Advance concept in nursing

Topic : Cardiovascular system

Iram shaheen
Myocardial infarction:

 ‘’It is an emergency condition characterized by an acute onset of myocardial ischemia that

results in myocardial death ‘’.
 Coronary occlusion , heart attack and myocardial infarction are used synonymously, the
preferred term is myocardial infarction .
Pathophysiology:

 In unstable angina there is reduced blood flow in coronary artery due to rupture of an
atherosclerotic plaque. A clot begins to form on the top of the coronary lesion , but the
artery is not completely occluded . This is an acute situation that results in chest pain and
other symptoms.
 In an MI , plaque ruptures and subsequent thrombus formation results in complete
occlusion of the artery , leading to ischemia and necrosis of myocardium supplied by that
artery.
 Vasospasm (sudden constriction or narrowing ) of the coronary artery , decreased oxygen
supply e.g (from acute blood loss ) and increased demand for oxygen . In each case a
profound imbalance exist between oxygen supply and demand.
 The area of infarction develops over minutes to hours. As the cells deprived of oxygen
ischemia develops cellular injury occurs , and the lack of oxygen results in infarction or the
death of he cells.
Pathophysiology:

 Various description are used to further identify an MI the type NSTEMI or STEMI, the
location of the injury to the ventricular wall inferior , anterior , posterior , lateral wall and
the point in time within the process of infarction, evolving or old) .
 The differentiation between STEMI OR NSTEMI is determined by the diagnostic tests.
 Non-ST-elevation myocardial infarction (NSTEMI) is a type of involving partial blockage
of one of the coronary arteries, causing reduced flow of oxygen-rich blood to the heart
muscle.
 An ST-elevation myocardial infarction (STEMI) is a type of heart attack that is more
serious and has a greater risk of serious complications and death.
Clinical manifestations:
 Chest pain that occurs suddenly and continues despite rest and medications is the presenting
symptom in most patients. Some of these patients have prodromal symptom or a previous
diagnosis of CAD but about half report no previous symptoms.
 Chest pain
 Shortness of breath
 Indigestion
 Nausea
 Anxiety
 Cool , pale and moist skin
 The heart rate and respiratory rate may be faster than normal these signs and symptoms which
are caused by stimulation of sympathetic nervous system may be present only for short period or
may persist.
 In most cases the sign and symptoms of MI cannot be distinguished from those of unstable
angina , hence the evolution of the term ACS.
Assessment and diagnostic findings:

 The diagnosis of ACS is generally based on the presenting symptoms

 12 lead ECG
 Laboratory tests( serial cardiac biomarkers)
 STEMI
 NSTEMI
 Physical examination is always conducted but examination alone does not confirm the
diagnosis.
 The prognosis depends on the severity of coronary artery obstruction and the presence and
extent of myocardial damage.
Patient history:

 The patient history includes the description of the presenting symptoms e.g pain.
 The history of the previous cardiac and other illness
 Family history of heart disease
 The history also include information about the patients risk factor for heart disease.
Electrocardiogram:

 The 12 lead ECG provides information that assists in ruling out or diagnosing an acute MI.
it should be obtained within 10 minutes a patient reports pain or arrives ED.
 By monitoring ECG changes over time, the location , evolution , and resolution of MI can
be identified and monitored.
 The ECG changes that occurs in MI are seen in the leads that involved surface of the heart.
The expected ECG changes are T-wave inversion , S-T segment elevation.
 Because infarction evolve over time the ECG changes also evolve over time. The first
ECG sign of an acute MI is seen in the T-wave and ST segment .
 As the area of injury becomes ischemic myocardial repolarization altered and delayed
causing the T-wave to invert. The ST segment is normally flat on ECG but in MI the
injured myocardial cells depolarize normally but repolarize rapidly causing the ST segment
rise at least 1mm above the isoelectric line (the area between the T wave and he next P
wave is used as the reference for isoelectric line).
 CONT..

 This change is measured 0.06 to 0.08 sec after the end of QRS complex a point called the J
point.
 An elevation in the two contiguous leads is a key diagnostic indicators for MI (STEMI).
 The appearnce of abnormal Q wave( represents initial depolarization of interventricular
septum) is another indication of MI . Q wave develops within 1 to 3 days because there is
no depolarization current conducted through necrotic tissues. Q wave is 0.04 sec or longer.
 During an acute MI, injury and ischemic changes are usually present . An abnormal Q
wave is present without ST segment and T wave changes which indicates an( old not acute)
MI.
 For some patients there are no persistent ST elevation OR other ECG changes therefore an
NSTEMI is diagnosed by blood levels of cardiac biomarkers.
Patients are diagnosed with the following changes:

 STEMI: the patient has ECG evidence of acute MI with characteristic changes in two
contiguous leads in 12 lead ECG. In this type of MI there is significant damage to the
myocardium.
 NSTEMI: the patient has elevated biomarkers e.g troponin but no definite ECG evidence
of acute MI there may be less damage to the myocardium.
 During recovering from an MI the ST segment is often first ECG indicator to return to
normal . Q wave alteration are usually permanent.
Echocardiogram:

 Echocardiogram is used to evaluate ventricular function. It may be used to assist in

diagnosing an MI especially when ECG is non diagnostic. The echocardiogram can detect
the hypokinetic and akinetic wall motion and can determine the ejection fraction.
Laboratory analysis:

 Cardiac enzymes and biomarkers such as troponin , Creatine kinase and myoglobin are used
to diagnose an MI. These tests are based on the release of cellular contents into the
circulation when the myocardial cells die.
 Troponin:
A protein found on the surface of myocardial cells regulate the myocardial contractile
process , an increase in the level of troponin in serum can be detected within a few hours of
during an cute MI. It remains elevated for long period often as long as 3 weeks , it can
therefore be used to detect a recent myocardial damage.
 Creatine kinase and its isoenzyme :
There are three CK isoenzyme CK-MM(skeletal muscle), CK-BB(brain tissues), CK-MB,
CK-MB is the specific cardiac isoenzyme which is present in cardiac cells and therefore
increases when there is a damage to cardiac cells . Elevated CK-MB is an indicator of an
acute MI the level begin to increase within a few hours and peaks within 24 hours of infarct.
Myoglobin:

 Myoglobin is a heme protein that transport oxygen ,like CK-MB it is also found in cardiac
and skeletal muscle. The myoglobin levels starts to increase within 1 to 3 hours and peaks
within 12 hours after the onset of symptoms. An increase in myoglobin is not very specific
in indicating an acute cardiac event however, negative results can be used to rule out an
acute MI.
Medical management:

 The goal of medical management is to minimize cardiac damage , restore cardiac function
and prevent complications. These goals are facilitated by the use of guidelines developed
by the American college of cardiology ACC and the AHA , in addition the joint
commission promotes the adherence to a set of core measures and interventions for
patients with acute MI that are associated with improved patient outcomes.
 The goal of treating patient is to minimize myocardial damage by reducing myocardial
oxygen demand and increasing oxygen supply with medications , oxygen administration
and bed rest.
 The resolution of pain and ECG changes indicate that demand and supply are in
equilibrium, they may also indicate reperfusion.
Initial management:

 The patient with suspected MI should immediately receive supplemental oxygen , aspirin ,
nitroglycerine and morphine . Morphine is the drug of choice in pain and reducing anxiety
and decrease the work of heart . The response to morphine is monitored carefully to asses
for hypotension and decrease in respiratory rate a beta- blocker may be used if dysrthytmia
occurs if a beta- blocker is not needed in initial management ,it should be introduced in 24
hours of admission , Once the hemodynamic have stabilized and patient have no
contraindication . Unfractionated heparin or LMWH may also be prescribed along with
platelet inhibiting factor to prevent further clot formation.
 Emergent percutaneous intervention:

 The patient with STEMI is taken directly to cardiac cathetrization laboratory for an
immediate PCI. this procedure is used to open an occluded coronary artery and to
promote the reperfusion of the area that has been deprived of oxygen . Superior outcomes
have been reported with the use of PCI when compared with the use of thrombolytic
agents. Early PCI has shown to be effective in patients of all ages including 75 years the
procedure treats underline an atherosclerotic lesion . Because of the oxygen deprivation
time determines the extent of cardiac cells damage so the time for patients arrival in ED to
PCI should be less than 60 minutes. This is frequently referred to as door- to-balloon time.
Thrombolytics:

 Thrombolytic therapy is initiated when primary PCI is not available . These agents are
administered IV according to the specific protocol. The thrombolytic agents are used most
often are ateplase and reteplase and tenecteplase .
 The purpose of thrombolytic is to dissolve the thrombus in coronary artery allowing the
blood flow through the coronary artery again ,minimizing the size of infarction and
preserving the ventricular function however ,the thrombolytic resolve the thrombus but
they do not affect the underlying atherosclerotic lesion. The patient may be referred to
cardiac cathetrization and other invasive procedures following the use of thrombolytic
agents.
 Thrombolytic should not be used if the patient is bleeding and having bleeding disorder.
They should be administered to 30 minutes of presentation to the hospital and often
referred to as door -to -needle time
Inpatient management:

 Following PCI or thrombolytic therapy , continuous cardiac monitoring is indicated

preferably in cardiac ICU.
 Continuing pharmacological management includes aspirin , beta blockers and
angiotension-converting enzyme inhibitors. The use of ACE inhibitors in an acute MI
decreases the mortality rates and prevents the remodeling of cardiac cells that are
associated with the onset of heart failure.
 Blood pressure, urine output , serum sodium , potassium and creatinine level should be
monitored closely.
 If ACE inhibitors are not suitable the angiotension receptor blockers should be prescribed .
 Nicotine receptor replacement therapy and smoking cessation counseling should also be
initiated in smokers.
Cardiac rehabilitation:

 After the patient has free of symptoms an active rehabilitation program is initiated. cardiac
rehabilitation is aimed at providing education to the patient and family about the risk
reduction., to extend life and improve quality of life.
 The immediate goal is to limit the effects and progression of atherosclerosis, return the
patient to work , and pre-illness life styles and enhance the patients psychosocial and
vocational status and prevent another cardiac event.
 Patients conditioning is achieved gradually overtime and are observes for chest pain,
dyspnea, weakness and fatigue, palpitations and are instructed to stop exercise if any of
these occur. Patients may also be monitored for increase in heart rate , an increase in
systolic or diastolic blood pressure of more than 20mmHg , a decrease in diastolic blood
pressure , onset of worsening of Dysarthria, or ST segment changes on ECG.
Cardiac rehabilitation program is categorized in three phases:

 Phase-1 begins with the diagnosing of atherosclerosis and to the education in

hospitalization includes the sign and symptoms that indicate the need to call an emergency
assistance , the medication regimen , rest –activity balance and follow up appointments
with the primary care provider.
 The amount and type of activity is recommended at discharge depends upon the patients
age and condition before the cardiac event , the extent of disease, the course of hospital
stay and the development of any complications.
 Phase-2 to occurs when the patient has been discharged the patient attends the session for
3 to 4 times a week for 4 to 6 weeks but may continue for as long as 6 months. This phase
also includes educational session for patients and families that are given by cardiologist ,
exercise physiologist, dietitians , nurses and other health care professionals.
Phase-3

 It is a long term outpatient program that focuses on maintaining cardiovascular stability

and long term conditioning. The patient is usually self directed during this phase and does
not require a supervised program.
Nursing management:

 Relieving pain and other sign and symptoms of ischemia

 Improving respiratory function
 Promote adequate tissue perfusion
 Reducing anxiety
 Monitoring and managing potential complications
 Promoting home and community based care.