Cardiac Exam 2

most common cause of MI

atherosclerotic plaque disruption

Management of ACS (2)

prevention! → risk assessment

activate EMS early - identify sx of MI

Sx of ACS

1. Chest discomfort (with or without radiation)

2. discomfort in one or both arms, back, neck, jaw, or stomach

3. SOB

4. sweating, N/V, lightheadedness

5. weakness

male ACS sx

“typical” cardiac sx = chest pain

female ACS sx

“associated” cardiac sx

• SOB, cough

• weakness, unusual fatigue

• cold sweat

• dizziness

• N/V, indigestion, loss of appetite

most common sx of acute MI in women

chest pressure (not pain)

• ache

• tightness

prodromal sx (women acute MI)

1 month prior to event

• unusual fatigue

• sleep disturbances

• SOB

• indigestion

• anxiety/scared feeling

Evaluation and physical exam in ED (MI)

hx - risk of bleeding

onset of sx (when did they start)

12 lead EKG within 10 min of arrival

Labs upon ED admission (MI)

hs-cTnI (troponin) - STAT

CBC

BMP

LFTs

lipid panel

urine toxicology screening (coke/meth)

stool guaiac (GI bleed suspected)

troponin cutoff for males

< 36 ng/L

troponin cutoff for females

< 15 ng/L

NSTEMI occlusion

not 100%

STEMI occlusion

100%

NSTEMI ST segment changes

depression or no change

STEMI ST segment changes

elevation

difference in diagnosing unstable angina vs NSTEMI

NSTEMI = troponin present

unstable angina = no troponin

NSTEMI clot composition

platelet rich

UA/NSTEMI presentation

angina for > 30 min

no response to SL NTG

ST depression or no change

normal to slight troponin = UA

elevated troponin = NSTEMI

STEMI clot composition

fibrin rich

STEMI infarction location

transmural ischemia (through all heart layers)

NSTEMI infarction location

subendocardial ischemia (inside layer of heart)

STEMI Q wave

may produce one

NSTEMI Q wave

may not produce one

ischemia of myocardial tissue

hypoxic myocardial tissue that may recover if circulation and O2 supply restored

no troponin release

injury to myocardial tissue

infarcting tissue where myocardial cell death is occurring due to continued ischemia

troponin release

infarction of myocardial tissue

necrotic, nonviable tissue

prominent Q-wave (STEMI)

anterior wall MI

anterior wall of LV (front)

anterior wall MI artery occluded

left anterior descending

MOST DEADLY

lateral wall MI

lateral (left) wall of LV

lateral wall MI artery occluded

left circumflex artery

inferior wall MI

inferior (right) wall and base of LV, may also involve RV

inferior wall MI artery occluded

right coronary artery (RCA)

cardiac biomarkers

cardiac troponin T and I

when is troponin released?

within 3-6 hours of sx onset

peaks at 12-16 hours

remains elevated for 5-9 days

high-sensitivity cardiac troponin (hs-cTn) 3 points

confirms diagnosis of MI when no ST segment elevation

differentiate between UA and NSTEMI

indicate size of infarction

how is troponin released?

troponin T and I is ECM → cells die and release troponin into bloodstream

when is hs-cTn ordered?

admission and again 1-3 hours later to assess change

keep checking until starts to decline (assess damage)

goals of acute treatment (MI)

early restoration of blood flow (salvage ischemic myocardium)

prevent coronary artery re-occlusion (hyperactive platelets)

prevent acute/chronic complications (HF, arrhythmia)

relieve chest pain/discomfort

MOANA

oral Antiplatelets

IV Anti-coagulant

IV NTG

Oxygen

IV Morphine

oral antiplatelets (MOANA)

ASA 324 (4 × 81 mg) chew and swallow ASAP and P2Y12 loading dose

IV anticoagulant (MOANA)

keep thrombus from growing, prevent further platelet activation and aggregation

LMWH, UFH → not DOAC

IV NTG (MOANA)

to reverse ischemia

even if took SL NTG

Oxygen (MOANA)

if hypoxic (Pox < 90%) AND symptomatic (SOB)

IV Morphine (MOANA)

if needed for severe pain despite IV NTG

avoid use if possible → do not want sedation/constipation

nitrate (anti-ischemic therapy) and dose

control BP, manage pulmonary congestion (acute HF)

IV infusion for first 24-48 hours, stop once BB started (better)

NTG contraindications (MI)

avoid SBP < 90 mmHg or decrease of SBP > 30% from baseline

avoid in patients with RV infarcts (dependent on preload)

analgesic (anti-ischemic therapy)

relieve pain/anxiety during hospitalization only

morphine/fentanyl → drug interactions with P2Y12 inhibitors

need stool softener when inpt

NO NSAIDS

acute reperfusion therapies (STEMI only)

primary PCI

fibrinolytics

emergent CABG

timing for Cath lab procedure if at institution

90 min to inflate with balloon

timing for Cath lab procedure if not at institution

120 min

stabilized then transported

timing of PPCI or UA/NSTEMI

depends on risk

not emergent, get drugs on board first

complications with PCI

arterial dissection, arterial perforation, thrombosis

bleeding from vascular access point (femoral/radial artery)

acute kidney injury from radioactive dye

stent restenosis complication

risk of thrombosis until stent covered up with skin

do not stop P2Y12 inhibitors

complete endothelialization

growth of endothelial cells over stent

good to prevent thrombosis

antithrombotic therapies after stent (PPCI)

DAPT → ASA + P2Y12 inhibitor

anticoagulant (UFH, Enoxaparin, etc.)

acute reperfusion

within 12 hrs of sx for STEMI pts only

PPCI

candidates for fibrinolytic

pts with STEMI who present within 12 hrs of onset

time to receiving hospital for PPCI > 120 min

2 best fibrinolytic options

alteplase

tenecteplase

how to monitor efficacy of fibrinolytic therapy

resolution of sx (CP, dizzy, sweating)

restoration of HR/BP

reduced in troponin

resolution of ST-segment elevation

restoration of flow

fibrinolytic side effects

angioedema (alteplase)

hypotension

bleeding

ICH (rare)

who has increased risk of ICH with fibrinolytic?

female

black

elderly

low BW (male < 80 kg, female < 65 kg)

h/o stroke, TIA

elevated BP

what therapy required with fibrinolytic?

antiplatelet and anticoagulant

broken clots release activated platelets and thrombin

MOA of thrombin

converts fibrinogen to fibrin

post-fibrinolytic efficacy monitoring

pain

hemodynamic stability

EKG

troponin

fibrin degradation products (should increase)

repercussion arrhythmias (means ischemic tissue getting blood flow)

post-fibrinolytic SE monitoring

BP

H/H (low indicates bleeding)

platelet count (can decrease)

aPTT (can increase, clotting time)

fibrinogen level

repercussion arrhythmia (continuous = bad)

purpose of antithrombotic therapy in ACS

prevent further damage from MI

purpose of antithrombotic therapy in PCI

prevent another clot from forming during procedure

protect stent

ASA dosing

324 mg non-EC STAT

prior to PCI

P2Y12 inhibitor for PCI (NSTE-ACS or STEMI)

ASA + ticagrelor (or prasugrel)

• ticagrelor most potent

• clopidogrel when ticagrelor or prasugrel not available

P2Y12 inhibitor for CABG

ASA + ticagrelor or clopidogrel (less potent)

• continue ASA through CABG, start P2Y12 when safe post-op

P2Y12 inhibitor for medically treated (no procedure)

ASA + ticagrelor

P2Y12 inhibitor for fibrinolytic in STEMI

ASA + clopidogrel

clopidogrel withdrawal time before major surgery (CABG)

5 days

prasugrel withdrawal time before major surgery (CABG)

7 days

ticagrelor withdrawal time before major surgery (CABG)

3-5 days

• reversibly binds

cangrelor withdrawal time before major surgery (CABG)

no delay

clopidogrel PCI dosing

600 mg prior to PCI or within 1 hour post

75 mg daily + ASA

prasugrel PCI dosing

60 mg load

10 mg daily + ASA

Ticagrelor PCI dosing

180 mg load

90 mg BID + ASA

prasugrel pts to use and avoid

Use: ACS (not CCS), DM

Avoid: elderly (>/= 75 yrs, use with caution), body wt < 60 kg (5 mg), h/o CVA or TIA

ticagrelor SE and pts to consider use

dyspnea SE

use: ACS (not CCS), DM

cangrelor

use during PCI to reduce risk of peri-procedural MI and stent thrombosis in pts not treated with oral P2Y12 inhibitor

DAPT duration for no PCI or > 12 months from ACS (stable)

lifelong ASA (81 mg)

DAPT duration for ACS with or without PCI

DAPT for min of 12 months

DAPT duration for PCI in CCS (low bleed risk)

drug eluding stent and DAPT for 6 months

then SAPT

DAPT duration for PCI in CCS (high bleed risk)

drug eluding stent and DAPT for 1-3 months

P2Y12 for months 3-12

then SAPT

DAPT therapy in first 12 months post discharge

ASA + ticagrelor/prasugrel for at least 12 months

DAPT therapy in first 12 months post discharge (bleeding risk reduction)

DAPT (ASA + ticagrelor)

discontinue ASA 1-3 months post PCI

SAPT (ticagrelor)

When is triple therapy used?

pts with AF (OAC indication)

DAPT + OAC therapy (first 12 months post discharge)

DAPT + OAC 1-3 months

discontinue ASA 1-4 wks post PCI

SAPT (clopidogrel) + OAC

therapy for CCS with PCI, OAC, low bleed risk

DOAC/clopidogrel/ASA less than 1 month

DOAC/clopidogrel 6 months

DOAC alone

IV anticoagulant for NSTEMI/UA

UFH

if HIT is concern → bivalirudin

IV anticoagulant for STEMI treated with fibrinolytics

IV anticoagulant continued for duration of hospital stay (8 days) or until revascularization performed

Pre-PCI therapies (antithrombotics)

DAPT

• ASA: yes if not taken already

• P2Y12i loading dose: oral LD can be held until coronary anatomy visualized and CABG ruled out

Anticoagulant

• UFH, enoxaparin, bivalirudin: Yes

Peri-PCI therapy (antithrombotics)

DAPT

• ASA: no

• P2Y12i: IV continued through procedure OR oral LD given within 1 hour of PCI completion

Anticoagulant

• UFH, enoxaparin, bivalirudin: yes, continue through procedure

Post-PCI therapies (antithrombotics)

DAPT

• ASA: start MD next day

• P2Y12i (oral): start MD later in evening (T) or next day (P,C)

Anticoagulant

• UFH, enoxaparin, bivalirudin: NO unless indication to transition to OAC (Afib, LV thrombus, etc.)

warfarin and DOAC place in therapy ACS

not indicated for long-term therapy unless indication present

• Afib (DOAC)

• VTE (DOAC)

• LV thrombus (DOAC)

• prior mechanical valve replacement (VKA)

what therapy should patients not be sent home with unless they have indication for it

DOAC

non-pharm management of ACS in hospital

continuous 3-lead ECG

12 lead ECG q 6-8 hours x 24 hrs

bed rest 12-24 hrs

hospitalization for 2-3 days

ECHO before discharge → gives EF

heart failure

inability of the heart to meet the metabolic demands of the body due to decreased CO