Unit 5 Module 04
APPLY THE NURSING PROCESS FOR A
PATIENT EXPERIENCING HEART FAILURE
-
CO = HR x SV
- Frank Starling mechanism: Good: ^ CO, Bad: ^ heart
muscle O2 demand
Cardiac reserve = the ability to increase CO to
meet demand
- ventricular hypertrophy: good: strong muscle to pump; bad:
thickens, can’t relax. ^ o2 demand. Cellular enlargement.
CO is effected by ANS, catecholamines and
thyroid hormones
- Neuroendocrine:
- ↓CO stimulates SNS and catecholamine release: good: ^
HR, BP, contractility; ^ vascular resistance and venous
return. Bad: v filling time, ^ vascular resistance and O2
demand/workload
-
Preload: Amt of blood in ventricles at the end of
diastole
-
Afterload: force needed to overcome to open
pulmonic and aortic valves
-
Contractility: natural ability of cardiac muscle to
shorten
-
Ejection fraction: % of blood ejected from LV
during systole
o
o
o
01.
- heart rate ^: rapid HR v ventricular filling, thus v SV and
CO
normal 50 – 70%
<40% in HF
<30% should be considered for automated
implantable cardioverter defibrillator
(AICD)
etiology and pathophysiology
Heart failure: Inability of the heart to fill and pump blood
to meet the metabolic needs of the body.
Diminished cardiac output results in inadequate peripheral
tissue perfusion.
Congestion of the lungs and periphery may occur, the pt
can develop acute pulmonary edema.
Higher prevalence and mortality in African Americans
than caucasions.
Life expectancy ~ 5-8 years; 6-9 times more likely to die of
sudden cardiac arrest; 1 in 9 death cert it’s the 1st or 2nd
cause of death.
- ↓ CO and v renal perfusion stimulate the RAAS. Good: ^
bp via vasoconstriction. Bad: ^ myocardial workload; renal
vasoconstriction causes v renal perfusion (visicous cycle)
- Angiotensin stimulates aldosterone release from the
adrenal cortex. Good: kidneys retain salt and water to ^
blood volume; vascular volume increases. Bad: ^ preload
and afterload r/t ^ volume, leading to … PULMONARY
CONGESTION.
- Kidneys release ADH, heart releases atrial natriuretic
factor. Good: v water excretion, ^ sodium excretion. Bad:
fluid retention leads to ^ preload and afterload.
- Blood flow shunted to vital organs (can lead to kidney
failure). v organ perfusion; v skin and muscle perfusion.
Can lead to ORGAN FAILURE (kidneys …)
All of the above result in:
- Increased HR
- Improved SV
- Arterial vasoconstriction
- Sodium and water retention
- Myocardial hypertrophy
Compensatory mechanisms contribute to ↑ myocardial
oxygen consumption; when this occurs, myocardial reserve
is exhausted and clinical manifestations of heart failure
develop.
Chronic = EF < 35% and NYHA class II to IV for longer
than 6 weeks. Related to cardiomyopathies, valve disease,
long term CAD ()
Heart failure caused by:
- untreated systemic hypertension (increased cardiac
workload, chronic ^ afterload
- Impaired cardiac contraction (infarct cardiomyopathies,
myocarditis)
- structural changes (valve disorders, congenital defects)
Left sided HF
- AKA CHF
- r/t HTN, CAD, valvular disease
- leads to v tissue perfusion, poor CO, pulmonary
congestion (pulmonary vein, lungs)
The following compensatory mechanisms kick in. These
restore CO initially but eventually have damaging effect on
pump action.
A.
Systolic : leads to problems with contraction and
ejection of blood
-problem w/ LV contractile force
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-reduced LVeF
-leads to ^ preload and afterload
-V tissue perfusion
-pulmonary congestion
-r/tischemia, infarction, cardiomyopathy,
inflammation
B.
Diastolic: failure leads to problems with the heart
relaxing and filling with blood
-inadequate ventricular relaxation
-stiff heart muscle can’t relax and fill
- left ventricular hypertrophy -> v vascular
compliance
- r/t chronic untreated HTN,
-less preload
-EF generally preserved >40%
-increased pressure congestion and pressure before
ventricle, pulmonary, backs up to lungs.
B.
Heart failure
Clinical Manifestations
Right sided failure evident in systemic circulation
- wheezes due to fluid overload
- edema (LE, pools when stand or dangle feet.
Sometimes ABD.)
- Anorexia/nausea: blood backs up from the liver
- Liver enlargement, URQ Pain
- Jugular distention (blood backing up in superior
and inferior vena cava)
- Night POLYURIA (ABN large amt urine)
- S3 often first sign
- Confusion, restlessness, insomnia (r/t electrolyte
imbalance)
- ^ BP r/t fluid volume
Right sided heart failure:
1. AKA Cor Pulmonale
2. Caused by: Left sided failure; RV myocardial
infarction; pulmonary HTN (b/c right ventricle
works against pulmonary tension). Often caused
by restricted bloodflow to lungs (COPD BIG RISK
FACTOR)
3. Blood backs up in organs and systemic venous
system
4. Right A and V become distended, can’t pump
Low output: HF caused by CAD, cardiomyopathy,
primary cardiac disorders
High output HF: occurs in pts in hypermetabolic states, not
structural problem:
 Hyperthyroidism
 Pregnancy
 Anemia
 sepsis
02.
clinical manifestations and nursing assessments
A.
Pulmonary edema
Clinical manifestations:
- severe dyspnea
- tachycardia, tachypnea
- nasal flaring, use of accessory breathing muscles
- wheezing and crackles on auscultation, gurgling
respirations
-Expectoration of large amounts of blood tinged, frothy
sputum
- acute anxiety, apprehension, restlessness
- profuse sweating
- cold clammy skin
- cyanosis
-distended jugular veins
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Left sided failure
- evident in the pulmonary system.
- Crackles due to pulmonary edema
- Systolic: weakness, fatigue, Activity intolerance r/t
v o2 perfusion
- Cold hands/feet, cyanosis hands and feet
- Day Oliguria (ABN small amt urine); Night
nocturia (FREQUENT peeing)
- S3
Assessments:
-Activity level, ask how many stairs, ADLs
-ABD distention (right)
- Lung sounds (left = crackles, right = wheezes_
-Pedal pulse (diminished – left, with cool extremities)
- Edema (right, LE)
Lower body:
Right:
Nausea, anorexia, nocturia
Left:
Fatigue, weakness, skin changes (color/temp, cyanotic,
cool, mottling)
03.
Diagnostic studies
A.
Pulmonary edema
- O2 sat below 90%
- CXR: alveolar fluid , large heart
- Echocardiogram -- > EF
- ABGs will show low O2
B.
Heart failure
- B-type natriuretic peptide: ↑ in CHF, produced when
ventricles stretched, to get rid of extra fluid
- ECG may show ischemia (T Wave inversion),
tachycardia or extrasystole (extra beats)
- CBC may show anemia (HgB less than 12 in females, 14
in males)
- chemistry may show renal problems, electrolyte
disturbance
 K+, Na+, (low Na+ r/t fluid overload, low K+ r/t
diuretics)
 Thyroid test
 Liver function (hepatomegoly)
 CBC (anemia)
 Urinalysis (microalbumuria, protein, early sign)
- CXR:
 left sided HF:
- pulmonary congestion
- enlarged left ventricle (LVH) because of ↑ stress
to pump blood
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cath”
Right sided HF
o Pulmonary congestion b/c of accumulation
of fluid in the lungs
o Accumulation of fluid in the pleural cavity
(pleural effusion)
-ECG:
 Left ventricular hypertrophy -> tall, big QRS
complex
-Echocardiogram (with or w/o bubble)
 Blood flow, valve issues, enlargement, muscle
thickness

STAGING/CLASS
04.
Describe medical/surgical management of
pulmonary edema/heart failure
- reduce vascular congestion
- ^ force of contraction
- ^ blood flow to peripheral organ
06.
A.

complications
Pulmonary edema
Hypoxia, organ failure
B.


Heart failure
Left sided - right sided
Paroxysmal nocturnal dyspnea:
o Left: pulmonary congestion
o Right: reabsorbed fluid too much for heart to
handle
o Teach to sit up, extra pillows
Multiorgan failure
o Right sided
o Hepatomegaly – liver failure
o Splenomegaly
o ^ ADB pressure (anorexia, nausea, nutrition
issues)
*Pulmonary edema (see above)


Monitoring:
-Hemodynamics:
 PA lines, Swan Ganz catheter ** transducer on
outside has to be at PHLEBOSTATIC ANGLE TO
BE BALANCED**
-Central venous pressure
 Right heart pressure
-Arterial pressure
 MAP = systolic + 2(diastolic) ÷ 3
-Pulmonary artery pressure
 PA line, cardiac catheterization (right) “right heart
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08.
A.
apply nursing interventions
Pulmonary edema
Heart failure:
- Assessment:
o VS
o I/O: effective diuresis
o Daily weight, make sure losing weight
o Lung sounds
o Heart sounds
 S3 and S4
- Nutrition: low sodium, cardiac diet, make sure
they follow
- Activity plan: move as much as possible
- Interdisciplinary
09.
Evaluate patients response to medical, surgical
and/or nursing interventions.
- **Tissue perfusion adequate
- Output > input
-losing weight
-lungs clear
10.
Discuss dietary management
- limit liquids to 1.5 to 2 liters
-low sodium diet to v fluid retention
- soups, bread, check labels, fried foods, egg yolks, shellfish,
deli meats
11.
Formulate a patient teaching plan for the
prevention of a recurrent heart failure.
A.
Signs of failure
B.
Medications








O2: Venturi face mask (5-6 L); nonreabreather (at
least 10L); CPAP; possibly intubation
Diuretics
Bronchodialators
ABGs (monitor for acidosis, CO2 retention)
CXR to confirm Dx
Vasodilators
Morphine (v anxiety, dilate peripheral vasc system)
Potential mech vent; potential hemodynamic
monitoring
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12.
Discuss the rehabilitation of a patient with heart
failure in terms of improving activity tolerance.
 Exercise will increase HDL, promote venous return,
weight mgmnt.
 Cardiac rehab is proven to improve outcomes
15.
Identify social, cultural and economic factors that
may impact the patient with heart failure.
- stress
- social limitations
- diuretics
- oxygen
- money for meds
- help with ADLs
- stoicism , not admitting need help
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