Cardiovascular AlterationsCoronary Artery Disease

Coronary Artery Disease

• An insidious, progressive disease of the coronary arteries resulting in narrowing or complete occlusion.

• Risk Factors• Pathophysiology

Manifestations of Coronary Artery Disease

• Sudden cardiac death• Angina pectoris• Myocardial infarction• The development of heart failure• Chronic arrhythmias• Conduction disturbances

Angina Pectoris

• A symptom of Coronary artery disease usually secondary to a blockage or a spasm of the coronary artery resulting in diminished blood supply to the myocardium.May also be caused by hypotension or other factors that cause ischemia to the muscle: aortic stenosis or insufficiency, anemia, polythemia

• Characteristics of pain: • Pain is usually relieved by rest and nitroglycerin

Types of AnginaStable

• Predictable and caused by the same types of activities.

• Usually begins gradually and reaches maximum intensity within minutes. Can be controlled by alleviating the precipitating factors and or by the administration of vasodilators.

• Usually caused by a fixed lesion.

Types of AnginaUnstable

• Defined as a change in the previously established stable pattern of angina or new onset severe angina.

• Pain relief usually requires more than nitrates.• This type of angina requires medical attention.

Types of AnginaVariant or Prizmetal’s Angina

• Caused by a coronary artery spasm with or without the presence of arteriosclerotic lesions.

• May be precipitated by smoking tobacco and ingesting alcohol and cocaine.

• Usually associated with ST segment elevation. • Treatment includes vasodilators such as nitrates and

calcium channel blockers.

Types of AnginaSilent

Defined as objective ECG changes of myocardial ischemia without the patient experiences symptoms.

Treatment of Angina

Goals of treatment:1. Increase coronary artery perfusion

- oxygen, nitrates,vasodilators, thrombolytics2. Decrease myocardial workload

- bed rest, beta blockers, ACE inhibitors, calcium channel blockers, morphine

3. Prevent myocardial infarction - All above interventions- reduce CAD risk factors

Acute Myocardial Infarction(AMI)

• Defined as irreversible myocardial necrosis resulting from an abrupt decrease or cessation of coronary blood flow to an area of the heart.

Diagnostic Indicators of an AMI

• Pain characteristics : usually last longer than 30 minutes and is not relieved by nitroglycerin or rest.

Diagnostic Indicators of an AMICardiac Enzymes

• CPK-MB: Proteins that are released from damaged myocardial tissue.– Elevate in 4-6 hours after injury– Peak at 6-12 hours– Remain elevated for 2-3 days after injury

Diagnostic Indicators of an AMICardiac Enzymes

• LDH1 and LDH2: Proteins that are released from damaged myocardial tissue later than CPK-MB. Useful in the late diagnosis of an MI.– Elevate in 10-12 hours after injury– Peak at 48-72 hours– Remain elevated for 10-14 days after injury

Diagnostic Indicators of an AMICardiac Enzymes

• Troponin-T: Found only in cardiac tissue, thus is more specific than CK-MB for detecting cardiac damage. – Elevates as soon as one hour after injury– Remain elevated for at least 14 days after injury

Diagnostic Indicators of an AMIEKG Changes

Baseline

Ischemia—tall or inverted T wave (infarct),ST segment may be depressed (angina)

Injury—elevated ST segment, T wave may invert

Infarction (Acute)—abnormal Q wave,ST segment may be elevated and T wavemay be inverted

Infarction (Age Unknown)—abnormal Q wave,ST segment and T wave returned to normal

EKG Changes with an AMI

Septal wall

V1, V2

Anterior wall

V1, V2, V3, V4, 1, AVL

Inferior wall

2, 3, AVF

Posterior Wall

Reciprocal changes in V1, V2

Lateral wall1, AVL, V5, V6

Treatment of AMI

Taken from American Heart Association’s ACLS Guidelines

Oxygen Used in Acute Coronary Syndromes

Oxygen Used in Acute Coronary Syndromes

Why?• Increases supply of oxygen to ischemic tissueWhen?• Always when AMI is suspectedHow?• Start with nasal cannula at 4 L/min• Remember one word: oxygen-IV-monitorWatch Out!• Rarely COPD patients with hypoxic

ventilatory drive will hypoventilate

Nitroglycerin: ActionsNitroglycerin: Actions

• Decreases pain of ischemia

• Increases venous dilation

• Decreases venous blood return to heart

• Decreases preload and cardiac oxygen consumption

• Dilates coronary arteries

• Increases cardiac collateral flow

Nitroglycerin: IndicationsNitroglycerin: Indications

• Class I: First 24 to 48 hours in patients with ST-segment elevation or depression including– LV failure (acute pulmonary edema or CHF)– Elevated BP (especially with signs of LV failure)– Large anterior infarction– Persistent ischemia

• Suspected ischemic chest pain• Unstable angina (change in angina pattern)• Acute pulmonary edema (if BP >90 mm Hg systolic)

Nitroglycerin: DoseNitroglycerin: Dose

• Sublingual: 0.4 mg; repeat every 5 minutes• Spray inhaler: 2 metered doses at 5-minute intervals• IV infusion: 10 to 20 mcg/min infusion, titrated

Nitroglycerin: PrecautionsNitroglycerin: Precautions

• Use extreme caution if systolic BP <90 mm Hg• Use extreme caution in RV infarction

– Suspect RV infarction with inferior ST changes

• Watch for headache, drop in BP, syncope, tachycardia

• Tell patient to sit or lie down during administration

Morphine Sulfate: Actions, IndicationsMorphine Sulfate:

Actions, Indications

• Why? (Actions)– To reduce pain of ischemia—by dilating smooth muscle.– To reduce anxiety– To reduce extension of ischemia by reducing

oxygen demands

• When? (Indications)– Continuing pain– Evidence of vascular congestion (acute pulmonary edema)– Systolic blood pressure >90 mm Hg– No hypovolemia

Morphine Sulfate: Dose, PrecautionsMorphine Sulfate: Dose, Precautions

• How? (Dose)– 2 to 4 mg titrated to effect

– Goal: Eliminate pain

• Watch out for (Precautions)– Drop in blood pressure, especially in patients with

• Volume depletion

• Increased systemic resistance

• RV infarction

– Depression of ventilation

– Nausea and vomiting (common)

– Bradycardia

– Itching and bronchospasm (uncommon)

Aspirin: ActionsAspirin: Actions

• Why? (Actions)– Blocks formation of thromboxane A2 (thromboxane A2

causes platelets to aggregate and arteries to constrict)

• These actions will reduce– Overall mortality from AMI

– Nonfatal reinfarction

– Nonfatal stroke

Aspirin: Indications, Dose, Precautions

Aspirin: Indications, Dose, Precautions

• When? (Indications) As soon as possible!– Standard therapy for all patients with new pain suggestive

of AMI– Give within minutes of arrival

• How? (Dose) 160- to 325-mg tablet taken as soon as possible• Watch Out! (Precautions)

– Relatively contraindicated in patients with active peptic ulcer disease or asthma

– Contraindicated in patients with known aspirin hypersensitivity– Bleeding disorders– Severe hepatic disease

ß-Blockersß-Blockers

• Mechanism of action– Blocks catecholamines from binding to

ß-adrenergic receptors

– Reduces HR, BP, myocardial contractility

– Decreases AV nodal conduction

– Decreases incidence of primary VF

ß-Blockersß-Blockers

• Severe CHF/PE • SBP <100 mm Hg• Acute asthma

(bronchospasm)• 2nd- or 3rd-degree

AV block

• Mild/moderate CHF• HR <60 bpm• History of asthma• IDDM• Severe peripheral

vascular disease

AbsoluteContraindications Cautions

HeparinHeparin

• Mechanism of action– Indirect thrombin inhibitor (with AT III)

• Indications– PTCA or CABG– With fibrin-specific lytics – High risk for systemic emboli

• Conditions with high risk for systemic emboli, such as large anterior MI, atrial fibrillation, or LV thrombus

ACE InhibitorsACE Inhibitors

• Mechanism of action– Reduces BP by inhibiting angiotensin-converting enzyme

(ACE)

– Alters post-AMI LV remodeling by inhibiting tissue ACE

– Lowers peripheral vascular resistance by vasodilatation

– Reduces mortality and CHF from AMI

Fibrinolytic TherapyFibrinolytic Therapy

• Breaks up the fibrin network that binds clots together• Indications: ST elevation >1 mm in 2 or more contiguous

leads or new LBBB or new BBB that obscures ST– Time of symptom onset must be <12 hours – Caution: fibrinolytics can cause death from brain hemorrhage

• Agents differ in their mechanism of action, ease of preparation and administration; cost; need for heparin

• 5 agents currently available: alteplase (tPA, Activase), anistreplase (Eminase), reteplase (Retavase), streptokinase (Streptase), tenecteplase (TNKase)

Antiplatelet AgentsAntiplatelet Agents

• Blocks glycoprotein IIb/IIIa receptors on platelets

• Blocked receptors cannot attach to fibrinogen

• Fibrinogen cannot aggregate platelets to platelets

• Indications: ACS with NO ST-segment elevation:– Non–Q-wave MI– Unstable angina managed medically

• Examples: abciximab (ReoPro), eptifibitide (Integrilin), tirofiban (Aggrastat)

Percutaneous Transluminal Coronary Angioplasty

Percutaneous Transluminal Coronary Angioplasty

• Direct treatment• Mechanical reperfusion

of infarct-related coronary artery

• Best outcome achieved for patients with AMI plus cardiogenic shock

Complications of AMI

Dysrhythmias

• 95% of all AMI patients will experience dysrhythmias.

• Site of the infarction will determine type of dysrhythmias:– right coronary artery- bradycardia, heart blocks,

PVCs– left anterior descending- PVCs, BBB, 2nd

degree blocks– circumflex- PVCs

Heart Failure and Cardiogenic Shock

• CHF: 20-30% mortality rate of all hospitalized AMI patients.

• Cardiogenic Shock: In patients with extensive myocardial damage it has a mortality rate of 80-90% despite aggressive treatment.

Ventricular Aneurysm

Papillary Muscle Rupture

Ventricular Septal Defect

Ventricular Free Wall Rupture

• 3-4% of all AMI deaths result from Ventricular free wall rupture.

• Usually occurs around the 5th post-MI day when leukocyte scavenger cells are removing necrotic trash. This thins the ventricular wall resulting in rupture.

• Cardiac tamponade cardiogenic shock and death are eminent.

Pericarditis

• Inflation of the pericardial sac secondary to irritation from a roughened epicardium.

• Signs and Symptoms:– pain (usually greater with deep inspiration)– pericardial friction rub at the sternal boarder

• Treatment:

– aspirin or other nonsteroidal antiinflammatory drug