chest pain and acute coronary syndromes

recent onset of pain/pressure/tightness in anterior thorax between xiphoid, suprasternal notch, both and midaxillary lines

acute chest pain

myocardial necrosis evident from elevation of cardiac biomarkers

acute myocardial infarction

clinical dx defined by chest pain or an equivalent (neck/upper extremity pain) from inadequate myocardial perfusion that is new or occurring w/ greater frequency, less activity, or at rest

unstable angina

door to balloon time

90 minutes

chest pain initial assessment

EKG w/i 10 min, vitals promptly and regularly, O2 via nasal cannula if <94%, cardiac monitoring, IV access, ABCs

retrosternal left anterior chest crushing/squeezing/tightness/pressure

classic/typical cardiac chest pain

clenched fist in front of chest

Levine’s sign, IDs ischemic chest pain

chest pain lasting for seconds, constant pains 12+ hours w/o intense waxing/waning, pain worsened by specific body movements/positions

nonclassic/atypical cardiac chest pain

what can new systolic murmur signify

papillary muscle dysfxn, flail leaflet of mitral valve w/ resultant mitral regurge, ventricular septal defect

marked difference in BP between arms suggests

aortic dissection

pts who present w/ acute chest pain and other sxs of myocardial ischemia, often w/ diagnostic/suggestive EKG changes of myocardial ischemia

acute coronary syndromes

ACS spectrum of dzs

stable angina to acute STEMI

what causes ACS

reduction of coronary artery blood flow due to arterial spasm, disruption of arteriosclerotic plaques, platelet aggregation, or thrombus formation

reversible myocardial ischemia w/o necrosis

unstable angina

myocardial ischemia w/ necrosis

AMI

left coronary artery divides into

left circumflex and left anterior descending branches

left anterior descending branch does what

courses down anterior aspect of heart providing main blood supply to anterior and septal regions of heart

circumflex branch does what

supplies blood to some of anterior wall and large portion of lateral wall of heart

right coronary artery does what

supplies right ventricle and provides some perfusion to inferior aspect of left ventricle through its continuation as right posterior descending artery

what determines whether pt develops myocardial ischemia w/ or w/o necrosis

degree and duration of O2 supply demand mismatch

STEMI, Q waves

transmural infarction

electric current directed towards endocardium, away from chest wall, negative EKG depression, ST segment depression, usually no Q waves, NSTEMI

only endocardium is injured

differentiate between unstable angina or NSTEMI

presence of cardiac injury enzyme

tall, pointed, upright T waves, ST elevation

few minutes after MI

inverted T waves, R voltage decreases, Q wave develops

few hours after MI

ST segment returns to normal

few days after MI

T wave may return to upright but Q wave remains

few weeks/months after MI

reciprocal EKG changes

in leads away from/opposite elevation area

reciprocal ST segment changes

subendocardial ischemia, larger area of injury risk, increased severity of CAD, more severe pump failure, higher likelihood of CV complications, increased mortality

T wave inversion, ST segment depression, T wave flattening, biphasic T waves

ischemia

ST segment elevation <1 mm in at least 2 contiguous leads, heightened/peaked T waves, directly related to portions of myocardium rendered electrically inactive

injury

when does anterior wall MI occur

anterior myocardial tissue usually supplied by left anterior descending artery dies due to lack of blood supply

when AWMI extends to septal and lateral regions as well the culprit lesion is usually

more proximal in LAD or in left main coronary artery, aka extensive anterior MI

ST elevation in anterior leads (V1-4), sometimes in septal and lateral leads, concave downward and frequently overwhelms T wave producing tombstoning appearance

AWMI

reciprocal ST segment depression in inferior leads (II, III, aVF)

AWMIA

inferior wall MI occurs when

inferior myocardial tissue supplied by right coronary artery dies due to thrombosis of that vessel

when IWMI extends to posterior regions what may occur

associated posterior wall MI

ST segment elevation in inferior leads (II, III, aVF)

IWMI

reciprocal ST segment depression in lateral and/or high lateral leads (I, aVL, V5, V6)

IWMI

posterior wall MI occurs when

posterior myocardial tissue, usually supplied by posterior descending artery dies due to thrombosis

PWMI frequently occurs w/

IWMI

ST segment depression in spetal and anterior precordial leads (V1-4)

PWMI

why does PWMI look like that

leads see MI backwards (upside down STEMI=PWMI)

lateral wall of LV is supplied by

branches of LAD and left circumflex arteries

infarction of the lateral usually occurs as

part of larger territory infarction like anterolateral STEMI

when might isolated lateral STEMIs occur

occlusion

lateral extension of anterior/inferior/posterior MI indicates

larger territory of myocardium at risk w/ consequent worse prognosis

ST elevation in lateral leads (I, aVL, V5-6)

LWMI

reciprocal ST depression in inferior leads (III, aVF)

LWMI

Wellen’s sign

pattern of abnormal T waves in precordial leads V2 and V3 associated w/ critical stenosis of LAD

abnormal T waves of Wellen’s syndrome usually visible when

pt is pain free and may normalize when pain recurs, repeat EKG when pain resolves/recurs

elevated in pts c ACS and can ID ACS pts who are at higher risk for adverse CV events, heart failure, or death

B type natriuretic peptide

serial high sensitivity troponin interval as short as 2 hours post presentation and low risk score

excludes AMI

general tx

EKG w/i 10 min, cardiac monitor, IV access, 162-324 mg aspirin, supplemental O2 if hypoxic, nitrates

give how much aspirin when

162+ mg (preferably 324 if naive) ASAP to all pts c STEMI, NSTEMI, unstable angina

pts w/ minor contraindications to aspirin during ACS?

give anyways lol

aspirin moa

prevents formation of thromboxane A2

AHA tx timing goals

90 min for pt at hospital w/ percutaneous coronary intervention capability or 120 min for pts at hospital w/o PCI capability

fibroanalysis should be given w/i

30 min of ED arrival if PCI cannot be accomplished w/i time frames

NSTEMI PCI when

w/i 24-48 hrs

when is PCI preferred method of reperfusion therapy

first medical contact to first balloon inflation time is 90-120 min

m/c PCI

coronary angioplasty w/ or w/o stent placement

balloon angioplasty alternatives

atherectomy, laser angioplasty

drug eluting stents are associated w/

decreased early vessel closure but higher delayed closure, particularly once antiplatelet agents are stopped

fibrinolytic therapy indication

reperfuse pts c STEMI if time to tx is w/i 6-12 hrs from sx onset and EKG has at least 1 mm of ST segment elvation in 2+ contiguous leads

fibrinolytic agents act on

acute thrombosis directly or indirectly as plaminogen activators

STEMI pts who received fibrinolytics should get

full dose anticoagulants for at least 48 hrs (unfractionated heparin, enoxaparin, fondaparinux)

intracranial hemorrhage is more common w/

tissue plaminogen activator than w/ streptokinase

fibrinolytic therapy absolute contraindications

prior intracranial hemorrhage, aortic dissection, major surgery/trauma w/i 2-4 wks, active bleeding/bleeding diathesis

fibrinolytic therapy relative contraindications

BP >180/110, oral anticoagulants and INR>1.5, major recent trauma/surgery, pregancy, non compressible recent vascular puncture, recent laser therapy of retina, cardiogenic shock

PCI vs fibrinolytics

PCI better, difference widens w/ duration of sxs

post MI tx w/i 24 hours

nitrates, BB/B adrenergic antagonists, angiotensin converting enzymes inhibitors, statins, anticoagulation

nitrates post MI

relax vascular smooth muscle, improves regional fxn, decreases CV complications

BB/B adrenergic antagonists post MI

antidysrhythmic, anti ischemic, antihypertensive, diminish myocardial O2 demand (decrease heart rate, systemic arterial pressure, myocardial contractility)

ACEI post MI

reduce LV dysfxn and LV dilatation, slow development of congestive HF during AMI

CV complications

acute pulmonary edema, cardiogenic shock, arrhythmia, bundle branch block, myocardial rupture, pericarditis (Dressler’s), systemic thromboembolism

inflammatory response of pericardium 1-6 wks post MI, low grade fever, pleuritic chest, pericardial

Dressler’s syndrome

tx Dressler’s

NSAIDs, corticosteroids, ASA

majority of sudden cardiac death is due to

fatal arrhythmias

thrombolytics general

tissue plasminogen activator, clot buster, start w/i 90 min of sxs

thrombolytics advantages

available at all hospitals, cheaper

thrombolytics disadvantages

hemorrhagic complications, reperfusion arrhythmias

thrombolytics limitations

original plaque still present, artery may still be occluded, re occlusion and re infarctions, recurrent ischemia, if no flow to blocked artery TPA can’t get to it

goals in ED for ACS

initial 12 lead EKG w/i 10 minutes of presentation, aspirin w/i 30 min, door to balloon w/i 90 min

global ST elevation

Dressler’s