Download Nursing Management of the Acute Congestive Heart Failure

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Proceeding of the NAVC
North American Veterinary Conference
Jan. 8-12, 2005, Orlando, Florida
Reprinted in the IVIS website with the permission of the NAVC
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Published in IVIS with the permission of the NAVC
The North American Veterinary Conference – 2005 Proceedings
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NURSING MANAGEMENT OF THE ACUTE
CONGESTIVE HEART FAILURE PATIENT
resulting in increased stroke volume provides some degree of
compensation for bradycardia.
Harold Davis, BA, RVT, VTS (ECC)
CONGESTIVE (BACKWARD) HEART FAILURE
Congestive heart failure refers to heart failure that is
accompanied by the backup of blood and fluid in tissues.
Increased in pulmonary or systemic venous capillary
pressure cause fluid to leak from capillary beds resulting in
edema (pulmonary or peripheral) or effusions (pleural,
peritoneal). Congestive heart failure can be characterized as
right or left (Table 1) depending on whether systemic or
pulmonary venous pressures are increased by heart disease.
Veterinary Medical Teaching Hospital
University of California, Davis, CA
Heart failure is the inability of the heart to supply adequate
blood flow to meet the metabolic demands of the body or to
provide adequate blood flow at the expense of excessive
increases in ventricular filling pressures. Heart failure exists
in three forms congestive (backward) failure, low output
(forward) failure or a combination of both. The veterinary
technician may be called upon to provide nursing care of the
acute congestive heart failure patient. An understanding of
this disease process will aid the veterinary technician in
providing nursing care.
CARDIOVASCULAR ANATOMY AND PHYSIOLOGY
The heart is a four-chambered pump. The tricuspid and
mitral valve separates the atria from the ventricles and
prevents back flow of blood when the ventricles contract.
The pulmonic and aortic valves prevent the backflow from the
pulmonary artery and aorta, respectively when the ventricles
relax. Unoxygenated blood enters the right atrium from the
anterior and posterior vena cavae. Blood is pumped into the
pulmonary vasculature from the right ventricle. Oxygenated
blood returns via the pulmonary vein into the left atrium. The
left ventricle then pumps blood into the arterial system.
Oxygenation of the heart muscle occurs through the coronary
arteries.
The heart generates electrical activity that induces
mechanical contraction. Sympathetic stimulation increases
heart rate, contractility, and conduction and contracts
vascular smooth muscle.
The sinoatrial node initiates
electrical impulses, which causes atrial contraction. The
electrical impulses travel down to the atrioventricular (AV)
node, through the purkinje fibers, to the ventricular muscles,
causing ventricular contraction.
Cardiac output is the product of stroke volume and heart
rate. It is the volume of blood pumped out of the heart per
minute.
Stroke volume is the amount of blood pumped out of the
heart with each beat and there are three primary
determinants of stroke volume: preload, contractility and
afterload. Preload is the effective distending or filling volume
of the ventricle as determined by the ventricular filling
pressure and ventricular compliance.
Preload affects
myocardial fiber length and directly influences contraction:
increased myocardial fiber length results in a more forceful
contraction and greater stroke volume up to a physiological
limit.
Contractility refers to the ability of heart to contract
independent of variations in preload and afterload.
Afterload is the resistance the ventricle has to overcome in
order to eject blood from the heart. As afterload increases,
stroke volume decreases, and vice versa.
Heart rate changes can cause rapid alterations in cardiac
output. An increase in heart rate can cause a two to threefold
increase in cardiac output. Excessive heart rates lead to
increased myocardial oxygen demand and decreased
ventricular filling time (causing decreased pre-load and stroke
volume). A decrease in heart rate can cause a decrease in
cardiac output. The increased time for ventricular filling
Table 1 Partial list of causes of heart failure
Dogs
Left heart failure
x Mitral regurgitation
x Dilated cardiomyopathy
x Infective endocarditis
Right heart failure
x Tricuspid regurgitation
x Pericardial disease
x Heartworm disease
Biventricular heart failure
x Dilated cardiomyopathy
Cats
x
x
x
Hypertrophic cardiomyopathy
Restrictive cardiomyopathy
Cardiomyopathy secondary to hyperthyroidism
LOW OUTPUT (FORWARD) HEART FAILURE
Low output failure, is a form of cardiogenic shock especially
when it is associated with hypotension. Low output failure
occurs when the heart cannot pump sufficient oxygenated
blood to the tissues.
PATIENT ASSESSMENT
It is important to remember that one of our goals is to
minimize the patient’s stress or not aggravate the patient. If it
appears that the patient can’t tolerate the physical
examination, imaging or electrocardiography then such
diagnostics should be postponed until the animal’s condition
has improved.
HISTORY / CLIENT COMPLAINT
The patient may or may not present with a pre-existing
history of heart disease. The most common owner complaint
for pets with heart failure includes: tachypnea, dyspnea,
weakness, collapse, and syncope. Additional complaints
include coughing (mostly in dogs), weight loss, abdominal
distention, and exercise intolerance.
PHYSICAL EXAM
Looking
By looking at the patient we can assess mucus membrane
(mm) color, capillary refill time (CRT), and jugular vein
distention. The mm color should be pink and the CRT should
be 1 - 2 seconds. Pale or white mm color suggests blood
loss, anemia, or vasoconstriction. CRT is an indicator of
peripheral perfusion and is a semi-quantitative evaluation of
vasomotor tone.
Vasoconstriction decreases tissue
perfusion. Causes of prolonged capillary refill time include
hypovolemia, poor cardiac output, hypoxia, hypothermia,
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Veterinary Technician
excitement, fear, pain and drugs. Anything that increases
sympathetic tone can prolong capillary refill. A CRT that is
faster than normal is due to vasodilation; in this instance the
patient will have brick red mucus membrane. Causes of
vasodilation include hyperthermia, sepsis, and vasodilator
therapy.
The jugular vein should be assessed with the patient
standing and the head in a normal position. Jugular vein
distention or pulses extending over one-third of the neck is
suggestive of right heart problems, pulmonic stenosis,
pericardial disease, or cranial vena cava obstruction.
Listening
Heart rate and rhythm can be determined by auscultation.
Increase in heart rate (tachycardia) may be caused by
hypovolemia (the tachycardia is a compensatory
mechanism), fever, excitement, exercise, pain and drugs.
Anything that increases sympathetic tone can cause
tachycardia. Tachycardia is generally defined as a heart rate
greater than 160 beats per minutes (bpm). Decrease in heart
rate (bradycardia) may be caused by high vagal tone, severe
electrolyte disturbances and atrioventricular conduction
blocks. Bradycardia is generally defined as a heart rate less
than 60 bpm. Auscultation of the heart may reveal murmurs
or arrhythmias.
Feeling
Palpation of pulses is a way of assessing stroke volume,
heart rate and rhythm. The height and width of the pulse
waveform is determined by stroke volume. Large bounding
(hyperkinetic) pulses usually indicate the rapid ejection of an
increased volume of blood from the left ventricle. Bounding
pulses may occur with exercise, fever, and cardiac disease
associated with increased stroke volume. Small or weak
(hypokinetic) pulses are due to diminished stroke volume and
may be a result of advance mitral disease.
When
irregularities in heart sounds are heard, the heart rate should
be compared to pulse rate and the difference in rates are
called pulse deficits.
Pulse deficits are indicative of
arrhythmias.
Hydration status can be assessed by checking skin turgor
and gum moisture. When interstitial deficits occur, skin turgor
will be decreased and gums will be tacky or dry.
Cool extremities may indicate decreased peripheral
perfusion.
Imagining
Radiography is useful in determining cardiovascular or
pulmonary changes. Heart and vessel enlargement may be
seen. The cardiac silhouette, takes on a soccer ball shape
with pericardial effusions. Pulmonary findings include pleural
effusions, and radiographic patterns suggestive of pulmonary
edema.
Ultrasonography is useful in determining chamber size,
function of the valves, contractility and ejection fraction
(percentage of the diastolic volume that is ejected form the
heart during systole). This diagnostic tool is also useful for
documenting, congenital defects, cardiac masses, pericardial
effusions, hepatomegaly and possibly ascites.
Imaging should not be performed at the expense of
stressing the patient.
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Electrocardiography
The ECG reflects electrical activity of the heart; it does not
measure mechanical activity. An arrhythmia is defined as an
irregular heart rhythm. When assessing an ECG you should
check the following: What is the heart rate?
•Is the rhythm regular or irregular?
•Is there a P wave for every QRS complex and is there a
QRS complex for every P wave?
•Is the P-R interval prolonged?
•Is the QRS complex form normal in size and shape?
•Are the T waves abnormally large?
•Is there S-T segment depression?
The heart rate defines the rhythm as a tachyarrhythmia or
a bradyarrhythmia. Wide, bizarre QRS complexes may
represent ventricular premature contractions (VPCs), right
ventricular hypertrophy or right bundle branch block. VPCs
are often not preceded by a P wave. Small but normal
appearing QRS complexes may be due to pericardial
effusion. Abnormally tall-tented T waves may be due to
hyperkalemia, hypoxia, or dilation. S-T segment slurring or
depression may be due to myocardial hypoxia.
PATIENT MANAGEMENT
The primary goal of therapy is to improve oxygen delivery.
This goal is achieved by improving oxygenation, reducing
effusion / pulmonary edema and optimizing cardiac output.
Oxygen Therapy
Maintaining oxygen saturation is one of the primary goals in
maintaining blood oxygenation. If there is any question
concerning a patient’s blood oxygenation, supplemental
oxygen should be provided until assessment of arterial blood
gases or hemoglobin saturation confirms that oxygen
supplementation is not necessary. When this equipment is
not available, assessment will have to be based on clinical
dyspnea or auscultable abnormalities and clinical signs of
hypoxia (cyanosis of the mucous membranes or dark colored
blood, tachypnea, tachycardia, and anxiety). Individually, the
clinical signs do not prove hypoxemia, but together they are
suggestive of hypoxemia. There are a variety of methods of
oxygen therapy. The method selected depends on the
expected duration of therapy, the demeanor of the patient,
and equipment availability.
Available methods include
facemask, oxygen bag (hood), oxygen cage, transtracheal,
and nasal insufflation. In the case of acute heart failure it is
perhaps best to use a technique that will be the least stressful
to the patient. The ultimate goal of oxygen therapy is to
provide adequate oxygen to the blood, using the lowest
possible inspired oxygen concentrations.
SEDATION
When the patient is anxious or stressed it may benefit from
sedation. Traditionally, morphine has been used in the dog.
In addition to its anxiolytic affects it redistributes blood away
from the lungs through venous vasodilation. Phenothiazine
tranquilizers such as acepromazine may be used to produce
similar effects. This drug can cause cardiovascular collapse
in Boxers and probably should not be used in that breed.
Reducing Pulmonary Edema and / or Effusion
Pulmonary edema is seen in left heart failure because of an
increase in pulmonary blood volume resulting in increased
capillary pressures. Diuretics will decrease the blood volume
and will decrease capillary pressures.
Furosemide, a
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commonly used loop diuretic is used to treat pulmonary
edema. It may be given intravenously or intramuscularly;
using doses up to 8 mg/kg and 4 mg/kg every few hours in
the dog and cat respectively. High dose administration is
discontinued once the respiratory rate decreases and / or
respiratory character improves. The patient is at risk for
developing mild hypokalemia and dehydration secondary to
high dose Furosemide administration. In dogs, this problem is
usually corrected once the pulmonary edema is resolved and
it resumes eating and drinking. Because cats do not readily
eat and drink, fluids may be administered judiciously to
correct dehydration.
Cardiogenic pleural effusion in dogs is usually secondary to
a combination of right and left heart failure. In the cat, left
heart failure secondary to hypertrophic cardiomyopathy is the
common cause for pleural effusion. Patients in respiratory
distress with pleural effusion should benefit from a
thoracentesis. The technician should be prepared to assist in
the thoracentesis. The technician should be familiar with the
indications, patient and procedure preparation, and
performance of the procedure and associated complications.
Ascites, secondary to severe right heart failure in the dog
may require abdominocentesis. The ascites makes the
patient feel uncomfortable and places pressure on the
diaphragm causing breathing difficulties. Enough fluid should
be removed to relieve the breathing difficulties and make the
patient comfortable. The technician’s role in this procedure is
similar to that in the thoracentesis.
Vasodilator Therapy
Vasodilating drugs are used to treat both congestive and
low output heart failure. Nitroglycerin is a venodilator.
Venodilators expands vascular capacity by dilating veins,
which, reduces preload and venous pressure. Venodilation
will reduce congestion but not improve cardiac output.
Nitroglycerin is applied transdermally.
Arterial
vasodilators
decrease
systemic
vascular
resistance, which reduces afterload and improves cardiac
output; in addition, it decreases the work of the heart.
Hydralazine is an arteriolar dilator. It is used to treat severe
mitral regurgitation. The drug is administered orally. The
vasodilating effect occurs within 30 minutes to 1 hour and
peaks in 3 hours. Nitroprusside is a potent veno and
arteriolar dilator. It is reserved for severe fulminant heart
failure. The drug has a short half-life and must be given as a
constant rate infusion. Adverse effects include hypotension
and cyanide toxicity. If the patient becomes hypotensive, the
drug is reduced or turned off and its effects will dissipate
within a few minutes.
Cyanide toxicity, resulting from
nitroprusside over-dosage, is characterized by hyperemia
and dyspnea. Because these drugs are potent vasoactive
substances blood pressure must be monitored.
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ACE Inhibitors
These drugs are balanced vasodilators, in other words they
work on the venous and arterial side. They work by
preventing the conversion of angiotensin I to angiotensin II.
Reduction in angiotensin II is what leads to the vasodilation
and ultimately the reduction in capillary pressure, edema
formation and increased perfusion.
Examples include
Captopril and Enalapril.
Positive Inotropes
Positive inotropic drugs such as dobutamine increase stoke
volume and ultimately cardiac output and blood pressure by
increasing contractility. Dobutamine increases contractility
without causing a significant increase in heart rate or vascular
resistance. Dobutamine has a short half-life and must be
administered as a constant rate infusion. It is indicated in
cases where the patient is showing signs of congestion and
diminished cardiac output.
Monitoring Therapy
Therapy should improve cardiac output or reduce
pulmonary edema. With improvement of cardiac output,
signs of increased perfusion should be evident. These signs
include normal capillary refill, good pulse quality, warm
extremities, and good urine production. More definitive
assessments include reduction in blood lactate, increased
venous oxygen tension or measured cardiac output.
If therapy has been effective in resolving the pulmonary
edema the patient’s attitude and mucous membrane color
should improve and the animal may be able to lie down and
sleep. If vasoactive drugs are utilized then blood pressure
must be measured. CVP is useful in determining an endpoint
for fluid administration or to measure the relative ability of the
heart to handle the fluids being returned to it.
Diuretic therapy should quickly produce increased urine
production. A baseline body weight and palpation of the
bladder should be performed to serve as a basis for
comparison. Acute changes in body weight are usually due
to fluid gains or losses.
Electrolyte and acid base
abnormalities can be caused by diuretic therapy; as a result
these parameters should be measured.
SUMMARY
The veterinary technician may be called upon to provide
nursing care of the acute congestive heart failure patient.
An understanding of this disease process, rationale of
therapy, and desired outcomes will aid the veterinary
technician in providing nursing care.
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