sputum

  • tachypnea

• Restlessness

• Confusion

• Orthopnea

• Tachycardia

• Exertional dyspnea

• Fatigue

• Cyanosis

Right ventricle is more vulnerable to volume overload than left ventricle. True or false?

True

Compare and contrast RV and LV

• 1/3 of contraction strength of RV is dependent on LV

• RV has lower pressure system than LV

• RV has thinner walls than left

If LV contraction is weak, RV contraction weakens too. True or false?

True

As left ventricle fails, pulmonary venous congestion increases RV work

• RV must generate more force to overcome pressure from increased venous congestion

• Systemic venous congestion occurs as venous congestion progresses backward into circulatory system

Right-sided HF due to impaired LV

Right-sided HF results in

Elevated jugular pressure, which causes liver congestion and peripheral edema

Right-sided HF due to RV failure that is isolated (not precipitated by LV failure)

• Leads to incomplete filling of LV → decreased CO; contributes to HF

• Cool extremities

• Poor distal pulse

• Exercise intolerance

• Syncope (fainting)

• Hepatomegaly (liver enlargement)

• Mesentery edema causes abd pain & loss of appetite

• Neck veins distend and jugular venous pressure increases

• Ascites and peripheral edema in the legs and back occur

This indicates what condition?

Clinical manifestations of right-sided HF

Clinical manifestations of right-sided HF

• Cool extremities

• Poor distal pulse

• Exercise intolerance

• Syncope (fainting)

• Hepatomegaly (liver enlargement)

• Mesentery edema causes abd pain & loss of appetite

• Neck veins distend and jugular venous pressure increases

• Ascites and peripheral edema in the legs and back occur

Symptoms of right-sided HF induced hepatomegaly

• NV → enlarged liver puts pressure on stomach

• RUQ becomes harder

• Liver enzymes elevate

• Liver function becomes impaired

Fluid accumulation in the abdominal cavity

Ascites

Other S&S of right-sided HF

• Fatigue

• Decreased urine output (oliguria)

• Exercise intolerance

• Increased periphery venous pressure

• Dizziness

• Syncope

• Difficulty falling or staying asleep

• Decreased distal pulses

• Cool or tepid skin

• Low BP (hypotension)

• Tachycardia

• Weight gain (sudden); weight loss (chronic)

• Enlarged liver and spleen

• Anorexia and GI distress (caused by pressure on abd from ascites)

• May be secondary to chronic pulmonary problems

Condition where ineffective contractions lead to decreased CO and decreases SV and EF; percentage of blood leaving LV is reduced

Systolic HF

AKA HF with reduced EF (HFrEF)

Systolic HF

Amount of blood pumped out of the heart with each beat (in ml)

Stroke volume (SV)

The percentage of blood ejected from the left ventricle with each contraction

Ejection fraction (EF)

AKA HF with preserved EF (HFpEF) 

Diastolic HF

In this condition, muscle contractility is preserved or only slightlyimpaired

Diastolic HF

Volume of blood in the ventricle at the end of diastole

Preload

Pressure in the aorta which the ventricle must overcome to eject into the aorta

Afterload

• HFpEF (muscle contractility preserved or only slightly impaired)

• Muscle remodeling and stiffness

  • Impaired ventricular filling

  • Decreased amount of blood in ventricle at end of diastole (preload)

  • Decreased SV and CO

• Problem is exacerbated when HR increases

  • Ventricular diastolic filling time shortens

  • SV decreases even more

HFpEF/Diastolic HF

Muscle remodeling & stiffness caused by HFpEF results in

• Impaired ventricular filling

• Decreased amount of blood in ventricle at end of diastole (preload)

• Decreased SV and CO

High output HF is more common than low output HF. True or false?

Fals

In this condition, heart pumps a large volume of blood, resulting in 

• Elevated CO

• Vasodilation of systemic blood vessels

• BP is decreased

• SNS and RAAS activation occurs

High-output HF

Heart cannot pump a sufficient amount of blood, resulting in

• CO reduction

• Tissue perfusion is decreased

• Cells do not receive sufficient oxygen and nutrients

• SNS and RAAS are activated

Low-output HF

Metabolic demands are normal but heart is unable to meet the need

Low-output HF

Metabolic demands are increased and the heart is unable to meet the need

High-output HF

These conditions create/cause low-output failure

Congenital, valvular, rheumatic, hypertensive, coronary and cardiomyopathic HF

These conditions create/cause high-output failure

Thyrotoxicosis, arteriovenous fistula, anemia, beriberi disease, Paget’s disease of the bone

HF is typically chronic. True or false?

True

Management of chronic HF

• Patients must manage aspects of their care

• Medication

• Low-sodium diet

• Symptom monitoring

• Weight and vital sign monitoring

• Health status decision making

Individuals with chronic HF may develop acute HF. True or false?

True

ADHF

Acute decompensated heart failure

Chronic HF that develops into acute HF; manifests as worsening HF symptoms that require hospitalization 

Chronic HF that develops into acute HF; manifests as worsening HF symtpoms that require hospitalization 

As chronic HF progresses,

ADHF becomes more frequent and precipitating events more subtle

Manifestations of this condition range from volume overload to cardiogenic shock

ADHF

This condition requires hospitalization and treatment of the cause of exacerbation

ADHF

This condition can be isolated (not precipitated by chronic HF)

Acute HF

Patients have typically developed a rapidly progressing critical illness, usually caused by

• MI

• Sudden cardiac death

• Myocarditis

• Drug toxicity

Acute HF

Treatment of acute HF focuses on

Resolving underlying cause of HF and providing supportive therapy until HF can be reversed

Some patients develop chronic HF after recovering from acute event. True or false?

True

Some patients recover from this condition, but must take inotropic medication or receive mechanical support

Acute HF

Isolated causes of acute HF

• Myocardial infarction

• Sudden cardiac death

• Myocarditis

• Drug toxicity 

In systolic failure, would you expect to see a thinner or thicker ventricle?

Thinner ventricular wall

The major problem in diastolic failure is    __________ and _________.

Stiffness; impaired ventricular filling

The most frequent cause of right ventricular failure is left ventricular failure. True or false?

True

Heart failure, no matter the cause, is essentially ____________.

Inability of the heart to perfuse the tissues/body adequately

Stroke volume is regulated via

Aldosterone; sodium and water reabsorption

Resistance, or PVR, is affected by

Vasoconstriction