Leanna R. Miller, RN, MN, CCRN-CSC, PCCN-CMC, CEN, CNRN, CMSRN, NP Education Specialist LRM Consulting Nashville, TN.

Leanna R. Miller, RN, MN, CCRN-CSC, PCCN-CMC, CEN, CNRN, CMSRN, NP

Education Specialist LRM Consulting

Nashville, TN

• Objectives– Evaluate common abnormalities that mimic

myocardial infarction.– Identify the criteria for pericarditis and evidence –

based interventions.– Differentiate between pulmonary embolus and

myocardial infarction using diagnostic criteria.

ST Segment Changes: Identifying MI Mimics

Acute Coronary Syndromes– Unstable Angina– Non ST segment Elevation MI

(NSTEMI)– ST segment Elevation MI

(STEMI)



Acute Coronary Syndromes– Clinical Symptoms

• typical• atypical


Acute Coronary Syndromes– Diagnostics

• Echocardiography• Lab

–ABGs–H & H–enzymes


Acute Coronary Syndromes– Diagnostics

• ECG (12 or 15 lead)–T wave inversion–ST segment elevation–Q wave–reciprocal ST segment depression




SITE INDICATIVE RECIPROCAL

Septal V1, V2 None

Anterior V2, V3, V4 None

Anteroseptal V1, V2, V3, V4 None

Lateral I, aVL, V5, V6 II, III, aVF

Anterolateral I, aVL, V3, V4, V5, V6 II, III, aVF

Inferior II, III, aVF I, aVL, V2, V3

Posterior None V1, V2


Variation to ST – Segment Elevation



High acute risk factors for progression to

myocardial infarction or death– recurrent chest pain at rest– dynamic ST-segment changes: ST-segment

depression > 0.1 mV or transient (<30 min) ST-segment elevation >0.1 mV

– elevated Troponin-I, Troponin-T, or CK-MB levels


High acute risk factors for progression to

myocardial infarction or death– hemodynamic instability within the observation

period– major arrhythmias (ventricular tachycardia,

ventricular fibrillation)– early post-infarction unstable angina– diabetes mellitus







AMI

LVH

BBB

Vpace

BER

Pericarditis

LV Aneurysm

Other


Acute Pericarditis

• Introduction

– causes physical discomfort

– predisposition to tachydysrhythmias


Acute Pericarditis

• ECG Criteria

– ST segment elevation

– PR segment depression

– T wave flattening or inversion

– atrial dysrhythmias


Acute Pericarditis

• ST segment elevation

– not isolated or discrete segments

– upward concavity

– may be notching at the junction of

QRS and ST segment

– no reciprocal ST segment depression


Acute Pericarditis

• PR interval

– interval between end of P wave and

beginning of QRS may be depressed

– most often seen in lead II and V

leads may be only ECG finding


Acute Pericarditis

• T wave flattening or inversion

– no T wave inversion during acute phase

– uncomplicated pericarditis: negative

T waves only occur in leads which usually

have negative T waves (aVR & V1)


Acute Pericarditis

• Atrial dysrhythmias

– SVT in postoperative open heart patient

– treat with low dose steroids



Acute Pericarditis

• Complications (pericardial effusion)

– dampening of electrical output

– low voltage in all leads

– ST segment & T wave changes


Acute Pericarditis

• Complications (pericardial effusion)

– freely rotating heart produces

electrical alternans


Dressler’s Syndrome

• Introduction

– postmyocardial infarction syndrome

– autoimmune process



• Clinical Presentation

–low – grade fever

–chest pain (worsens with deep

breath; lessens with sitting up

and leaning forward)

–pericardial friction rub



• 12 – lead ECG

– diffuse ST segment elevation across the precordial leads



• Treatment

– corticosteroid administration

– monitor for complications (effusion)


Pulmonary Embolus

• Introduction

– sudden massive PE produces ECG changes

– must get 12 – lead to rule out MI


Pulmonary Embolus

• ECG Findings

– RVH with strain

– RBBB pattern in V1

– large S wave in Lead I; large Q wave in Lead

III (S1Q3 pattern)




Ventricular Aneurysm

• Introduction (etiology)

– myocardial infarction

– congenital

– cardiomyopathy

– inflammatory

– idiopathic



• Introduction

– infereolateral wall of LV

– symptoms include CHF & exercise –

induced syncope (VT)



• ECG Findings

– persistent ST segment elevation

– small q wave in II, III, & aVF

– sustained VT with RBBB morphology






• Treatment

– surgical resection

– antidysrhythmics

– anticoagulants

– treat heart failure

– ablation therapy



Left Bundle Branch Block (LBBB)

• QRS duration > 0.12 second

• absence of septal q waves and S wave

in I, aVL, & V5 – 6 (+ complex usually

notched)

• broad QS or rS in V1 – 3 (- complex)



• S – T, T wave changes in leads I,

aVL & V5 – 6 (T wave opposite QRS)

• delayed intrinsicoid deflection over

left ventricle (V6); normal over V1



• hypertensive heart disease

• aortic stenosis

• degenerative changes of the conduction

system

• coronary artery disease







LBBB with Acute Myocardial Infarction


Left Ventricular Hypertrophy



Left Ventricular Hypertrophy


• Brugada Syndrome – autosomal dominant inheritance (SCN5A)

gene– sodium channel involvement in 25% of the

patients– Asian populations (58%)– high incidence of polymorphic ventricular

tachycardias


• Brugada Syndrome – found in right precordial leads– prominent J wave– ST – segment elevation in the absence of

structural heart disease– three types


• Brugada Syndrome – Type I: ST – segment elevation is

triangular and T waves may be inverted in V1 – V3

– Type II: downward displacement of ST – segment (does not reach baseline)

– Type III: middle part of ST segment touches baseline



Brugada Syndrome


LBBB• Infarction Resemblance

– ST segment elevation in the negatively deflected leads, (V1 – V3)

– QS complexes in the negatively deflected leads, (V1 – V3)

• Recognition– Wide QRS

– QS in V1


Ventricular Rhythms• Infarction Resemblance


– QS complexes in the negatively deflected leads, (V1 – V3)

• Recognition– Wide QRS following pacer spike

– Negative V1 (RV paced)


LVH• Infarction Resemblance


• Recognition– Choose deepest S wave from V1 and V2

– Choose tallest R wave from V5 and V6

– Add deflections of tallest R wave and deepest S wave

– Suspect LVH if total is > 35


Pericarditis• Infarction Resemblance

– ST segment elements in multiple leads

• Recognition– ST segment elevation not in anatomical

grouping– PR segment deprewsion– Notching of the J point


Acute Pulmonary Emboli • Infarction Resemblance

– RVH with strain pattern

– RBBB pattern in V1

– S1Q3 on frontal plane

• Recognition– Patient is symptomatic with atypical

cardiac pain– Elevates BMP– r/o with spiral CT/angiogram


Ventricular Aneurysm• Infarction Resemblance

– High risk for ventricular dysrhythmias (VT with RBBB pattern)

– Inferolateral MI– Persistent ST segment elevation– Small q wave in II, III, aVL

• Recognition– Structural abnormality on ECHO– CHF & exercise – induced syncope (VT)


Brugada Syndrome• Infarction Resemblance

– Ventricular dysrhythmias (polymorphic VT)– ST segment elevation in right precordial

leads

• Recognition– Autosomal dominant– Asian culture– No structural abnormality noted on ECHO


• Prominent J with ST segment elevations – septal MI– RV cardiomyopathy– pericardial effusion– hypercalcemia


• Prominent J with ST segment elevations – hyperkalemia– acute pulmonary embolism– subarachnoid hemorrhage– tricyclic antidepressant intoxication



• In Conclusion

– is the patient having a MI?– a variety of conditions can mimic

infarctionST segment changes


Leanna R. Miller, RN, MN, CCRN-CSC, PCCN-CMC, CEN, CNRN, CMSRN, NP Education Specialist LRM Consulting Nashville, TN.

Documents

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