Learning Station 1 Cardiovascular Emergencies Case 1

1999 American Heart Association

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Acknowledgments

Janice Ritchie Saia, RN, EMT-P, of St. Petersburg, FL, first developed these materials. She has generously donated her work to the AHA. Steve Anderson, MD, of Auburn, WA, provided helpful scripts for this case. Mary Fran Hazinski, RN, MSN, and John Field, MD, provided many refinements during final review. We appreciate the hard work of each of these people.

Learning Objectives
After completing this learning station you should be able to Apply the Five Quadrads Approach to patients with complex cardiovascular emergencies Discuss, assess, and manage acute MI Identify ECG changes consistent with Myocardial ischemia/infarction Location of infarct Infarct-related coronary artery
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Case History

Mr. B. Skimmer, age 45, complains of chest discomfort, nausea, severe fatigue Past Med Hx: hypertension (poor control), 2 to 3 pack/day cigarettes, high stress job Refuses coworkers assistance States: Its just the flu Goes to break room to rest
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Case Progression

One hour later a coworker finds Mr. Skimmer lethargic, pale, profusely diaphoretic Coworker offers to drive Mr. Skimmer to ED, only 3 minutes away Should Mr. Skimmer go to ED by ALS ambulance? WHY?
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Case Progression

Mr. Skimmer arrives at your ED with O2 via NRB; IV LR @ KVO Received MONA in field; BP dropped alarmingly, near syncope Triaged as urgent Placed in ED critical care bed
What should you as the key ACLS provider do first?
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The Five Quadrads Approach to ACLS-EP

1. 2. 3. 4. 5. Primary ABCD Survey Secondary ABCD Survey OxygenIVmonitorfluids TempBPHRRR Tanktankpumprate

Assessment
Five Quadrads Approach

Primary Survey Airway: adequate Breathing: present with equal chest rise, adequate tidal volume Circulation: pulse present carotid and radial Defibrillation: not needed
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Assessment
Five Quadrads Approach

Secondary Survey
Airway: adequate Breathing: lung sounds clear Oxygen sat 97% with NRB Circulation: sinus rhythm 2-mm ST-elevation in leads II, III, aVF BP 126/84 mm Hg; IV access present Differential diagnosis: AMI. Others?
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Assessment
Five Quadrads Approach

OxygenIVmonitorfluids Started by EMS; continued in ED Vital signs T=99.1F, BP=126/84 mm Hg, HR=74 bpm, RR=28/min Tanktankpumprate Consider sources of hemodynamic compromise
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What would you like to do NOW?

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Immediate ED Assessments

O2IVmonitorfluids (done by EMS) Grade chest pain: character, intensity H & P: focus on thrombolytic screening VS frequent recordings Multilead ECG? (12, 15, or 22 leads) First set serum markers Electrolytes; coagulation studies Portable chest film
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12-Lead ECG Findings

1. ST-segment elevation or new LBBB strongly suspicious for injury

2. ST-segment depression/dynamic T-wave inversion; strongly suspicious for ischemia

3. Nondiagnostic or normal ECG; chest pain strongly suspicious for ischemia

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Localizing Ischemia or Injury

I lateral

aVR

V1 septal

V4 anterior

II inferior

aVL lateral

V2 septal
V3 anterior

V5 lateral
V6 lateral

III inferior

aVF inferior

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ECG 1: Interpretation?

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ECG 1: elevated ST segments; inferior leads (II, III, aVF); ST depression: precordial leads V2-V5; lateral leads I, aVL Suspect occlusion right coronary artery

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Coronary Artery Distribution

Left

Right

Septal wall of LV Anterior and lateral walls of LV Inferior wall LV (10%) Both bundle branches

Inferior wall of LV Posterior wall of LV (90%) AV node (90%) Right ventricle

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Cardiac Anatomy in Relation to Coronary Artery

Anterior wall V3-V4
Left main coronary artery Right coronary artery

Circumflex artery Left anterior descending artery Lateral wall I, aVL, V5-V6
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Septal wall V1-V2

Posterior View of the Heart

Circumflex artery (from left coronary artery) Posterior wall
NOTE 1: Inferior wall supplied by either the right (85% to 90% of people) or left coronary artery. NOTE 2: If there is acute injury in inferior leads (II, III, aVF), unknown whether left or right coronary artery is blocked.

NOTE 3: KEY you must obtain a RIGHTRight coronary SIDED ECG at once.

Lateral wall Inferior wall Leads II, III, aVF

artery

Posterior descending artery

HOW TO GET RIGHT-SIDED ECG?

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Lead Placement for a Right-sided ECG

V1

V2

V3R
V6R V5R V4R

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Right Ventricular Infarction

Inferior lead changes RV infarction? Use lead V4R (ST elevation >1 mm) Clinical significance: Increased mortality Preload dependence Vasodilators may cause severe hypotension What is management of RV infarction?
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How would you manage this patient?

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Treatments to Consider for Acute Coronary Syndromes

Oxygen/airway Nitroglycerin Analgesia Aspirin -Blockers Heparin

ACE inhibitors Magnesium Lidocaine Reperfusion therapy PTCA Thrombolytics

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Nitroglycerin

Mechanism of action Indications Administration Cautions

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Narcotic Analgesia

Morphine sulfate readily available Effects Relieves pain and anxiety Reduces myocardial oxygen needs Administration 2 to 5 mg IV q 5 minutes (slow) Caution N & V, low BP, respiratory depression
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Aspirin

Aspirin inhibits platelet cyclo-oxygenase decreases thromboxane A2 production Aspirin benefits Reduces overall mortality in AMI Reduces incidence of nonfatal reinfarction Dose: 160 to 325 mg PO ASAP

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-Blockers
Mechanism of action Block catecholamines from binding to -adrenergic receptors Nonselective and cardioselective Reduce HR, BP, myocardial contractility, and oxygen consumption Decrease AV nodal conduction
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-Blockers
Absolute Cautions contraindications Mild/moderate CHF Severe CHF/PE Bradycardia Hypotension (HR <60 bpm) (SBP <100 mm Hg) Hx asthma Bronchospasm IDDM 2nd- or 3rd-degree Severe peripheral AV block vascular disease
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Heparin
Mechanism of action Indirect thrombin inhibitor (with AT III) Indications PTCA or CABG With fibrin-specific lytics (eg, alteplase) High risk for systemic emboli Large anterior MI, atrial fib, LV thrombus

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ACE Inhibitors
Mechanism of action Lower BP by inhibiting angiotensinconverting enzyme (ACE) Attenuate LV remodeling by inhibiting tissue ACE Lower peripheral vascular resistance by vasodilatation mechanism Reduce mortality from AMI
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Potassium and Magnesium Sulfate

Potassium deficiency but not magnesium deficiency associated with arrhythmias, sudden death Recent studies suggest no reduction in AMI mortality with magnesium administration

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Case Progression

Is Mr. Skimmer a candidate for thrombolysis?

What information do you need to make this decision?

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Contraindications to Thrombolytic Therapy

Absolute contraindications

Relative contraindications

Previous hemorrhagic stroke any time Other stroke, CVA within 1 year; IC neoplasm Active internal bleeding (not menses) Suspected aortic dissection

Severe uncontrolled hypertension (>180/110) Current use of anticoagulants Recent trauma (2 to 4 wk); major surgery <3 wk Recent internal bleeding, active peptic ulcer Pregnancy Streptokinase allergy
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Percutaneous Transluminal Coronary Angioplasty

Direct treatment Mechanical reperfusion of infarct-related coronary artery Best outcome achieved for patients with AMI plus cardiogenic shock

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Case Progression

Mr. Skimmer received oxygen, aspirin, metoprolol IV, and heparin No nitroglycerin or morphine in ED Now pain-free; stable BP; O2 sat 98% Reperfusion therapy: t-PA + heparin

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ECG 2: Interpretation?

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Case Progression

Mr. Skimmer transferred to CCU Uneventful night No chest pain or shortness of breath No arrhythmias Treatment: Oxygen at 2 L/min Heparin, ACE inhibitors, -blockers Nitroglycerin not given
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The next day

In CCU Mr. Skimmer begins complaining of Chest pressure Light-headedness Increasing intensity over 20 minutes What should you do now?

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The Five Quadrads

Primary Survey: no CPR or defibrillation indicated Secondary Survey Airway: adequate Breathing: dyspnea, + JVD, rales in lower third of lung fields Circulation: diaphoretic; peripheral pulses weak Differential diagnosis: obtain 12-lead ECG
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The Five Quadrads

OxygenIVmonitorfluids Vital signs BP 76/64 mm Hg, HR 80 bpm, RR 32/min Tanktankpumprate What is the nature of the problem? Check 12-lead ECG

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ECG 3: Interpretation?

SR with ST-segment elevation in leads II, III, aVF; reciprocal changes throughout

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Treatment Considerations
Acute Pulmonary Edema With Hypotension
First-line Actions

Second-line Actions

Oxygen Furosemide Avoid, if possible, nitroglycerin or morphine, especially if patient is hypotensive

Dopamine

Dobutamine PEEP (caution) CPAP

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Treatment Considerations

Priority actions Thrombolytic therapy (repeat t-PA) Coronary angiography and angioplasty or emergency surgical revascularization Intra-aortic balloon pump

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Differential Diagnosis

Reocclusion RCA; infarct extension Mechanical complications (eg, mitral regurgitation, VSD) Low cardiac output Pulmonary embolus

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Case Progression

Pulmonary edema persists Cardiogenic shock continues Patient remains hypotensive ECG: ST elevation consistent with reocclusion Strategy: coronary angiography Outcome: angioplasty and stent proximal RCA

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Summary

Five Quadrads
Layered approach; guides actions and thinking Apply whenever you arrive at an emergency setting

Goals of coronary syndrome treatment

Early reperfusion therapy (myocardial salvage) when indicated Reduce morbidity and mortality through adjunctive agents (ASA, -blockers, ACE, statins) Recognize and anticipate serious early complications: unstable post-MI angina, CHF, late VT/VF
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Summary

A focused history and assessment facilitates early initiation of reperfusion therapy The 12-lead ECG may be used to localize injury and guide therapy Serum markers may be used to triage patients and assess prognosis

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Summary

Several treatments help patients by Decreasing mortality Limiting extent of infarction Limiting incidence of reinfarction Knowledge of complicated AMIs enables us to Anticipate complications Care for patients with complex acute coronary syndromes
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