Extern interesting case: STEMI
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Transcript of Extern interesting case: STEMI
71-year-old Thai womanwith chest discomfort
case presentation
Ext.Ekkapot Jitpun
1 July 2009
History
• อาการสำ�าคั�ญ : เจ็�บแน่�น่หน่าอก หายใจ็เหน่��อย 3 ชั่��วโมงก�อนมาโรงพยาบาล
• ประว�ติ�ป�จจ�บ�น : ผู้��ป วยหญ�งอาย� 71 ป" • underlying hypertension ,TIA
3 hr PTA ขณะก�าล�งน��งดู�โทรท�ศน) ผู้��ป วยม*อาการเจ,บแน�นหน�าอก บร�เวณกลางอก ไม�ร�าวไปท*�ใดู ไม�ปวดูหล�ง ล�กษณะเป1นแบบแน�นๆเหม3อนม*อะไรมาท�บ เหน3�อยหายใจไม�ออก ม*อาการเหง3�อแติกใจสำ��น ติ�วเย,น คัล3�นไสำ� อาเจ*ยน
ผู้��ป วยไม�ไดู�ใชั่�ยาใดูเพ3�อบรรเทาอาการ อาการแน�นหน�าอกหายใจไม�ออกเป1นอย��ติลอดูเวลา
History
• ร� �สำ4กแน�น หายใจเหน3�อย นอนราบไม�ไดู� หากนอน ราบจะร� �สำ4กแน�นหายใจไม�ออก ติ�องนอนยกห�วสำ�ง
ไม�ม*หายใจเสำ*ยงดู�ง หร3อหายใจม*เสำ*ยงว*5ดู• อาการเหน3�อยเป1นมากข45นขณะเดู�น• ไม�เคัยม*อาการเจ,บหน�าอก หร3อหายใจล�าบากมา
ก�อน• เดู�มผู้��ป วยนอนหน�นหมอน 2 ใบอย��แล�ว• ก�อนม*อาการผู้��ป วยเป1นคันท*�เหน3�อยง�าย เหน3�อย
เวลาเดู�น ร�วมก�บม*อาการปวดูเข�า จ4งไม�คั�อยเดู�น
• Underlying disease– hypertension on moduratic ½ x 1, atenolol ¼ x1 ,
adalat 1 x 2 ก�นยาไม�สำม��าเสำมอ คัวามดู�นเดู�มอย��ท*�150/80
– TIA• ปฏิ�เสำธโรคัเบาหวาน ไขม�นในเล3อดูสำ�ง• ปฏิ�เสำธโรคัห�วใจในคัรอบคัร�ว• No alcohol, no smoking
History
Physical Examination
• V/S : T37.2, PR 86/min, RR 26/min, BP 140/80 mmHg• GE : Obese Thai female, good consciousness,
dyspnea ,cold skin, diaphoresis, not pale, no jaundice, no pitting edema
• RS : Equal breath sound, Coarse crepitation both lungs• CVS : normal S1S2 , no murmur( ไดู�ย�น heart sound ไม�
ชั่�ดูเจนเน3�องจาก chest wall หนา), no carotid bruit, no engorge neck vein , JVP not elevated, peripheral pulse 2+ all extremities
• Abd : soft, not tender, liver and spleen not palpable, no abdominal bruit
Problem list
1.Severe substernal discomfort 3 hr
2.Diaphoresis, Nausea vomiting, Coolness of skin
3.Crepitation both lungs4.Underlying HT , TIA
Differential diagnosis
??? Y__Y
Acute chest discomfort
Typical clinical features
Typical clinical features
Differential diagnosis
Acute ischemic heart disease
Pros• Prolonged and severe typical anginal
chest pain• Typical associated symptoms
• Diaphoresis• Nausea,vomiting• Cold skin• Dyspnea
• Crepitation : possible complication of IHD
• Risk factor : old age,obesity,hypertension
Cons : none
Differential diagnosis
Acute aortic dissection
Pros• Acute and severe chest pain• Risk factor : hypertension
Cons• Character of chest pain : sharp pain
radiate to the back• Grade I hypertension• Normal peripheral pulse
Differential diagnosis
Pulmonary embolism
Pros• Acute and severe chest
pain (most are lateral and pleuritic but in massive PE can be substernal pain)
• Dyspnea
Cons• No detectable source of emboli (no
murmur, no vascular bruit, no embolic sign)
• Usually pleuritic chest pain
Differential diagnosis
Pneumothorax
Pros• Sudden onset , several hour chest pain• Dyspnea• may occur without a precipitating
event in persons without lung disease
Cons• Character of chest pain : pleuritic,
often unilateral• Physical exam : decreased breath
sound
Initial Investigation
EKG
EKG
• Normal sinus rhytm rate 100/min • Left axis deviation• ST segment elevation at V1-V5• No LVH by voltage criteria
Laboratory Investigation
• CBC : Hb 12.0 , Hct 38.6 , WBC 11150 ,N 63,L 29Plt 441,000
• Blood chemistry : Na 137, K 3.8, Cl 105, HCO3 19
• CK 36, Troponin T 1.80• F/U CK, Troponin T every 6 hr– CK 2750, Troponin T >2– CK 6685, Troponin T >2
• FBS 104, cholesterol 177, TG 95, HDL 48 ,LDL 110
Ischemic heart diseaseChroni
c stable angina
Acute coronar
y syndro
me
Ischemic heart disease
Acute coronary syndrome
Unstable anginaNon-ST elevation MI ST elevation MI
Spectrum of acute coronary syndrome
Dx UA NSTEMI STEMI
Coronary trombosis subtotal total
History Angina that is new onset,crescendo or at rest,usually < 30 min
Angina at rest usually>30 min
EKG ± ST depression and/or T wave inversion ST elevation
Troponin/CK-MB - + ++
Acute coronary syndrome• Clinical manifestation– Typical angina : • retrosternal pain/pressure/tightness ± radiation to
neck,jaw or arms • precipitate by exertion, emotional stress• Relieved within 5-15 min by rest and/or sublingual
nitroglygerinIn acute coronary syndrome :• Angina pectoris or equivalent ischemic discomfort with at least
one of three feature1. It occurs at rest (or with minimal exertion) usually lasting>10 min2. It’s severe and of new onset3. It occurs with crescendo pattern (more severe,prolonged,or
frequent than previously)
• Clinical manifestation– Associated symptoms • Dyspnea• Diaphoresis• Nausea/vomiting• Palpitation• Lightheadedness
Acute coronary syndrome
• Other less common presentations– Painless ACS is greater in patients with DM, old age– In elderly, ACS may present as sudden onset
breathlessness– Sudden loss of consciousness– Confusion– Sensation of profound weakness– Arrhythmia– Evidence of peripheral embolism– Unexplained drop in arterial blood pressure
Acute coronary syndrome
• Physical finding– Most are anxious,restless , attempting
unsuccessfully to relieve the pain by moving about in bed, altering their position
– Pallor, coolness of skin– Diaphoresis– Precordium is usually quiet ,apical impulse may be
difficult to palpate
Acute coronary syndrome
• Physical finding– Sign of ischemia : S4, new MR murmur secondary
to papillary muscle dysfunction– Sign of heart failure : crepitation, ↑ JVP, S3– Sign of other area of atherosclerotic disease :
carotid or femoral bruit, ↓ distal pulse
Acute coronary syndrome
Laboratory findings
EKG
Serum cardiac biomarkers
Imagings
Nonspecific index of tissue necrosis and inflammation
EKG• A 12-lead ECG should be performed and shown
to an experienced emergency physician within 10 minutes of ED arrival on all patients with chest discomfort
• If the initial ECG is not diagnostic of STEMI but the patient remains symptomatic, and there is a high clinical suspicion for STEMI, serial ECGs at 5- to 10-minute intervals or continuous 12-lead ST-segmentmonitoring should be performed to detect the potential development of ST elevation
EKGDefinitionSTEMI or new LBBB: • EKG ท*�ม* ST segment elevation ≥ 1mm (0.1 mV)
ติ�ดูก�นไม�น�อยกว�า 2 leads• New LBBB ( ม* EKG เปร*ยบเท*ยบว�าเดู�มไม�เคัยม* LBBB
sinus at about 80 bpm with marked ST elevations in I, aVL and VI-V5. ST depressions, consistent with reciprocal changes, are seen in II, III and aVF
sinus rhythm at about 90 bpm with acute ST elevations in leads I, aVL and V2-V6Q waves are present in leads V3-V6. Borderline left axis deviation is present
Sinus bradycardia, left bundle branch block (LBBB ) with ST-T wave changes
Ischemic ST segment depression in UA/NSTEMI• ST segment depression ≥ 0.5mm (0.05 mV) • หร3อม* dynamic T wave inversion ในขณะท*�ม*เจ,บหน�าอก
sinus rhythm, rate 90 bpm ,marked ST segment depressions in leads V2-4 with T wave inversions in leads V3-6
Localization of MIAnatomic area EKG leads with STE Coronary artery
Septal V1-V2 Proximal LAD
Anterior V3-V4 LAD
Apical V5-V6 Distal LAD,left circumflex or RCA
Lateral I , aVL Left circumflex
Inferior II,III,aVF RCA, Left circumflex
RV V1-V2 & V4R Proximal RCA
Posterior ST depression V1-V2 RCA or left circumflex
Cardiac biomarkers
Cardiac biomarkers
Cardiac enzyme Advantage Disadvantage
Cardiac troponin 1. Greater sensitivity and specificity than CK-MB
2. Detection of recent MI up to 2 wk after onset
3. Useful for selection of therapy4. Detection of reperfusion
1. Low sensitivity in very early phase of MI (less than 6 hr after symptom onset) and require repeat measurement at 8 to 12 hr if negative
2. Limited ability to detect late minor reinfarction
CK-MB 1. Rapid ,cost effective accurate assay
2. Ability to detect early reinfarction
1. Loss of specificity in setting of skeletal muscle disease or injury, including surgery
2. Low sensitivity during very early MI (less than 6 hr after onset) or later after symptom onset (more than 36 hr) and for minor myocardial damage (detectable with troponin
Cardiac enzyme Advantage Disadvantage
Myoglobin 1. High sensitivity2. Useful in early detection of
MI3. Detection of reperfusion4. Most useful in ruling out MI
1. Very low specificity in setting of skeletal muscle injury or disease
2. Rapid return to normal range limits sensitivity for later presentation
STEMIManagement
Initial management : pre-hospital
• ACC/AHA Practice Guidelines 2004 for STEMI recommends empirical treatment of patients with suspected STEMI with Morphine, Oxygen, Nitroglycerin,and Aspirin (MONA)
Initial management : ER
• Monitor EKG, เติร*ยมชั่�ดู CPR , defribrillator ให�พร�อม• ติรวจว�ดู V/S, O2 sat• EKG 12 leads• ให� O2 4 LPM (keep O2 sat> 90℅)• ให� Aspirin Gr V (300 mg) เคั*5ยวท�นท* ถ้�าผู้��ป วยไม�ม*ประว�ติ�แพ�
ยา aspirin หร3อ ไม�ม*ประว�ติ� active bleeding• Sublingual NTG (Up to three doses of 0.4 mg should be
administered at about 5-min intervals )• Morphine 2-5 mg IV ถ้�าให� NTG แล�วย�งม* chest pain• เป9ดูเสำ�นเล3อดู เจาะเล3อดูเก,บไว� เป9ดูเสำ�นเล3อดูเพ3�อเติร*ยมให� IV
Management of STEMI
Copied slide from E.Antman ppt on reperfusion therapy with STEMI Pt ,Nov 30,2007,AHA
patients from an urban area
patients from rural areas
patients from the study areawho received prehospital fibrinolysis
Management of STEMI
Assessment of reperfusion options in patient with STEMI
Copied slide from E.Antman ppt on reperfusion therapy with STEMI Pt ,Nov 30,2007,AHA
Reperfusion therapy : PCI• PCI usually angioplasty and/or stenting without preceding
fibrinolysis, referred to as primary PCI• effective in restoring perfusion in STEMI when carried out on
an emergency basis in the first few hours of MI. • It has the advantage of being applicable to patients who have
contraindications to fibrinolytic therapy but otherwise are considered appropriate candidates for reperfusion.
• It appears to be more effective than fibrinolysis in opening occluded coronary arteries and, when performed by experienced operators [75 PCI cases (not necessarily primary) per year] in dedicated medical centers (36 primary PCI cases per year), is associated with better short-term and long-term clinical outcomes. Compared with fibrinolysis,
• primary PCI is generally preferred when – the diagnosis is in doubt, – cardiogenic shock is present,– bleeding risk is increased, – or symptoms have been present for at least 2–3 h when the
clot is more mature and less easily lysed by fibrinolytic drugs.
• However, PCI is expensive in terms of personnel and facilities, and its applicability is limited by its availability, around the clock, in only a minority of hospitals.
Reperfusion therapy : PCI
Reperfusion therapy : fibrinolysis
• If no contraindications are present fibrinolytic therapy should ideally be initiated within 30 min of presentation
• The principal goal of fibrinolysis is prompt restoration of full coronary arterial patency.
• The fibrinolytic agents tissue plasminogen activator (tPA), streptokinase, tenecteplase (TNK), and reteplase (rPA) have been approved for intravenous use in patients with STEMI.
• These drugs all act by promoting the conversion of plasminogen to plasmin, which subsequently lyses fibrin thrombi
• Fibrinolytic therapy can reduce the relative risk of in-hospital death by up to 50% when administered within the first hour of the onset of symptoms of STEMI, and much of this benefit is maintained for at least 10 years.
• When appropriately used, fibrinolytic therapy appears to reduce infarct size, limit LV dysfunction, and reduce the incidence of serious complications such as septal rupture, cardiogenic shock, and malignant ventricular arrhythmias
• Although reduction of the mortality rate is more modest, the therapy remains of benefit for many patients seen 3–6 h after the onset of infarction, and some benefit appears to be possible up to 12 h, especially if chest discomfort is still present and ST segments remain elevated.
• Compared with PCI for STEMI (primary PCI), fibrinolysis is generally the preferred reperfusion strategy for patients presenting in the first hour of symptoms
Reperfusion therapy : fibrinolysis
Copied slide from E.Antman ppt on reperfusion therapy with STEMI Pt ,Nov 30,2007,AHA
Fibrinolytic drugs
• Fibrinolytics ท*�น�ยมใชั่�มากท*�สำ�ดูในประเทศไทย คั3อstreptokinase– Non-selective fibrinolytics – 90 ℅patency rate : 50 ℅ , TIMI 3 flow : 32℅• 90 นาท* ท*�ผู้��ป วยไดู� SK ถ้�าไปฉี*ดูสำ*ดู�จะม*เพ*ยงคัร4�งเดู*ยวเท�าน�5น
ท*�หลอดูเล3อดูเป9ดูดู*– ราคัาถ้�กกว�า fibrinolytics ชั่น�ดูอ3�นๆ– ว�ธ*การให� คั3อ ให�ชั่�าๆผู้สำมใน NSS หร3อ 5℅D/W 100 ml
IV drip in 1 hr– อาจให� hydrocortisone 100 mg ก�อนให� SK เพ3�อลดู
reaction
• Streptokinase– ติ�อง monitor EKG และ blood pressure ติลอดู เพราะ
อาจเก�ดู arrhythmia ระหว�างหยดูยาไดู�ติลอดูเวลา โดูย เฉีพาะ VT และ VF หร3ออาจเก�ดู bradycardia ไดู�
– ก�อนให�หร3อหล�งให�ไม�คัวรท�าห�ติถ้การติ�างๆ ถ้�าติ�องการ ท�าห�ติถ้การจร�งๆคัวรรอหล�งให�ยาไปแล�วนานกว�า 24
ชั่��วโมง– ไม�จ�าเป1นติ�องให� heparin หร3อ LMWH ติ�ออ*ก
Fibrinolytic drugs
• t-PA– Fibrin specific fibrinolytic drug– ประสำ�ทธ�ถ้าพดู*กว�า และ patency rate สำ�งกว�า– โอกาสำเก�ดู intracerebral hemorrhage สำ�งกว�า– ราคัาแพงกว�ามาก– ใชั่�ไดู�ง�าย เพราะให�เป1น bolus dose ติามน�5าหน�กติ�วไดู�– Side effect น�อยกว�า– จ�าเป1นติ�องให� unfractionated heparin (UFH) หร3อ
LMWH ติ�อ
Fibrinolytic drugs
Adjunct medications
• คัวรให�ในท�กรายท*�ไม�ม*ข�อห�าม เพราะ ลดูmortality rate, infarct size และ reinfarction• ข�อห�าม : heart block, heart failure, bronchospasm
Beta-blockers
• ลดู ventricular remodelling และปร�บเปล*�ยนhemodynamic ของheart failureให�ดู*ข45น• ข�อคัวรระว�งคั3อ BP ไม�คัวร <100, คัวรให�หล�ง 24 hrแรก•ARB ไดู�ผู้ลเหม3อน ACEI ใชั่�เม3�อทนผู้ลของ ACEI ไม�ไดู�
ACEI/ARB
Adjunct medications
• ให�แทน aspirin ไดู� เม3�อม*ข�อห�ามของการให�aspirin• การให� clopidogrel ร�วมก�บ aspirin ลดูการ
เก�ดู recurrent infarction ไดู�ดู*กว�าการให�aspirin อย�างเดู*ยว
Clopidogrel
• ลดู inflammation และ complication ติ�างๆ เชั่�น reinfarction, recurrent angina,
arrhythmia•ให�ไดู�อย�างปลอดูภั�ยแม�จะไม�ม*ไขม�นในเล3อดูสำ�ง
HMG-CoA reductase inhibitor (statin)
Adjunct medications
•IV NTG is indicated in the first 48 hours after STEMI for treatment of persistent ischemia, CHF, or hypertension• ไม�ชั่�วยลดู mortality rate•Intravenous, oral, or topical nitrates are useful beyond the first 48 hours after STEMI•Nitrates should not be administered to patients with systolic blood pressure less than 90 mm Hg or greater than or equal to 30 mm Hg below baseline, severe bradycardia (less than 50 bpm), tachycardia (more than 100 bpm), or RV infarction
nitroglycerin
Adjunct medications
•Intravenous UFH or LMWH should be used in patients after STEMI who are at high risk for systemic emboli (large or anterior MI, AF, previous embolus, known LV thrombus, or cardiogenic shock)•It is reasonable that STEMI patients not undergoing reperfusion therapy who do not have a contraindication to anticoagulation be treated with IV or SC UFH or with SC LMWH for at least 48 hours
Antithromboti
cs
Killip classificationKillip class description Hospital mortality rate
I no signs of pulmonary or venous congestion
0–5%
II moderate heart failure as evidenced by rales at the lung bases, S3 gallop, tachypnea, or signs of failure of the right side of the heart, including venous and hepatic congestion
10–20%
III severe heart failure, pulmonary edema 35–45%
IV shock with systolic pressure <90 mmHg and evidence of peripheral vasoconstriction, peripheral cyanosis, mental confusion, and oliguria.
85–95%
Our patient
ICU เติ,ม
• Morphine 3 mg IV stat• O2 canula 3 LPM• ISDN 5 mg SL stat
then ISDN (10) 1 tab tid pc• ASA Gr V 1 tab oral stat then
ASA (80) 1 tab oral OD
• Plavix (75mg) 4 tab oral stat then 1 tab oral OD
• NTG (1:10) IV drip 5 mdrop/min x 3 d• Enoxaparin 0.6 ml SC q 12 hr X 5 d• Enalapril (5) 1 tab oral OD • Lasix 40 mg V stat
with lasix(40) 1 tab oral bid and prn dose
• Simvastatin (20) 1 tab oral hs• Ativan(0.5) 1 tab oral hs• MOM 30 cc prn for constipation
Progression
• 1 day after admission :– Clinical chest pain ลดูลงมาก ย�งม*เหน3�อยเล,กน�อย– อาการกระสำ�บกระสำ�ายลดูลง ผู้��ป วยพ�ดูไดู� ไม�ม*ติ�วเย,น
systemic perfusion ดู*ข45น– ย�งม* crepitation both lung ประเม�นว�าย�งม* volume
overload– Vital sign stable : BP 150/90, RR 26– Lab : FBS WNL, lipid profile : OK– CK,Trop T increased
• 4 days after admission– Clinical stable, no chest pain, no dyspnea– Increased BUN,Cr : BUN 38.8,Cr 3.1– CXR : cardiomegaly , no congestion , R/O lung
mass– Rx : Off enalapril, lasix , เปล*�ยน antihypertensive
เป1น HDZ– Plan D/C
Progression