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PRESENTED BY:
DR.MD.NOOR-E-KHUDA
MD Final part student
cardiology,DMCH
 A 62 yrs old male is brought to the ED with
sudden onset chest pain, exessive sweating,
nausea and dyspnoea
 No other medical history is known.
 He is agitated upon presentation and is unable to
give any history.
 Vital signs upon arrival: HR 135bpm, BP
80/60mmHg, RR>40/min, SpO2 62% on
room air.
 Cold clammy skin,cyanosed extremities
 Gallop rhythm present.
 Bilateral Diffuse crackles
o Cardiogenic shock is a state of systemic
hypotension persisting >30minutes, with
reduced end-organ perfusion due to low
cardiac output despite adequate filling
pressures.
 Persistent (>30 minutes) hypotension with
systolic arterial pressure <90mm Hg
 Reduction in cardiac index <2.2 litres/min/m2
 Presence of elevated left ventricle filling
pressure(PCWP>18 mm Hg)
 Signs and symptoms of end organ
hypoperfusion (restlessness,confusion,cold
cyanotic extremeties,oliguria<30ml/hr)
 Acute MI
 LV Systolic failure
 RV infraction
 Papillary muscle rupture(1%)
 Acute VSD(1-3%)
 Free wall rapture(1-6%)
 Non infract related LV failure
 Critical ischaemia without MI
 End stage cardiomyopathy
 Acute myocarditis
 Drug toxicity(e.g.-beta blocker)
 Obstructed cardiac output
 Critical aortic stenosis
 Prosthetic valve obstruction/failure
 Massive pulmonary embolism
 Other mechanical causes
 Tamponade
 Aortic dissection
Predominant LV Failure
79%
Acute Severe MR
7%
VSR
4%
Isolated RV Shock
3%
Tamponade/rupture
1%
Other
7.5%
Shock Registry
JACC 2000 35:1063
 Extensive damage to left myocardium (large anterior
wall MI)->40% LV mass loss
 Age > 70 years
 SBP < 120 mmHg
 Sinus tachycardia rate > 110/min.
 Bradycardia rate < 60/min.
 Increased time from onset of STEMI
 H/O Hypertension, diabetes mellitus
 Multi vessel coronary artery disease
 Prior MI or angina
 Prior diagnosis of heart failure
 History :
 Recent MI ?
 Previous HF?

Valvedisease/prosthesis/cardiomyopathy?
 Thrombolysis given?any symptoms of
internal bleeding?anaphylaxis?
 Timing.day 2-3 post MI
 Sudden onset when previously
stable:suspect rupture,VSR,
 Fluid balance
 Drugs
 G/E- decreased conscious
level,confusion,cyanosis,diaphoresis,
pale,cool pheripheries
 Tachycardia or bradycardia
 Tachypnoea
 Systolic BP<90mm Hg with narrow pulse
pressure
 Elevated JVP
 AUSCULTATION-
Precordium :
Apex -dyskinetic in anterior MI /LV aneurysm
-hyperdynamic in VSR and MR
-absent in tamponade
Thrill / murmur : ventricular septal rupture/MR
S3 gallop when LA pressure is high
Systolic murmur- louder upon valsalva and
prompt standing (HOCM)
Chest :
Bilateral crackles
 Acute coronary syndrome : STEMI, NSTEMI, RV
infarction
 Cardiomyopathy
 Arrhythmia
 Chest X-ray-
1. Cardiac shadow is enlarged in TD
(silhouette can be normal)
2. Pulmonary vascular congestion
and pulmonary edema
3. Pericardial effusion
4. Bilateral pleural effusion
1. VSD
2. severe MR
3. Aortic dissection with AR
4. PE or tamponade
5. Ruptured free wall
6. RV infarct:RV dilation and asynergy, abnormal
interventricular and interatrial septal motion,
7. Both PA systolic pressure and wedge
pressure can be accurately estimated with
Doppler echocardiography, and in particular,
the finding of a short mitral deceleration time
(≤140 ms) is highly predictive of pulmonary
capillary wedge pressure ≥20 mm Hg in CS
 Elevated CKMB ,Troponin I
 RFT-s.creatinine,U&E: progressively derranged
 LFT-markedly elevated transaminases
 Increased lactate levels
 Anion gap. metabolic acidosis compensated by
respiratory alkalosis
 ABG:Arterial hypoxemia
 Exclude other causes of shock
 Diagnosis of cardiogenic shock
1-PCWP > 18mmHg, CI < 2.2L/min/m2
2-Large V wave on PCWP, very high PCWP = severe MR
3-Step up in oxygen saturation from RA to RV, large V wave on RA pressure-
Ruptured Ventricular septum
4-High right sided filling pressure in the absence of elevated PCWP(RA > 10
and > 80% of PCWP) = RV infarct
5-Classic sign of cardiac tamponade (equalization of diastolic pressure among
the cardiac chambers) = free wall ruptured.
6. Low mixed venous O2 saturations and elevated AV O2 difference-low CI and
high fractional O2 extraction
 GENERAL MEASURES
 TEMPORARY SUPPORT
1. Vasopressor
2. Mechanical support
 SPECIFIC MEASURES
1. Fibrinolysis
2. Revascularization- PCI/CABG
3. Cardiac transplantation
 Rapid correction of haemodynamic
compromise is essential,to avoid organ
damage from hypoperfusion: ATN,MI
extension,shock liver
 Management of reversible cause : 5H’s,5T’s
Hypoxia,hypovolemia,hypokalemia,hypothermia,hydrog
en ion,tamponade,t.pneumothorax,toxins,thrombosis
 Maintain SBP >90mm Hg and PCWP <20mm Hg
 Correct hypoxia, acidosis- ventilatory support if
required.
 Control arrhythmias- brady or
tachyarrhythmias
 Control hyperglycemia by insulin.
 If condition persists despite optimal LV
filling, inotropic support is usually needed
 High PCWP,in the presence of shock,
necessitates inotropic or mechnical support
DRUG INITIAL
DOSE
MAINTENANC
E DOSE
COMMENTS
DOPAMINE 1-2 mcg//kg/min
4-5mcg/kg/min
2-4 mcg/kg/min
5-10 mcg/kg/min
10-20mcg/kg/min
Inotropy,vasodilation,tachycardia,hypot-
ension,arrythmia
Increased contractility and heart rate
Inotropy,vasoconstriction,tachycardia,h
y-potension, arrythmia
NORADRENALINE 0.2-1.5mcg/kg/min Vasoconstriction,inotropy,tachycardia,
less arrythmia
DOBUTAMINE 1-2mcg/kg/min 2-20mcg/kg/min. Inotropy,vasodilation,tachycardia,hypot
ension, arrythmia
EPINEPHRINE 0.05-0.5mcg/kg/min Vasoconstriction,inotropy,tachycardia,h
ypotension
VASOPRESSIN 0.1-0.4 units/min
LEVOSIMENDAN 12mcg 0.2 Mcg/kg.min Vasodilation,inotropy,tachycardia,hypot
ension
MILRINONE 25-75mcg/kg
bolus
0.1-0.75mcg/kg/min Vasodilation,inotropy,tachycardia,hypot
ension
Clinical Signs: Shock, Hypoperfusion, CHF, Acute Pulm Edema
Most likely major underlying disturbance?
Acute Pulmonary
Edema
Hypovolemia Low-output
cardiogenic shock
Arrhythmia
Administer
Furosemide
Morphine
Oxygen intubation
Nitroglycerin
Dopamine
Dobutamine
Administer
Fluids
Blood transfusions
Cause-specific
interventions Check Blood Pressure
Brady
cardia
Tachy
cardia
Check Blood Pressure
Systolic BP
(>100 mm Hg)
Systolic BP
≥90mm Hg
Mean arterial
BP>70mmHg
(signs/sympto
ms of shock)
Systolic BP <90
mm
Hg+Oliguria+oth
ers signs/sympt
oms
of shock)
SBP (<70 mm Hg +
tachycardia+others
signs/symptoms of
shock)
Manage accordingly
ACE
Inhibitors
Dobutamine Dopamine
Norepinephrine
33
 INTRA –AORTIC BALLOON PUMP(IABP)
 PERCUTANEOUS VENTRICULAR ASSIST
DEVICES (pVAD)
 EXTRACORPOREAL MEMBRANE
OXYGENATION(ECMO)
 BRIDGE TO RECOVERY-Cardiogenic
shock refractory to optimal medical
management and reasonable
expectation that myocardial injury is
reversible and temporary(acute
MI,acute myocarditis, postcardiotomy
cardiogenic shock.
 BRIDGE TO TRANSPLANTATION:- In whom
myocardial function is unlikely to recover(Long
standing ischemic,valvular cardiomyopathy,or
myocarditis)
39
40
- The end of the balloon should be just distal (1-2 cm) to the takeoff
of the left subclavian artery
- Position should be confirmed by fluoroscopy or chest x-ray
Positioning
 Inflation occurs at aortic dicrotic notch and
deflation occurs immediately before systole for
maximum augmentation in diastole and maximum
systolic unloading
 Timing is usually adjusted as 1:2(one inflation in 2
beats)
 Significant aortic regurgitation or AV shunting
 Abdominal aortic aneurysm or aortic dissection
 Uncontrolled sepsis
 Uncontrolled bleeding disorder
 Severe bilateral PVD
 Bilateral femoral popliteal bypass grafts
 Percutaneous LVADs may rapidly reverse the
hemodynamic compromise seen in patients with
CS that is refractory to IABP and vasopressor
support.
o Left atria-to-femoral arterial
LVAD
 Low speed centrifugal
continuous flow pump
 Maximum flow 4L/minute
 The TandemHeart removes blood from the left
atrium using a cannula placed through the femoral
vein and into the left atrium via transseptal
puncture.
 Blood is then returned to a systemic artery,
usually the femoral artery with retrograde
perfusion of the abdominal and thoracic aorta.
IMPELLA LP 2.5 & LP
5.0
 Helical propellar-axial flow
 Minimally –invasive,percutaneous
catheter LVADs.
 Insertion similar to IABP but device
rests across the aortic valve,with
the tip in the LV cavity.
 FDA approved for high risk
PCI,post PCI,cardiogenic
shock,myocarditis &bridge to
decision.
 Axial flow pump
 Much simpler to use
 Increases cardiac output & unloads LV
◦ Maximum 5L flow
Pressure Lumen
Motor
Blood outlet
Blood Inlet
 A procedure in which blood is taken from a
patient's circulation to have a process applied to it
before it is returned to the circulation.
 The drainage cannula is commonly placed in
IVC(via IJV or Femoral vein)
 Blood is returned to patient through cannula in
ascending aorta(central) or femoral
artery(peripheral)
 As in MI with shock, earlier revascularization is
better (<75 years-class I,≥75 yrs-class IIa)
 Presentation 0 to 6 hours after symptom onset
was associated with the lowest mortality among
CS patients undergoing primary PCI
 In the SHOCK trial, there appeared to be
increasing long-term mortality as time to
revascularization increased from 0 to 8 hours.
 However, there is a survival benefit as long as 48
hours after MI and 18 hours after shock onset
JAMA.
2006;295:2511–2515.
AGENT FIBRIN
SPECIFIC
ITY
FIBRINOG
EN
DEPLETI
ON
ANTIGENI
C
PATENCY
RATE
Tenecteplase ++++ Minimal No 85%
Reteplase ++ Moderate No 84%
Alteplase ++ Mild No 73-84%
Streptokinase No Marked Yes 60-68%
Circulation. 2004;110:588–636
ACC/AHA
Guidelines
(1) cardiogenic shock requiring mechanical
support or high-dose inotropic or
vasopressor drugs (in which case the
irreversibility of their course is usually
clear);
 Cardiogenic Shock secondary to RV Infarct has
better prognosis than LV Pump Failure
 IV Fluid Administration
 Dobutamine
 IABP
 Maintain A-V Synchrony
 Mortality with Successful Reperfusion = 2%
 Unsuccessful Reperfusion = 58%
 Class I
1. Early revascularization, either PCI or CABG, is
recommended for patients < 75 years old with ST
elevation or new LBBB who develop shock
2. Fibrinolytic therapy should be administered to STEMI
patients with cardiogenic shock who are unsuitable for
further invasive care and do not have contraindications
for fibrinolysis.
3. Echocardiography should be used to evaluate
mechanical complications unless assessed by
invasively.
1. Pulmonary artery catheter monitoring can be useful for the
management of STEMI patients with cardiogenic shock.
2. Early revascularization, either PCI or CABG, is reasonable for
selected patients > 75 years with ST elevation or new LBBB who
develop shock < 36 hours of MI and who are suitable for
revascularization that is performed < 18 hours of shock.
 Cardiogenic shock is a treatable illness with a
reasonable chance of full recovery.
 The literature has traditionally focused on the
very high mortality associated with this diagnosis.
 It is important to recognize that although patients
with CS are at very high risk for early death, great
potential exists for salvage.
Management of Cardiogenic shock

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Management of Cardiogenic shock

  • 1. PRESENTED BY: DR.MD.NOOR-E-KHUDA MD Final part student cardiology,DMCH
  • 2.  A 62 yrs old male is brought to the ED with sudden onset chest pain, exessive sweating, nausea and dyspnoea  No other medical history is known.  He is agitated upon presentation and is unable to give any history.
  • 3.  Vital signs upon arrival: HR 135bpm, BP 80/60mmHg, RR>40/min, SpO2 62% on room air.  Cold clammy skin,cyanosed extremities  Gallop rhythm present.  Bilateral Diffuse crackles
  • 4.
  • 5.
  • 6. o Cardiogenic shock is a state of systemic hypotension persisting >30minutes, with reduced end-organ perfusion due to low cardiac output despite adequate filling pressures.
  • 7.  Persistent (>30 minutes) hypotension with systolic arterial pressure <90mm Hg  Reduction in cardiac index <2.2 litres/min/m2  Presence of elevated left ventricle filling pressure(PCWP>18 mm Hg)  Signs and symptoms of end organ hypoperfusion (restlessness,confusion,cold cyanotic extremeties,oliguria<30ml/hr)
  • 8.  Acute MI  LV Systolic failure  RV infraction  Papillary muscle rupture(1%)  Acute VSD(1-3%)  Free wall rapture(1-6%)
  • 9.  Non infract related LV failure  Critical ischaemia without MI  End stage cardiomyopathy  Acute myocarditis  Drug toxicity(e.g.-beta blocker)  Obstructed cardiac output  Critical aortic stenosis  Prosthetic valve obstruction/failure  Massive pulmonary embolism
  • 10.  Other mechanical causes  Tamponade  Aortic dissection
  • 11. Predominant LV Failure 79% Acute Severe MR 7% VSR 4% Isolated RV Shock 3% Tamponade/rupture 1% Other 7.5% Shock Registry JACC 2000 35:1063
  • 12.
  • 13.
  • 14.
  • 15.  Extensive damage to left myocardium (large anterior wall MI)->40% LV mass loss  Age > 70 years  SBP < 120 mmHg  Sinus tachycardia rate > 110/min.  Bradycardia rate < 60/min.  Increased time from onset of STEMI  H/O Hypertension, diabetes mellitus  Multi vessel coronary artery disease  Prior MI or angina  Prior diagnosis of heart failure
  • 16.
  • 17.
  • 18.
  • 19.  History :  Recent MI ?  Previous HF?  Valvedisease/prosthesis/cardiomyopathy?  Thrombolysis given?any symptoms of internal bleeding?anaphylaxis?  Timing.day 2-3 post MI  Sudden onset when previously stable:suspect rupture,VSR,  Fluid balance  Drugs
  • 20.  G/E- decreased conscious level,confusion,cyanosis,diaphoresis, pale,cool pheripheries  Tachycardia or bradycardia  Tachypnoea  Systolic BP<90mm Hg with narrow pulse pressure  Elevated JVP
  • 21.  AUSCULTATION- Precordium : Apex -dyskinetic in anterior MI /LV aneurysm -hyperdynamic in VSR and MR -absent in tamponade Thrill / murmur : ventricular septal rupture/MR S3 gallop when LA pressure is high Systolic murmur- louder upon valsalva and prompt standing (HOCM) Chest : Bilateral crackles
  • 22.  Acute coronary syndrome : STEMI, NSTEMI, RV infarction  Cardiomyopathy  Arrhythmia
  • 23.  Chest X-ray- 1. Cardiac shadow is enlarged in TD (silhouette can be normal) 2. Pulmonary vascular congestion and pulmonary edema 3. Pericardial effusion 4. Bilateral pleural effusion
  • 24. 1. VSD 2. severe MR 3. Aortic dissection with AR 4. PE or tamponade 5. Ruptured free wall 6. RV infarct:RV dilation and asynergy, abnormal interventricular and interatrial septal motion, 7. Both PA systolic pressure and wedge pressure can be accurately estimated with Doppler echocardiography, and in particular, the finding of a short mitral deceleration time (≤140 ms) is highly predictive of pulmonary capillary wedge pressure ≥20 mm Hg in CS
  • 25.  Elevated CKMB ,Troponin I  RFT-s.creatinine,U&E: progressively derranged  LFT-markedly elevated transaminases  Increased lactate levels  Anion gap. metabolic acidosis compensated by respiratory alkalosis  ABG:Arterial hypoxemia
  • 26.  Exclude other causes of shock  Diagnosis of cardiogenic shock 1-PCWP > 18mmHg, CI < 2.2L/min/m2 2-Large V wave on PCWP, very high PCWP = severe MR 3-Step up in oxygen saturation from RA to RV, large V wave on RA pressure- Ruptured Ventricular septum 4-High right sided filling pressure in the absence of elevated PCWP(RA > 10 and > 80% of PCWP) = RV infarct 5-Classic sign of cardiac tamponade (equalization of diastolic pressure among the cardiac chambers) = free wall ruptured. 6. Low mixed venous O2 saturations and elevated AV O2 difference-low CI and high fractional O2 extraction
  • 27.
  • 28.  GENERAL MEASURES  TEMPORARY SUPPORT 1. Vasopressor 2. Mechanical support  SPECIFIC MEASURES 1. Fibrinolysis 2. Revascularization- PCI/CABG 3. Cardiac transplantation
  • 29.  Rapid correction of haemodynamic compromise is essential,to avoid organ damage from hypoperfusion: ATN,MI extension,shock liver
  • 30.  Management of reversible cause : 5H’s,5T’s Hypoxia,hypovolemia,hypokalemia,hypothermia,hydrog en ion,tamponade,t.pneumothorax,toxins,thrombosis  Maintain SBP >90mm Hg and PCWP <20mm Hg  Correct hypoxia, acidosis- ventilatory support if required.  Control arrhythmias- brady or tachyarrhythmias  Control hyperglycemia by insulin.
  • 31.  If condition persists despite optimal LV filling, inotropic support is usually needed  High PCWP,in the presence of shock, necessitates inotropic or mechnical support
  • 32. DRUG INITIAL DOSE MAINTENANC E DOSE COMMENTS DOPAMINE 1-2 mcg//kg/min 4-5mcg/kg/min 2-4 mcg/kg/min 5-10 mcg/kg/min 10-20mcg/kg/min Inotropy,vasodilation,tachycardia,hypot- ension,arrythmia Increased contractility and heart rate Inotropy,vasoconstriction,tachycardia,h y-potension, arrythmia NORADRENALINE 0.2-1.5mcg/kg/min Vasoconstriction,inotropy,tachycardia, less arrythmia DOBUTAMINE 1-2mcg/kg/min 2-20mcg/kg/min. Inotropy,vasodilation,tachycardia,hypot ension, arrythmia EPINEPHRINE 0.05-0.5mcg/kg/min Vasoconstriction,inotropy,tachycardia,h ypotension VASOPRESSIN 0.1-0.4 units/min LEVOSIMENDAN 12mcg 0.2 Mcg/kg.min Vasodilation,inotropy,tachycardia,hypot ension MILRINONE 25-75mcg/kg bolus 0.1-0.75mcg/kg/min Vasodilation,inotropy,tachycardia,hypot ension
  • 33. Clinical Signs: Shock, Hypoperfusion, CHF, Acute Pulm Edema Most likely major underlying disturbance? Acute Pulmonary Edema Hypovolemia Low-output cardiogenic shock Arrhythmia Administer Furosemide Morphine Oxygen intubation Nitroglycerin Dopamine Dobutamine Administer Fluids Blood transfusions Cause-specific interventions Check Blood Pressure Brady cardia Tachy cardia Check Blood Pressure Systolic BP (>100 mm Hg) Systolic BP ≥90mm Hg Mean arterial BP>70mmHg (signs/sympto ms of shock) Systolic BP <90 mm Hg+Oliguria+oth ers signs/sympt oms of shock) SBP (<70 mm Hg + tachycardia+others signs/symptoms of shock) Manage accordingly ACE Inhibitors Dobutamine Dopamine Norepinephrine 33
  • 34.  INTRA –AORTIC BALLOON PUMP(IABP)  PERCUTANEOUS VENTRICULAR ASSIST DEVICES (pVAD)  EXTRACORPOREAL MEMBRANE OXYGENATION(ECMO)
  • 35.  BRIDGE TO RECOVERY-Cardiogenic shock refractory to optimal medical management and reasonable expectation that myocardial injury is reversible and temporary(acute MI,acute myocarditis, postcardiotomy cardiogenic shock.
  • 36.  BRIDGE TO TRANSPLANTATION:- In whom myocardial function is unlikely to recover(Long standing ischemic,valvular cardiomyopathy,or myocarditis)
  • 37.
  • 38.
  • 39. 39
  • 40. 40 - The end of the balloon should be just distal (1-2 cm) to the takeoff of the left subclavian artery - Position should be confirmed by fluoroscopy or chest x-ray Positioning
  • 41.  Inflation occurs at aortic dicrotic notch and deflation occurs immediately before systole for maximum augmentation in diastole and maximum systolic unloading  Timing is usually adjusted as 1:2(one inflation in 2 beats)
  • 42.  Significant aortic regurgitation or AV shunting  Abdominal aortic aneurysm or aortic dissection  Uncontrolled sepsis  Uncontrolled bleeding disorder  Severe bilateral PVD  Bilateral femoral popliteal bypass grafts
  • 43.  Percutaneous LVADs may rapidly reverse the hemodynamic compromise seen in patients with CS that is refractory to IABP and vasopressor support.
  • 44. o Left atria-to-femoral arterial LVAD  Low speed centrifugal continuous flow pump  Maximum flow 4L/minute
  • 45.  The TandemHeart removes blood from the left atrium using a cannula placed through the femoral vein and into the left atrium via transseptal puncture.  Blood is then returned to a systemic artery, usually the femoral artery with retrograde perfusion of the abdominal and thoracic aorta.
  • 46. IMPELLA LP 2.5 & LP 5.0  Helical propellar-axial flow  Minimally –invasive,percutaneous catheter LVADs.  Insertion similar to IABP but device rests across the aortic valve,with the tip in the LV cavity.  FDA approved for high risk PCI,post PCI,cardiogenic shock,myocarditis &bridge to decision.
  • 47.  Axial flow pump  Much simpler to use  Increases cardiac output & unloads LV ◦ Maximum 5L flow Pressure Lumen Motor Blood outlet Blood Inlet
  • 48.
  • 49.  A procedure in which blood is taken from a patient's circulation to have a process applied to it before it is returned to the circulation.
  • 50.
  • 51.  The drainage cannula is commonly placed in IVC(via IJV or Femoral vein)  Blood is returned to patient through cannula in ascending aorta(central) or femoral artery(peripheral)
  • 52.  As in MI with shock, earlier revascularization is better (<75 years-class I,≥75 yrs-class IIa)  Presentation 0 to 6 hours after symptom onset was associated with the lowest mortality among CS patients undergoing primary PCI  In the SHOCK trial, there appeared to be increasing long-term mortality as time to revascularization increased from 0 to 8 hours.  However, there is a survival benefit as long as 48 hours after MI and 18 hours after shock onset JAMA. 2006;295:2511–2515.
  • 53. AGENT FIBRIN SPECIFIC ITY FIBRINOG EN DEPLETI ON ANTIGENI C PATENCY RATE Tenecteplase ++++ Minimal No 85% Reteplase ++ Moderate No 84% Alteplase ++ Mild No 73-84% Streptokinase No Marked Yes 60-68%
  • 55. (1) cardiogenic shock requiring mechanical support or high-dose inotropic or vasopressor drugs (in which case the irreversibility of their course is usually clear);
  • 56.  Cardiogenic Shock secondary to RV Infarct has better prognosis than LV Pump Failure  IV Fluid Administration  Dobutamine  IABP  Maintain A-V Synchrony  Mortality with Successful Reperfusion = 2%  Unsuccessful Reperfusion = 58%
  • 57.  Class I 1. Early revascularization, either PCI or CABG, is recommended for patients < 75 years old with ST elevation or new LBBB who develop shock 2. Fibrinolytic therapy should be administered to STEMI patients with cardiogenic shock who are unsuitable for further invasive care and do not have contraindications for fibrinolysis. 3. Echocardiography should be used to evaluate mechanical complications unless assessed by invasively.
  • 58. 1. Pulmonary artery catheter monitoring can be useful for the management of STEMI patients with cardiogenic shock. 2. Early revascularization, either PCI or CABG, is reasonable for selected patients > 75 years with ST elevation or new LBBB who develop shock < 36 hours of MI and who are suitable for revascularization that is performed < 18 hours of shock.
  • 59.  Cardiogenic shock is a treatable illness with a reasonable chance of full recovery.  The literature has traditionally focused on the very high mortality associated with this diagnosis.  It is important to recognize that although patients with CS are at very high risk for early death, great potential exists for salvage.

Editor's Notes

  1. Hypotension and elevated left-sided filling pressures result in decreased coronary perfusion and increased ischemia. Vasopressors may increase myocardial oxygen demand, worsen ischemia, and result in arrhythmias. May require invasive arterial pressure monitoring, especially with pressors and inotropes.