SGD 1: AMI

CL, 55y/o M, CEO, severe substernal chest

heaviness

SGD 1: AMI

SALIENT FEATURES 55 y/o M, CEO severe substernal chest heaviness

accompanied by nausea and vomiting

History of having episodes of mild substernal chest tightness for the last 5 yrs a known hypertensive for 6 yrs (Usual BP: 130/80, Highest BP: 170/100)

Irregular intake of Nifedipine 30mg

SALIENT FEATURES 40 pack years of cigarette smoking heavy alcohol beverage drinker Family History

(+ ) premature CAD sister, 38 and brother, 45 (+ ) HTN father (+ ) DM mother

SALIENT FEATURES Soft S1 murmur on PE Laboratory tests

12 lead ECG: NSR, ST segment elevation I, aVL, V1-V6; ST segment depression II, III, aVF Troponin I – 1.5ng/mL CPK-MB – 256u/L CXR: cardiomegaly

SALIENT FEATURES• Cont’d

Echo –Doppler: Eccentric LVH w/ segmental wall motion abnormality

Ejection fraction at 48%Doppler evidence off

impaired LV relaxationDilated LADilated Aortic RootAortic Sclerosis

Ischemic Cardiac Disease with an Eccentric Left Ventricular

Hypertrophy with segmental wall motion abnormality, a Dilated Left Atrium and Aortic Root, and Aortic Sclerosis with evident ST Elevation Myocardial Infarction (STEMI) and

Normal Sinus Rhythm, of Class IV-D Functional Disability

Diagnosis

2. Differentiate between ATHEROGENESIS and ATHEROTHROMBOSIS

Atherogenesis The process of forming atheromas, plaques in the

inner lining (the intima) of arteries. It involves elements of inflammation , a process that provides a unifying theme in the pathogenesis of atherosclerosis

Atherogenesis

AtherothrombosisCharacterized by an unpredictable, sudden

disruption (rupture or erosion/fissure) of an atherosclerotic plaque, which leads to platelet activation and thrombus formation. It is the underlying condition that results in events leading to myocardial infarction, ischemic stroke, and vascular death.

Atherothrombosis

3. What are the risk factors for CAD?

RISK FACTORS OF CAD

RISK FACTORS PRESENT IN THE PATIENT (+) Family history of

premature CAD (sister at age 38 and brother at age 45)

Sex (Male)

Age (55 years old)

Known hypertensive for 6 years Highest BP = 170/100

mmHg Irregular intake of

Nifedipine 30 mg

Forty (40) pack years of cigarette smoking

Stress Occupation: CEOHad an argument

during regular board meeting

Heavy alcoholic beverage drinker

4. What are the WHO criteria for acute myocardial infarction?

Are they present in this patient?

WHO CRITERIA FOR AMI (1979):

1. Clinical history of ischemic type of chest pain lasting for more than 20 minutes.

A patient is diagnosed with myocardial infarction if two (probable) or three (definite) of the following criteria are satisfied:


2. Changes in serial ECG tracings.



3. Rise and fall of serum cardiac biomarkers such as creatinine kinase-MB fraction and troponin.


REDEFINED WHO CRITERIA FOR AMI (2000):

Cardiac troponin rise

accompanied by

either:

Typical symptoms

Pathological Q waves

ST elevation or

depression

Coronary intervention

The WHO criteria were refined in 2000 to give more prominence to cardiac biomarkers.

IN THE PATIENT:• Severe substernal heaviness (experienced about 1 hour)

• ST segment elevation I, aVL, V1-V6

• Troponin I: 1.5ng/mL (NV: 0 – 0.4 ng/mL)• CPK-MB: 256 u/L (NV: <1 u/L)

• ST segment depression II, III and aVF

• Clinical history of ischemic type chest pain lasting > 20 mins

• Changes in serial ECG tracings

• Rise and fall of cardiac biomarkers

• Cardiac troponin rise accompanied by ST depression

CRITERIA:

5.What are the clinical features(Sx and PE) of AMI? Are

they present in this patient?

Symptoms and PE of AMI• Chest pain

– described as a pressure sensation, fullness, or squeezing in the midportion of the thorax

– may radiate to the arms, jaw or teeth, shoulder, and/or back

• Associated diaphoresis or sweating palpitations, weakness

Substernal chest pain for >30 mins and diaphoresis strongly suggests STEMI

• Presence of a precipitating factor:– Vigorous physical activity– Emotional stress– Illness: medical or surgical

Symptoms and PE of AMI• Associated with dyspnea or shortness of breath• Associated epigastric discomfort with or without

nausea and vomiting• Syncope or near-syncope without other cause• Impairment of cognitive function without other

cause lightheadedness or loss of consciousness a look of anxiety, or a sense of impending doom or death

• It may occur at any time of the day, but most appear to be clustered around the early hours of the morning, are associated with demanding physical activity, or both

PESigns of ventricular dysfunction:

(+) S3 and S4Decreased intensity of S1Paradoxical splitting of S2

Transient midsystolic or late systolic apical systolic murmur (mitral valve apparatus dysfunction)

Anterior infraction (1/4 of pxs): sympathetic hyperactivityTachycardia, hypertension

Posterior infarction (1/2 of pxs): parasympathetic hyperactivityBradycardia, hypotension

Carotid pulse decreased in volume (reduced stroked volume)

1st week after STEMI: temp. up to 38 ⁰Cin transmural STEMI: (+) pericardial friction rub

Symptoms and PE of AMI

Symptoms and PE seen in AMI which is present in our patient(+) precipitating factor

Emotional stress: started after argument during board meeting

(+) Chest pain (severe substernal chest heaviness) not relieved by rest

(+) weakness, sweating ( due to sympathetic activity), nausea, vomiting anxiety

Soft S1

6. What is the ECG pattern of STEMI and NSTEMI?

Normal ECG PAttern

STEMI ECG FINDINGSST-segment elevation of at least 1 mm in two or more limb leads

STEMI ECG FINDINGSAt least 2 mm ST segment elevation in two or more precordial leads

STEMIST segment elevationQ – wave inversion

ECG NSTEMI

In UA,ST-segment

depressiontransient ST-

segment elevation

T-wave inversion

Non-ST Elevation Infarction

ST depression & T-wave inversion

The ECG changes seen with a non-ST elevation infarction are:

Before injury Normal ECG

ST depression & T-wave inversion

ST returns to baseline, but T-wave inversion persists

Ischemia

Infarction

Fibrosis

Classify AMI as to location based on ECG.

Location

Leads Vessel

Anterior

V3-V4 LCA

Septal V1-V2 LAD

Inferior

II, III, AVF RCA

Lateral V5-V6L circumflex

Posterior

II, III, AVF, rV4 or marked depression V1-V4

RCA

ACUTE ANTERIOR MYOCARDIAL INFARCTION

ACUTE INFERIOR MYOCARDIAL INFARCTION

POSTEROLATERAL MYOCARDIAL INFARCTION

What is the location of the AMI in this patient based on his

ECG?

Location of AMI based on ECG –ANTERIOR

ECG of the PatientST segment depression on II, III and aVFMarked ST elevation on I, aVL, V1-V6

Early Management of AMIKey pointsRecognition of symptoms by the patient

and prompt seeking of medical attentionRapid deployment of emergency medical

team capable of performing resuscitative measures

Expeditious transport of patient to hospitalEarly treatment without more delay

Early Management of AMI

Goals of ManagementControl of cardiac discomfort

Rapid identification of patients in need of urgent reperfusion therapy

Early Management of AMITreatment:1. Aspirin- rapidly inhibits COX-1 in

platelets and reduces thromboxane A2.- chewed 160- 325 mg tablet

2. Presence of hypoxemia- Oxygen supplementation (2-4 L/ min)

3. Nitroglycerin(sublingual) – 3 doses of 0.4 mg at 5 min intervals to relieve chest pain and decrease preload and dilate infarcted coronary or collateral vessels.

Early Management of AMI4. Nitroglycerin (intravenous)- given when

there is return of chest pain accompanied with ST-segment of T-wave shifts.

5. Beta-blockers- diminish myocardial O2 demand and ischemia, reduces the risk of ventricular fibrillation.

6. Reperfusion therapy- by fibrinolysis or primary Percutaneous Coronary Intervention.- done if ST- segment elevation is at least 2mm in 2 contiguous precordial leads and 1 mm in 2 adjacent limb leads present

8. What are the possible complications of AMI?

Complications• Ventricular remodeling

• left ventricle undergoes a series of changes in shape, size, and thickness in both the infarcted and noninfarcted segments

• Precedes clinically evident CHF in months to years after infarction

• Progressive dilation and its clinical consequences may be ameliorated by therapy with ACE inhibitors and other vasodilators (e.g., nitrates).

• Ventricular premature beats– Infrequent, sporadic ventricular premature depolarizations occur

in almost all patients with STEMI and do not require therapy. – hypokalemia and hypomagnesemia are risk factors for

ventricular fibrillation in patients with STEMI; the serum potassium concentration should be adjusted to approximately 4.5 mmol/L and magnesium to about 2.0 mmol/L.

ComplicationsVentricular tachycardia and fibrillations

Within the first 24 h of STEMI, ventricular tachycardia and fibrillation can occur without prior warning arrhythmias.

The occurrence of ventricular fibrillation can be reduced by prophylactic administration of intravenous lidocaine.

Ventricular arrhythmias, including the unusual form of ventricular tachycardia known as torsades des pointes, may occur in patients with STEMI as a consequence of other concurrent problems (such as hypoxia, hypokalemia, or other electrolyte disturbances) or of the toxic effects of an agent being administered to the patient (such as digoxin or quinidine)

ComplicationsAccelerated idioventricular rhythm (AIVR, "slow

ventricular tachycardia") Ventricular rhythm with a rate of 60–100 bpm, occurs in 25% of

patients with STEMI.Often occurs transiently during fibrinolytic therapy at the time of

reperfusion. Benign and does not presage the development of classic

ventricular tachycardia. Most episodes do not require treatment if the patient is monitored

carefully, as degeneration into a more serious arrhythmia is rare.

Sinus bradycardiaTreatment of sinus bradycardia is indicated if hemodynamic

compromise results from the slow heart rate. Atropine is the most useful drug for increasing heart rate and should be given intravenously in doses of 0.5 mg initially.

Complications• Recurrent chest discomfort

– Recurrent angina develops in ~25% of patients hospitalized for STEMI.

– Higher in patients who undergo successful fibrinolysis.

– Since recurrent or persistent ischemia often heralds extension of the original infarct or reinfarction in a new myocardial zone and is associated with a near tripling of mortality after STEMI, patients with these symptoms should be referred for prompt coronary arteriography and mechanical revascularization.

– Repeat administration of a fibrinolytic agent is an alternative to early mechanical revascularization.

Complications• Pericarditis

– Pericardial friction rubs and/or pericardial pain are frequently encountered in patients with STEMI involving the epicardium.

– It is important to diagnose the chest pain of pericarditis accurately, since failure to recognize it may lead to the erroneous diagnosis of recurrent ischemic pain and/or infarct extension, with resulting inappropriate use of anticoagulants, nitrates, beta blockers, or coronary arteriography.

– Pain radiating to either trapezius muscle is helpful since such a pattern of discomfort is typical of pericarditis but rarely occurs with ischemic discomfort.

– Managed with aspirin (650 mg four times daily). Anticoagulants should not be used since it can produce tamponade

Complications• Thromboembolism

– Clinically apparent thromboembolism complicates STEMI in ~10%

– Embolic lesions are found in 20% of patients in necropsy series, suggesting that thromboembolism is often clinically silent.

– Considered to be an important contributing cause of death in 25% of patients with STEMI who die after admission to the hospital.

– Arterial emboli originate from LV mural thrombi, while most pulmonary emboli arise in the leg veins.

– Occurs in association with large infarcts (especially anterior), CHF, and a LV thrombus detected by echocardiography.

– Arterial embolism often presents as a major complication, such as hemiparesis when the cerebral circulation is involved or hypertension if the renal circulation is compromised.

– Systemic anticoagulation for 3–6 months is probably prudent

Complications• Left Ventricular Aneurysm

– dyskinesis or local expansile paradoxical wall motion– Complications of LV aneurysm do not usually occur

for weeks to months after STEMI • they include CHF, arterial embolism, and ventricular

arrhythmias.

– Apical aneurysms are the most common and the most easily detected by clinical examination.

– The physical finding of greatest value is a double, diffuse, or displaced apical impulse. Ventricular aneurysms are readily detected by two-dimensional echocardiography, which may also reveal a mural thrombus in an aneurysm.

– readily detected by two-dimensional echocardiography

Documents

SGD 1: AMI