(a p advanced concept of nursing-...

Advanced Concept of Nursing- IIUNIT-3

ADVANCE NURSING MANAGEMENTOF CARDIOVASCULAR DISEASES.

In The Name of God

(A PROJECT OF NEW LIFE COLLEGE OF NURSING KARACHI)

UNIT-3ADVANCE NURSING MANAGEMENT

OF CARDIOVASCULAR DISEASES.Shahzad Bashir

RN, BScN, DCHN,MScN (Std.DUHS)Instructor

New Life College of NursingUpdated; March 22, 2015

Objectives• At the end of the unit, students will be able to:1. Utilize Functional health pattern to identify patients

problems related to cardiovascular disorders including:1. Myocardial infarction (MI)2. Coronary heart disease (CHD) and Coronary artery disease

(CAD)3. Valvular heart disease

2. Integrate pathophysiology and pharmacology concepts ofcardiovascular disease

3. Apply nursing process with support on Evidence-BasedNursing (EBN) to provide to the clients with CV disorders

4. Discuss the holistic approach for nursing management ofthe patient with cardiovascular diseases

5. Develop a teaching plan for a client experiencing disordersof the CV disorders.

• At the end of the unit, students will be able to:1. Utilize Functional health pattern to identify patients

problems related to cardiovascular disorders including:1. Myocardial infarction (MI)2. Coronary heart disease (CHD) and Coronary artery disease

(CAD)3. Valvular heart disease

2. Integrate pathophysiology and pharmacology concepts ofcardiovascular disease

3. Apply nursing process with support on Evidence-BasedNursing (EBN) to provide to the clients with CV disorders

4. Discuss the holistic approach for nursing management ofthe patient with cardiovascular diseases

5. Develop a teaching plan for a client experiencing disordersof the CV disorders.

8/22/2016 2Shahzad Bashir, Lecturer NLCON

INTRODUCTION• Myocardial infarction (MI)refers to the process by whichareas of myocardial cells in theheart are permanently destroyed.

• It occurs when myocardialtissues are abruptly andseverely deprived of oxygen.

• Myocardial infarction is adiseased condition which iscaused by reduced blood flowin a coronary artery due toatherosclerosis and occlusionof an artery by an embolus orthrombus.

• Myocardial infarction (MI)refers to the process by whichareas of myocardial cells in theheart are permanently destroyed.

• It occurs when myocardialtissues are abruptly andseverely deprived of oxygen.

• Myocardial infarction is adiseased condition which iscaused by reduced blood flowin a coronary artery due toatherosclerosis and occlusionof an artery by an embolus orthrombus.


Coronary arteries of heart


CHD or CAD• Coronary artery disease is a narrowing or

obstruction of one or more coronary arteries asa result of atherosclerosis, which is anaccumulation of lipid-containing plaque in thearteries.• The disease causes decreased perfusion of

myocardial tissue and inadequate myocardialoxygen supply leading to hypertension, angina,dysrhythmias, MI, heart failure, and death.

• Coronary artery disease is a narrowing orobstruction of one or more coronary arteries asa result of atherosclerosis, which is anaccumulation of lipid-containing plaque in thearteries.• The disease causes decreased perfusion of

myocardial tissue and inadequate myocardialoxygen supply leading to hypertension, angina,dysrhythmias, MI, heart failure, and death.


Cont…• Symptoms occur when the coronary artery is

occluded to the point that inadequate bloodsupply to the muscle occurs, causing ischemia.• Coronary artery narrowing is significant if the

lumen diameter of the left main artery isreduced at least 50%, or if any major branch isreduced at least 75%.• The goal of treatment is to alter the

atherosclerotic progression.

• Symptoms occur when the coronary artery isoccluded to the point that inadequate bloodsupply to the muscle occurs, causing ischemia.• Coronary artery narrowing is significant if the

lumen diameter of the left main artery isreduced at least 50%, or if any major branch isreduced at least 75%.• The goal of treatment is to alter the

atherosclerotic progression.


Angina• Angina is chest pain resulting from myocardial

ischemia caused by inadequate myocardialblood and oxygen supply.

• Angina is caused by an imbalance betweenoxygen supply and demand.

• Causes include obstruction of coronary bloodflow resulting from atherosclerosis, coronaryartery spasm, or conditions increasingmyocardial oxygen consumption.

• Angina is chest pain resulting from myocardialischemia caused by inadequate myocardialblood and oxygen supply.

• Angina is caused by an imbalance betweenoxygen supply and demand.

• Causes include obstruction of coronary bloodflow resulting from atherosclerosis, coronaryartery spasm, or conditions increasingmyocardial oxygen consumption.


Patterns of angina• 1. Stable angina(Also called exertional angina)– Occurs with activities that involve exertion or emotional

stress; relieved with rest or nitroglycerin– Usually has a stable pattern of onset, duration, severity, and

relieving factors• 2. Unstable angina (Also called preinfarction angina)– Occurs with an unpredictable degree of exertion or emotion

and increases in occurrence, duration, and severity over time– Pain may not be relieved with nitroglycerin– Associated with acute coronary insufficiency– Lasts longer than 15 minutes– Symptom of worsening cardiac ischemia– Occurs after an MI, when residual ischemia– May cause episodes of angina

• 1. Stable angina(Also called exertional angina)– Occurs with activities that involve exertion or emotional

stress; relieved with rest or nitroglycerin– Usually has a stable pattern of onset, duration, severity, and

relieving factors• 2. Unstable angina (Also called preinfarction angina)– Occurs with an unpredictable degree of exertion or emotion

and increases in occurrence, duration, and severity over time– Pain may not be relieved with nitroglycerin– Associated with acute coronary insufficiency– Lasts longer than 15 minutes– Symptom of worsening cardiac ischemia– Occurs after an MI, when residual ischemia– May cause episodes of angina


Cont…

• 3. Variant angina (Also called Prinzmetal’sor vasospastic angina)– Results from coronary artery spasm–May occur at rest OR Sleep– Attacks may be associated with ST segment

elevation noted on the electrocardiogram (ECG).

• 3. Variant angina (Also called Prinzmetal’sor vasospastic angina)– Results from coronary artery spasm–May occur at rest OR Sleep– Attacks may be associated with ST segment

elevation noted on the electrocardiogram (ECG).


Valvular Heart Disease• Valvular heart disease occurs when the heart

valves cannot fully open (stenosis) or closecompletely (insufficiency or regurgitation).• Valvular heart disease prevents efficient blood

flow through the heart.• Types:• 1. Mitral stenosis: Valvular tissue thickens

and narrows the valve opening, preventingblood from flowing from the left atrium to theleft ventricle.

• Valvular heart disease occurs when the heartvalves cannot fully open (stenosis) or closecompletely (insufficiency or regurgitation).• Valvular heart disease prevents efficient blood

flow through the heart.• Types:• 1. Mitral stenosis: Valvular tissue thickens

and narrows the valve opening, preventingblood from flowing from the left atrium to theleft ventricle.


Conti…• 2. Mitral insufficiency, regurgitation: Valve is

incompetent, preventing complete valve closureduring systole.• 3. Mitral valve prolapse: Valve leaflets protrude

into the left atrium during systole.• 4. Aortic stenosis: Valvular tissue thickens and

narrows the valve opening, preventing blood fromflowing from the left ventricle into the aorta.• 5. Aortic insufficiency: Valve is incompetent,

preventing complete valve closure duringdiastole.

• 2. Mitral insufficiency, regurgitation: Valve isincompetent, preventing complete valve closureduring systole.• 3. Mitral valve prolapse: Valve leaflets protrude

into the left atrium during systole.• 4. Aortic stenosis: Valvular tissue thickens and

narrows the valve opening, preventing blood fromflowing from the left ventricle into the aorta.• 5. Aortic insufficiency: Valve is incompetent,

preventing complete valve closure duringdiastole.


Location / types of myocardial infarction

Obstruction of the left anterior descending artery(LAD) results in anterior or septal wall MI.


Cont…..

Obstruction of the circumflex artery results inposterior wall MI or lateral wall MI.Obstruction of the right coronary artery results

in inferior wall MI.

Obstruction of the circumflex artery results inposterior wall MI or lateral wall MI.Obstruction of the right coronary artery results

in inferior wall MI.


ETIOLOGY


ETIOLOGY

NON-MODIFIABLERISK

FACTORS

MODIFIABLERISK

FACTORS


NON-MODIFIABLE RISKFACTORS

AGE

FACTOR

SEXFAMILYHISTORY


AGE: More than 40 years.

FAMILY HISTORY:Myocardial infarction canbe inherited from parentsto children.

GENDER: Myocardialinfarction is 3 times morein men than women.

AGE: More than 40 years.

FAMILY HISTORY:Myocardial infarction canbe inherited from parentsto children.

GENDER: Myocardialinfarction is 3 times morein men than women.


MODIFIABLE RISK FACTORS

HIGHBLOODLIPIDSLEVEL

HYPER-TENSIONSTRESS

FACTOR

SMOKING

PHYSICALINACTIVITYOBESITY

DIABETESMELLITUS


HIGH BLOOD CHOLESTROL LEVEL

LIPIDS(LIPOPROTIENS)

LOW DENSITYLIPOPROTEIN

(LDL)DANGEROUS

HIGH DENSITYLIPOPROTEIN

(HDL)8/22/2016 22Shahzad Bashir, Lecturer NLCON

HDL is not dangerous because it containsmore proteins & very less lipids.Secondly it carry lipids away from arteries tothe liver for metabolism. So it prevents lipidsaccumulation within arteries.LDL is dangerous because it contains morelipids & has capacity to deposit fat withinarteries.So, LDL level more than 160mg/dl will place aperson at a risk of myocardial infarction.

HDL is not dangerous because it containsmore proteins & very less lipids.Secondly it carry lipids away from arteries tothe liver for metabolism. So it prevents lipidsaccumulation within arteries.LDL is dangerous because it contains morelipids & has capacity to deposit fat withinarteries.So, LDL level more than 160mg/dl will place aperson at a risk of myocardial infarction.


HYPERTENSION

If a person’s blood pressure is more than140/90 mmHg continuously for 4-5 yearsSustained stress on arterial walls injuryto endothelial lining atherosclerosisnarrowed & thickened arterial wallsrisk of M.I.Also salt consumption 5gms/ day cause M.I.

If a person’s blood pressure is more than140/90 mmHg continuously for 4-5 yearsSustained stress on arterial walls injuryto endothelial lining atherosclerosisnarrowed & thickened arterial wallsrisk of M.I.Also salt consumption 5gms/ day cause M.I.


SMOKING

Smoking nicotine catecholamine(epinephrine & nor epinephrine) releaseincreases heart rate & blood pressure increasescardiac workload.

+CO decreases O2 available to myocardium

Injury to myocardium

Smoking nicotine catecholamine(epinephrine & nor epinephrine) releaseincreases heart rate & blood pressure increasescardiac workload.

+CO decreases O2 available to myocardium

Injury to myocardium8/22/2016 25Shahzad Bashir, Lecturer NLCON

PHYSICAL INACTIVITY

Improper lipid metabolism

LDL level increases

Starts accumulatingin blood vessels

Risk of M.I.

Improper lipid metabolism

LDL level increases

Starts accumulatingin blood vessels

Risk of M.I.


OBESITY

More lipids are produced

LDL level increases

Atherosclerosis

Risk of M.I.

More lipids are produced

LDL level increases

Atherosclerosis

Risk of M.I.


DIABETES MELLITUS

Glucose molecules may stick tolumen of artery

Blockage of artery

Risk of having M.I.

Glucose molecules may stick tolumen of artery

Blockage of artery

Risk of having M.I.


STRESS

SNS stimulation

Release of catecholamine

Increases heart rate & intensify the force ofmyocardial contraction

Increases O2 demand

Cell death

Risk of M.I.

SNS stimulation

Release of catecholamine

Increases heart rate & intensify the force ofmyocardial contraction

Increases O2 demand

Cell death

Risk of M.I.8/22/2016 29Shahzad Bashir, Lecturer NLCON

PATHOPHYSIOLOGY


Causative factor: Obesity

Atherosclerosis

Narrowing of lumen

ed heart insufficient blood flow to myocardiumContractility ed O2 demand of myocardial cells

Inadequate creates an O2 deficitBlood supply

myocardial cell death inflammationOliguria

CK-MB & Troponine released Fever

Causative factor: Obesity

Atherosclerosis

Narrowing of lumen

ed heart insufficient blood flow to myocardiumContractility ed O2 demand of myocardial cells

Inadequate creates an O2 deficitBlood supply

myocardial cell death inflammationOliguria

CK-MB & Troponine released Fever8/22/2016 31Shahzad Bashir, Lecturer NLCON

Anaerobic glycolysis

Accumulation of lactic acid

Irritation of myocardial nerve fibers

Transmission of pain massage tomyocardium

Chest pain & radiation towards shoulder &arm

Anaerobic glycolysis

Accumulation of lactic acid

Irritation of myocardial nerve fibers

Transmission of pain massage tomyocardium

Chest pain & radiation towards shoulder &arm


Stimulation of vomiting SNS Stimulationcenter

increasedNausea & Vomiting catecholamine

Diaphoresis Increased(perfuse sweating) Heart Rate

Cold & Clammy skin“Cold Sweat”

Stimulation of vomiting SNS Stimulationcenter

increasedNausea & Vomiting catecholamine

Diaphoresis Increased(perfuse sweating) Heart Rate

Cold & Clammy skin“Cold Sweat”


Clinical manifestations

Cardiovascular- Chest pain/Discomfort Palpitations Elevated BP ECG may show tachycardia, bradycardia and

dysarrythmia

Cardiovascular- Chest pain/Discomfort Palpitations Elevated BP ECG may show tachycardia, bradycardia and

dysarrythmia


Cont…..Respiratory- Shortness of breath Dyspnea/Tachypnea Crackles Pulmonary edema-may be present

Gastrointestinal- Nausea Vomiting

Respiratory- Shortness of breath Dyspnea/Tachypnea Crackles Pulmonary edema-may be present

Gastrointestinal- Nausea Vomiting


Cont…..

Genitourinary- Decreased urinary output

Skin- Cool, clammy skin Diaphoresis Pallor, Cyanosis Coolness of extremities

Genitourinary- Decreased urinary output

Skin- Cool, clammy skin Diaphoresis Pallor, Cyanosis Coolness of extremities


Cont…..

Neurogenic- Anxiety, restleness Light- headedness Headache Visual Disturbances Altered speech Altered motor functions Altered level of consciousness

Neurogenic- Anxiety, restleness Light- headedness Headache Visual Disturbances Altered speech Altered motor functions Altered level of consciousness


PAIN

Characteristics: Severe,immobilizing chest pain.Usually prescribed as heaviness,pressure, tightness, burning.Location: Substernal,Retrosternal or Epigestric.Radiation: It may radiate toneck, jaw, arm or back.Duration: Lasts for 20 minutesor more.

Characteristics: Severe,immobilizing chest pain.Usually prescribed as heaviness,pressure, tightness, burning.Location: Substernal,Retrosternal or Epigestric.Radiation: It may radiate toneck, jaw, arm or back.Duration: Lasts for 20 minutesor more.


NAUSEA & VOMITING

Stimulation of vomiting center by severepain causes nausea & vomiting.

FEVER100.4 to 102.2°FIt is due to inflammatory process caused byMyocardial cell death.

Stimulation of vomiting center by severepain causes nausea & vomiting.

FEVER100.4 to 102.2°FIt is due to inflammatory process caused byMyocardial cell death.


SYMPATHETIC NERVOUS SYSTEMSTIMULATION

Increased catecholamine releases.

Diaphoresis (perfuse sweating).

Cold & clammy skin (“cold sweat”).

Increased catecholamine releases.

Diaphoresis (perfuse sweating).

Cold & clammy skin (“cold sweat”).


CARDIOVASCULAR MANIFESTATIONS

Hypotension

Decrease cardiac output

Shock

Urine output (Oliguria): <30ml/day.Dyspnoea

Hypotension

Decrease cardiac output

Shock

Urine output (Oliguria): <30ml/day.Dyspnoea


DIAGNOSTIC TESTS


Assessment/diagnostic findings It is generally based on presenting symptoms, ECG and

laboratory test results. Patient history-it includes

• Description of presentingsymptoms

• History of previous illness,family health history

It is generally based on presenting symptoms, ECG andlaboratory test results. Patient history-it includes

• Description of presentingsymptoms

• History of previous illness,family health history


Cont…..

Electrocardiogram-ECG provides information thatassists in diagnosing acute MI.The classic ECG changes are- T wave inversion ST segment elevation Abnormal Q wave

Electrocardiogram-ECG provides information thatassists in diagnosing acute MI.The classic ECG changes are- T wave inversion ST segment elevation Abnormal Q wave


SERUM CARDIACMARKERS

TROPONINE-C,T,I(PROTEIN)CK-MB (ENZYME) TROPONINE-C,T,I(PROTEIN)

Troponin I especially has a high affinity for myocardial injury; it rises within3 hours and persists for up to 7 to 10 days. Normal values lower than 0.6ng/mL


Cont…..• CK-MB(creatine kinase, myocardial muscle)-

increases 3-6 hrs after onset of chest pain,peaks in 12-18 hrs & return to normal within3-4 days.– Normal value is 0% to 5% of total; total CK is 26

to 174 units/L.

• Cardiac troponin T- increases 7-14 hrs after MI& persists for 5-7 days.– Normally ranging from 0 to 0.2 ng/mL;

• CK-MB(creatine kinase, myocardial muscle)-increases 3-6 hrs after onset of chest pain,peaks in 12-18 hrs & return to normal within3-4 days.– Normal value is 0% to 5% of total; total CK is 26

to 174 units/L.

• Cardiac troponin T- increases 7-14 hrs after MI& persists for 5-7 days.– Normally ranging from 0 to 0.2 ng/mL;


Cont…..• LDH(Lactate dehydrogenase)- it increases 14-

24 hrs after onset of MI, peak within 48-72 hrs& slowly return to normal over next 7-14 days.

• Leukocytosis- (10,000-20,000/mm3 ) appearson second day after MI & diappears in 1 wk.

• LDH(Lactate dehydrogenase)- it increases 14-24 hrs after onset of MI, peak within 48-72 hrs& slowly return to normal over next 7-14 days.

• Leukocytosis- (10,000-20,000/mm3 ) appearson second day after MI & diappears in 1 wk.


MEDICAL MANAGEMENT

MEDICALMANAGEMENT

DRUGTHERAPY FIBRINOLYTIC

THERAPY


MEDICAL MANAGEMENT

The goal of medical management is to minimizemyocardial damage, preserve myocardial functionand prevent complications. Pharmacological management- Thrombolytics Analgesics ACE Inhibitors(ACE-I)

The goal of medical management is to minimizemyocardial damage, preserve myocardial functionand prevent complications. Pharmacological management- Thrombolytics Analgesics ACE Inhibitors(ACE-I)


DRUG THERAPYANALGESIC: Morphine Sulphate.NITRATESI/V Nitroglycerine: 4 ampules of NTG are dissolved in100 ml normal saline to reduce pain by dilatingcoronary arteries.Sublingual Nitroglycerine: (Sorbitrate)At one time patient can take 3 tablets.if pain relieved If pain not relieved

Take second Tab. After 10 take next Tab. at same timeminutes

ANALGESIC: Morphine Sulphate.NITRATESI/V Nitroglycerine: 4 ampules of NTG are dissolved in100 ml normal saline to reduce pain by dilatingcoronary arteries.Sublingual Nitroglycerine: (Sorbitrate)At one time patient can take 3 tablets.if pain relieved If pain not relieved

Take second Tab. After 10 take next Tab. at same timeminutes


BETA ADRENERGIC BLOCKERS

(Propanolol) it inhibit SNS stimulation of heart.reduces both heart rate & contractility

CALCIUM CHANNEL BLOCKERS

(Verapamil, Nifedipine)It causes coronary artery vasodilatation & decreasesmyocardial contractility.Increases blood supply to myocardium & decreasesO2 demand of myocardium.

LOW-MOLECULAR-WEIGHT HEPARIN(Fragmine)These inhibit conversion of fibrinogen into fibrin.

(Propanolol) it inhibit SNS stimulation of heart.reduces both heart rate & contractility

CALCIUM CHANNEL BLOCKERS

(Verapamil, Nifedipine)It causes coronary artery vasodilatation & decreasesmyocardial contractility.Increases blood supply to myocardium & decreasesO2 demand of myocardium.

LOW-MOLECULAR-WEIGHT HEPARIN(Fragmine)These inhibit conversion of fibrinogen into fibrin.


FIBRINOLYTIC THERAPY

TIME OFADMINISTRATION:Thrombolytics are given to thepatient upto 12 hours of onsetof chest pain but for bestresults it should be givenwithin 1 hr after onset of chestpain.ACTION: These will dissolve& do lysis of thrombus incoronary artery.It includes streoptokinase,urokinase, t-PA, alteplase.After thrombolytic therapy,IV heparin is continued.

TIME OFADMINISTRATION:Thrombolytics are given to thepatient upto 12 hours of onsetof chest pain but for bestresults it should be givenwithin 1 hr after onset of chestpain.ACTION: These will dissolve& do lysis of thrombus incoronary artery.It includes streoptokinase,urokinase, t-PA, alteplase.After thrombolytic therapy,IV heparin is continued.


SURGICAL MANAGEMENT

PTCA (PercutaneousTransluminalCoronaryAngioplasty)

PTCA (PercutaneousTransluminalCoronaryAngioplasty)


STENT PLACEMENT


Conti….CORONARY

ARTERYBYPASS

GRAFT (CABG)A portion ofsaphenous veinfrom leg isremoved & isanastmosedproximally to theascending aorta &distally tocoronary artery.

CORONARYARTERYBYPASS

GRAFT (CABG)A portion ofsaphenous veinfrom leg isremoved & isanastmosedproximally to theascending aorta &distally tocoronary artery.


COMPLICATIONS

Dysrrythmias

Cardiogenic shock

Heart failure

Pulmonary embolism

Recurrent MI

Dressler’s syndrome

Dysrrythmias

Cardiogenic shock

Heart failure

Pulmonary embolism

Recurrent MI

Dressler’s syndrome


NURSING MANAGEMENT

Nursing assessmnet-SUBJECTIVE DATA:Past history of M.I., Angina, hypertension.Medication: use of nitrates, calcium channelblockers, antihypertensive drugs.Chest pain: squeezing, sharp & radiation tojaw, neck, arm.OBJECTIVE DATA:General: anxiety, diaphoresis.Integumentary: cool, clammy skin.Cardiovascular signs & findings

Nursing assessmnet-SUBJECTIVE DATA:Past history of M.I., Angina, hypertension.Medication: use of nitrates, calcium channelblockers, antihypertensive drugs.Chest pain: squeezing, sharp & radiation tojaw, neck, arm.OBJECTIVE DATA:General: anxiety, diaphoresis.Integumentary: cool, clammy skin.Cardiovascular signs & findings


Conti….

Nursing interventions in acute stage-

Obtain a description of chest discomfort Assess vital signs Assess cardiovascular status Place client in semi-fowler’s position Administer oxygen Establish I/V access Administer NTG as prescribed

Nursing interventions in acute stage-

Obtain a description of chest discomfort Assess vital signs Assess cardiovascular status Place client in semi-fowler’s position Administer oxygen Establish I/V access Administer NTG as prescribed


Conti….

• Administer Morphine Sulfate as prescribed.• Obtain 12-lead ECG• Administer I/V and anti-dysrrythmics as prescribed• Monitor thrombolytic therapy• Monitor for signs of bleeding• Monitor lab values• Assess distal peripheral pulses• Monitor intake-output• Assess resp. rate and breath sounds• Provide reassurance to client and family

• Administer Morphine Sulfate as prescribed.• Obtain 12-lead ECG• Administer I/V and anti-dysrrythmics as prescribed• Monitor thrombolytic therapy• Monitor for signs of bleeding• Monitor lab values• Assess distal peripheral pulses• Monitor intake-output• Assess resp. rate and breath sounds• Provide reassurance to client and family


Conti….

Interventions following acute stage-

Maintain bed rest for 24-36 hrs. Provide range of motion exercises Monitor for complications Encourage client to verbalize feelings regarding

MI

Interventions following acute stage-

Maintain bed rest for 24-36 hrs. Provide range of motion exercises Monitor for complications Encourage client to verbalize feelings regarding

MI


Nursing diagnosis• Acute pain R/T myocardial ischemia resulting from

coronary artery occlusion• Outcome- the client will experience improved comfort

as evidenced by dec. in pain rating scale.• Interventions- assess characteristics of pain• Assess respiration, BP, heart rate with each episode of

chest pain.• Obtain 12 lead WCG on admission & on each episode

of chest pain.• Monitor respond to drug therapy.• Limit visitors.• As morphine as ordered.• Administer nitrates as ordered.

• Acute pain R/T myocardial ischemia resulting fromcoronary artery occlusion• Outcome- the client will experience improved comfort

as evidenced by dec. in pain rating scale.• Interventions- assess characteristics of pain• Assess respiration, BP, heart rate with each episode of

chest pain.• Obtain 12 lead WCG on admission & on each episode

of chest pain.• Monitor respond to drug therapy.• Limit visitors.• As morphine as ordered.• Administer nitrates as ordered.8/22/2016 64Shahzad Bashir, Lecturer NLCON

Conti….• Ineffective tissue perfusion R/T thrombus in

coronary artery• Outcome- the client will demonstrate

improved cardiac tissue perfusion as evidencedby dec. rating of pain.• Interventions- provide bed rest.• Administer oxygen as prescribed.• Administer thrombolytics.• Monitor ST segments.

• Ineffective tissue perfusion R/T thrombus incoronary artery• Outcome- the client will demonstrate

improved cardiac tissue perfusion as evidencedby dec. rating of pain.• Interventions- provide bed rest.• Administer oxygen as prescribed.• Administer thrombolytics.• Monitor ST segments.8/22/2016 65Shahzad Bashir, Lecturer NLCON

Conti….• Dysrrhythmias R/T electrical instability or

irritability secondary to infarcted tissue• Outcome- the client will have no dysrrythmias as

evidenced by normal sinus rhythm.• Interventions- teach client & family about need

for continous monitoring.• Assess apical heart rate.• Give antidysrrythmic agents as ordered.• Monitor effects of antidysrrythmics.• Monitor serum K levels.• Maintain patent IV line.• Monitor ST segments & document changes.

• Dysrrhythmias R/T electrical instability orirritability secondary to infarcted tissue• Outcome- the client will have no dysrrythmias as

evidenced by normal sinus rhythm.• Interventions- teach client & family about need

for continous monitoring.• Assess apical heart rate.• Give antidysrrythmic agents as ordered.• Monitor effects of antidysrrythmics.• Monitor serum K levels.• Maintain patent IV line.• Monitor ST segments & document changes.8/22/2016 66Shahzad Bashir, Lecturer NLCON

Conti….• Decreased cardiac output R/T negativ einotropic

changes in heart secondary to myocardial ischemia.• Outcome- the client will have improved cardiac output

as evidenced by normal cardiac rate, rhythm &hemodynamic parameters.• Interventions- assess mental status of pt.• Assess lung sounds for crackles & ronchi.• Monitor BP .• Assess heart sounds for murmur.• Monitor urine output.• Assess for peripheral perfusion-cyanosis, peripheral

pulses.• Monitor ABG.• Maintain hemodynamic stability & duration.

• Decreased cardiac output R/T negativ einotropicchanges in heart secondary to myocardial ischemia.• Outcome- the client will have improved cardiac output

as evidenced by normal cardiac rate, rhythm &hemodynamic parameters.• Interventions- assess mental status of pt.• Assess lung sounds for crackles & ronchi.• Monitor BP .• Assess heart sounds for murmur.• Monitor urine output.• Assess for peripheral perfusion-cyanosis, peripheral

pulses.• Monitor ABG.• Maintain hemodynamic stability & duration.8/22/2016 67Shahzad Bashir, Lecturer NLCON

Conti….• Impaired gas exchange R/T decreased cardiac

output.• Outcome- the client will demonstrate improved

gas exchange as evidenced by absence ofdyspnea.• Interventions- administer oxygen as ordered.• Monitor ABG.• Continue to assess client’s skin, capillary refill &

level of consciousness.• Assess respiratory status for dyspnea & crackles.• Prepare for intubation & mechanical ventilation if

hypoxia inc.

• Impaired gas exchange R/T decreased cardiacoutput.• Outcome- the client will demonstrate improved

gas exchange as evidenced by absence ofdyspnea.• Interventions- administer oxygen as ordered.• Monitor ABG.• Continue to assess client’s skin, capillary refill &

level of consciousness.• Assess respiratory status for dyspnea & crackles.• Prepare for intubation & mechanical ventilation if

hypoxia inc.


Conti….• Risk for bleeding R/T coagulopathies with

thrombolytic therapy.• Powerlessness R/T a near-death experience &

anticipated lifestyle changes.• Anxiety & fear R/T hospital admission & fear of

death.• Risk for constipation R/T bed rest, pain

medications & NPO or soft diet.• Ineffective health maintenance R/T MI &

implications for lifestyle changes.• Risk for activity intolerance R/T an imbalance

b/w oxygen supply & demand.

• Risk for bleeding R/T coagulopathies withthrombolytic therapy.• Powerlessness R/T a near-death experience &

anticipated lifestyle changes.• Anxiety & fear R/T hospital admission & fear of

death.• Risk for constipation R/T bed rest, pain

medications & NPO or soft diet.• Ineffective health maintenance R/T MI &

implications for lifestyle changes.• Risk for activity intolerance R/T an imbalance

b/w oxygen supply & demand.8/22/2016 69Shahzad Bashir, Lecturer NLCON

Conti….• Risk for heart failure R/T disease progress as

evidenced by tachycardia, hypotension orhypertension.• Excess fluid volume R/T reduced GFR,

decreased cardiac output, increased ADHhormone & sodium & water retention.• Risk for impaired skin integrity R/T bed rest &

decreased tissue perfusion.

• Risk for heart failure R/T disease progress asevidenced by tachycardia, hypotension orhypertension.• Excess fluid volume R/T reduced GFR,

decreased cardiac output, increased ADHhormone & sodium & water retention.• Risk for impaired skin integrity R/T bed rest &

decreased tissue perfusion.


References• Porter, P. A & Perry, A. G. (2003). Basic

Nursing: Essentials for practice (5th ed.) St.Louis: Mosby.• Erb, G. K., (2000). Fundamentals of Nursing:

Concept, process and practice (5th ed.).Addison: Wesley.• Bruner, L.S., & Suddarth, D.S. (2001). Text

book of Medical-Surgical Nursing (9th Ed.).Philadelphia: Lippincott.

• Porter, P. A & Perry, A. G. (2003). BasicNursing: Essentials for practice (5th ed.) St.Louis: Mosby.• Erb, G. K., (2000). Fundamentals of Nursing:

Concept, process and practice (5th ed.).Addison: Wesley.• Bruner, L.S., & Suddarth, D.S. (2001). Text

book of Medical-Surgical Nursing (9th Ed.).Philadelphia: Lippincott.


THANKSTHANKS THANKS


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