INTRODUCTION

Cardiovascular disease is the number one killer of adults. Prompt recognition and initiation of
appropriate treatment can save lives during six of the most deadly cardiac emergencies: angina
pectoris, myocardial infarction, cardiac arrest, carcinogenic shock, cardiac temponant, acute
coronary syndrome

ANATOMY AND PHYSIOLOGY OF CIRCULATORY SYSTEM

Heart

The heart is a roughly cone-shaped hollow muscular organ. It is about 10 cm long and is
about the size of the owner’s fist. It weighs about 225 g in women and is heavier in men (about
310 g). Position. The heart lies in the thoracic cavity in the mediastinum (the space between the
lungs). It lies obliquely, a little more to the left than the right, and presents a base above, and an
apex below. The apex is about 9 cm to the left of the midline at the level of the 5th intercostal
space, i.e. a little below the nipple and slightly nearer the midline. The base extends to the level
of the 2nd rib.
Structure

The heart wall is composed of three

layers of tissue pericardium,
myocardium and endocardium.

1. Pericardium
The pericardium is the
outermost layer and is made up of two sacs. The outer sac consists of fibrous tissue and the
inner of a continuous double layer of serous membrane. The outer fibrous sac is continuous
with the tunica adventitia of the great blood vessels above and is adherent to the diaphragm
below.

2. Myocardium
The myocardium is composed of specialised cardiac muscle found only in the heart. It is
not under voluntary control but is striated, like skeletal muscle. Each fibre (cell) has a
nucleus and one or more branches. The myocardium is thickest at the apex and thins out
towards the base. This reflects the amount of work each chamber contributes to the pumping
of blood.

1. Endocardium
It is innermost layer of the heart. This lines the chambers and valves of the heart. It is a
thin, smooth, glistening membrane that permits smooth flow of blood inside the heart. It
consists of flattened epithelial cells, and it is continuous with the endothelium lining the
blood vessels.

The cardiac cycle

At rest, the healthy adult heart is likely to beat at a rate of 60–80 bpm. During each
heartbeat, or cardiac cycle the heart contracts and then relaxes. The period of contraction is
called systole and that of relaxation, diastole. Stages of the cardiac cycle Taking 74 bpm as an
example, each cycle lasts about 0.8 of a second

Flow of blood through the heart

The two largest veins of the body, the superior and inferior vena cava, empty their
contents into the right atrium. This blood passes via the right atrio- ventricular valve in to the
right ventricle, and from there is pumped into the pulmonary artery or trunk (the only artery in
the body which carries deoxygenated blood). The opening of the pulmonary artery is guarded by
the pulmonary valve, formed by three semi-lunar cusps. This valve prevents the backflow of
blood into the right ventricle when the ventricular muscle relaxes. After leaving the heart the
pulmonary artery divides into left and right pulmonary arteries, which carry the venous blood to
the lungs where exchange of gases takes place: carbon dioxide is excreted and oxygen is
absorbed. Two pulmonary veins from each lung carry oxygenated blood back to the left atrium.
Blood then passes through the left atrio-ventricular valve into the left ventricle, and from there it
is pumped into the aorta, the first artery of the general circulation. The opening of the aorta is
guarded by the aortic valve, formed by three semi-lunar cusps.

Function of heart

 Generating blood pressure

 Routing blood –heart separates pulmonary and systematic circulation,
 Ensuring one way blood flow-heart valves ensure one way flow
 Regulating blood supply- changes in contraction rate and force match blood delivery to
changing metabolic needs.

CLASSIFICATION OF CARDIAC EMERGENCY

a) Angina Pectoris
b) Cardiac Tamponade
c) Myocardial Infarction
d) Cardiac Arrest
e) Cardiogenic shock
ANGINA PECTORIS

DEFINITION

A disease marked by brief sudden attacks of chest pain or discomfort caused by deficient
oxygenation of the heart muscles usually due to impaired blood flow to the heart.

PREVALENCE

The prevalence of CAD has been steadily increasing, and India is no exception to this. 1 In the
last three decades, the prevalence of CAD has significantly increased. The prevalence of CAD in
urban areas was 2.5% 12.6% and in rural areas, it was 1.4% 4.6%.

TYPES:

1) Stable Angina
2) Unstable Angina
3) Variant angina.
4) Angina decubitus
5) Intractable angina
6) Post infraction angina

1) Stable Angina
Stable angina is paroxysmal chest pain or discomfort triggered by a predictable
degree of exertion (e.g., walking 20 feet) or emotion. Char- acteristically, a stable pattern of
onset, duration, severity, and relieving factors is present. Normally, stable angina is relieved
with rest or nitroglycerin, or both.
 2) Unstable angina.

Unstable angina (preinfarction angina, crescendo angina, or intermittent coronary syndrome)

is paroxysmal chest pain triggered by an unpredictable degree of exertion or emotion, which
may occur at night. Unstable angina attacks characteristically increase in number, duration,
and severity over time. If unstable angina occurs, it must be treated as a medical emergency
with the client receiving immediate medical attention.

3) Variant angina.

Variant angina (Prinzmetal's angina) is chest discomfort similar to classic angina but of
longer duration; it may occur while the client is at rest. These attacks tend to happen between
mid- night and 8 AM. Variant angina results from coronary artery spasm and may be
associated with elevation of the ST segment on the electrocardiogram (ECG). Nocturnal
angina. Nocturnal angina is possibly associated with rapid eye movement (REM) sleep
during dreaming

4) Angina decubitus.

Angina decubitus is paroxysmal chest pain that occurs when the client reclines and lessens
when the client sits or stands up.

5) Intractable angina

Intractable angina is chronic incapacitations angina that is unresponsive to intervention

6) Postinfraction angina

Pain occurs after MI, when residual ischemia may cause episodes of angina.

ETIOLOGY

Angina pectoris is associated with atherosclerotic lesions and is a manifestation of CHD.

Angina can be caused either by chronic or acute blockage of a coronary artery or by coronary
artery spasm. Chronic blockages are associated with fixed calcified (type Vb) or fibrotic (type
VC) atherosclerotic lesions that occlude more than 75% of the vessel lumen.

When fixed blockages are present in the coronary arteries, conditions that increase
myocardial oxygen demand (e.g., physical exertion, emotion, exposure to cold) may precipitate
episodes of angina. Because the severely stenosed arteries cannot dilate to deliver enough
oxygen to meet the increased demand, ischemia results. In contrast, acute blockage of a coronary
artery results from rupture or disruption of vulnerable atherosclerotic plaques that cause platelet
aggregation and thrombus formation. Acute blockages are associated with unstable angina and
AMI.

Development of atherosclerosis; Coronary artery disease is thought to begin with damage

or injury to the inner layer of a coronary artery, sometimes as early as childhood

The damage may be caused by various factors, including:

 Smoking
 High blood pressure
 High cholesterol
 Diabetes or insulin resistance
 Sedentary lifestyle

RISK FACTORS:

MODIFIABLE RISK FACTORS:

 Tobacco use
 High blood cholesterol or triglyceride levels
 Lack of exercise
 Obesity
 Stress

NONMODIFIABLE RISK FACTORS:

 Family history of heart disease

 Older age
  Diabetes
 High blood pressure

PATHOPHYSIOLOGY

Angina is usually caused by atherosclerotic disease. Almost invariably angina is associate with a
significant obstruction of at lest one major coronary artery. Normally, the myocardium extracts a
large amount of oxygen from the coronary circulation to meet its continuous demands. When
demand increases, flow through the coronary arteries needs to be increased. When there is a
blockage in a coronary artery, flow cannot be increased and ischemia result.

Predisposing factor

Obstruction in coronary artery

Ischemia

Hypoxia

Reduced oxygen demand Angina

Thrombolyisis Unstable angina

CLINICALMANIFESTATION

Angina is a clinical syndrome characterized by discomfort in the chest, jaw, shoulder, back, or
arm. Angina pectoris produces transient paroxysmal attacks of substernal or precordial pain with
the following characteristics:
Onset. - Angina can develop quickly or slowly. Some clients ignore the chest pain, thinking that
it will go away or that it is indigestion. Ask what the client was doing when the pain began.

Location:-. Nearly 90% of clients experience the pain as retrosternal or slightly to the left of the
sternum

Radiation. - The pain usually radiates to the left shoulder and upper arm and may then travel
down the inner aspect of the left arm to the elbow, wrist, and fourth and fifth fingers. The pain
may also radiate to the right shoulder, neck, jaw, or epigastric region. On occasion, the pain may
be felt only in the area of radiation and not in the chest. Rarely is the pain localized to any one
single small area over the precordium.

Duration. - Angina usually lasts less than 5 minutes. However, attacks precipitated by a heavy
meal or extreme anger may last 15 to 20 minutes squeezing, burning, pressing, choking, aching,
or bursting pressure. The client often says the pain feels like gas, heartburn, or indigestion.
Clients do not describe anginal pain as sharp or knife-like.

Severity. - The pain of angina is usually mild or mod- erate in severity. It is often called
"discomfort," not "pain." Rarely is the pain described as "severe."

Associated characteristics. - Other manifestations that may accompany the pain include
dyspnea, pallor, sweating, faintness, palpitations, dizziness, and digestive disturbances.

Atypical presentation. - Women, older adults, and clients with diabetes may have atypical
presentations of CHD that are equivalent to angina. In women, CHD may be manifested as
epigastric pain, dyspriea, or back pain, whereas older adults frequently experience dyspnea,
fatigue, or syncope.

Relieving and aggravating factors. Angina is aggra- vated by continued activity, and most
anginal attacks quickly subside with the administration of nitroglycerin and rest. The typical
exertion-pain, rest-relief pattern is the major clue to the diagnosis of angina pectoris.
Treatment. :-Treatments to reduce the demand on the heart, such as rest, or treatments that
dilate then coronary arteries will commonly reduce the pain. The client may have used
nitroglycerin and the client should be asked if the angina subsided.

DIAGNOSTIC EVALUATION

 ECG: - The ECG tracings remain normal in more than 50% of clients with angina
pectoris at rest. An ECG recorded in the presence of pain may document transient
ischemic attacks with ST-segment elevation or depression. An ECG recorded during an
episode of pain also suggests coronary artery involvement and the extent of cardiac
muscle affected by the ischemic event
 Exercise Electrocardiography
During a stress test, the client exercises on a treadmill or stationary bicycle until reaching
85% of maximal heart rate. ECG or vital sign changes may indicate ischemia. Exercise
electrocardiography is less sensitive in women and older adults.
 Radioisotope Imaging
Various nuclear imaging techniques are used to evaluate myocardial muscle. Regions of
poor perfusion or ischemia appear as areas of diminished or absent activity (cold spots).
 Tomography (EBCT)
This non-invasive method enables detection of the amount of calcium in coronary
arteries. Because calcification occurs with atherosclerotic plaque formation,
measurement of coronary calcium may reflect the extent of coronary atherosclerosis.
High coronary calcium values have been associated with obstructive coronary disease.
 Coronary Angiography
Angiography remain the most accurate test to diagnose the percentage of blockage in
coronary arteries because of atherosclerosis.

 Chest X-Ray
 Chest x-rays are an inexpensive technique that allows detection of cardiomegaly and
noncardiac causes of chest pain (e.g. pleuritis or pneumonia).

MEDICAL MANAGEMENT

Various drugs can be used to treat coronary artery disease, including:

Vasodilators (These drugs acts as blood vessel dilator):

1. Nitrates: - Nitrates are used to treat the chest pain associated with angina and to ease the
symptoms of congestive heart failure (CHF).

 Nitroglycerin (such as Nitro-Dur, Nitrolingual, Nitrostat).

 Isosorbide (such as Dilatrate, Isordil).
 Nitroprusside (such as Nitropress).

2. Beta-Blockers (Decrease work load in heart): Beta blockers block the release of the stress
hormones adrenaline and noradrenaline. They are widely prescribed for angina, heart failure and
some heart rhythm disorders, and to control blood pressure.

Examples of beta blockers

 Acebutolol (Sectral)
 Atenolol (Tenormin)
 Bisoprolol (Zebeta)
 Metoprolol (Lopressor, Toprol XL)
 Nadolol (Corgard)
 Nebivolol (Bystolic)

3. Propranolol 20-40 mg:- Propranolol oral tablet reduces your heart's workload and helps it

beat more regularly. It's used to treat high blood pressure, angina, and atrial fibrillation

Calcium channel blocker (They improve coronary blood flow):

Nifedipine: - nifedipine helps to prevent future heart disease, heart attacks and
strokes. Nifedipine is also used to prevent chest pain caused by angina. Occasionally, it's used
to treat Raynaud's phenomenon and chilblains. The medicine is only available on prescription.

Anticoagulant Drugs:

Heparin :- Heparin (heparin sodium injectable) is a heterogeneous group of straight-chain

anionic mucopolysaccharides, called glycosaminoglycans that have anticoagulant properties used
to help prevent clot formation (for example, venous thrombosis, pulmonary embolisms,
coagulopathies and coronary artery clots).

ANTIHYPERTENSIVE MEDICINES-

 Methydopa - This medication is used alone or with other medications to treat high
blood pressure (hypertension). Lowering high blood pressure helps prevent strokes,
heart attacks, and kidney problems.Methyldopa works by relaxing blood vessels so
blood can flow more easily.
 Sodium nitroprusside- It is used for lowering the blood pressure.
 Amlodipine- Amlodipine is used with or without other medications to treat high blood
pressure. Lowering high blood pressure helps prevent strokes, heart attacks, and kidney
problems. Dose-10 mg,20 mg

NURSING MANAGEMENT

 Instruct the client regarding the purpose of diagnostic medical & surgical
procedures and the pre- & post procedure expectations.
 Assist the client to identify risk factors that can be modified, and set goals that
will promote change in lifestyle to reduce the impact of risk factors.
 Instruct client regarding a low-calorie, low-sodium, low-cholesterol, low-fat diet
with an increase in dietary fiber. Stress that dietary changes are not temporary and
must be maintained for life.
 Provide community resources to client regarding exercise, smoking cessation and
stress reduction.
PREVENTION:

 Quitting smoking
 Monitoring and controlling other health conditions, such as high blood pressure, high
cholesterol and diabetes
 Eating a healthy diet and maintaining a healthy weight
 Increasing physical activity. Aim for 150 minutes of moderate activity each week. Plus,
it's recommended that person get 10 minutes of strength training twice a week and to
stretch three times a week for 5 to 10 minutes each time.
 Reducing stress level
 Limit alcohol consumption to two drinks or fewer a day for men, and one drink a day or
less for women.
 Get an annual flu shot to avoid heart complications from the virus

NURSING DIAGNOSIS
1. Impaired gas exchange related to decreased blood flow as evidenced by breathlessness
2. Acute pain related to disease condition as evidenced by patient verbalization
3. Impaired physical mobility related to weakness as evidenced by patient is unable to
perform daily activity.
4. Imbalanced nutrition less than body requirement related to less intake of food as
evidenced by weight loss
5. Disturbed sleep pattern related to hospitalization as evidenced by patient verbalization
6. Anxiety related to hospitalization as evidenced by patient asking too many question.
7. Knowledge deficit related to disease process and treatment as evidenced by patient is
having many doubts
CARDIAC TAMPONADE

• DEFINATION

Cardiac tamponade is a life threatening complication caused by accumulation of fluid in the

pericardium

This fluid ,which can be blood.pus ,or air in the pericardial sac, accumulates fast enough and in
sufficient quantity to compress the heart and restrict blood flow in and out of the ventricles. This
a cardiac emergency.

INCIDENCE

The incidence of cardiac tamponade is 2 cases per 10,000 population in the United States.
Approximately 2% of penetrating injuries are reported to result in cardiac tamponade.

ETIOLOGY

 In this condition, blood or fluid collects in the pericardium, the sac surrounding the heart.
This prevents the heart ventricles from expanding fully. The excess pressure from the
fluid prevents the heart from functioning normally. As a result, the body does not receive
enough blood.
 Cardiac tamponade can occur due to:
o -Dissecting aortic aneurysm (thoracic)
o -End-stage lung cancer
o Heart attack (acute MI)
o -Heart surgery
o -Pericarditis caused by bacterial or viral infections
o Wounds to the heart
 Other possible causes include:
 -Heart tumors
 -Hypothyroidism
  -Kidney failure
 -Leukemia
 -Placement of central lines
 -Radiation therapy to the chest
 -Recent invasive heart procedures
 -Recent open heart surgery
 -Systemic lupus erythematosus

PATHOPHYSIOLOGY

Cardiac tamponade results from an accumulation of pericardial fluid under pressure, leading to

impaired cardiac filling and haemodynamic compromise. Findings during physical examination
are included in Beck´s triad (sinus tachycardia, elevated jugular venous pressure, low blood
pressure) and pulsus paradoxus.
CLINICAL MANIFESTATION

 Elevated venous pressure (increased venous pressure}

 Distended neck veins Kussmaul's sign{distended neck veins
 Hypotension
 Tachycardia
 Narrow pulse pressure
 Dyspnoea
 Cyanosis of lips and nails
 Restlessness and anxiety
 Diaphoresis
 Muffled heart sounds
  pulses paradoxus:- fall of systolic blood pressure of >10 mmHg during the
inspiratory phase.
 Decreased QRS voltage:- QRS complex amplitudes of <0.5 mV in all frontal
leads and/or <1.0 mV in all precordial leads, is present in about 1% to 2% of
normal lean individuals.
 Beck's triad (cardiology):- Beck's triad is a collection of three medical signs
associated with acute cardiac tamponade, an emergency condition wherein fluid
accumulates around the heart and impairs its ability to pump blood.
 The signs are low arterial blood pressure, distended neck veins, and distant,
muffled heart sounds.

DIAGNOSTIC EVALUATION

The following tests are also used for diagnosis:

Echocardiogram –a test that uses high-frequency sound waves (ultrasound) to

examine the size, shape, and motion of the heart.
This is the primary test used to diagnose and manage cardiac tamponade.
Cardiac catheterization -a tube-like instrument inserted into the heart through a
vein or artery (usually in the arm or leg) to detect problems with the heart and its
blood supply
Chest x-ray -a test that uses radiation to take a picture of structures inside the
body, especially bones
CT scan -a type of x-ray that uses a computer to make pictures of structures
inside the chest
MRI scan -a test that uses magnetic waves to make pictures of structures inside
the chest
Coronary angiography –x-rays taken after a dye is injected into the arteries;
allows the doctor to look for abnormalities in the arteries
Electrocardiogram (ECG, EKG–a test that records) the heart's activity by
measuring electrical currents through the heart muscle
MANAGEMENT

Treatments are administered to:

 Save the patient's life

 Improve heart function
 Relieve symptoms
 Treatments that are administered for cardiac tamponade include:
 Pericardiocentesis -a procedure to drain the fluid around the heart. Fluids to maintain
normal blood pressure
 Antibiotics
 Medications to help increase blood pressure to normal levels
 Oxygen to reduce workload on the heart.

ASSESSMENT

 Pulsusparadoxus> 10 mm Hg (hallmark)
 Narrowed pulse pressure (<30 mm Hg)
 Hypotension
 Neurologic
 Anxiety
 Confusion
 Obtunded if decompression is advanced

NURSING DIAGNOSIS

1. Ineffective Breathing Pattern related to: hyperventilation

Goal: Patterns breath effectively as evidenced by no tachypnea, vital signs are within normal
ranges

NURSING INTERVENTIONS-

I. Monitor strictly vital signs, especially respiratory frequency.

 II. Monitor the contents breathing, chest expansion, regularity of breathing, mouth
breathing and muscle use a respirator.
III. Give the semi-Fowler position if not contraindicated.
 Rationale: Facilitates lung expansion
IV. Teach clients a deep breath.
 Rationale: With the deep breathing exercise can increase oxygen intake.
V. Give oxygen as indicated.
 Rationale: Oxygen adequate to avoid the risk of tissue damage.
VI. Give medication as indicated.
 Rationale: Medications that can affect the respiratory ventilation.

 Monitor for pulsusparadoxus via arterial tracing or during manual BP reading.

 Monitor urine output hourly; a drop in urine output may indicate decreased renal
perfusion as a result of decreased stroke volume secondary to cardiac compression

2. Decreased cardiac output related to reduced ventricular filling secondary to increased intra-
pericardial pressure.

GOALS-To maintain cardiac output of the patient as evidenced by client HR,BP,Pulse pressure

NURSING INTERVENTIONS-

I. Continuously monitor ECG for dysrhythmia formation, which may result of myocardial
ischemia secondary to epicardial coronary artery compression.
II. Monitor the BP every 5 to 15 minutes during the acute phase.
III. Note the color, presence / quality of the pulse.
IV. Auscultation of breath sounds and heart sounds. Listen to the murmur.
V. Maintain bedrest in a comfortable position during the acute period.
VI. Provide adequate rest periods / adequate. Assess the form of self-care activities, if
indicated.
VII. Assess signs and symptoms of CHF.
3. Activity intolerance related to restlessness, fatigue

GOAL-To increase the ability of Client to perform activities of daily routine

NURSING INTERVENTION

I. Assess the ability of client to perform activities of daily life.

II. Assess patient's need for assistive devices.
III. Assess the degree of ability performed by client
IV. Assess the degree of ability performed by client
V. Help the people closest to identify the risk of hazards that may arise.
VI. Minimize the sources of the hazards in the environment.

4. Deficient knowledge related to disease condition

GOALS - To increase knowledge of the patient

NURSING INTERVENION

I. Assess the level of knowledge of the patient

II. Educate the patient about the disease condition
III. Educate the patient about the treatment
IV. Educate the patient about the pericardiocentesis
V. Encourage the patient to ask questions
Myocardial Infarction

Definition of myocardial infarction

Acute Coronary Syndrome and Myocardial Infarctionis an emergent situation characterized by

an acute onset of myocardial ischemia thatresults in myocardial death (i.e., MI) if definitive inter
ventionsdo not occur promptly.

OR

A myocardial infarction Occurs as a result of sustained ischemia, causing irreversible myocardial

cell death (necrosis).

Epidemiology

 In industrial countries MI accounts for 10-25% of alldeaths.

 Incidence is higher in elderly people, about 5% occurs atpeople under age 40.
 Males have higher risk.
 Women during reproductive period have low risk.
 In 2006, studies revealed a prediction that India wouldaccount for 40-60% of
cardiovascular diseases burden withinnext 10-15 years.
 Over last 30 years, the rate of diseases increased from 26% in rural population and 4-12%
in urban population.
 Classification
 Type 1 - spontaneous MI related to ischemia due to a primarycoronary event such as
plaque erosion and/or rupture,fissuring, or dissection
 Type 2 - MI secondary to ischemia due to either increasedoxygendemand or decreased
supply, e.g. coronary artery spasm,coronary embolism, anemia, arrhythmias,
hypertension, orhypotension
 Type 3 – sudden unexpected cardiac death, including cardiac arrestbut death occurring
before blood samples could beobtained
 Type 4 - associated with PCI (percutaneous coronary intervention)
 Type 4a - MI associated with the procedure of PCI(percutaneous coronary intervention)
  Type 4b - MI associated with stent thrombosis
 Type 5 - MI associated with CABG

Etiology of myocardial infarction

1. Acute coronary thrombosis (partial or total) associated with 90% of MIs.
 Severe atherosclerosis (>70% narrowing of the artery) precipitates thrombus.
 Thrombus formation begins with plaque rupture and platelets' adhesion to the
damaged area.
 Activation of the exposed platelets causes expression of glycoprotein IIb/Illa
receptors that bind fibrinogen.
 Further platelet aggregation and adhesion occurs, enlarging the thrombus and
occluding the artery.
2. Other etiologic factors include coronary artery spasm, coronary artery embolism,
infectious diseases causing arterial inflammation, hypoxia, anemia, and severe exertion or
stress on the heart in the presence of significant CAD (ie, surgical procedures, shoveling
snow).
3. Different degrees of damage occur to the heart muscle
4. Other etiological factor include, Tobacco smoking Hypertension, Drug abuse, Obesity,
Stress, alcohol, diabetes, family history of ischemic heart disease.
5. Chronic kidney disease.

Pathophysiology of myocardial infarction

In unstable angina, there is reduced blood flow in a coronaryartery, often due to rupture
of an atherosclerotic plaque. A clotbegins to form on top of the coronary lesion, but the arteryis
not completely occluded. This is an acute situation that canresult in chest pain and other
symptoms that may be referredto as pre-infarction angina because the patient will likely have an
MIif prompt interventions do not occur.

In an Ml, plaque rupture and subsequent thrombus formation result in complete occlusion
of the artery, leading to ischemia and necrosis of the myocardium supplied by that artery.
Vasospasm (sudden constriction or narrowing) of a coronary artery% decreased oxygen supply
(e.g, from acute blood loss, anaemia, or low blood pressure), and increased demand for oxygen
(e.g, From a rapid heart rate, thyrotoxicosis,or ingestion of cocaine) are other causes of MI in
each case a profound imbalance exists between myocardial oxygen supply and demand

Clinical Manifestations of Myocardial infarction

1. Pain:- Severe, immobilizing chest pain not relieved by rest, position change, or nitrate
administration is the hallmark of an MI. Persistent and unlike any other pain, it is
usually described as a heaviness, pressure, tightness, burning, constriction, or crushing.
Common locations are sub sternal, retrosternal, or epigastric areas.
2. Not everyone has classic symptoms. Some patients may not experience pain but may
have "discomfort," weakness, or shortness of breath. Although women and men have
more similarities in their symptoms of an acute M than differences, some women may
experience atypical discomfort, shortness of breath, or fatigue
3. Patients with diabetes are more likely to experience silent (asymptomatic) MIs due to
cardiac neuropathy and present with atypical symptoms (e.g., dyspnea)
4. An older patient may experience a change in mental status (e.g., confusion), shortness
of breath, pulmonary edema, dizziness, or a dysrhythmia
5. 5. Sympathetic Nervous System Stimulation. During the initial phase of MI,
catecholamines (norepinephrine and epinephrine) are released from the ischemic
myocardial cells that normally contain varying quantities of these substances. The
increased sympathetic nervous system stimulation results in release of glycogen,
diaphoresis, and vasoconstriction of peripheral blood vessels. On physical examination,
the patient's skin may be ashen, clammy, and cool to touch
6. 6. Cardiovascular Manifestations. In response to the release of catecholamines, the
BP and HR may be elevated initially. Later, the BP may drop because of decreased
cardiac output (CO). If severe enough, this may result in decreased renal perfusion and
urine output. Crackles may be noted in the lungs, persisting for several hours to several
days, suggesting left ventricular dysfunction. Jugular venous distention, hepatic
engorgement, and peripheral edema may indicate right ventricular dysfunction
 7. Cardiac examination may reveal abnormal heart sounds that may seem distant.
Careful auscultation may reveal splitting of heart sounds. Other abnormal sounds
suggesting ventricular dysfunction are S3 and S4. In addition, a loud holosystolic
murmur may develop and may indicate a septal defect or mitral valve dysfunction
8. Nausea and Vomiting. The patient may be nauseated and vomit Nausea and
vomiting can result from reflex stimulation ol the vomiting center by the severe pain.

9. Fever. The temperature may increase within the first 24 hours up to 100.4°F (38°C)
and occasionally to 102.2°F (39°C). The temperature elevation may last for as long as
week This increase in temperature is a systemic manifestation of the inflammatory
process caused by myocardial cell death.

Diagnostic evaluation of myocardial infarction

 Patient History

The patient history includes the description of the presenting symptom (e.g., pain), the
history of previous cardiac and other illnesses, and the family history of heart disease. The
history should also include information about the patient's risk factors for heart disease.Patients
with typical acute MI usually present with chest pain and may have prodromal symptoms of
fatigue, chest discomfort, or malaise in the days preceding the event; alternatively, typical ST-
elevation MI (STEMI) may occur suddenlywithout warning.

 Physical examination

Physical examination findings for myocardial infarction (MI) can vary; one patient may be
comfortable in bed, with normal examination results, whereas another patient may be in
severe pain, with significant respiratory distress and a need for ventilatory support.

 The patient's heart rate is often increased.

 Depressed heart rate may also be present in some cases
 Alternatively, hypotension can also beseen.
 Fever is usually present within 24-48
 hours, with the temperature curve generally parallel to the time course of elevations
of creatine kinase (CK) levels in the blood. 
 The respiratory rate may be increased in response to pulmonary congestion or
anxiety.
 On palpation, lateral displacement of the apical impulse, dyskinesis, a palpable
S4 gallop, and a soft S1 sound may be found.
 A pericardial friction rub may be audible as a to-and-fro rasping sound; it is produced
through sliding contact of inflammation-roughened surfaces.
 Electrocardiogram

The ECG changes that occur with an MI are seen in the leads that view the involved surface
of the heart. The expected ECG changes are T-wave inversion, ST-segment elevation, and
development of an abnormal Qwave Because infarction evolves over time, the ECG also
changes over time.

Using the information presented, patients are diagnos with one of the following forms of ACS:

*Unstable angina: The patient has clinical manifestations coronary ischemia, but ECG and
cardiac biomarkers show no evidence of acute MI.

*STEMI: The patient has ECG evidence of acute MI with characteristic changes in two
contiguous leads on a 12-lead ECG. In this type of MI, there is a significant damage to the
myocardium.

*NSTEM: The patient has elevated cardiac biomarkers (e.g. troponin) but no definite ECG
evidence of acute MI. In this type of MI, there may be less damage to the myocardium. During
recovery from an MI, the ST segment often is the first ECG indicator to return to normal. Q-
wave alterations are usually permanent. An old STEMI is usually indicated by an abnormal Q
wave or decreased height of the R wave without ST-segment and T-wave changes.

 Echocardiogram
 The echocardiogram is used to evaluate ventricular function. It may be used to assist in
diagnosing an MI, especially when the ECG is nondiagnostic. The echocardiogram can detect
hypokinetic and a kinetic wall motion and can determine the ejection fraction.

 Laboratory Tests :-Cardiac enzymes and biomarkers, which includecreatine kinase

(CK), and myoglobin, are used to an acute MI. Cardiac biomarkers can be analyzed
expediting an accurate diagnosis. These tests are based on the release of cellular contents
into the circulation when myocardial cells die. Fig shows the time courses of cards
enzymes and biomarkers.
 Troponin:- Troponin, a protein found in myocardial cells, regulates the myocardial
contractile process. There are three isomers of troponin :C, I and T. Troponins I and T are
specific for cardiac muscle, and these biomarkers are currently recognized a Reliable and
critical markers of myocardial injury.
Creatine Kinase and Its Isoenzymes :-There are three CK isoenzymes: CK-MM
(skeletal muscle), CK-MB (heart muscle), and CK-BB (brain tissue). CK-MB is the
cardiac-specific isoenzyme; it is found mainly in cardiac cells and therefore increases
when there has been damage to these cells. Elevated CK-MB is an indicator of acute
MI; the level begins to increase within a few hours and peaks within 24 hours of an
infarct

Medical management
1. IV Nitroglycerin. IV nitroglycerin is used in the initial treatment of the patient with ACS.
The goal of therapy is to reduce anginal pain and improve coronary blood flow. It has an
immediate onset of action and can be titrated to prevent, treat, and stop UA.IV
nitroglycerin is usually titrated to relieve pain. Because hypotension is a common side
effect, BP is closely monitored during this time.

2. Morphine Sulfate. Morphine sulfate is given for chest pain that is unrelieved by
nitroglycerin. As a vasodilator, it decreases cardiac workload by lowering myocardial
oxygen consumption, reducing contractility, and decreasing BP and HR. In addition,
morphine can help reduce anxiety and fear. In rare situations, morphine can depress
 respirations. Patients should be monitored for signs of bradypnea or hypoxia, a condition
to be avoided in myocardial ischemia and infarction.

3 B Adrenergic Blockers. B-Adrenergic blockers are used to decrease myocardial

oxygen demand by reducing HR, BP, and contractility. The use of these drugs in the first
hours of MI have shown to reduce the size of the infarction and incidence of
complications. The continuation of B-adrenergic blockers indefinitely is recommended.

4 Angiotensin-Converting Enzyme Inhibitors. ACE inhibitors (e.g., captopril) are

recommended following anterior wall MIs or MIs that result in decreased left ventricular
function (ejection fraction [EF] <40%) or pulmonary congestion. ACE inhibitors should be
continued indefinitely. For patients who cannot tolerate ACE inhibitors, angiotensin receptor
blockers (e.g., losartan) should be considered.

5. Antidysrhythmia Drugs. Dysrhythmias are the most common complications after an

MI. In general, they are not treated aggressively unless they are life threatening.

6. Cholesterol-Lowering Drugs. A fasting lipid panel should be obtained on all patients

admitted with ACS. Cholesterol lowering drugs are recommended for all patients with
elevated LDL cholesterol.

7. Stool Softeners. After an MI, the patient may be predisposed to constipation as a result
of bed rest and opioid administration. Stool softeners such as docusate sodium are given to
facilitate and promote the comfort of bowel evacuation. This prevents straining and the
resultant vagal stimulation from the ValsalvamaneuverVagal stimulation produces
bradycardia and can provoke dysrhythmias.

SURGICAL MANAGEMENT
1. Coronary Artery Bypass Graft Surgery. CABG surgery consists of the construction of
new conduits (vessels to transport blood) between the aorta, or other major arteries, and the
myocardium distal to the obstructed coronary artery (or arteries). Ihe procedure involves one
or more grafts using the internal mammary artery, saphenous vein, radial artery,
gastroepiploic artery, and/or inferior epigastric artery.
CABG surgery requires a sternotomy (opening of the chest cavity) and the use of
cardiopulmonary bypass (CPB). CPB involves diverting (bypassing) the patient's blood from
the heart to the CPB machine. Here blood is oxygenated and returmed (via a pump) to the
patient. In this way, vital organs are perfused while the surgeon operates on a nonbeating,
bloodless heart
2. Minimally Invasive Direct Coronary Artery Bypass. With recent efforts to reduce cost,
length of hospital stay, and morbidity, newer approaches to CABG surgery have been
developed. Minimally invasive direct coronary artery bypass (MIDCAB) is a technique that
offers the patient with singlevessel disease (i.e., left anterior descendng or ight coronary
artery disease) an approach to surgical treatment that does not involve a sternotomy and
CPB.
3. Off-Pump Coronary Artery Bypass. The off-pump coronary artery bypass (OPCAB)
procedure uses full or partial sternotomy to enable access to all coronary vessels. OPCAB is
also performed on a beating heart using mechanical stabilizers and without CPB.

4. Transmyocardial Laser Revascularization.Transmyocardial laser revascularization (TMR)

is an indirect revascularization procedure used for patients with advanced CAD who are not
candidates for traditional bypass surgery and who have persistent angina after maximum
medical therapy.The procedure involves the use of a high-energy laser that is triggered
electro cardio graphically to create channels between the left ventricular cavity and the
coronary microcirculation (ventricularcoronary anastomoses). The channels allow blood to
flow into ischemic areas. The procedure may be performed during cardiac catheterization as
a percutaneous TMR or during surgery using a left anterior thoracotomy incision. Optimal
result are seen at about 3 to 6 months.

Nursing management
RELIEVING PAIN AND OTHER SIGNS AND SMPTOMS

1. Balancing myocardial oxygen supply with demand (e.g, as evidenced by the relief of chest
pain) is the top priority the care of the patient with an ACS.

2. Oxygen should be given along with medication therapy to assist with relief of symptoms.
Administration of oxygen raises the circulating level of oxygen to reduce pain associated with
low levels of myocardial oxygen.

3.The route of administration (usually by nasal cannula) and the oxygen flow rate are
documented. A flow rate of 2 to 4 L/min is usually adequate to maintain oxygen saturation levels
of at least 959% unless chronic pulmonary disease is present.

4. A Vital signs are assessed frequently as long as the patient is experiencing pain and other signs
or symptoms of acute ischemia

5. Physical rest in bed with the head of the bed elevated or in a supportive chair helps decrease
chest discomfort and dyspnea. Elevation of the head and torso is benefhicial for the following
reasons:

 Tidal volume improves because of reduced pressure from abdominal contents on the
diaphragm and better lung expansion.
 Drainage of the upper lung lobes improves,
Venous return to the heart (preload) decreases, reducing the work of the heart.

AMPROVING RESPIRATORY FUNCTION

Regular and careful assessment of respiratory function detects early signs of pulmonary
complications. The nurse monitors fluid volume status to prevent fluid overload and
encourages the patient to breathe deeply and change position frequently to maintain effective
ventilation throughout the lungs. Pulse Oximetry guides the use of oxygen therapy.

PROMOTING ADEQUATE TISSUE PERFUSION

 Bed or chair rest during the initial phase of treatment helps reduce myocardial oxygen
consumption. This limitation on mobility should remain until the patient is pain free and
hemodynamically stable. Skin temperature and peripheral pulses must be checked frequently
to monitor tissue perfusion.

REDUCING ANXIETY

Alleviating anxiety and decreasing fear are important nursingfunctions that reduce the
sympathetic stress response. Less sympathetic stimulation decrease the workload of the heart,
which may relieve pain and other signs and symptoms of ischemia.

Preventing a Second MI

The American Heart Association recommends five stepsthat may reduce risk of a second MI:

 Take medications as prescribed

 Maintain follow-up appointments with healthcareproviders
 Participate in cardiac rehabilitation
 Get support
 Manage risk factors feeded, such as hypertension, hyperlipidemia, and diabetes, and
maintain healthy weight.

Nursing diagnosis

1. Acute pain related to increased myocardial oxygen demand and decreased

myocardial oxygen supply
2. Risk for decreased cardiac tissue perfusion related to reduced coronary blood flow
3. Risk for imbalanced fluid volume deficient related to body requirement secondary
to disease condition
4. Risk for ineffective peripheral tissue perfusion related to decrease cardiac output
from left ventricular dysfunction.
5. Anxiety related to cardiac event and possible death

CARDIAC ARREST

DEFINITION
Cardiac arrest is the cessation of normal circulation of the blood due to failure of the
heart to contract effectively. Medical personnel can refer to an unexpected cardiac
arrest as a sudden cardiac arrest or SCA

INCIDANCE

There are more than 356,000 out-of-hospital cardiac arrests (OHCA)[1] annually in the
U.S., nearly 90% of them fatal, according to the American Heart Association's newly
released Heart Disease and Stroke Statistics - 2018 Update
It was found that in the SCD cohort there was a large prevalence of coronary risk
factors without traditional risk factors known to be associated with sudden death.
Extrapolating the data to national mortality figures, it can be roughly estimated that
annually about 7-lakh SCD cases occur in India....

ETIOLOGY
Cardiac causes
a) Coronary heart disease
-Approximately 60-70% of SCD is related to coronary heart disease.
- Among adults, ischemic heart disease is the predominant cause of arrest.
b) Non ischemic heart disease
- cardiomyopathy,
 - cardiac rhythm disturbances (VT/VF/ Asystole/PÉA)
- hypertensive heart disease
- congestive heart failure.
Non-cardiac causes
-SCD is unrelated to heart problems
in 35% of cases.
- Trauma
- Non-trauma related bleeding (such as gastrointestinal bleeding, aortic rupture, and
intracranial hemorrhage)
- Medication Overdose ( Ca channel blockers, Digitalis,Beta-blockers)
- Drowning
-Pulmonaryembolism

RISK FACTORS
 Sex :The lifetime risk is three times greater in men (12.3%) than women (4.2%)
 Smoking
 Lack of physical exercise
 Obesity
 Diabetes
 Familyhistory.

Hs and Ts
Hs end Ts" is Ine name for a mnemonic used to Aid in remembering the possible
treatable or reversible causes of cardiac arrest.

Hs Ts
 Hypovolemia  Tablets or Toxins
Hyрoxia  Cardiac Tamponade
Hydrogen ions  Tension
Hyperkalemia  Pneumotharax
Hypokalemia
 Thrombosis
Hypothermia
 Thromboembolism
Hypoglycemia
 Trauma
Hyperglycemia.

CLASSIFICATION
Cardiac arrest is classified based upon the ECG rhythm into:
1. Shockable :- Ventricular fibrillation and Pulseless ventricular tachycardia
2. Non-shockable:- Asystole and Pulseless electrical activity
3.
CLINICAL MANIFESTATION
 In cardiac arrest, consciousness, pulse, and blood pressure are lost immediately.
 Breathing usually ceases, but ineffective respiratory gasping may occur. The pupils of the
eyes begin dilating in less than a minute, and seizures may occur.
 Pallor and cyanosis are seen in the skin and mucous membranes.
 The risk of organ damage, including irreversible brain damage, and of death increases
with every minute that passes.
 A patient's age and overall health determine his or her vulnerability to irreversible
damage. As soon as possible, the diagnosis of cardiac arrest must be made and action taken
immediately to restore circulation.
The most reliable sign is absence of pulse.
 Unconsciousness
 No breathing
  No Blood Pressure
 Pupils begin dialating within 45 seconds
 Seizures may/maynot occur
 Death - like appearance
Lips & nail buds turn blue

DIAGNOSTIC EVALUATION
 Cardiac arrest is synonymous with clinical death.
 Lack of carotid pulse is the gold standard for diagnosing cardiac arrest.
 Cardiac arrest is usually diagnosed
clinically by the absence of a pulse, but lack of a pulse (particularly in the peripheral
pulses) may be a result of other conditions (e.g. shock), or simply an error on the part of
the rescuer.

PATHOPHYSIOLOGY
Cardiac arrest

No blood flow and oxygenation

Brain sustain damage for 4 min and after 7 min irreversible damage

After 1-2 hours cells of the body die

CPR

Blood is manually forced to circulate to brain

and heart
 Enough oxygen Allows heart to
to brain remain responsive
delay brain death till defibrillation

MANAGEMENT

Sudden cardiac arrest may be treated via attempts at resuscitation.

This is usually carried out based upon:

 Basic life support (BLS):-

The 2010 AHA Guidelines for CPR and ECC recommend a change in the BLS sequence of
steps from A-B-C (Airway, Breathing, Chest compressions) to C-A-B (Chest compressions,
Airway, Breathing) for adults, children, and infants (excluding the newly born; see Neonatal
Resuscitation section). The purpose of BLS is to maintain sufficient blood circulation and
breathing through a clear airway. If you are responding to an emergency, having a basic life
support certification will assure the patient that you are qualified to help them.
 Advanced cardiac life support (ACLS):- What is the difference between BLS and
ACLS? Basic Life Support (BLS) is the generic term for any form of CPR and is required for
all registered nurses. Advanced Cardiac Life Support (ACLS) is primarily required for RNs
who work in a hospital setting and care for critically ill adults.
 Cardiopulmonary resuscitation (CPR):- Cardiopulmonary resuscitation (CPR) is a
lifesaving technique that's useful in many emergencies, such as a heart attack.

1. Position your hand (above). Make sure the patient is lying on his back on a firm surface. ...
2. Interlock fingers
3. Give chest compressions
4. Open the airway
5. Give rescue breaths
6. Watch chest fall
7. Repeat chest compressions and rescue breaths.

Defibrillation":- Defibrillation is an emergency treatment for ventricular fibrillation and

other life-threatening arrhythmias (abnormal heartbeats). ... It will cause cardiac arrest
and death within a few minutes if not treated immediately. Defibrillation restores a
normal heartbeat by shocking the heart with electricity. Defibrillators are devices that
restore a normal heartbeat by sending an electric pulse or shock to the heart. They are
used to prevent or correct an arrhythmia, a heartbeat that is uneven or that is too slow or
too fast. Defibrillators can also restore the heart's beating if the heart suddenly stops

PREVENTION
 As the prime causes of cardiac arrest being ischemic heart disease
 Efforts to promote a healthy diet
 exercise
 smoking cessation
 For people at risk of heart disease
 Blood pressure control
 Cholesterol lowering.

CARDIOGENIC SHOCK

Definition of shock
Shock is defined as failure of the circulatory system tomaintain adequate perfusion of
vital organs. Disordersleading to inadequate tissue perfusion result in
decreasedoxygenation at the cellular level. Inadequate oxygenationresults in anaerobic
cellular metabolism and accumulated waste products in cells. If this condition is
untreated, celldeath and organ death occur.

Prevalence

Prevalence of clinically diagnosed shock was 1.5 % (n = 622) and overall bolus use was
0.9 % (n = 366); 41 % (256/622) of children with clinically diagnosed shock did not
 receive a fluid bolus (but had a fluid plan for management of dehydration). Identified
cases appeared mostly to be hypovolaemic shock secondary to dehydration/diarrhoea
(94 %, 582/622), with a high case fatality (34 %, 211/622). Overall mortality for all
admitted children was 5 % (2115/42,937) and was 7.9 % (798/10,096) in children with
dehydration/diarrhea.

Classification of shock

Hypovolemic shock
Cardiogenic shock
Anaphylactic shock
Distributive shockshock
neurogenic
septic shock

DEFINITION OF CARDIOGENIC SHOCK

Cardiogenic shock is a condition in which heart suddenly can't pump enough blood to
meet the body's needs.

INCIDENCE:
 Cardiogenic shock occurs as a serious complication in 5% to 10% of patients
hospitalized with acute myocardial infarction.
► Historically, mortality for cardiogenic shock had been 80% to 90%, but recent studies
indicate that the rate has dropped to 56% to 67% due to the advent of thrombolytics,
improved interventional procedures, and better therapies.

CLASSIFICATION:
Coronary: Coronary cardiogenic shock is more common than non-coronary
cardiogenic shock and is seen most often in patients with acute myocardial infarction.
Non-coronary:
Non-coronary cardiogenic shock is related to conditions that stress the myocardium as
well as conditions that result in an ineffective myocardial function.

ETIOLOGY :
 Myocardial ischemia: Compensatory mechanisms may initially stabilize the
patient but later on would cause deterioration with the rising demands of oxygen
of the already compromised myocardium.
Myocardial infarction(MI): Regardless of the underlying cause, left ventricular
dysfunction sets in motion a series of compensatory mechanisms that attempt to increase
cardiac output, but later on leads to deterioration.

Other possible causes of cardiogenic shock include:

 Inflammation of the heart muscle (myocarditis)
 Infection of the heart valves (endocarditis)
 Weakened heart from any cause.
Drug overdoses or poisoning with substances that can affect your heart's pumping ability.

CLINICAL MANIFESTATION
 Clammy skin.
 Decreased systolic blood pressure
 Tachycardia
 Rapid respirations
 Oliguria.
 Cyanosis.
 Mental confusion
o Other Symptoms are:
 Rapid breathing
 Severe shortness of breath
 Sudden, rapid heartbeat (tachycardia)
 Loss of consciousness
 Weak pulse
 Low blood pressure (hypotension)
 Sweating
 Pale skin
 Cold hands or feet
 Urinating less than normal or not at all

PATHOPHYSIOLOGY
 DIAGNOSTIC EVALUATION

 History collection:-collect the all history regarding past and present history of patient.
 Physical examination :- Findings in patients with cardiogenic shock include the
following: Altered mental status, cyanosis, cold and clammy skin, mottled extremities
Peripheral pulses are faint, rapid and sometimes irregular if there is an underlying
arrhythmia, Jugular venous distension, Diminished heart sounds
 Diagnostic assessments of clients in shock should include oxygenation, organ perfusion,
and fluid balance.
 Assessment of respiratory status can be accomplished tosome degree by noninvasive
procedures such as spirometry, pulse oxymetry. Other noninvasive assessment
andmonitoring tools are the cardiac monitor and the 12-leadelectrocardiogram (ECG).
Laboratory studies include acomplete blood cell count, blood chemistry, and blood and
body fluid cultures for certain clients.

 Spirometry :- test used to assess how well lungs work by measuring how much air
inhale, how much exhale and how quickly exhale
 Pulse oxymetry:- a noninvasive and painless test that measures oxygen saturation level,
or the oxygen levels in blood. It can rapidly detect even small changes in how efficiently
oxygen is being carried to the extremities furthest from the heart, including the legs and
the arms.

 12-lead electrocardiogram (ECG):-a representation of the heart's electrical activity

recorded from electrodes on the body surface. This section describes the basic
components of the ECG and the lead system used to record the ECG tracings
 ABG analysis may also be done to determine whether the metabolic acidosis that occurs
with shock is being effectively combated by hyperventilation. A low Paco2, along with
low pH and bicarbonate levels (metabolic acidosis), indicates that hyperventilation is
trying to com pen sate. However, an increasing Paco2 in the presence of a persistently
low pH indicates that respiratory assistance is needed. It is also important to monitor
Pao2 levels to determine whether the client being adequately oxygenated .
 CVP measurement is one of the first invasive assessments made in the presence of
shock to estimate fluid loss.

 A pulmonary artery or swan-ganz catheter;- it may also be inserted to assist with

assessment of fluid status, cardiac function and tissue oxygen consumption.

MEDICAL MANAGEMENT
 Vasodilators (These drugs acts as blood vessel dilator): Some drugs used to treat
hypertension, such as calcium channel blockers — which prevent calcium from
entering blood vessel walls — also dilate blood vessels. But
the vasodilators that work directly on the vessel walls are hydralazine and
minoxidil.
  Nitrates:- Essentially, nitrates dilate – that is, widen or relax – the arteries and
the veins not only in the heart but also elsewhere in the body. By dilating the
blood vessels of the heart, nitrates can reduce the stress on the heart by
improving blood flow to the heart muscle.
 Beta-Blockers (Decrease work load in heart): Beta blockers are a class of
medications that are predominantly used to manage abnormal heart rhythms,
and to protect the heart from a second heart attack after a first heart attack.
 Propranolol 20-40 mg
 Calcium channel blocker (They improve coronary blood flow):
 Nifedipine:- Nifedipine is a medicine used to treat high blood pressure. If have
high blood pressure, taking nifedipine helps to prevent future heart disease,
heart attacks and strokes. Nifedipine is also used to prevent chest pain caused by
angina.
 Antiplatelet medication.
These drugs similar to aspirin to help prevent new clots from forming.
 Thrombolytic Drugs:
Thrombolytic drugs are a group of drugs used to dissolve certain types of blood
clots. Ex. streptokinase, Urokinase
MEDICAL PROCEDURE:
Angioplasty and stenting. If a blockage is found during a cardiac catheterization, the
doctor can insert a long, thin tube (catheter) equipped with a special balloon through an
artery, usually in your leg, to a blocked artery in the heart. Once in position, the balloon
is briefly inflated to open the blockage.

ANGIOPLASTY
Angioplasty for coronary artery disease
Balloon pump. The doctor inserts a balloon pump in the main artery off of the heart
(aorta). The pump inflates and deflates within the aorta, helping blood flow and
taking some of the workload off the heart.

SURGICAL MANAGEMENT
 1. coronary artery bypass surgery
Coronary bypass surgery redirects blood around a section of a blocked or partially
blocked artery in heart. The procedure involves taking a healthy blood vessel from leg,
arm or chest and connecting it below and above the blocked arteries in heart. With a
new pathway, blood flow to the heart muscle improves.
2. Ventricular assist device.

A mechanical device can be implanted into the abdomen and attached to the heart to
help it pump. This might extend and improve the lives of some people with end-stage
heart failure

Nursing management
General Measures

Critical factors in the successful management of a patient experiencing shock relate to the early
recognition and treatment of the shock state. Prompt intervention in the early stages of shock
mayprevent the decline to the progressive or refractory stage. Successful management of the
patient in shock includes the following:

1. Identification of patients at risk for the development of shock

2. Integration of the patient's history, physical examination, andclinical findings to establish a

diagnosis

3. Interventions to control or eliminate the cause of the decreasedperfusion

4. Protection of target and distal organs from dysfunction

5. Provision of multisystem supportive care.

Oxygen and Ventilation.

Oxygen delivery is dependent onCO. available hemoglobin, and arterial oxygen saturation
(SaO2). Methods to optimize oxygen delivery are directed atincreasing supply and decreasing
demand. Supply can beincreased by

(1) Optimizing the Co with drug therapy or fluid replacement,

(2) Increasing the hemoglobin by the transfusionof blood or packed red blood cells (RBCs),
and/or (3) Increasing the arterial SaO2 with supplemental oxygen and mechanicalventilation

Fluid Resuscitation.

Except for cardiogenic and neurogenicshock, all other classifications of shock involve decreased
circulating blood volume. The cornerstone of therapy for septic, hypovolemic administration of
the appropriate fluid

When large amounts of fluids are required, the patient must be protected against
complications. Two major complications are hypothermia and coagulopathy. The patient can be
protected fromhypothermia by warming both crystalloid and colloid solutionsused during
massive fluid resuscitation.

Nutritional therapy

A patient with shock should be weighed daily on the same scale at the same time of day. If the
patient experiences a significant weightloss, dehydration should be ruled out before additional
calories areprovided. Large weight gains are common because of third spacingof fluids.
Therefore daily weights may function better as an indicator of fluid status than caloric needs and
balance. Serum protein,nitrogen balance, BUN, serum glucose, and serum electrolytes areall
used to assess nutritional status.

NURSING DIAGNOSIS:

1. Impaired gas exchange related to decreased blood flow as evidenced by

breathlessness
2. Acute pain related to disease condition as evidenced by patient verbalization
 3. Impaired physical mobility related to weakness as evidenced by patient is unable to
perform daily activity.
4. Imbalanced nutrition less than body requirement related to less intake of food as
evidenced by weight loss
5. Disturbed sleep pattern related to hospitalization as evidenced by patient
verbalization

HEALTH EDUCTION

DIET

1. Eat a variety of fruits, vegetables and grain products, especially whole grains.
2. Consume fat-free and low-fat dairy products, fish, beans, skinless poultry and lean
meats.
3. Limit foods high in saturated fat, trans fat and cholesterol.
4. Eat less than 6 grams of salt a day.
5. Maintain a healthy lifestyle: Eat a well-balanced diet and exercise regularly to avoid
heart diseases.
6. Prevent injuries: Wear protective gears while driving, playing sports, or working
with dangerous equipment to prevent injuries.
Shock can be prevented by reducing the incidence of the causes, such as heart failure,
injuries, dehydration, etc. The following measures may help to prevent the causes:
Maintain a healthy lifestyle: Eat a well-balanced diet and exercise regularly to avoid
heart diseases.

Exercise:-

Choose an aerobic activity such as walking, swimming, light jogging, or biking. Do this

at least 3 to 4 times a week. Always do 5 minutes of stretching or moving around to
warm up muscles and heart before exercising. Allow time to cool down after exercise.
Exercise also increases levels of HDL cholesterol, the "good" cholesterol that lowers heart
disease risk by flushing the artery-clogging LDL or "bad" cholesterol out of system. Along with
lowering risk for heart disease, exercise: Keeps weight down. Improve mood.
Medication: -

Regular medication is very important for any disease condition. Medication takes as per doctor
order. The initial management and stabilization of the patient in the early and critical phase of
acute myocardial infarction (MI), the goals of care for these patients is to restore normal
activities, prevent long-term complications, as well as aggressively modify lifestyle and risk
factors.

Fallow up :-

A return to all normal activities, including work, may take a few weeks to 2 or 3 months,
depending on condition. A full recovery is defined as a return to normal activities. This will
depend on how active were before heart attack, the severity of the attack, and body's response to
it.

SUMMARY
Today we discuss about the topic of cardiac emergency in this topic we seen definition of cardiac
emergency, anatomy of pelvis and femur, circulatory system, classification of cardiac emergency
and it can be done by asking question to the group and getting feedback from the group.

CONCLUSION
 Emergency happen every day and these 5 items will better prepare student to know how to react
in cardiac and first aid emergencies. It is not safe to practice CPR techniques on other student so
training aids are necessary.
REFERENCE

1. Lewis, textbook of medical and surgical nursing, chintamani,page no ;805 ,

806,810,811,806,820.823,634
2. Brunner and suddarth’s, textbook of medical and surgical nursing, volume 1,south Asian
edition page no:-553, 558,559,561,564
3. Black M. textbook of medical and surgical nursing volume 2, 8 th edition,page no:-
1485,1482,1486,1488
4. Black M. textbook of medical and surgical nursing volume 2, 7th edition,page no:-1708
5. Ross and willsons,textbook of anatomy and physiology, 12 the edition page no:-78
6. www.pinterest.com
7. www.slideshare.org
8. www.wikipedia.com
9. www.ajajournal.org
General objective

After completion of practice teaching students will be able to gain knowledge regarding
cardiac emergency and will be able to apply in practice.

Specific objective

1. Review the anatomy and physiology of circulatory system.

2. Enlist the classification of cardiac emergency.
a. Angina pectoris
1. Define angina pectoris.
2. Discuss the prevalence of angina pectoris.
3. Enlist the type of angina pectoris.
4. Explain the etiology of angina pectoris.
5. Discuss the pathophysilogy of angina pectoris.
6. Enumerate the clinical manifestation of angina pectoris.
7. Discuss the diagnostic evaluation of angina pectoris.
8. Explain the medical management of angina pectoris.
9. Discus the nursing management of angina pectoris.
b. Cardiac Tamponade
1. Define Cardiac Tamponade.
2. Discuss the incidence of Cardiac Tamponade.
3. Explain the etiology of Cardiac Tamponade.
4. Discuss the pathophysiology of Cardiac Tamponade.
5. Enumerate the clinical manifestation of Cardiac Tamponade.
6. Discuss the diagnostic evaluation of Cardiac Tamponade.
7. Explain the management of Cardiac Tamponade.
8. Discuss the nursing management of Cardiac Tamponade
c. Myocardial Infarction.
 1. Define myocardial infarction.
2. Discuss the epidemiology of myocardial infarction.
3. Enlist the classification of myocardial Infarction.
4. Explain the etiology of myocardial Infarction.
5. Discuss the pathophysiology of myocardial Infarction.
6. Enumerate the clinical manifestation of myocardial Infarction.
7. Discuss the diagnostic evaluation of myocardial Infarction.
8. Explain the Medical management of myocardial Infarction.
9. Explain the surgical management of myocardial Infarction..
10. Explain the nursing management of myocardial Infarction.

d. Cardiac Arrest
1. Define cardiac arrest.
2. Discuss the incidence of cardiac arrest.
3. Enlist the classification of cardiac arrest
4. Explain the etiology of cardiac arrest.
5. Discuss the pathophysiology of cardiac arrest.
6. Enumerate clinical manifestation of cardiac arrest.
7. Discuss the diagnostic evaluation of cardiac arrest.
8. Explain the management of cardiac arrest.
e. Cardiogenic Shock
1. Define shock.
2. Discuss the prevalence of shock.
3. Enlist the classification of shock.
4. Define cardiogenic shock.
5. Enlist the classification of cardiogenic shock.
6. Explain the etiology of cardiogenic shock.
7. Discuss the pathophysiology of cardiogenic shock.
8. Enumerate the clinical manifestation of cardiogenic shock.
9. Discuss the diagnostic evaluation of cardiogenic shock.
10. Explain the medical management of cardiogenic shock.
 11. Explain the surgical management of cardiogenic shock.
12. Discuss the nursing management of cardiogenic shock.

3. Discuss the health education of for the patient