Coronary Heart Disease NUR -224 - PowerPoint Presentation

Slide1

Coronary Heart Disease

NUR -224Slide2

Coronary Heart Disease

Affects 16 million people

Causes more than 600,000 death annually

Caused by impaired blood flow to the myocardium

Accumulation of atherosclerotic plaque in the coronary arteries usual cause.

May be asymptomatic or may lead to angina pectoris, acute coronary care syndrome, myocardial infarction (MI/heart attack), dysrhythmias, heart failure and even sudden deathSlide3

Coronary Atherosclerosis

Atherosclerosis is the abnormal accumulation of lipid deposits within arterial walls and lumen.

In coronary atherosclerosis, blockages and narrowing of the coronary vessels reduce blood flow to the myocardium. Slide4

Coronary Heart Disease

Risk Factors

age (over 50)

heredity

smoking

obesity

high serum cholesterol levels

hypertension

diabetes mellitusSlide5

Angina Pectoris

Characterized by chest pain and usually precipitated by exercise and relieved by rest.

Myocardial oxygen needs are greater than partially occluded vessels can supply, myocardial cells become ischemic and shift to anaerobic metabolism



produces lactic acid that stimulates the nerve endings in the muscle

 pain

Pain subsides when oxygen supply meets myocardial demand.Slide6

Angina Pectoris

Chest pain

 reduced coronary blood flow  temporary imbalance between myocardial blood supply and demand

This causes temporary/reversible myocardial ischemia.

More than 30 minutes of ischemia irreversibly damages myocardial cells (necrosis)Slide7

Types of Angina

Stable angina

Unstable angina

Silent Ischemia

Variant angina (

Prinzmetal’s

angina)Slide8

Stable Angina

Occurs with a predictable amount of activity or stress

Predictable and common

Occurs when the work of the heart

is

increased by physical exertion, exposure to cold, or by stress

Sensation may

occur



neck, jaw, shoulders

Lasts for few minutes – 5/15 minutes

Relieved by rest and/or nitratesSlide9

Unstable Angina

Occurs with increasing frequency, severity and duration

Pain is unpredictable and occurs with decreasing levels of activity or stress and may occur at rest.

Patients at risk for myocardial infarction

May not be relieved by NTG or restSlide10

Variant Angina (Prinzmetal’s)

Atypical angina that occurs unpredictably

Caused by coronary artery spasm with/out atherosclerotic lesion

Often occurs at night Slide11

Silent IschemiaOccurs in the absence of any subjective

symptoms (asymptomatic)

Patient reports no

pain

May occur with either activity or mental stressSlide12

Clinical Manifestations

Chest pain

Precipitated by an identifiable event.

Classic sequence

Women frequently present with atypical symptoms of anginaSlide13

Angina Pain

Manifestations

Chest Pain

Quality

Associated manifestations

Atypical manifestations

Precipitating factors

Relieving factorsSlide14

Assessment/Diagnostic Findings

Past medical history/family history

Comprehensive description of chest pain

Presence of risk factors

Electrocardiography

Echocardiography

Cardiac stress testing

Cardiac AngiographySlide15

Medical Management

Focus on maintaining coronary blood flow and cardiac function

Measures to restore coronary blood flow (later)

Pharmacologic therapy

* nitrates

* beta blockers

* calcium channel blockers

* aspirin Slide16

Nitrates

SL NTG -> acute angina attacks (

Buccal

spray)

Acts within 1-2 minutes

Long acting nitroglycerin

Used to prevent attacks not treat an acute attack.

Headache, hypotension, nausea, dizziness

NTG,

Nitrostat

, Nitro-bidSlide17

NitratesNursing Responsibilities

Patient TeachingSlide18

B –Adrenergic Blockers

Decrease myocardial contractility, HR, BP

 which will reduce myocardial oxygen demand

Side

effects  bradycardia, hypotension, wheezing, GI complaints.

Contraindicated for patient with asthma

Metoprolol

(

L

opressor), Atenolol(Tenormin),

Carvedilol

(Coreg)Slide19

Beta Blockers

Nursing Responsibilities

Patient TeachingSlide20

Calcium Channel Blockers

Decrease the workload of the heart

Relax blood vessels

 decrease BP and increase coronary perfusion

Potent coronary

vasodilator

Amlodipine (Norvasc),

Diltiazem

(Cardizem),

Felodipine

(

Plendil

)

Used to treat Variant Angina Slide21

Aspirin

Prevent platelet aggregation/thrombus formation

Reduces the incidence of MI

80-325 mg of aspirin as soon as dx.

i

s made

If patient is taking Tylenol – should continue to take aspirin

GI upset – H2 blocker, PPISlide22

Nursing Diagnosis

Ineffective Cardiac Tissue Perfusion

Deficient

Knowledge

Risk for Ineffective Therapeutic Regimen ManagementSlide23
Slide24

Acute Coronary Syndrome

Condition of unstable cardiac ischemia

Includes unstable angina and acute myocardial ischemia c/out significant injury of myocardial tissue

Coronary blood flow is acutely reduced, but not fully occluded. Myocardial cells are injured by the acute ischemia that results.

Most people have stenosis of one or more coronary arteries.Slide25

Acute Coronary Syndrome

Cardinal manifestation

Chest pain

– substernal/epigastric

Dyspnea

Diaphoresis

Pallor

Cool skin

Tachycardia

HypotensionSlide26

Acute Coronary Care Syndrome

Diagnosis

ECG

Cardiac Markers

*Cardiac muscle troponins (sensitive indicators

of myocardial damage)

* Creatine Kinase (CK) & CK-MB (specific to

myocardial muscle)Slide27

MedicationsReduce myocardial ischemiaReduce risk for blood clotting

Nitrates

Beta blockers

Antiplatelet (

po

/IV)Slide28

Oral Antiplatelet -Medication

Aspirin

Clopidogrel

(Plavix)

Ticlopidine

(

Ticlid

)

Suppress platelet aggregation, prevents the development of thrombus.

Nursing responsibilities

Patient EducationSlide29

IV Antiplatelet Tirofiban

(

Aggrastat

)

Eptifibatide

(

Integrilin

)

IV

antiplatelets

more effective than oral administered meds but the risk of bleeding is greaterSlide30

Heparin

Prevents the formation of new clots

Reducers the occurrence of MI

IV bolus/then continuous infusion

Infusion based on PTT – 2-2.5 times the normal PTT value (25-35 sec.)

LMWH – Lovenox/Fragmin

All increase the risk of bleeding : bleeding precautionsSlide31

Revascularization ProceduresSeveral procedures may be used to restore blood flow and oxygen to ischemic tissue.Nonsurgical techniques:

percutaneous coronary revascularization

coronary

atherectomy

intracoronary stents

coronary

artery bypass

graft (surgical procedure may be used) Slide32

Percutaneous Coronary Revascularization

Is recommended for patients:

Fail medical management

Have left main coronary artery/three vessel disease

Are not candidates for PCI

Have failed PCI with ongoing chest painSlide33

Percutaneous Coronary InterventionGoal: open the affected artery within 90 minutes of arrival to a facility

Advantages:

Alternative to surgical intervention

Performed with local anesthesia

Patient is ambulatory 24 hours after the procedure

Hospital stay shorter

Patient can return to workSlide34

Percutaneous Coronary Revascularization

A balloon-tipped catheter is threaded over the

guide wire

Balloon is inflated for about 30 sec.-2 minutes to compress the plaque against the arterial wall

The stent is then placed over a balloon catheter and expanded as the balloon is inflated

It remains in the artery when the

balloon is

removed.Slide35

Percutaneous Coronary Intervention

Post procedure care:

Assess vital signs

Bedrest

/ flat in bed

Affected leg straight

Pressure dressing applied

Monitor for bleeding/hematoma

Resume self-care activities/ambulation few hours after procedure Slide36

Percutaneous Coronary RevascularizationSlide37

AtherectomyRemove plaque from the identified lesionCatheter shaves the plaque off vessels walls using a rotary cutting head

-

retaining the fragments in it compartment and removing them from the vessel.

Rotation catheter

pulverize

the

plaque into particles small enough to pass through the coronary microcirculation.Slide38
Slide39

CABG

Involves using a section of a vein /artery to create a connection (bypass) between the aorta and the coronary artery beyond construction.

This allows blood to perfuse the ischemic portion of the heart.

Internal mammary artery in the chest/saphenous vein from the leg are the vessels most commonly used.Slide40

CABG Surgery

Internal mammary artery – is commonly used.

Remains palliative treatment and not a cure.

Improves quality of life/patient outcomes

Postoperative complications/mortality increase as a function of age.

Women have a higher mortality rate than menSlide41
Slide42

CABGSlide43

Patient teaching

Lifestyle changes and reduction of risk factors

Explore, recognize, and adapt behaviors to avoid to reduce the incidence of episodes of ischemia

Teaching regarding disease process

Cardiac rehabilitation

Stress reduction

When to seek emergency careSlide44
Slide45

Myocardial InfarctionAn area of the

myocardium

is permanently destroyed

 necrosis of the myocardial cells. If circulation to the affected myocardium is not promptly restored , the heart loses the ability to maintain effective cardiac output.

Life-threatening event

May lead to cardiogenic shock and deathSlide46

Myocardial InfarctionAnnually 785,000 experience their first MIMajority of deaths from MI occur during the initial period after symptoms begin:

60% within the first hour

40% prior to hospitalization

Medical treatment and training in CPR are vital to decrease deaths due to

MI.Slide47

Myocardial Infarction

The area of infarction develops over minute to hours.

Cellular ischemia  affects conduction and myocardial contractility

Myocardial contractility decreases, increasing the risk for dysrhythmias, subsequently reducing cardiac output, B/P, and tissue perfusionSlide48

Myocardial Infarction

When a larger artery is compromised, collateral vessels connecting smaller arteries in the coronary system dilate to maintain blood flow to the cardiac muscle.

The degree of collateral circulation determines the extent of myocardial damage.

Occlusion of coronary artery without any collateral vessels

 massive tissue damage and death

Slide49

Clinical Manifestations

Pain – sudden and usually not associated with activity

Women/older adults

atypical chest

pain,

elevated

BP & HR initially, then ↓

’

es

Nausea/vomiting

Fever

Dyspnea, shortness of breath

Anxiety , sense of impending doomSlide50
Slide51
Slide52

Collaborative CareGoalsRelieve chest pain

Reduce the extent of myocardial damage

Maintain cardiovascular stability

Decrease cardiac workload

Prevent complicationsSlide53

Assessment/ Diagnostic FindingsECG

Laboratory tests— serum cardiac biomarkers

CK-MB

Myoglobin

Troponin

CBC

EchocardiogramSlide54

Laboratory Tests

Serum Cardiac Markers

Are proteins released into the blood from necrotic heart muscle

They occur after cellular death indicates cardiac damage

Creatine

kinase (CK-MB) and troponin are measured to diagnose an MI.Slide55

Serum Cardiac Markers

Creatine kinase (CK )

Important enzyme for cellular function

Found mainly in cardiac muscle (skeletal muscle/brain)

Begin to rise rapidly with damage to these tissues at about 4/6 hours after an MI , peak at about 12/24 hours and return to normal within 36/48 hours

CK correlates with the size of the infarctionSlide56

Serum Cardiac MarkersCPK-MB

Subset of CK specific to cardiac muscle

Most sensitive indicating of MI

Elevated CK –alone is not specific for MI

Elevated CPK-MB

 positive indicator of MI

Does not normally rise with chest pain from angina or other causes other than MISlide57

Serum Cardiac Markers

Troponin

Regulates the myocardial contractility process

Proteins released during myocardial infarction – are sensitive indicators of myocardial damage.

Necrosis of cardiac muscle, troponins are released and blood levels rise.

Is a

highly cardiac specific

indicator of an MI

Increases with 4-6 hours during an acute MI, remains elevated for a long period -- 3 weeksSlide58

Serum Cardiac Markers

Myoglobin

Helps transport oxygen

Found in cardiac and skeletal muscle

Levels start to increase within 1-3 hours of symptom onset return to normal within 24 hours after onset of symptoms.

Is one of the first cardiac markers to appear after MI, it lacks cardiac specificity.

Kidneys rapidly excrete it in urine

 blood levels return to normal range within 24 hours.Slide59

Ischemia, Injury , InfarctionSlide60

COMPLICATIONS

Heart failure

Cardiogenic shock

Dysrhythmias and cardiac arrestSlide61

Interdisciplinary Care

Immediate treatment goals for the MI

Relieve the chest pain

Reduce the extent of myocardial damage

Decrease the cardiac workload

Prevent complications Slide62

Treatment of Acute MI

Obtain diagnostic tests including ECG within 10 minutes of admission to the ED

Oxygen

Aspirin, nitroglycerin, morphine, beta-blockers

fibrinolytic

therapy

Revascularization Procedures

As indicated: IV heparin, LMWH

Bed restSlide63

Nursing Interventions Pain stimulates the SNS, increasing cardiac work. Pain relief is a priority.

Acute Pain

Assess for verbal and nonverbal signs of pain

Administer oxygen2-5L/min via nasal cannula

Promote physical and psychologic rest

Titrate IV nitroglycerin as ordered

Administer morphine by IV push for chest pain as neededSlide64

Nursing Interventions

Ineffective Tissue Perfusion

Assess and document vital signs

Assess for changes in LOC

Auscultate heart and breath sounds

Monitor ECG



Administer

antidysrhythmic

medications

Monitor oxygen saturationSlide65

Nursing Interventions

Fear

Acknowledge the client’s perception of the situation

Encourage questions/ provide consistent, factual answers

Encourage self-care

Administer anti-anxiety medications as ordered

Teach non-pharmacologic methodsSlide66
Slide67

HEART FAILURESlide68

Heart Failure

Complex syndrome resulting from cardiac disorders that impair the ventricles’ ability to fill and effectively pump blood

Inability of the heart to pump sufficient blood to meet the metabolic demands of the body.

5.7 million people in the US have heart disease.

HF is increasing in incidence and prevalence.

Primarily a disease of older adults.

HF is associated with high morbidity/mortality ratesSlide69

HEART FAILURE

Heart failure develops

 cardiac output falls  decrease in tissue perfusion

.

Is a disorder of cardiac function

Hypertension and CHD are the leading causes of heart failure

The prognosis for the client with heart failure depends on the underlying cause and how effectively the precipitating factors can be treated.

Most clients with heart failure die within 8 years of the diagnosis.

Ejection fraction – provides information about the (L) ventricle during systole. Normal 55-65%.Slide70

PathophysiologyDecrease cardiac output

 activation of compensatory mechanisms 

neurohormonal

response decrease in renal perfusion & increase vasoconstriction  sodium and water retention  fluid overload increase the workload of the heartSlide71
Slide72

Etiology

CAD and advancing age are the primary risk factors for HF

CAD is found in more than 60% of patients

Other factors: hypertension, diabetes, cigarette smoking, obesity, Slide73

Manifestations of Heart FailureCHD/hypertension are common causes of

L-sided heart failure

whereas

R-

heart failure

caused by conditions that restrict blood flow to the lungs (acute/chronic pulmonary disease).

Left sided heart failure can lead to right sided heart failure.Slide74

Classification of Heart Failure

Left-sided heart failure

Most common form of HF

LV

cannot pump blood effectively to the systemic circulation. Pulmonary venous pressures increase and result in pulmonary congestion with dyspnea, cough, crackles, and impaired oxygen exchange

.

This increase pulmonary pressure  pulmonary congestion and edemaSlide75

Types of Heart Failure

Manifestation of

L-sided heart failure

result from pulmonary congestion (backward effects) and decreased cardiac output (forward effects).

Fatigue and activity intolerance

Dizziness and syncope

Pulmonary congestion

Cyanosis

Rales

/wheezing Slide76
Slide77

Types of Heart Failure

Right sided heart failure

Causes a back up of blood to the ( R) atrium

RV

cannot eject sufficient amounts of

blood into the pulmonary circulation 

blood backs up in the venous system.

Increase venous pressure causes abdominal organs to become congested /peripheral edema develops

This results

in

peripheral

edema,

® upper quadrant pain, ascites

, anorexia, nausea, weakness, and weight gain

.Slide78
Slide79

Multisystem Effects of Heart Failure

Neurologic

Respiratory

Cardiovascular

Gastrointestinal

Genitourinary

Integumentary

Metabolic Slide80

Diagnostic Studies

BNP levels – key diagnostic indicator of HF

Serum electrolytes

Liver function tests

Echocardiogram

Chest x-ray

ElectrocardiogramSlide81

Heart Failure

Hemodynamics Monitoring

Used to assess cardiovascular function in the critically/unstable client and evaluate their interventions

Hemodynamic parameters

 heart rate, arterial blood pressure, central venous pressure, pulmonary pressure and cardiac outputSlide82
Slide83

Management of Heart FailureEliminate or reduce etiologic or contributory factors.

Reduce the workload of the heart by reducing afterload and preload.

Optimize all therapeutic regimens.

Prevent exacerbations of heart failure.

Medications are routinely prescribed for heart failure.Slide84

Medications

Angiotensin-converting

enzyme inhibitors

Angiotensin II receptor blockers

Beta-blockers

Diuretics

Digitalis

Other medicationsSlide85

Other Treatment

Surgery

Circulatory assistance

Cardiac transplantation

Hemodynamic MonitoringSlide86

ComplicationsCompensatory Mechanism

Hepatomegaly/splenomegaly

Dysrhythmias

Pulmonary problemsSlide87

Nursing interventions

Decreased Cardiac Output

Excess Fluid Volume

Activity Intolerance

DietSlide88
Slide89

ACUTE CORONARY SYNDROME

ACS

 occurs when ischemia is prolonged and not immediately reversible resulting in myocardial cell death .

The spectrum of ACS encompasses: unstable angina(UA), non-ST-segment-elevation MI (NSTEMI), ST-segment-evaluation MI (STEMI).