Name: Perfecto Pandacan Balili Room and Bed #: CCU bed 1
Age: 60 y.o. Attending Physician: Dr. Voltaire Egnora
Sex: Male Institution: Davao Medical Center
Diagnosis: CAD, AMIK II, (+) LVH, (+) LVD, FC III Date and
Time Cues Need Nursing Diagnosis Objective Nursing Intervention Evaluation
Novembe and reactive to light
Acute pain related to decreased myocardial blood flow as
evidenced by reports of chest pain
secondary to CAD, AMI
Rationale:
Pain is an unpleasant
sensory and
emotional experience arising from actual or potential tissue damage.
Acute Myocardial Infarction (AMI) occurs when coronary blood flow decreases
1. Administer medication as indicated (antianginal, beta-blocker, analgesics) R: Immediate response in relief of pain.
2. Administer
supplemental oxygen as indicated
R: Increases amount of oxygen available for myocardial uptake and thereby may relieve discomfort associated with tissue ischemia.
3. Monitor characteristics of pain, noting verbal reports, nonverbal cues,
and hemodynamic
response.
R: Variation of appearance and
Goal Met
- Crackles thrombotic occlusion of a coronary artery previously narrowed by atherosclerosis.
Infarction occurs
when an thrombogenesis, so that a mural thrombus forms at the site of
serotonin) promote platelet activation.
There is production
behavior may occur.
Respirations may be increased as a result of pain and associated anxiety, while release of stress induced catecholamines will increase heart rate and BP.
4. Review history of previous angina or MI pain R: May differentiate current pain from preexisting patterns, as well as identify complications such as extension of infarction, pulmonary embolus, or pericarditis.
5. Instruct patient to report pain immediately
R: Delay in reporting pain hinders pain relief or may require increased dosage of medication to achieve relief.
Severe pain may induce shock by stimulating the sympathetic nervous system, thereby creating further damage and interfering with diagnostics and relief of pain.
6. Provide quiet
environment, calm
noted potential resistance to thrombolysis.
The coagulation cascade is activated on exposure of tissue factor in damaged endothelial cells at the site of the ruptured thrombin, which then converts fibrinogen to fibrin. The culprit coronary artery eventually becomes occluded by a thrombus containing platelet aggregates and fibrin strands.
This occlusion will impede the flow of blood to the cardiac muscles. Decrease cardiac functioning will lead to imbalance between myocardial oxygen supply and
activities and comfort measures.
R: Decreases external stimuli, which may aggravate anxiety and cardiac strain and limit coping abilities and adjustment to current situation.
7. Assist in relaxation techniques such as deep breathing, visualization and guided imagery
R: Helpful in decreasing perception of pain. Provides a sense of having some control over the situation, increase in positive attitude.
8. Check vital signs before and after narcotic medication
R: Hypotension or respiratory depression can occur as a result of narcotic administration.
These may increase myocardial damage in presence of ventricular insufficiency.
9. Place patient at complete rest during anginal episodes
R: Reduces myocardial oxygen demand to minimize risk of
Yap, Novelynne Joy
demand wherein the heart is unable to meet
the metabolic
demands of the body.
Lack of blood and oxygen supply in the cardiac muscle will lead to ischemia and thus to experience of pain.
Source:
Pathophysiology:
Concepts and
Applications for
Health Care
Professionals, 3rd Edition by Nowak Harrison’s Internal Medicine, 5th Edition
tissue injury or necrosis.
10. Elevate head of bed if patient is short of breath R: Facilitates gas exchange to decrease hypoxia and resultant shortness of breath.
11. Monitor heart rate and rhythm
R: Patient may have acute life-threatening dysrhythmias, which occur in response to ischemic changes or stress.
12. Stay with the patient who is experiencing pain or appears anxious
R: Anxiety releases
catecholamines, which increase myocardial workload and can prolong ischemic pain.
Presence of nurse can reduce feelings of fear and helplessness.
13. Provide light meals.
Have patient rest for 1 hour after meals
R: Decreases myocardial workload associated with work of digestion, reducing risk of anginal attack.
14. Monitor serial ECG changes
R: Ischemia during anginal attack may cause transient ST segment depression or elevation and T wave inversion. Serial tracing verify ischemic changes, which may disappear when patient is pain-free. They also provide a baseline with which to compare later pattern changes.
Source:
- Nursing Care Plan, 4th Edition by Doenges
- Nurse’s Pocket Guide, 8th Edition by Doenges
Name: Perfecto Pandacan Balili Room and Bed #: CCU bed 1
Age: 60 y.o. Attending Physician: Dr. Voltaire Egnora
Sex: Male Institution: Davao Medical Center
Diagnosis: CAD, AMIK II, (+) LVH, (+) LVD, FC III Date and
Time
Cues Need Nursing Diagnosis Objective Nursing Intervention Evaluation
November and reactive to light
- Pale conjunctiva noted - O2
inhalation at 5 lpm via nasal
Decrease Cardiac Output related to altered heart rate and rhythm as evidenced by atrial fibrillation in slow to moderate ventricular response with ST elevation pattern secondary to CAD, AMIK II
Rationale:
Acute Myocardial Infarction (AMI) generally occurs when coronary blood flow decreases abruptly after a thrombotic occlusion of a coronary artery previously narrowed by atherosclerosis.
When a coronary
1. Determine baseline vital signs
R: Provide opportunities to track changes.
2. Auscultate BP,
compare both arms and dysfunction, hypoperfusion of the myocardium, and vagal stimulation. However, hypertension is also a common phenomenon, possibly related to pain, anxiety, catecholamine release, and/or preexisting vascular problems. Orthostatic hypotension may be associated with complications of infarct.
3. Evaluate quality and
cough noted site of vascular injury, this injury is
produced or
facilitated by factors such as cigarette smoking,
hypertension, and lipid accumulation.
Infarction occurs
when an thrombogenesis, so that a mural thrombus forms at the site of
serotonin) promote platelet activation.
After agonist
4. Auscultate heart sound;
note development of S3 and S4
R: S3 is usually associated with HF, but it may also be noted with mitral insufficiency and left ventricular overload that can accompany severe infarction. S4 may be associated with myocardial ischemia, ventricular heart. Presence of rub with an infarction is all associated with inflammation.
6. Auscultate breath sounds
- Temp=35. potential resistance to thrombolysis.
The coagulation cascade is activated on exposure of tissue factor in damaged endothelial cells at the site of the ruptured plaque.
Factors VII and X are activated, ultimately leading to the
conversion of
prothrombin to thrombin, which then converts fibrinogen to fibrin. Fluid-phase and clot-bound thrombin participate
in an activity, as well as developing complications/dysrhythmias, which could compromise cardiac function or increase ischemic damage. Acute or chronic atrial flutter/fibrillation may be seen with coronary artery or valvular involvement and may or may not be pathogenic.
8. Place on moderate high back rest oxygen consumption/demand and can compromise myocardial function.
10. Provide bedside
the coagulation cascade. The culprit coronary artery eventually becomes occluded by a thrombus containing platelet aggregates and fibrin strands.
This occlusion will impede the flow of blood to the cardiac muscle and other parts of the body. Therefore there is inadequate blood pumped by the heart to meet the metabolic demands of the body. This cardiac problem also alters the cardiac rate and rhythm as the body reacts to the lack of blood carrying oxygen in which the occlusion results to tissue
ischemia and
eventually to necrosis.
The infracted area in AMI will eventually heal and the necrotic myocardial cells will
commode if unable to use bathroom
R: Attempts at using bedpan can be exhausting and psychologically stressful, thereby increasing oxygen demand and cardiac workload.
11. Provide small or easily digested meals. Restrict can increase heart rate.
12. Avoid activities such as isometric exercises, rectal stimulation, vomiting, spasmodic coughing.
Administer stool softeners as ordered.
be replaced by dense fibrous connective tissue (scarring). This area cannot contribute to pumping except to maintain the integrity of the ventricular wall.
Source:
Pathophysiology:
Concepts and
Applications for
Health Care
Professionals, 3rd Edition by Nowak Harrison’s Internal Medicine, 5th Edition
myocardial uptake, reducing ischemia and resultant dysrhythmias.
14. Maintain IV access as indicated
R: Patent line is important for administration of emergency drugs in presence of persistent dysrhythmias or chest pain.
15. Administer
antidysrhythmic drugs and ACE inhibitors as ordered.
R: Dysrhythmias are usually treated symptomatically, except for PVCs, which are often treated prophylactically.
Early inclusion of ACE inhibitor therapy enhances ventricular output, increases survival and may slow progression of heart failure.
Source:
- Nursing Care Plan, 4th Edition by Doenges
- Nurse’s Pocket Guide,
8th Edition by Doenges
Name: Perfecto Pandacan Balili Room and Bed #: CCU bed 1
Age: 60 y.o. Attending Physician: Dr. Voltaire Egnora
Sex: Male Institution: Davao Medical Center
Diagnosis: CAD, AMIK II, (+) LVH, (+) LVD, FC III Date and
Time
Cues Need Nursing Diagnosis Objective Nursing Intervention Evaluation
Novembe
“Dali ko makapoy ug lisod mulihok”
as verbalized by and reactive to light
- Pale conjunctiva noted - O2
inhalation at 5 lpm via nasal
Activity Intolerance related to decrease cardiac functioning as evidenced by irregular cardiac rate and psychological energy to endure or complete required or desired daily activities.
Acute Myocardial Infarction (AMI) occurs when coronary blood flow decreases abruptly after a thrombotic occlusion of a coronary artery
1. Determine baseline vital signs
R: Provide opportunities to track changes.
2. Record or document heart rate, rhythm, and BP changes before, during, and after activity as indicated. indicate myocardial oxygen deprivation that may require
Limit activities on basis of pain or hemodynamic response. Provide nonstress diversional activities
expansion
previously narrowed by atherosclerosis.
Infarction occurs
when an thrombogenesis, so that a mural thrombus forms at the site of
serotonin) promote platelet activation.
After agonist
workload or oxygen
consumption, reducing risk of complications
4. Limit visitors and/or visiting by patient, initially R: Lengthy or involved conversations can be very taxing for the patient; however, periods of quiet visitation can be therapeutic.
5. Instruct patient to avoid increasing abdominal pressure like straining during defecation
R: Activities that require holding of breath and bearing down can result in bradycardia, temporarily reduced cardiac output and rebound tachycardia with elevated BP.
6. Explain pattern of graded increase of activity level like getting up in chair when there is no pain, progressive ambulation, and resting for 1 hour after meals.
rough skin potential resistance to thrombolysis.
The coagulation cascade is activated on exposure of tissue factor in damaged endothelial cells at the site of the ruptured thrombin, which then converts fibrinogen to fibrin. The culprit coronary artery eventually becomes occluded by a thrombus containing platelet aggregates and fibrin strands.
This occlusion will impede the flow of blood to the cardiac muscles. Decrease cardiac functioning will lead to imbalance between myocardial oxygen supply and irregularities, development of chest pain, or dyspnea may indicate need for changes in exercise regimen or medication
8. Place on moderate high back rest oxygen consumption/demand and can compromise myocardial function.
10. Provide bedside commode if unable to use bathroom
R: Attempts at using bedpan can be exhausting and
Yap, Novelynne Joy
demand wherein the heart is unable to meet
the metabolic
demands of the body.
Performing activities increases oxygen consumption from the body in which an individual with such imbalance will have difficulty performing the task.
Professionals, 3rd Edition by Nowak Harrison’s Internal Medicine, 5th Edition
psychologically stressful, thereby increasing oxygen demand and cardiac workload.
11. Provide small or easily digested meals. Restrict can increase heart rate.
12. Plan care with rest periods in between
R: reduce fatigue
13. Encourage patient to maintain positive attitude;
suggest use of relaxation
myocardial uptake, reducing ischemia and resultant dysrhythmias.
15. Maintain IV access as indicated
R: Patent line is important for administration of emergency drugs in presence of persistent dysrhythmias or chest pain.
Source:
- Nursing Care Plan, 4th Edition by Doenges
- Nurse’s Pocket Guide, 8th Edition by Doenges
PROGNOSIS
MI may be associated with a mortality rate as high as 30%, with more than half of deaths occurring in the prehospital setting. Prognosis is highly variable and depends on a number of factors related largely on infarct size, left ventricular function and the presence or absence of ventricular arrhythmias. Prognosis is significantly worsened if a mechanical complication (papillary muscle rupture, myocardial free wall rupture, and so on) were to occur.
Overall, the prognosis is poor. This is for the reason that the patient’s condition has been transpiring for years. He had attacks in the past and his condition has complications already.
Regardless of the patient’s willingness to comply with all the medical regimens that would possibly help his condition there is only small hope that normal cardiac rate and rhythm would be achieved basing on the amount of myocardial tissue that has already been damaged. The family also lacks the financial support that they would need for medical intervention and this is also with respect to the patient’s age.
CRITERIA ACTUAL JUSTIFICATION
Poor Fair Good
Duration of illness √
The patient already had four attacks prior to the present hospitalization. This implies that the condition of the patient continuously deteriorates every after the attack. In addition, it only indicates that the patient is unable to meet the necessary interventions to prevent having another attack.
Willingness to
take medication √
The patient is very willing to take all the available prescribed medications. In fact, he always asks questions regarding it. He would ask for the purpose of his medicines before taking it.
Age √
The patient is not getting any younger and at his current age (60 y.o.) there is a higher risk for acquiring such illness. Since the patient’s immune system and other bodily functions deteriorates as he continuously age he will no longer be able to fight against infection or inflammation that could also trigger the aforementioned illness.
Expectations to √
The patient wanted to go home with ordered medications however, he is also aware of the
illness reality that his condition is worsening. He and his family still hopes that Mr. Perfecto would fully recover from his illness.
Environment √
The patient lives in an air conditioned room and is provided with his oxygen tank. There is no air pollutant present that could worsen his respiratory problems and the patient already stopped all his vices ever since he had his attack.
Family support √
The family is always there to provide assistance and support the patient. Although this is the case the family still lacks assistance on other matter such as financial aid. The help the patient gets from his daughter is not enough to sustain all that should necessarily be done to achieve optimal health.
BIBLIOGRAPHY
Harrison’s Internal Medicine
Marilynn E. Doenges, Mary Frances Moorehouse, Alice C. Geissler-Murr, Nurses’ Pocket Guide, Diagnoses, Interventions and Rationales. 9th Edition
Marilynn E. Doenges, Mary Frances Moorehouse, Alice C. Geissler-Murr, Nursing Care Plan Guidelines for Individualizing Nursing Care 6th Edition
Nowak, Thomas. Pathophysiology: Concepts and Application for Health Care Professionals, 3rd Edition
Rod Seeleys, Trent D. Stephens, Philip Tate, Essentials of Anatomy and Physiology 4th Edition Suzanne C. Smeltzer, Brenda G. Bare, Brunner and Suddhart’s Textbook on Medical-Surgical
10th Edition
Sylvia A. Price, Lorraine M. Wilson, Pathophysiology Clinical Concepts of Disease Process 4th Edition
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http://www.cvphysiology.com/Heart%20Disease/HD002.htm
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http://www.emedicine.com/EMERG/topic327.htm http://en.wikipedia.org/wiki/Myocardial_infarction
http://circ.ahajournals.org/cgi/content/abstract/111/25/3481
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