case study part 2

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HEART FAILURE


NUR 41500

Heart Failure

  • Costs estimated >$35 billion in the US
  • Leading cause of hospitalization of patients over 65 years in age.

  • Condition usually progresses with time

Function of the heart

  • Moves deoxygenated blood from the venous system through the right heart into the pulmonary circulation
  • Moves the oxygenated blood from the pulmonary circulation through the left heart into the arterial system
  • Right and left heart must maintain an equal output to function properly.

Heart Failure

Heart Failure Physiology

  • Heart unable to maintain adequate CO to meet body demands

  • Action of compensatory mechanisms

CO = HR x SV

(amount blood pumped every minute)

Heart Failure

Caused by any condition that reduces the pumping ability of the heart.

The consequence

 stroke volume and ejection fraction from

 increase in the residual volume left in the ventricle at the end of systole.

Over time, this extra remaining volume begins to dilate the ventricle.

COMPENSATORY Mechanisms--Early

Sympathetic Nervous System Stimulation

A. Reflex stimulation of SNS occurs in HF

  • Autoregulation

B. Helps perfuse heart & brain –

  • Blood gets diverted from skin, kidneys & GI tract to coronary & cerebral circulation

C. When HF persists too long & SNS overused:

  • May cause dysrhythmias
  • May wear out SNS nerve endings & exhaust supply of norepinephrine

COMPENSATORY Mechanisms--Early

Salt & Water Retention:

A: ↑ circulatory volume  ↑ venous return

in an attempt to ↑ CO

B: In HF, this mechanism makes heart work harder by ↑ blood volume & giving heart more blood to pump

C: The diversion of blood from kidneys & reduced CO both cause reduced renal perfusion

COMPENSATORY Mechanisms-Early

Renin-Angiotensin Aldosterone Mechanism.

  • This reduced renal perfusion leads to stimulation of Renin Angiotension cycle

  • Angiotensin II acts as vasoconstrictor, stimulating release of ADH (antidiuretic hormone)  retains water in circulation

  • RA cycle leads to release of aldosterone which ↑ tubular reabsorption of Na+ & water follows Na+ - end result is retention of sodium & water

COMPENSATORY Mechanisms--Early

Frank-Starling mechanism

Increases ventricular preload causing greater stroke volume (Increases CO)

This mechanism is only adaptive to a point.

Eventually mechanism fails as ventricle becomes overfilled & muscle becomes overstretched .

COMPENSATORY Mechanisms

CHF: classifications

  • Left/Right
  • High-output/Low-output
  • Systolic/Diastolic

Right-sided vs.
Left-sided failure

Classified as to which side of heart is failing

  • However, whether left or right, eventually, the failure becomes general & involves both sides

Right-sided Failure

Represents failure of the right heart to pump blood forward into the pulmonary circulation

Blood backs up in the systemic circulation

Causes peripheral edema (dependent extremities) and venous congestion of the abdominal organs

Also Manifests as weight gain

1000mL = 1 Kg (2.2#)

If congestion & edema severe enough 

engorged liver with death of liver cells,

external jugular veins remain engorged even when the person stands (JVD)

Ascites, hepatomegaly

Left-sided Failure

  • Represents failure of the left heart to move blood from pulmonary circulation into systemic circulation
  • Blood backs up in the pulmonary circulation
  • Fluid moves out of capillaries into surrounding alveoli
  • Excess fluid in lung tissue interferes with gas exchange
  • More respiratory signs (DOE, SOB) & Pulmonary Edema (complication)

The Role of

Increased Afterload (PVR) on the Pathogenesis of Heart Failure

Afterload: the amount of resistance the blood must overcome to be pumped out of the heart

HF Video

S/S of CHF

1.Edema – (right sided)

  • Mostly due to capillary pressure with fluid leaking into surrounding tissues

  • Salt & water retention adds to pressure –

  • Nocturia (Urination during nighttime)

  • when person is lying down dependent fluid in extremities is redistributed to central circulation & can then be excreted

S/S of CHF

2.Respiratory Symptoms – (left sided)

Dyspnea: Nocturnal dyspnea may occur when dependent edema 1st returns to general circulation & overloads pulmonary circulation

Bronchospasm may occur

May need several pillows to sleep(orthopnea)

S/S of CHF

3. Fatigue & weakness – (> w/ Left)

May occur with left-sided failure

CO is less

CO may be so low that circulation to brain may be impaired which leads to CNS disturbances  memory, confusion, ..... (Left or right sided)

5. Cardiac Arrhythmias

S/S of CHF

6. Renal impairment-- In most cases this is a pre-renal cause of AKI

7.Cachexia (> w/ right sided)

Cardiac wasting due to poor intake of food & congestion of GI organs 

Impairing digestion & absorption

8. Cyanosis - (either / both)

Late sign of failure

due to poor oxygenation of blood &/or low output failure

The American Heart Association & the American College of Cardiology Stages of HF (2001)

Stage A: Patients at high risk (risk factors present) for developing HF in future but no functional or structural heart disorder

Stage B: Diagnosed by an ejection fraction (amount of blood pumped out of left ventricle w/ each heartbeat) below 40% (norm 55 % or >) but no past or current symptoms.

Stage C: Heart failure diagnosed, with past or current symptoms, including SOB, fatigue, & reduced exercise tolerance.

Stage D: Advanced symptoms of heart failure after receiving optimal medical care, requiring hospital-based support, heart transplant or palliative care.

New York Heart Association
Classification of HF

Rank from Class I to IV according to functional limitations & severity of symptoms.

Class Patient Symptoms
Class I (Mild) No limitation of physical activity. Ordinary physical activity does not cause undue fatigue, palpitation, or dyspnea (shortness of breath).
Class II (Mild) Slight limitation of physical activity. Comfortable at rest, but ordinary physical activity results in fatigue, palpitation, or dyspnea.
Class III (Moderate) Marked limitation of physical activity. Comfortable at rest, but less than ordinary activity causes fatigue, palpitation, or dyspnea.
Class IV (Severe) Unable to carry out any physical activity without discomfort. Symptoms of cardiac insufficiency at rest. If any physical activity is undertaken, discomfort is increased.

CHF DIAGNOSIS

Diagnosed primarily by clinical picture:

Assess Risk factors (common causes)

Ischemic Heart Disease / CAD (over 50%)

Hypertension

Cardiac Arrhythmias

Cigarette Smoking

Obesity

Diabetes

Congenital Heart Disease

Valvular Heart Disease

(much higher in older populations)

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CHF Diagnostics

Blood Test

  • B-type Natriuretic Peptide (BNP)

BNP is a substance secreted from the ventricles in response to changes in pressure (stretching) – protective mechanism

Occurs when heart failure develops & worsens.

The level of BNP in the blood increases when heart failure symptoms worsen, & decreases when the heart failure condition is stable.

  • Half-life of 20 minutes (measures current ventricular status)

  • When released this polypeptide decreases systemic vascular resistance and central venous pressure by

  • Increasing diuresis
  • Vasodilatation

BNP

BNP level in a person with heart failure - even someone whose condition is stable - is higher than in a person with normal heart function.

Patients with CHF, BNP values will generally be above 100 pg/ml

Results

BNP levels below 100 pg/mL - no heart failure

BNP levels of 100-300 pg/mL - suggest heart failure is present

BNP levels above 300 pg/mL - indicate mild heart failure

BNP levels above 600 pg/mL - indicate moderate heart failure.

BNP levels above 900 pg/mL - indicate severe heart failure.

CHF DIAGNOSIS

EKG to see if underlying rhythm or conduction problems (r/o MI)

Chest X-Ray

Echocardiogram (assesses pumping strength and EF)

Hemodynamic monitoring to assess fluid overload

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