CAD and ACS

Problems of Oxygenation
Ventilation-pulmonary
Transport-hematologic
Perfusion-cardiovascular
Coronary Artery Disease and
Acute Coronary Syndrome
- Atherosclerosis: Coronary Artery disease (CAD ) Clinical Manifestation…angina, acute coronary
syndrome and sudden cardiac death

CAD- Risk Factors

Unmodifiable Modifiable
Age Lipid levels
Gender HTN
Ethnicity Smoking
Genetics Obesity
Physical inactivity
 Daily Stress
DM

CAD- Risk Factors

Risk Factor reduction remains most important to change the course CAD
Decreasing blood pressure…high blood pressure cause changes in our vascular system
Lowering cholesterol levels…helps reduce the amount of plaque that is form in the blood vessels
Smoking cessation…smoking narrows our blood vessels, making them less compliant
Increasing activity levels…help reduce coronary artery disease
Tighter control of DM…hemoglobin a1c

C-Reactive Protein (hsCRP) bloodtest…measure level in the blood stream that has something to do with
inflammation
Inflammation may play a part in development of Atherosclerosis
CRP is an acute phase protein released during systemic inflammation, infection, and acute injury
The higher the level of hsCPR the greater the risk of developing MI (PREDICTIVE, not
DIAGNOSTIC…this could be a modifiable risk factor)may be able to help change some of their
lifestyle to bring down c-reactive protein, putting them at less risk
Hypothesized that infection may contribute or cause atherosclerosis
< 1.0 mg/L = Low Risk
1.0 -3.0 mg/L = Moderate Risk
3.0 mg/L = HIGH Risk

CAD-Risk Factors
Homocysteine…blood level
Amino acid synthesized during protein catabolism (breakdown of protein)
High levels toxic to endothelial lining of arterial walls
May lead to plaque formation and platelet aggregation
N= 4-17 micromole/liter
Moderate: 16-30
Intermediate: 31-100
Severe: >100
Vitamin B6 and B12

CAD: Etiology and Pathophysiology

Narrowing of Coronary Arteries…major vessel that supply blood and nutrient to the heart muscle
Build up of plaques within vessels
Plaques rupture, trigger blood clot or thrombus blocking blood flow
Development of collateral circulation r/t chronic ischemia

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Progression of Atherosclerosis: Coronary Circulation/ Myocardial Oxygenation
Supply and Demand
Increase in demand for O2 –or-…exercise, exertion
Decrease in supply of O2…low BP, hypovolemic, shock
Both lead to Myocardial Ischemia or lack of oxygen supply to the heart…particuly when we have
compromised vessels
Cause: narrowing of coronary arteries by atherosclerosis
Usually 75% occluded before ischemia occurs

More about ISCHEMIA

Myocardium becomes cyanotic in 10 sec!
ECG changes occur
Contractility at the site stops after several minutes
No GLUCOSE for aerobic metabolism
Anaerobic metabolism begins
Lactic Acid is produced, irritates nerve fibers
Pain impulses sent to cardiac nerves and upper thoracic nerve roots
Cardiac cells viable for 20 min
Ischemic changes are reversible if blood flow is restored

Angina: two types stable and unstable (chest pain)

Precipitating Factors
Physical exertion- less time in diastole (filling time)
Temperature extremes- increases workload
Strong emotion- increases SNS
Heavy meal- blood diverted to GI, decreases coronary flow
Smoking- increase HR, vasoconstriction, catecholamines
Sexual activity- increases workload and SNS
Stimulants- HR, and O2 demand

Angina: Pain Characteristics

Vague sensation, strange feeling, pressure or ache in chest
Constrictive, squeezing, heavy, choking, suffocating
Can be accompanied by indigestion or burning
Substernal can radiate to jaw, shoulders, down arms, between shoulder blades

Angina: Symptoms
Anxiety
SOB
Cold sweat
Weakness or paresthesia of one arm/hand

Angina: Stable
Results from reversible cell injury
Occurs intermittently over long periods of time…pt will be on nitrate, to prevent stable angina from
occurring
SAME pattern of:
1. Onset
2. Duration
3. Intensity of symptoms
Pain:
subsides when precipitating factor is relieved
usually 3-5 min
for this pain to occur at rest is Unusual…not doing anything
ST segment depression

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 Controlled with medication…nitrate
Relieved with rest

Angina: Unstable
NEW in onset
Occurs at Rest
Worsening pattern
Unpredictable…can happen with exertion or without
Ruptured plaque
Not relieved by rest

Unstable angina can result from Acute Coronary Syndrome or myocardial infarction

Acute Coronary Syndrome

2002, 34% of US population has some form of CV disease
Each year 700,000 will have new “heart attack”; 500,000 will have recurrent
Cost: direct and indirect, >$400 billion annually
Leading cause of death in US

Myocardial Infarction
Occurs d/t sustained ischemia
Causes irreversible cell death (necrosis)
Cell death begins after 20 minutes
Contractile function stops in the area of necrosis
Degree of contractile dysfunction is related to
 How big area of cardiac tissue involved…the bigger the area of infarct, the more muscle tissue
we are taking out, the more it will effect contractile and cardiac output
 the size of infarct
Location and area of infarct correlate to coronary circulation involved
- anterior wall infarct…will cause a large area necrosis by occluding this vessel
- inferior wall infarct…the entire inferior wall

Signs and Symptoms

Pain:
1. Severe, immobilizing, not relieved by rest, position change or SL nitrates
2. Heaviness, pressure, tightness, burning, constriction, crushing
3. Substernal, retrosternal, epigastric
4. Radiate: neck, jaw, arms, back
5. While active, rest, or asleep
6. Women present atypical: discomfort, SOB, fatigue…women present in a different fashion
7. pulmonary system (pneumonia, pleuritis), musculoskeletal issues
 chest pain related to MI are not relieved by nitrates

Nausea and Vomiting

1. Stimulation of reflex vomiting center caused by pain
2. Or vasovagal reflexes initiated from infarct site
SNS
Epinephrine/norepinephrine released
Stimulates SNS
1. Diaphoresis
2. Vasoconstriction of peripheral blood vessels, that result in…

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 3. Ashen skin color, clammy, cool, called “cold sweat”
Fever
1. Rises within first 24 hrs
2. Up to 100.4 F or 38 C
3. Lasts up to one week
4. Results from inflammatory process caused by cell death

Cardiovascular
HR/BP elevated initially, then decreased if drop in Cardiac Output…due to stimulation SNS, the heart is
trying to compensate
Decreased urine output
Heart failure:
JVD
pulmonary congestion
Peripheral edema
Hepatic engorgement
Distant heart sounds
Murmurs may develop d/t papillary muscle ischemia (valves have muscle that hold them in place an
help them to work)
Abnormal precordial movement
Abnormal sounds: S3, S4 d/t ventricular dysfunction

Complications
Dysrhythmias…the main complication that can result from/after MI
Most common complication, 80% of MI patients
Caused by
Ischemia…primary
Electrolyte imbalances…K+, calcium, magnesium
SNS stimulation
HTN
Hypoxia
Bradycardia…most common post MI
Tachycardia
Irregular beats (PVCs)
Ventricular dysrhythmias are life-threatening
Require immediate treatment

Congestive Heart Failure (CHF)…pump failure

Inability of the heart to pump effectively…if we have killed of a large portion of our myocardium, we
have killed off a large portion of our pumping ability
R/T severity and extent of injury
Symptoms of CHF
Dyspnea
Restlessness
Agitation
JVD
Crackles
Extra heart sounds (S3, S4)

Cardiogenic Shock
High mortality rate
Lack of oxygen and nutrients to tissue d/t severe L ventricular failure (pump failure)
Treat aggressively with circulatory support and vasoactive medications

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Pericarditis
Inflammation of visceral and/or parietal pericardium
Cause cardiac compression, decrease ventricular filling and emptying, cardiac failure
Occurs 1-2 days post-MI
Severe pain aggravated by inspiration, coughing, movement, relieved by sitting forward
Friction rub, may have fever
Treatment: pain relief, corticosteroids or NSAIDS

Pulmonary Embolism…high mortality rate

Source usually rough endocardium or leg veins
Early detection is vital
Watch for pallor or cyanosis, unexplained pleural effusion and/or heart failure unresponsive to treatment
Sudden severe dyspnea, usually fatal

MI: Diagnostics
Three components for diagnosis of Acute MI
Patient’s HISTORY of pain, risk factors, and health history

Serial 12 Lead ECGs consistent with acute MI: ST segment elevation of 1mm or more in two contiguous leads

Serial measurement of CARDIAC MARKERS

MI: Diagnostics

Electrocardiogram
1. Serial 12 Lead ECGs (looks at the electrical activity of the heart form 12 different perspectives) needed to
“rule out” or confirm MI
2. Look for changes in:
a. Q wave: > .04 sec or > 1/3 the amplitude of the QRS
b. ST segment: depression (ischemia) or elevation (injury)
c. T wave: inverted (full thickness ischemia)
3. ECG may be normal initially, repeated every 8 hrs X 3
Serum Cardiac Markers…blood test, that will help diagnose MI
1. Proteins that are released into the blood stream in large amounts from necrotic heart muscle
2. Important for diagnosis of acute MI
3. Have established peaks and durations
4. Repeated q 8 hrs x 3 (8hrs for 24hrs)
Creatine Kinase (CK)…not real specific to cardiac
Levels rise 3-12 hrs post MI
Peak in 24 hrs; Normal in 2-3 days
CK-MB
More specific to cardiac cells, more specially, necrosis quantifies damage…the higher it is the worst
> 3% indicate MI
Troponin
Also proteins released after injury
Highly specific indicator of MI
Greater sensitivity and specificity than CK-MB
Rises quickly, elevated for 2 weeks

MI: Medications
Remember: MONA
1. Morphine Sulfate
2. Oxygen
3. Nitroglycerine

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 4.
Aspirin
Then…Add Thrombolytics, Beta Blockers, ACE inhibitors

Morphine Sulfate…create vasodilation (decreasing the workload)

Narcotic: opioid analgesic
Acute chest pain
Added effect of vasodilation, decreases BP
Decreases myocardial oxygen demand
Given IV, titrated to effect (gradually increase the dose, monitoring the patient BP (don’t want BP to bottom,
but we want the chest pain to go away)
Oxygen
Improves tissue oxygenation
Dose by pulse oximetry and ABGs
Nasal cannula 1-6 L/min
Face mask 8-10 L/min

Nitroglycerine…short acting vasodilators

Short-acting Nitrate: relax arterial and venous smooth muscle
Initially given SL q 5 min for up to three doses
Given IV infusion in acute care setting (ED, ICU)
Titrated to effect, elimination of chest pain
Vasodilation, decreased amount of blood returning to the heart, less for ventricles to pump
Decreases workload and myocardial oxygen demand

Aspirin
Anticoagulant, platelet aggregation inhibitor…low dose, once a day
180-325 mg given as soon as MI is suspected
Use following MI shown to dramatically decrease mortality rates
Increase risk of bleeding, gastritis, GI bleed
• can be given right away and known to be

Beta-Blockers
-OLOL: atenolol, metoprolol, propranolol
Slow HR, decrease contractility, reduce BP
Reduce myocardial oxygen demand
Can slow impulse conduction, suppressing dysrhythmias
Reduce mortality rate if given within 8 hr of MI onset

Thrombolytics…relates to PE…break down or dissolve clot

t-PA, alteplase, Activase
Promote fibrinolysis or clot destruction
Most effective when given as soon as possible after clot formation: ideally within 4 hours
Non-specific: will dissolve any clot that exists
Narrow margin of safety
Monitor VS closely and for signs of BLEEDING
Cerebral hemorrhage (huge complication): change in LOC, neuro status
Observe for “reperfusion dysrhythmias”…vessel is unblocked and creating new blood flow…restored blood
flow to area…this is a good thing
Administered in ICU or ED
Exclusion criteria:
Recent trauma
Surgery/biopsy
Arterial emboli
Recent cerebral emboli
Hemorrhage
Thrombocytopenia
Childbirth (within 10 days)

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ACE Inhibitors…given later in the treatment
-PRIL: captopril, lisinopril
Improve survival post-MI if started 1-2 days following onset of symptoms
Usually after thrombolytics are completed
• found to decrease mortality rate

Discharge Teaching
Cardiac Rehabilitation is returning to optimal state
of functioning…usually started in the hospital
Focus on ‘abilities’ rather than ‘disabilities’
Six areas:
Physiologic
Psychologic
Mental
Spiritual
Economic
Vocational
Patient and family involvement
Anatomy and physiology of heart
Cause and effect of atherosclerosis
Terms
S & S of angina and MI
Healing process
Risk factors and how to decrease them
Tests and treatments
Expectations about rehab and recovery
Resuming work, physical activity, sexual activity
Gradual progression of activity
When to seek help