Cardiogenic Shock

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Case Presentation :

Cardiogenic Shock

dr. David Hutagaol Sp.BTKV, K-VE


Patient
Identity

 Name : Mrs. AB
 DOB : January 13th, 1950
 Age : 74years
 Gender : Female
Anamnesis
 Chief complaint
- Chest pain

 History of the present illness


Patient is referred from Carolus Hospital with recurrent chest pain for
about 1 year. Chest pain is triggered with activity and relieved with rest.
Patient experiences shortness of breath during heavy work activity. Patient
has underwent cardiac catheterization in November 2023, no stenting.

 Past medical history


- Hypertension and Diabetes since 30 years ago, controlled
PE
 Compos mentis
 Hemodynamic: BP 120/80, HR 68 x/min, RR 18x/min, T 36,7oC
 Eye : anemic conjunctiva (-/-), icteric sclera (-/-)
 Neck : JVP 5 +2 cmH2O
 Cor and pulmo : within normal range
 Abdomen : within normal range
 Extremity : no edema, CRT within normal range
ECG

EKG
Pre-op

SR, HR 72x/min, T inverted V1-V4


Echocardiography
Comment:
 Cardiac chamber dimension : no LV dilatation
 LV wall thickness: IVS wall thickening
 LV wall motion: hypokinetic septal, anteroseptal, segment, basal, mid, apical
 Cardiac valves: mild PR
 LV systolic function: poor (EF: 41 %)
 LV diastolic function: impaired relaxation (E/A: 0,9, E/E’: 7,4)
 RV systolic function : good (TAPSE: 34,1)
 Trombus (-), PE (-)
Conclusion:
 Eccentric hypertrophy
 Low EF (41%)
 Segmental hypokinetic
 Poor LV systolic function
 Grade 1 LV diastolic dysfunction
Cor - angiography
 LM : 30% mid stenosis, short LM
 LAD : osteal CTO, heavy calcified,
collateral flow from LCx
 LCx : 80% osteal stenosis, 70-80%
proximal stenosis , 80% distal
stenosis, 80% OM2 stenosis
 RCA : CTO from proximal with
collateral bridging
 Conclusion :
 CAD 3 VD
Cardiac
Conference
Conference :
• CABG

Surgical approach : Urgency status :
LIMA  LAD
• SVG  OM2 median sternotomy Elective
• SVG  distal RCA

Note : EURO Score 6


(Mortality Risk 4.81%)
Diagnosis

 CAD 3VD
 HHD with HF
Operation
 Preoperative diagnosis : CAD 3VD, HT, CHF fc II
 Postoperative diagnosis : CAD 3VD, HT, CHF fc II
 Operation : CABG x 3
 Complication during operation: clamp off, DC shock 1x20 Joule . VT 2x after
aortic cross
 CPB Time: 110 min, AoX clamp: 77 min
ICU
Day 1
Monitoring
Follow Up
4 pm 8 pm
• Patient was admitted to the ICU • Unstable hemodynamic : BP
with dopamine 5 mcg/kg/min. 90/45 mmHg, MAP 55, HR 90
• PE : sedated, warm extremities bpm, CVP 9, t 36oC on
• Hemodynamic status : BP 145/70 Dopamine 3 mcg/kg/min.
mmHg, MAP 90, HR 70 bpm, • PE : sedated, cold extremities
CVP 8 mmHg, t 35oC. • ECG : sinus rhythm
• ECG : sinus rhythm
• UO last 1 hour : 0.6
• UO last 1 hour : 1.5 mL/kg/h
mL/kg/h.
• Th :
• Th :
• Dopamine was tapered down to
• Gelofusin 300 cc/1 h
3 mcg/kg/min
• Morphine 20 mcg/kg/h • Uptitrated dopamine to 5-10
mcg/kg/min
• Morphine 10 mcg/kg/h
Follow Up
3 am 4 am

• Hemodynamic status : BP • Hemodynamic status : BP


95/40 mmHg, MAP 55, 122/45 mmHg, MAP 70,
HR 82 bpm, CVP 7 HR 69 bpm, CVP 7
mmHg, t 35.9oC on mmHg, t 36.3oC on
Dopamine 10 mcg/kg/min Dopamine 5 +
• ECG : sinus rhythm epinephrine 0.01
• UO : 0.5 mL/kg/h mcg/kg/min
• ECG : sinus rhythm
• Th :
• UO : 2.5 mL/kg/h
• Dopamine 10
• Th :
mcg/kg/min
• Morphine 10 mcg/kg/h • Dopamine 10
• Start epinephrine 0.01 mcg/kg/min
• Morphine 5 mcg/kg/h
mcg/kg/min
• epinephrine 0.02
mcg/kg/min
Laboratory
PH 7.32
findings
PCo2 35.2
PO2 154.9
SO2% 99
Hct 34 Laboratory ( July 3, 2021)
Hb 11.2 1. Elevated Lactate
Na 137
K 4.91
2. Slight decline of pCO2
Cl 109.1
Ca2+ 1.11
Mg2+ UC 3. Incline of pO2
Glu 185
Lac 5 4. Slight decline of HCO3
HCO3- 21
ICU Day 1
Time Blood Pressure MAP HR (bpm) UO Medications
(mmHg) (mL/
kg/h)
8 pm 90/40 56,7 70 0.6 Dopamin
9 pm 130/55 80 73 0.6 Dopamin
10 pm 120/55 76,7 70 0.5 Dopamin
11 pm 105/40 61,7 70 0.7 Dopamin
12 pm 105/40 61,7 75 0.5 Dopamin
1 am 115/40 65 70 0.5 Dopamin
2 am 110/45 63,3 75 0.5 Dopamin
3 am 90/40 55 82 0.5 Dopamin + E
4 am 122/45 70,7 69 2.5 Dopamin + E
5 am 145/50 81,7 69 5.7 Dopamin + E
6 am 140/55 85 70 3.5 Dopamin + E

GCS at 20.00 = E4M6V Ett


GCS at 07.00 = E4M6V5
Follow Up
9 am 11 am

• Hemodynamic status : BP
105/65 mmHg, MAP 78, • Hemodynamic status : BP
HR 70 bpm, CVP 7 mmHg, 105/45 mmHg, MAP 65,
t 36.2oC on Dopamine 5 HR 75 bpm, CVP 8 mmHg,
mcg/kg/min + epinephrine t 36.1oC
0.01 mcg/kg/min • ECG : sinus rhythm
• ECG : sinus rhythm
• UO : 0.9 mL/kg/h
• UO : 1.1 mL/kg/h
• Th :
• Th :
• Dopamine 5 mcg/kg/min
• Dopamine 5 mcg/kg/min
• Morphine 7 mcg/kg/h
• Morphine 10 mcg/kg/h
• epinephrine off
• Plan  transfer to IW
ICU Day 2
Time Blood Pressure MAP HR UO Medications
(mmHg) (bpm) (cc/h)
7 am 115/40 65 75 3.5 Dopamin + E
8 am 112/42 65,3 65 1.5 Dopamin + E
9 am 105/65 78 70 1.8 Dopamin + E
10 am 105/40 61,7 70 1.7 Dopamin + E
11 am 105/45 65 75 1.1 Dopamin
Transfer to IW
Cardiogenic
Shock
Clinical
Definition of
Cardiogenic
Shock

Source :
van Diepen S, Katz JN, Albert NM, Henry TD, Jacobs AK, Kapur NK, et al. Contemporary Management of Cardiogenic Shock. Circulation. 2017;136:e232-68.
Cardiogenic
Shock

 Cardiogenic shock (CS) is a common cause of mortality, and


management remains challenging despite advances in
therapeutic options.
 CS is caused by severe impairment of myocardial
performance that results in diminished cardiac output, end‐
organ hypoperfusion, and hypoxia
 CS complicates 5% to 10% of cases of acute MI and is the
leading cause of death after MI.
Diagnosing
Cardiogenic
Shock

 Frank or Relative hypotension (BP < 80-90 mmHg or reduction


MAP of 30 mmHg)
 Inadequate cardiac index
 Elevated EDP on the right (10-15 mmHg) and/or the left (>18
mmHg)
 Evidence of end-organ hypoperfusion

Source: Mann. Zipes. Libby. Braunwald's Heart Disease 12 th ed. Boston: SAUNDERS; 2021.
Clinical
Presentation
Pathophysiology
from MI to
Cardiogenic
Shock

Source : Mann. Zipes. Libby. Braunwald’s Heart Disease 12th ed. Boston: SAUNDERS; 2021.
Pathophysiology from MI to
Cardiogenic Shock

Impaired Systolic Function


Dyssynchrony  hypokinesis  Dyskinesis
(impaired CO)

Impaired Diastolic function


LVEDP (higher)  congestion  hypoxemia
ischaemia

Source : Mann. Zipes. Libby. Braunwald's Heart Disease. Boston: SAUNDERS; 2018.
Oliguria ↓ Cardiac output

Compensatory renin- Adequate or ↑ SVR Cathecolamine


aldosterone (ADH) ↑ blood volume compensatory release

Systemic and pulmonary


↑ Preload, stroke volume, and heart rate
edema

↑ Myocardial O2 requirement
Dyspnea
↓ Cardiac output
↓ Blood pressure ↓ Ejection fraction
Cold
extremities
Low BP ↓ Tissue perfusion

Ischemia
Impared cellular
↑ Lactate
metabolism

Myocardial
infarction
Sign of shock  Low systolic and diastolic blood pressure.
(Low cardiac output)
in the patient
 Weak Pulse and cold extremities.
(Low cardiac output and realocation)

 Oliguria
(Low cardiac output)
Cor - angiography
Findings
• LM : 30% mid stenosis, short LM
• LAD : osteal CTO, heavy calcified,
collateral flow from LCx
• LCx : 80% osteal stenosis, 70-80%
proximal stenosis , 80% distal
stenosis, 80% OM2 stenosis
• RCA : CTO from proximal with
collateral bridging
ECG Findings

1. ST elevasi pada v1
dan v2
2. T inverted pada
sadapan I dan AVL.
3. ST elevasi pada II,
III, AVF
Laboratory findings
PH 7.32
PCo2 35.2
PO2 154.9
SO2% 99
Laboratory ( July 3, 2021)
Hct 34
1. Slight decline of HCO3
Hb 11.2
Na 137
and PH
K 4.91
Cl 109.1 2. Slight decline of pCO2
Ca2+ 1.11
Mg2+ UC 3. Incline of pO2
Glu 185
Lac 5
HCO3- 21
4. Elevated Lactate
Patophysiology
from laboratory
findings

 Elevated lactate  sign of anaerob


metabolism
 Decline of PCO2  sign of compensatory of
decline HCO3  prevent acidosis metabolic.
 Incline of PO2  the use of controlled
ventilation.
Management of Cardiogenic Shock

CO = SV x HR

Preload Contractility

Afterload
Source : Thiele H, Ohman EM, Desch S, Eitel I, Waha S De. Clinical update Management of cardiogenic shock. Eur Heart J. 2015;36:1223–30
1. Intravenous fluid
2. Oxygenation and Ventilation
3. Vasopressor Support
Stabilization
and
Resuscitation
Strategy
Stabilization
and
1. Intravenous fluid
Resuscitation
 Fluid resuscitation strategy is a clinical challenge
Strategy
in the early management.
 In right‐sided heart failure, right atrial pressures
and pulmonary artery wedge pressures are poor
predictors of fluid response.
 If hypovolemia is present, conservative boluses
of crystalloids (250–500 mL) are reasonable
while the patient is being stabilized for cardiac
catheterization.
Stabilization and Resuscitation Strategy
2. Oxygenation and Ventilation
 Continuous pulse oximetry should be used
to monitor for respiratory compromise.
 Oxygen goals vary depending on patient
comorbidities, but in the acute care setting
blood oxygen saturations of >90% are
acceptable.
 When non‐invasive forms of oxygenation
and ventilation are inadequate, invasive
ventilation is required.
Stabilization and Resuscitation Strategy
3. Vasopressor Support
 Vasopressors should be titrated to a mean
arterial pressure with a typical goal of
>65 mm Hg.
 When using these agents invasive blood
pressure monitoring is required as they can
rapidly induce hypotension
Source :van Diepen S, Katz JN, Albert NM, Henry TD, Jacobs AK, Kapur NK, et al. Contemporary Management of Cardiogenic Shock. Circulation. 2017;136:e232-68.
Vasopressor and Inotropes

Vasocon-
Vasopressor SVR ↑ MAP ↑
striction ↑

Cardiac Cardiac
Inotropes
contractility ↑ output ↑
Hemodynamic
Monitoring
 Goals of hemodynamic monitoring should be focused
on hemodynamic modification to produce stable vital
signs and adequate tissue perfusion.
 Continuous blood pressure monitoring with an arterial
line, telemetry, continuous pulse oximetry,
temperature, respiratory rate, and urinary output are
rudimentary parameters to monitor.
Mechanical Circulatory Support
Options for acute percutaneous MCS include:
 the intra‐aortic balloon pump (IABP),
 axial flow pumps (Impella LP 2.5, Impella CP),
 left atrial‐to‐femoral arterial ventricular assist
devices (Tandem Heart)
 venous‐arterial extracorporeal membrane
oxygenation (ECMO)
Intra Aortic Balloon Pump

• Can be placed preoperative and


intraoperatively.
• Indication inadequate performance despite
of max dose of dopamine (10 mg/kgbb/min).
• Prophylaxis IABP low LVEF, Acute MR,
ventricular rupture
• Contraindication IABP  aortic regurgitation,
aortic dissection, PAD.
Intra Aortic Balloon Pump
Intra Aortic Balloon Pump
 Assist cardiac cycle by
 Assist diastolic by inflation of balloon cause the
increasing of coronary perfusion rate  oxygen supply
increased.
 Assist systolic by deflation of balloon cause reduction
in afterload  oxygen supply decrease.
Conclusion

 Diagnosis of the patient are CAD 3VD, Hypertension,


HHD with HF
 Patient with low EF is more likely to have CS post
surgery
 One of the most common cause of CS is perioperative
myocardial infarction
 Several treatments available for patient with CS post surgery
are the use of fluid, ventilation, inotropic-vasoactive agents,
and IABP.
Thank You

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