Professional Documents
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Book 1 Complete
Book 1 Complete
Angina pectoris is a term used to describe chest pain, characterized by transient and paroxysmal. The
chest pain is produced by insufficient blood flow to the myocardium resulting in myocardial ischemia.
Risk factors
Pathophysiology
1. Decrease supply
❖ Hypotension (Spinal anesthesia, drugs, blood loss)- | blood return to the heart
2. Increased demand:
- Increase cardiac output e.g., exercise, emotion, digestion of a large meal, anemia and hyperthyroidism
- Increased myocardial need of 02 e.g. HTN, hypertrophy of the myocardium, thyrotoxicosis, strong
emotion, heavy exertion
Classifications
■ Stable angina: it is also called exertional angina. It occurs with activities that involve
coronary artery spasm and may occur at rest. The attacks may be associated with ST
interventions
■ Angina usually causes chest pain that is like pressure, crushing, tightness, squeezing
substemally with possible radiation to the neck, jaw, back, and arms and relieved by
rest.
Diagnosis
• History of chest pain, aggravating factors (e.g. exercise, emotion, heavy meal),
• Chest X -ray
The objectives of the management of angina are: (1) Relief from acute attack (2) Prevention of
further attack for reducing the risk of MI. The treatment is focused on decreased oxygen demand
1. Pharmacological management
given by different routes such as sublingual, oral, IV, topical to reduce myocardial
afterload.
► Anti-ischemic agents
2. Dietary management: low saturated fat and low cholesterol diet. Increase the intake of
3. Surgery: Revascularization therapy can be considered in patients with left main artery
stenosis greater than 50%, 2- or 3-vessel disease and LV dysfunction (ejection fraction,
< 45%), poor prognostic signs during noninvasive studies, or severe symptoms despite
stenting,
Nursing management
1. Assess pain, vital signs, dysrhythmias, cardiac output, anxiety, dyspnea, level of
consciousness, pallor, and diaphoresis. During pain assessment, find out the
information about location, intensity, radiation, frequency, aggravating factors,
alleviating factors.
P Position, location, provocation Where is the pain? Can you point it? What were you
doing when pain began?
Q Quality and quantity How would you describe the pain? Has the pain been
constant or relieved with rest?
R Radiation and relief Had pain radiated to another site? Had pain relieved
after rest?
S Severity and symptoms How much do you rate your pain in 0-10 pain scale or
mild, moderate, severe? Did you notice any other
symptoms with pain?
2. Provide bed rest and place the patient in semi to high Fowler’s position
8. Instruct the client to notify the physician if pain occurs and persists, despite rest and
medication
9. Provide teaching
❖ If no relief with 1 tablet, take additional tablets at 5-minute intervals, but no more than 3
tablets within 15 minutes.
❖ Keep the bottle tightly capped and prevent exposure to air, light, heat
■ Gradually increase activities and exercise. Can participate in regular exercise program
Evaluation
" The patient does not exhibit manifestations that indicate high level of anxiety
Myocardial infarction
Myocardial infarction (MI), commonly known as a heart attack, is the irreversible necrosis of heart
muscle secondary to prolonged ischemia.
MI usually results from an imbalance in oxygen supply and demand, which is most often caused by
plaque rupture with thrombus formation in a coronary vessel, resulting in an acute reduction of blood
supply to a portion of the myocardium when myocardial tissue is abruptly and severely deprived of 02.
Risk factors
Nonmodifiable
• Advance age
• Male
Modifiable factors
• Diabetes mellitus
• Hypertension
• Dyslipidemia
Contributing factors
• Obesity
• Sedentary lifestyle
• Psychosocial stress
• Type A personality
Pathophysiology
I
Activates the platelets
Formation of thrombus
Myocardial ischemia
Myocardial cell death -> Anaerobic glycolysis -> lactic acid production -> severe chest pain.
Decreased myocardial contractility -> stimulation of CNS -> HR -> O2 demands? Afterload
Shock
Death
The degree of symptoms ranges from asymptomatic (in diabetic patient) to sudden cardiac death.
In spite of the variation of manifestations, majority of the signs and symptoms are as follows:
■ Pain usually substernal with radiation to the neck, arm, jaw or back, severe, crushing,
viselike with sudden onset, unrelieved by rest or nitrates
Complications
heart tissues)
Diagnosis
Diagnosis criteria of MI (WHO, 2000): a cardiac troponin rise accompanied by typical symptoms,
■ History: chest discomfort, types, nature of chest pain, aggravating and alleviating
■ Physical examination: vital signs, heart sound, lung sound, JVP, skin condition etc
■ Cardiac enzyme:
> CK-MB level rises within 3-12 hours of the onset of chest pain, reach peak values
within 24 hours, and return to baseline after 48-72 hours (50- 325 unit/L
> Troponin levels increase within 3-12 hours from the onset of chest pain, peak at
> LDH level rises 24 hrs. after MI, peaks between 48-72 hours and falls to normal in
7 days (normal value- troponin I <0.6ng/ml
> Myoglobin level rises within 1 hour after cell death, peaks in 4-6 hours and return
Management
1. Restoration of the balance between the oxygen supply and demand to prevent further
ischemia
2. Pain relief
■ 02 therapy: to reduce myocardial work load and maintain SP02 > 90%
■ Morphine: Usually morphine (opioid) is given I/V, to relieve pain and anxiety.
vasodilator effects
decreasing heart rate & BP and force of myocardial contraction. Monitor pulse/heart
rate & BP
■ Calcium channel blocker can be used after beta blocker and nitrates.
■ Antidysrhythmic and inotropes may be used according to the changes in ECG, BP and
pulse.
■ A defibrillator may be used to restore a normal rhythm if the patient has arrhythmias
chest pain of less than 12 hours, it dissolves the thrombus in a coronary artery &
■ Stool softeners; reduce stress during defecation and reduce myocardial workload.
■ H2 antagonist
■ Diuretics: can help get rid of excess fluids that sometimes accumulate when the heart is
not pumping effectively. Usually taken orally, they cause the body to dispose fluids
through urination.
soon as possible.
■ M- morphine
■ O-oxygen
■ N- nitrate
■ A- antiplatelets
■ B- beta blockers
■ H- heparin
■ A- atorvastatin
■ I- inotropes (dopamine, dobutamine)
Surgical management
(PC1/PTCA).
Nursing management
The focus of the plan of care tor MI patient includes Recognize and treat potentially life
therapeutic critical care environment. Identify the psychosocial impact of the MI on the client and
significant others. Educating the client in lifestyle changes and rehabilitation after the MI.
Assessment
■ Physical examination- position of the patient, sweating, BP, pulse, temperature, heart
sound
Nursing diagnosis
■ Acute chest pain may be related to myocardial ischemia resulting from coronary artery
occlusion with loss/restriction of blood flow to an area of the myocardium and necrosis
changed heart rate, |BP, jtemperature, changed skin color, dyspnea, impaired capillary
■ Ineffective coping may be related to acute illness, anticipated life style change
■ Anxiety may be related to hospitalization, fear of death
■ High risk for activity intolerance may be related to imbalance between 02 supply and
demand
■ Risk for constipation may be related to bed rest, medication, NPO, soft diet
Nursing interventions
straining
6. Need to report the following symptoms; increased persistent chest pain, dyspnea,
Rehabilitation: The overall goal of the cardiac rehabilitation is to help the patient (1) Live as full,
vital and productive life as possible (2) Remain within the limits of the heart’s ability to respond
to increase in activity and stress. This program has six important sub goals which are as follows:
2. Teach the patient and significant others concerning cause, prevention and
treatment of CAD
6. Change the psychosocial factors adversely affecting the recovery from CAD
A heart healthy life-style includes; a low-fat diet, regular exercise, maintaining a healthy weight,
no smoking, moderate drinking, no illegal drugs, controlling hypertension and managing stress.
Valvular heart disease occurs when the heart valves cannot fully open (stenosis) or close
completely (insufficiency or regurgitation). Valvular heart disease prevents efficient blood flow
through the heart. Chronic valvular heart disease develops in at least half of those affected by
rheumatic fever with carditis. Two thirds cases occur in women. Mitral valve is affected in more
than 90% cases, followed by aortic, tricuspid and then pulmonary valves in decreasing order of
frequency. Valvular heart disease is categorized according to the anatomical name and functional
Insufficiency.
Mitral stenosis (MS)
Mitral stenosis occurs if valvular tissue thickens and narrows the valves MS is characterized by
obstruction to left ventricular inflow at the level of mitral valve due to structural abnormality of
Primarily a result of rheumatic fever and rarely congenital. Rheumatic heart disease causes
scarring & fusion of valve apparatus. Pure or predominant MS occurs in approximately 40% of
all patients w.th rheumatic heart disease and two-thirds of all patients with MS are female.
• Moderate mitral stenosis: MVA 1.0-1.5 cm2 usually does not produce symptoms at rest
• Severe mitral stenosis: MVA <1.0 cm and 2 symptoms occur even at rest.____________
Pathophysiology
I
Decreased cardiac output
Activity intolerance
• Pulmonary edema
• SOB/Cough
• Increased JVP
• Edema
> Orthopnea
> Edema
■ Systemic embolism
■ Atrial fibrillations
Diagnosis
■ ECHO: Thickened immobile cusps; reduced valve area, reduced rate of diastolic filling
of LV
passed from the femoral vein through the arterial septum to the mitral valve. The
balloon is inflated to enlarge the orifice. It is effective for long term improvement.
Mechanical or Bioprosthetic
Nursing management
> Monitor closely for signs of bleeding, cardiac output, sings of heart failure.
> Administer medications as prescribed and monitor incision and report any redness
❖ Avoid: any dental procedure for six months. Heavy lifting (>10 lb) and
reduce risk of infective endocarditis. Brush teeth twice daily with a soft
Aortic stenosis
Aortic stenosis is a narrowing of the aortic valve in the heart. This restricts the blood flow through
the valve. The heart then needs to squeeze (contract) harder to pump blood into the aorta.
Causes
Pathophysiology
Normally the aortic valve consists of three cusps or leaflets and has an opening of 3-42cm. When
the left ventricle contracts, it forces blood through the valve into the aorta When the left ventricle
expands again, the aortic valve closes and prevents the blood in the aorta from regurgitating into
Partial restriction of blood flow from the left ventricle into the aorta
Diagnosis
■ Aortic stenosis is diagnosed by heart murmur, chest X-ray (calcification around the
Management
Management of the patient depends upon the clinical manifestation, if there is no symptom then
may not need any treatment. If the patient develops symptoms or complications, medicines and
Nursing management
■ Provide nursing care according to physical status of the patient and pre-post operative
Aortic regurgitation
Regurgitation is due to incompetence of the aortic valve or any disturbance of the valvular
apparatus. Blood is leaked each time from the aortic valve when the left ventricle relaxes.
Regurgitation of aortic valve allows the blood to flow in two directions. Oxygen-rich blood flows
out through the aorta to the body as it should, but some flows backwards from the aorta into the
Incompetent closure of the aortic valve can result from intrinsic disease of the cusp, diseases of
the aorta, or trauma. An increase in systolic stroke volume and low diastolic aortic pressure
produces an increased pulse pressure. The heart will have to do more work to compensate for the
blood leaked back into the left ventricle. The walls of the ventricle will sometimes thicken
(hypertrophy), and a thickened heart muscle is a less effective pump. Eventually, the heart maybe
unable to pump enough to meet the body’s need for blood, leading to heart failure.
Mild aortic regurgitation may be treatable with medications to reduce blood clotting and reduce
Cardiomyopathy
Cardio: heart Disease of the heart muscles (myocardium) which inhibit effective
Pathy: disease
Cardiomyopathy is a subacute or chronic disease of the heart muscle, associated with cardiac
dysfunction (heart loses effectiveness as a pump). In cardiomyopathy, the heart muscle becomes
enlarged, thick or rigid. When condition becomes worse, the heart becomes weaker and less able
to pump blood through the body and maintain a normal electrical rhythm. The result can be heart
failure, or arrhythmias. Problems also arise in heart valves due to a weakened heart. Treatment is
palliative, not curative, and the client needs to deal with numerous lifestyle changes and a
Causes
Classifications
hypercontraction of the left ventricle and rigid walls that causes obstruction of the left
ventricular outflow.
Pathophysiology
■ Decreased stroke volume stimulates the sympathetic nervous system and the renin
and increased sodium and fluid retention, which places an increased workload on the
heart.
a result, the heart cannot pump blood to the rest of the body, which causes heart failure.
■ The heart loses its ability to pump blood and, in some instances, heart rhythm is
Dilated cardiomyopathy
• Shortness of breath
• Activity intolerance
• Blood clots in the dilated left ventricle because of pooling of the blood
Hypertrophic myopathy
• Exertional dyspnea, syncope
• Palpitation
• Chest pain is prolonged, unrelated to exertion and not relieved by nitrates dysrhythmias
Restrictive myopathy
• Shortness of breath (at first with exercise; but over time it occurs at rest)
• Fatigue, weakness
• Activity intolerance
• Weight gain
• Palpitations
Diagnosis
■ Medical and family history of heart disease and physical exam- swelling of the ankles,
feet, legs, abdomen or veins in the neck suggests fluid buildup, which is a sign of heart
failure.
■ Myocardial Biopsy
Treatment includes
output
■ Instruct the patient to report any signs of dizziness of fainting, which may indicate a
dysrhythmia
■ Instruct the patient to avoid ingestion of alcohol because of cardiac depressant effect
■ Beta blockers and calcium antagonists decrease the outflow obstruction and decrease
C = Calcium channel blocker (end in -dipine, -zem, -amil) e.g., nifidipine, diltizem.
verapamil
Assessment
■ Vital signs, SOB, restlessness, chest pain, ECG, level of anxiety, alertness
Nursing diagnosis
dysrhythmias
Nursing interventions
> skin warmth, color, and capillary refill time, chest discomfort because myocardial
> heart and lung sounds to evaluate the degree in heart failure.
■ Monitor:
> Urinary output every hour to evaluate status of cardiac output and effects of
medications.
> The patient’s activities and nursing interventions that may adversely affect
oxygenation.
■ Monitor serum potassium before and after the administration of loop diuretics.
Heart failure
Heart failure or cardiac failure is inability of the heart to pump an adequate supply of blood to
meet the metabolic needs of the body. It is a clinical syndrome, which is developed due to
accumulation of the blood in front of the left or right parts of the heart.
• MI
• Hypertension
• Mitral stenosis
Right sided
• COPD
• Pulmonic stenosis
• Pulmonary embolism
Pathophysiology
■ The common pathophysiologic state that perpetuates the progression of heart failure is
■ Only when this network of adaptations becomes overwhelmed does heart failure ensue.
Ventricular dysfunction limits a patient's ability to perform the routine activities.
• Tachycardia
• Possible S3
• Cyanosis, pallor
• Bounding pulses
• Hepatomegaly
• Cool extremities
• Oliguria
Class II: Slight limitation of physical activity. Comfortable at rest, but ordinary physical
Class III: Marked limitation of physical activity. Comfortable at rest, but less than ordinary
Class IV: Unable to carry out any physical activity without discomfort. Symptoms of cardiac
Diagnosis
■ Physical examination: vital signs, abnormal heart and lung sounds, swelling, weight gain
■ ECG
■ Chest x-ray
■ Echocardiography
> Digitalis
> Dopamine and dobutamine- facilitate myocardial contractility and enhance stroke volume
> Diuretics-|preload
> ACE inhibitors- suppress RAAS-frenal blood flow &|renal vascular resistance-dieresis
lifestyle e.g. rest, exercise, reduce weight, quit smoking, goal setting etc
> Create realistic goal: Have patients set their own goals of what they would like to
> Encourage them to participate in activities e.g. daily weight check, regular
follow up
Nursing management
Assessment
■ Vital signs, fatigue, dyspnea, exertional dyspnes, swelling, restlessness, dietary pattern,
■ Fluid volume excess may be related to reduced GFR, decreased cardiac output,
■ High risk for decreased peripheral tissue perfusion may be related to decreased cardiac
■ High risk for activity intolerance may be related to reduced cardiac output
■ High risk for impaired skin integrity may be related to immobility, swelling
Nursing interventions
pulmonary edema):
> Monitor ECG, vital signs, daily weight, CVP, electrolyte, peripheral edema,
■ Provide teaching
> Medical regimen including name, purpose, dosage, frequency, and side effects
Shock
Shock is an abnormal physiologic state where an imbalance between the amount of circulating
blood volume and the size of vascular bed results in circulatory failure and oxygen and nutrient
dysfunction of organs vital to survival. The effects of shock are initially reversible, but rapidly
Classification of shock
volume lead to decrease in diastolic filling pressure and volume which results in
adequate cardiac output hypotension and shock e.g., hemorrhage, severe diarrhea or
vomiting etc
■ Cardiogenic: failure of the heart to pump properly; marked by the reduced cardiac
in preload that leads to hypotension with a normal or increased cardiac output such as
injury etc.
> Anaphylactic: massive vasodilatation resulting from allergic reaction due to
> Septic: release of bacterial toxins that act directly on the blood vessels producing
massive vasodilation and pooling of blood results usually occurs in gram negative
septicemia.
■ Impaired metabolism: tissue anoxia leads to anaerobic metabolism causing lactic acid
■ Impaired organ function e.g. renal failure (decreased perfusion in kidneys), shock lung
(ARDS)
■ Cool, pale moist skin (in hypovolemic and cardiogenic shock); warm, dry and pink skin
■ BP may be normal in the early stage due to compensatory mechanisms and BP drops in
■ Decreased temperature
Nursing interventions
■ Promote restoration of blood volume; administer fluids (crystalloid solutions. RL, NS;
> Elevate lower extremities to 45° to promote venous return to heart, thereby
> Promote rest by using energy conservation measures and maintain quiet
environment as possible
> Monitor urine output, CVP, ECG and report significant changes e.g., decrease
> Check laboratory reports: CBC, electrolytes, BUN, creatinine, blood gases
■ Provide psychological support to the patient and family; reassure the patient to relieve
apprehension
Drugs used to treat shock
Cardiac arrest
Cardiac arrest is the condition where the heart’s pumping function is “arrested,” or stopped. It is a
sudden, sometimes temporary, cessation of the heart's functioning due to malfunction of the
It is a condition of sudden, unexpected cessation of breathing and adequate circulation of blood by the
heart. Cardiac arrest, also known as cardiopulmonary arrest or circulatory arrest, is the cessation of
normal circulation of the blood due to failure of the heart to contract effectively.
Arrested blood circulation prevents delivery of oxygen to the body. Lack of oxygen to the brain causes
loss of consciousness, which then results in abnormal or absent breathing. Brain injury is likely to
happen if cardiac arrest goes untreated for more than five minutes. For the best chance of survival and
neurological recovery, immediate and decisive treatment is imperative.
Causes
■ Cardiac causes
■ Non cardiac causes: drug overdose, pulmonary embolism, poisoning, hypo/hyperkalemia, hypoxia etc.
Pathophysiology
Brain death
■ Pallor, cyanosis
■ Dilation of pupils
Management
■ Assess level of consciousness, pulse and respiration to find out cardiac arrest
protocol
compress/minute
■ Defibrillation
■ Drug therapy:
> Adrenaline (ephinephrine): the first drug given in all causes of cardiac arrest to
ventricular fibrillation
VT/VF
> Atropine sulfate to reduce vagus nerve’s control over the heart, thus increasing the
heart rate
> Sodium bicarbonate: administered during the first few moments of a cardiac arrest
> Calcium chloride: calcium ion helps the heart beat more effectively by enhancing
> Maintain oxygen saturation (>94%), fluid volume (systolic pressure > 90 mmHg),
> For a low blood pressure, consider one or more of these treatments:
system
■ Rapid defibrillation
Nursing management
> Assist with administration of and monitor effects of additional emergency drugs
> Manage the airway, provide oxygen and maintain oxygen saturation >94%.
> Keep IV line open and administered IV fluids and medication as prescribed.