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)
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
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
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
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
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)
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.
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
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.