Presentation is loading. Please wait.

Presentation is loading. Please wait.

โรงพยาบาลสรรพสิทธิ ประสงค์ อุบลราชธานี. How to manage ACS Complications นพ. วีระ มหาวนากูล กลุ่มงานอายุรกรรม โรงพยาบาลสรรพสิทธิประสงค์ อุบลราชธานี

Similar presentations


Presentation on theme: "โรงพยาบาลสรรพสิทธิ ประสงค์ อุบลราชธานี. How to manage ACS Complications นพ. วีระ มหาวนากูล กลุ่มงานอายุรกรรม โรงพยาบาลสรรพสิทธิประสงค์ อุบลราชธานี"— Presentation transcript:

1 โรงพยาบาลสรรพสิทธิ ประสงค์ อุบลราชธานี

2 How to manage ACS Complications นพ. วีระ มหาวนากูล กลุ่มงานอายุรกรรม โรงพยาบาลสรรพสิทธิประสงค์ อุบลราชธานี

3 Complications of Acute Coronary Syndrome Arrhythmic complications of ACS Mechanical complications of ACS Pump failure Right ventricular infarction Left ventricular aneurysm Left ventricular pseudoaneurysm Pericardial complications Complications involving bleeding Complications of percutaneous coronary intervention

4

5 Complications of Myocardial Infarction arrhythmic mechanical inflammatory (early pericarditis and post-MI syndrome) right ventricular (RV) infarction and cardiogenic shock left ventricular mural thrombus (LVMT)

6 Arrhythmic Complications 90% of patients  cardiac arrhythmia immediate or during MI 25% of patients  first 24 hr The incidence of arrhythmia: STEMI > NSTEMI Most peri-infarct arrhythmias are benign  self- limited Hypotension  myocardial oxygen requirements  malignant ventricular arrhythmias (aggressively monitored and treated)

7 Pathophysiology autonomic dysfunction  enhanced automaticity of the myocardium and conduction system Electrolyte imbalances (hypoK and hypoMg) and hypoxia  cardiac arrhythmia damaged myocardium = substrate  re- entrant circuits (tissue refractoriness) Arrhythmic Complications

8 Peri-infarction arrhythmias Supraventricular tachyarrhythmias Accelerated junctional rhythms Bradyarrhythmias Atrioventricular (AV) blocks Intraventricular blocks Ventricular arrhythmias Reperfusion arrhythmias

9 Supraventricular tachyarrhythmias Sinus Tachycardia enhanced sympathetic activity  transient hypertension or hypotension Causes: Pain Anxiety Heart failure Hypovolemia Hypoxia Anemia Pericarditis Pulmonary embolism

10 Treatment strategies: adequate pain medication, diuresis  heart failure Oxygenation volume repletion  hypovolemia anti-inflammatory agents  pericarditis Beta-blockers and/or nitroglycerin  relieve ischemia Supraventricular tachyarrhythmias Sinus Tachycardia

11 Premature atrial contractions (PAC’s) PAC’s  paroxysmal SVT, atrial flutter, or atrial fibrillation ↑left ventricular (LV) diastolic pressure or pericarditis (inflammation)  atrial distention No specific therapy: ?? occult heart failure ?? Supraventricular tachyarrhythmias

12 Paroxysmal supraventricular tachycardia (PSVT) Incidence in AMI < 10% No Hypotension  Adenosine (No data) No significant LV failure  IV diltiazem or beta-blocker severe heart failure or hypotension  synchronized electrical cardioversion Supraventricular tachyarrhythmias

13 Supraventricular Tachycardia

14

15 Atrial flutter < 5% of AMI. Transient Sympathetic overstimulation of the atria Treatment strategies: atrial fibrillation  ventricular-rate control with drugs is less easily synchronized electrical cardioversion: with 50 J, or the biphasic equivalent  relatively promptly decrease coronary blood flow and/or hemodynamic compromise refractory to medication  overdrive atrial pacing Supraventricular tachyarrhythmias

16 Atrial Flutter

17

18

19 Atrial fibrillation 10-15% in AMI Onset < 1 hour  caused by LV failure, ischemic injury to the atria, or RV infarction Pericarditis & conditions ↑left atrial pressure  atrial fibrillation ↑mortality and stroke: Anterior wall MI. Supraventricular tachyarrhythmias

20 Atrial fibrillation

21

22 unstable condition worsening ischemic pain and/or hypotension  electrical cardioversion Synchronized electrical cardioversion 200 J or the biphasic equivalent Conscious sedation (preferred) or general anesthesia is advisable Supraventricular tachyarrhythmias Atrial fibrillation

23 stable condition immediate objective  controlling the ventricular response Not respond to cardioversion  IV amiodarone or IV digoxin (in patients with LV dysfunction or heart failure)  achieve rate control. IV beta-blocker & IV diltiazem  alternative for slowing the ventricular rate, with caution in moderate-to-severe heart failure Supraventricular tachyarrhythmias Atrial fibrillation

24 AF & atrial flutter  ↑risk of thromboembolism Anticoagulation: unfractionated heparin or low molecular weight heparin (LMWH) (If no contraindications) Transient AF  ??? Anticoagulation Supraventricular tachyarrhythmias Atrial fibrillation

25 Accelerated Junctional Rhythm ↑ automaticity of the junctional tissue  heart rate of /min. most common in inferior MI Treatment  correcting the underlying ischemia

26 Accelerated Junctional Rhythm

27 Arrhythmic Complications Bradyarrhythmias Sinus bradycardia Junctional bradycardia

28 Sinus bradycardia common in acute inferior or posterior MI first 1-2 hours after AMI Mechanism: stimulation of cardiac vagal afferent receptors  efferent cholinergic stimulation of the heart (↓ myocardial oxygen demand)  bradycardia and hypotension  ventricular arrhythmias (treated aggressively) Arrhythmic Complications Bradyarrhythmias

29 No adverse signs or symptoms  therapy is typically unnecessary HR < 40 bpm with hypotension  atropine sulfate mg IV every 3-5 min. (maximum of mg/kg) inability to reverse hypotension with atropine in inferior MI  volume depletion and/or RV infarction Arrhythmic Complications sinus bradycardia

30 atropine is ineffective  transcutaneous or transvenous pacing Transplanted hearts do not respond to atropine  require cardiac pacing Additional pharmacologic intervention  dopamine 5-20 mcg/kg/min IV, epinephrine mcg/min, and/or dobutamine.

31 Junctional bradycardia  a protective AV junctional escape rhythm, rate of bpm in inferior MI Usually not associated with hemodynamic compromise Treatment:not required Arrhythmic Complications Junctional bradycardia

32 Arrhythmic Complications AV and Intraventricular Blocks SA node ปกติรับเลือดจาก right coronary artery (RCA) ประมาณ 60% และรับจาก left circumflex artery (LCX) ประมาณ 40% AV node ปกติรับเลือดจาก RCA ประมาณ 90% และรับจาก LCX ประมาณ 10% His bundle ส่วนใหญ่ได้รับเลือดจาก RCA และ ส่วนน้อยจาก septal perforators จาก left anterior descending artery (LAD)

33 Main bundle branch และ Right bundle branch รับเลือดจาก septal perforators จาก LAD ส่วน น้อยได้รับ collateral circulation จาก LCX และ RCA Posterior fascicle ได้รับ dual blood supply จาก AV nodal artery และ septal perforators จาก LAD Anterior fascicle ส่วนใหญ่ได้รับเลือดจาก septal perforators และส่วนน้อยจาก AV nodal artery Arrhythmic Complications AV and Intraventricular Blocks

34

35

36 First-degree AV block 15% of AMI, most common  inferior wall MI conduction disturbances above the His bundle  CHB or asystole is rare CCB & ß-blockers  cause or exacerbate 1˚AV block  stopped if hemodynamic impairment /higher-degree block No specific therapy, atropine if BP ↓ cardiac monitoring: possible  higher block.

37

38 Arrhythmic Complications AV and Intraventricular Blocks Second-degree AV block Mobitz type I (Wenckebach) AV block  10% of AMI (most common  inferior MI), 90% of 2˚ AV block in AMI Not affect overall prognosis Not require treatment. If HR is inadequate for perfusion  atropine mg IV Transcutaneous/temporary transvenous pacing  Rare

39

40 AV Block 1 st AV block 2nd AV block Mobitz I (Wenckebach)

41 Arrhythmic Complications AV and Intraventricular Blocks Mobitz type II AV block accounts: < 1% in AMI (10% of all second-degree AV blocks) associated with anterior infarction poor prognosis ( ถ้าร่วมกับมี complete heart block  mortality rate ประมาณ 80%) immediately  transcutaneous pacing/atropine Atropine helps in 50% of cases, but occasionally worsens the block

42

43 Mobitz I & II AV Block

44 Arrhythmic Complications AV and Intraventricular Blocks Third-degree AV block 5-15% in AMI (anterior or inferior MI) inferior MI: gradually progress from 1˚AV block / Mobitz I AV block most patients  supranodal or intranodal  escape rhythm  stable, narrow QRS & rates > 40 bpm 30%  below the His bundle  escape rhythm < 40 bpm & wide QRS complex

45 Third degree heart block

46 Arrhythmic Complications AV and Intraventricular Blocks CHB in inferior MI usually responds to atropine resolves within a few days without the need for a temporary or permanent pacemaker Mortality rate for inferior MI + CHB  15% (Higher in RV infarction) Atropine  may not help & worsen the block  Temporary transcutaneous / transvenous pacing

47 Complete Heart Block

48 Arrhythmic Complications AV and Intraventricular Blocks persistent symptomatic bradycardia /unresolved with lysis or percutaneous coronary intervention  Permanent pacing anterior MI: intraventricular block / Mobitz type II AV block  third-degree AV block  high mortality rate Immediate treatment: atropine and/or transcutaneous / temporary transvenous pacing If survive  often permanent pacemaker

49 Arrhythmic Complications AV and Intraventricular Blocks Intraventricular blocks 1 or more fascicular block  15% of AMI Isolated left anterior fascicular block (LAFB)  3-5% of AMI (complete AV block uncommon) Isolated left posterior fascicular block (LPFB)  1-2% of AMI (blood supply of the posterior fascicle is larger than that of the anterior fascicle  relatively large infarct and high mortality rate)

50 Arrhythmic Complications AV and Intraventricular Blocks The right bundle branch: dominant blood supply from the left anterior descending (LAD) artery. new RBBB  2% of AMI, suggests a large infarct territory  cardiogenic shock & Death RBBB with LAFB (bifascicular block)  เกิดจาก occlusion of the proximal LAD coronary artery (Mortality related to the amount of muscle loss, CHB-uncommon)

51 Arrhythmic Complications RBBB

52 Arrhythmic Complications AV and Intraventricular Blocks Bifascicular block + first-degree AV block  trifascicular block (40%  complete heart block)

53 Trifascicular Block

54

55 Acute phase arrhythmia เกิดใน 48 ชั่วโมงแรก สาเหตุส่วนใหญ่จะเป็น reversible cause เช่น ภาวะ ischemia, left ventricular wall stress ถ้า ได้รับการแก้ไขก็จะไม่มีผลต่อการพยากรณ์โรค ในระยะยาว Chronic phase arrhythmia มักจะเป็น monomorphic VT กลไกการเกิดเป็น reentry ซึ่ง เกิดจากการที่มีแผลเป็นในผนังกล้ามเนื้อหัวใจ ผู้ป่วยกลุ่มนี้มีการพยากรณ์โรคระยะยาวไม่ดี มี โอกาสเกิด sudden cardiac death สูงในอนาคต Arrhythmic Complications: Ventricular Arrhythmias

56 Premature ventricular contractions (PVC’s) prophylactic suppression of PVCs with antiarrhythmic drugs (lidocaine, etc)  not recommended. Prophylaxis  ↑ risk of fatal bradycardia /asystole  suppression of escape pacemakers (lidocaine เพื่อรักษา PVCs กลับทำให้อัตราตายเพิ่ม สูงขึ้นจาก bradyarrhythmia และ asystole ปัจจุบัน จึงมีที่ใช้น้อยมาก ) attention  correct electrolytic or metabolic abnormalities, identify & treat recurrent ischemia.

57 PVC’s

58

59 Arrhythmic Complications: Ventricular Arrhythmias Accelerated idioventricular rhythm (AIVR) 20% of AMI wide QRS complex /regular escape rate faster than the atrial rate, but < 100 bpm AV dissociation is frequent Slow, nonconducted P waves unrelated to the fast, wide QRS rhythm short & terminate spontaneously

60 Arrhythmic Complications: Ventricular Arrhythmias

61 Accelerated idioventricular rhythm SA node or AV node  sustain structural damage & depress nodal automaticity and/or an abnormal ectopic focus in the ventricle  dominant pacemaker Do not affect prognosis No definitive evidence  untreated occurrence increases the incidence of ventricular fibrillation or death

62 Arrhythmic Complications: Ventricular Arrhythmias Accelerated idioventricular rhythm พบบ่อยใน early reperfusion  neither sensitive nor specific marker for reperfusion Suppression  bradycardia or asystole  left untreated

63 Arrhythmic Complications Nonsustained ventricular tachycardia 3 or more consecutive ventricular ectopic beats, > 100 bpm and lasting < 30 sec multiple runs of nonsustained VT  sudden hemodynamic collapse antiarrhythmic  No morbidity/mortality benefit > 48 hr after infarction in LV systolic dysfunction (LVEF < 0.40)  ↑ risk for sudden cardiac death  electrophysiologic testing & appropriate therapy

64 Arrhythmic Complications Nonsustained ventricular tachycardia Multiple episodes of nonsustained VT  intensified monitoring & attention to electrolyte imbalances Keep Serum K > 4.5 mEq/L, and Mg > 2.0 mEq/L Ongoing ischemia  aggressively be sought and corrected

65

66 Arrhythmic Complications Sustained ventricular tachycardia 3 or more consecutive ventricular ectopic beats,rate > 100 bpm and lasting > 30 sec or causing hemodynamic compromise that requires intervention 20% hospital mortality rate Rapid polymorphic VT ( >150 bpm) associated with hemodynamic instability  immediate unsynchronized cardioversion of 200 J (or biphasic energy equivalent)

67 Arrhythmic Complications Sustained ventricular tachycardia Monomorphic VT  synchronized 100 J (or biphasic energy equivalent) Antiarrhythmic therapy: amiodarone (drug of choice) or procainamide may be attempted before electrical cardioversion Correct electrolyte abnormalities, acid-base disturbances, hypoxia, or medication Persistent/recurrent VT  overdrive pacing

68 lidocaine mg/kg bolus และให้ทาง iv drip ต่อ 2-4 mg/min ให้ลดขนาดยาในผู้สูงอายุ, มี ภาวะ CHF หรือ hepatic dysfunction amiodarone 150 mg iv ใน 10 นาทีและให้ iv drip ต่อ 1 mg/min ใน 6 ชั่วโมง ต่อไปให้ 0.5 mg/min Arrhythmic Complications Sustained ventricular tachycardia

69

70

71 Arrhythmic Complications ventricular fibrillation Primary VF  greatest in the first hour, 60% of episodes occur within 4 hours, and 80% occur within 12 hours Secondary or late VF  48 hr after an MI  usually associated with pump failure and cardiogenic shock, large infarct, an intraventricular conduction delay, and an anteroseptal MI (In-hospital mortality rate of 40-60%)

72 Arrhythmic Complications ventricular fibrillation Treatment: unsynchronized electrical countershock J (or biphasic energy equivalent) electromechanical dissociation (EMD) or pulseless electrical activity (PEA)  extensive myocardial ischemia/necrosis or cardiac rupture IV amiodarone/lidocaine  facilitate successful electrical defibrillation & prevent recurrent/ refractory episodes, continued IV infusion for hr early use of ß-blockers in MI  ↓ ventricular fibrillation/death

73

74 Arrhythmic Complications Reperfusion Arrhythmias believed to be a marker of successful coronary reperfusion high incidence in patients with AMI in whom coronary reperfusion is unsuccessful neither sensitive nor specific for reperfusion  treated Accelerated Idioventricular Rhythm (AIVR) อาจจะเป็น PVCs, AIVR, VT หรือ VF

75 Mechanical Complications of MI Ventricular free wall rupture (VFWR) ventricular septal rupture(VSR) papillary muscle rupture with severe mitral regurgitation (MR)

76 Ventricular free wall rupture (VFWR) most serious complication of AMI VFWR leads to acute hemopericardium and death from cardiac tamponade incidence %  declined with better 24 hour systolic blood pressure control; ↑use of reperfusion therapy, beta blockers, and ACE inhibitors; and ↓use of heparin Percutaneous transluminal coronary angioplasty (PTCA) had an incidence of free wall rupture < receiving thrombolytic therapy.

77 ส่วนใหญ่ 1st week after AMI Involve: anterior or lateral wall Acute  severe chest pain, abrupt electromechanical dissociation, asystole, hemodynamic collapse, and death Subacute  pseudoaneurysms (vary in size,high risk to rupture) syncope, hypotension, shock, arrhythmia, prolonged & recurrent chest pain Ventricular free wall rupture (VFWR)

78 Risk factors Age > 70 years Female no previous MI Q waves on ECG Hypertension during the initial phase of STEMI Corticosteroid/NSAID use Fibrinolytic therapy > 14 hr after STEMI onset Ventricular free wall rupture (VFWR)

79 Echocardiography  moderate-to-large pericardial effusion with signs of impending tamponade Most important prevention strategy: early reperfusion therapy IABP, IV fluids, inotropic agents, emergency pericardiocentesis. Stable  emergency surgical repair mortality rate: high & depend on preoperative hemodynamic status Ventricular free wall rupture (VFWR)

80 ventricular septal rupture(VSR) high mortality rate Bimodal: high incidence in the first 24 hr, another peak on days 3-5 (rarely > 2 weeks) median time (onset of AMI to septal rupture): 1 Day in GUSTO-I, 16 hr in SHOCK-Trial most common in large anterior MI (occlusion of the LAD artery causing extensive septal infarcts)  ST-segment elevations and Q waves in inferior leads (II, III, aVF)

81 Risk factors Age >65 y Female Single-vessel disease Extensive MI Poor septal collateral circulation RV involvement ventricular septal rupture(VSR)

82 Clinical presentation chest pain, shortness of breath, hypotension, biventricular failure & shock with (hours to days) new, loud & harsh holosystolic murmur  LLSB & palpable parasternal systolic thrill, S3 gallops ( เทียบกับ acute MR  soft systolic murmur at the apex, without thrill) กรณี cardiogenic shock  identify murmur ยาก ventricular septal rupture(VSR)

83 Echocardiography (color Flow)  Tool of choice Cardiac catheterization  confirm Dx, ประเมิน degree of left-to-right shunt, ตำแหน่งของ VSR, แยกโรค VSR จากภาวะ MR, ดู coronary artery lesion ventricular septal rupture(VSR)

84 Key management: prompt diagnosis & an aggressive approach to hemodynamic stabilization, angiography, and surgery Oxygen, IABP use of vasodilators (↓ afterload & LV pressure & left-to-right shunt) diuretics, and inotropic agents Medical therapy  temporary stabilization before surgery ventricular septal rupture(VSR)

85 GUSTO-I  30-day mortality rate ของผู้ป่วยที่ รักษาโดย surgical repair = 47% VS medical = 94% และ 1-year mortality rate = 53% vs 97% Current guidelines of the ACC/AHA  patients with septal rupture complicating AMI  urgent surgical intervention, regardless of their clinical status Percutaneous closure of septal rupture  relatively new approach ventricular septal rupture(VSR)

86 acute mitral regurgitation MR is a common complication, results from local and global LV remodeling  predictor of heart failure & death เกิด 7-10 days หลัง MI, onset may vary according to the mechanism of MR. MR จาก Papillary muscle rupture เกิดในช่วง 1-14 วัน (median 1 วัน ) Mild-to-moderate MR  silent, พบจากการทำ Doppler echocardiography Severe acute MR (rupture of papillary muscles or chordae tendineae)  abrupt hemodynamic deterioration with cardiogenic shock  อัตราตาย สูง

87 Risk factors: advanced age, female, large infarct, previous AMI, recurrent ischemia, multivessel coronary artery disease & heart failure Posteromedial papillary muscle > anterolateral papillary muscle (PM มี single blood supply ขณะที่ AL มี dual supply) Papillary muscle rupture  flailing or prolapse of the leaflets  severe MR acute mitral regurgitation

88 Papillary muscle dysfunction due to scarring or recurrent ischemia  MR in the subacute and chronic phases, resolve spontaneously Large posterior infarctions  acute MR จาก asymmetric annular dilation and altered function and geometry ของ papillary muscle Dx: Echocardiography with color flow Doppler imaging CXR  pulmonary edema without cardiac enlargement acute mitral regurgitation

89 Presentation: mild or moderate MR  asymptomatic acute severe MR  shortness of breath, fatigue, a new apical holosystolic murmur (may be early-to-mid systolic, no thrill), flash pulmonary edema & shock

90 Cardiac catheterization should be performed to determine the extent and severity of coronary artery disease Treatment: Determination of hemodynamic stability & exact mechanism of MR Medication: afterload reduction diuretics, sodium nitroprusside & nitrates in no hypotension Intra-aortic balloon counterpulsation (IABP) in hemodynamic compromise acute mitral regurgitation

91 Emergency surgical intervention is the treatment of choice for papillary muscle rupture MV repair ดีกว่า Replacement ในกรณีไม่มี papillary necrosis emergency surgery avoided กรณี intermittent MR due to recurrent ischemia  angioplasty or coronary artery bypass grafting (CABG) acute mitral regurgitation

92 Etiologies, Prevalence, and Mortality* CausesIncidenceMortality Predominant left ventricular failure 78%59% Severe mitral regurgitation 6.9%55% Ventricular septal rupture 3.9%87% Isolated right ventricular shock 2.8%55% Free wall rupture and tamponade 1.4%55% Average 60% *Hochman JS, Buller CE, Sleeper LA, Boland J, Dzavik V, Sanborn TA, et al. Cardiogenic shock complicating acute myocardial infarction-- etiologies, management and outcome: a report from the SHOCK Trial Registry. SHould we emergently revascularize Occluded Coronaries for cardiogenic shocK. J Am Coll Cardiol 2000;36(3 Suppl A):

93 Left Ventricular Aneurysm a localized area of myocardium with abnormal outward bulging and deformation during both systole and diastole approximately 3-15% Risk factors: female, total occlusion of the LAD artery, single-vessel disease & absence of previous angina 80%  anterolateral wall (asso. CTO of LAD)

94 ECG  ST elevation persists several weeks after AMI & same leads showing the acute infarct Echocardiography  93% sensitivity & 94% specificity cardiac catheterization  standard for Dx Left Ventricular Aneurysm

95 Inferior wall aneurysm

96 small or clinically insignificant aneurysms  conservative, close follow-up Medical therapy: angiotensin-converting enzyme (ACE) inhibitors  reduce afterload, infarct extension & LV remodeling Anticoagulation  severe LV dysfunction and/or thrombus in the LV or aneurysm Surgical resection: if severe heart failure, ventricular tachyarrhythmias refractory to medical treatment, recurrent thromboembolism Left Ventricular Aneurysm

97 Left ventricular mural thrombus anterior wall infarcts 20-40% (60% in large anterior-wall AMIs, not treated with anticoagulant therapy) high risk of systemic embolization (Anticoagulant therapy  ↓ rate of embolic events by 33% เทียบกับไม่ได้ anticoagulation) most common presentation  Stroke (within the first 10 days after AMI)

98 Transthoracic echocardiography  modality of choice (92% sensitivity, 88% specificity) Management  heparin treatment followed by oral warfarin therapy for 3-6 months, lifelong anticoagulation if a mural clot persists. Left ventricular mural thrombus

99 Apical LV thrombus

100 Pericarditis ≈10%, ภายใน hr inflammation of pericardial tissue overlying infarcted myocardium severe chest pain (pleuritic) & pericardial friction rub ECG  diffuse ST-segment ↑ in all or nearly all of leads Echocardiography may reveal a small pericardial effusion

101 Treatment  aspirin & NSAIDs Colchicine  in recurrent pericarditis Post-MI syndrome (Dressler syndrome)  autoimmune process, fever, chest pain, signs & symptoms of pericarditis เกิด 2-3 weeks after AMI. incidence 1-5%, ลดลงหลังมีการรักษาด้วย thrombolysis และ coronary angioplasty Management: hospitalization & observation for any evidence of cardiac tamponade, rest, NSAIDs, and/or steroids Pericarditis & Dressler syndrome

102 Management of RV Infarction Early maintenance of right ventricular preload Reduction of right ventricular afterload Inotropic support of the dysfunctional right ventricle Early pharmacological and percutaneous mechanical reperfusion

103 Blood pressure <90 mm Hg for at least 1 hour, not improved with fluid administration Signs of hypoperfusion (cold extremities), altered mental status: restlessness, agitation Reduces urine output (<20 cc/h) Cardiac index of <2.2 L/min/m2 Diagnostic Criteria for Cardiogenic Shock

104 Acute anterior wall MI and multisite MI with decreasing systolic BP (most common) Decreasing systolic BP in patients with history of prior MI (old MI) Decreasing systolic BP in patients with acute inferior wall MI Decreasing systolic BP with clear lungs due to acute right ventricular infarction (very rare) Suspicious of Early Cardiogenic Shock by ECG

105 Management of Cardiogenic Shock 1.Early recognition of cardiogenic shock 2.Stabilization of patient by correction of arrhythmia, electrolyte imbalance, acid-base abnormality 3.Insertion of intra-aortic balloon pump (IABP) in the left femoral artery, for possible angioplasty in the right femoral artery 4.Early intubation and mechanical ventilation to decrease the work of the respiratory muscles and myocardial oxygen consumption 5. Right, left heart catheterization and coronary angiography 6.Early mechanical intervention or coronary artery bypass surgery (CABG)

106


Download ppt "โรงพยาบาลสรรพสิทธิ ประสงค์ อุบลราชธานี. How to manage ACS Complications นพ. วีระ มหาวนากูล กลุ่มงานอายุรกรรม โรงพยาบาลสรรพสิทธิประสงค์ อุบลราชธานี"

Similar presentations


Ads by Google