Monitoring

of Cardiogenic
Shock in ICCU: Non Invasive to
Invasive
dr. Wayan Aryadana, SpJP (K)
Frequency
of CS in HF
Registries
 Mortality rates from different causes of CS from SHOCK Registry
Hochman et al. CS complicating acute MI. JACC Vol. 36, No. 3, Suppl A
 ALARM-HF vs EHS-HF II: In-Hospital Mortality
according to ESC Classification of AHFS
Sample = EHS HF II (3,580), All ALARM-HF patients (4,953)
45%
40% 40%
40%
35%
30%
25%
20%
15% 12% 13%
11% 10%
10% 7% 7%
6%
5% 2%
0%
EHS HFAll AHFADCHF De ADHF P-OE Cardio EHS HF HT AHF RV HF
II NOVO shock II C-
AHF Shock

Mebazaa A, Parissis J, Porcher R, et al. Intensive Care Med 2011 Feb;37(2):290-301

 EuroHeart Survey HFII: Long-term mortality in the
different clinical classes of AHF

Mebazaa A, Parissis J, Porcher R, et al. Intensive Care Med 2011 Feb;37(2):290-301

Definition of Cardiogenic Shock

Van Diepen et al. Circulation. 2017;136:e232–e268

 Etiology of Cardiogenic Shock
Cardiac output not adequate for metabolic demands of body

• The most common etiology of CS is ACS with or without mechanical

complication (80 %)
• The other causes of CS include:
o Severe decompensation of chronic heart failure
o Valvular disease
o Cardiac tamponade
o Cardiac disrhythmia
o Myocarditis
o Pulmonary embolism
Mebazaa et al. Intensive Care Med (2016) 42:147–163
Mebazaa et al. Intensive Care Med (2016) 42:147–163
 Current understanding suggests that 3 aspects of treatment should be
addressed to potentially improve chances of survival:
1. Circulatory support
To treat tissue hypo-perfusion and avoid accumulation of lactic
acid and other metabolic products of anaerobic metabolism.
2. Ventricular unloading
Normalizing filling pressures, in addition to improving CO, &
minimize the remodeling process and favorably impact prognosis;
therefore, using and adjusting devices by their effect on PCWP or
central venous pressure might be beneficial.
3. Myocardial perfusion
Revascularization is essential, and allowing for higher DBP and
lower LVEDP may shift the coronary pressure gradient toward
increased myocardial perfusion.

Hemodynamics in Cardiogenic Shock

Clinical Evaluation of Cardiogenic Shock
• Increased preload caused by pump failure
o Tahypneic, dyspnea, rales
o Distended JVP
o Congestion of visceral organ (hepatomegaly) and pedal edema
• Decreased organ perfusion
o Reduced cerebral perfusion (altered mental status; restlessness, agitation)
o Cool, clammy skin
o Reduced urine output
o Increased heart rate / dysrhythmia
o Weak peripheral arterial pulse
o Hypo- or hyperthermic
o Hypotension
Clinical Evaluation of Cardiogenic Shock

High jugular venous pressure

Peripheral Vasoconstriction
Haemodynamic findings:
Low cardiac output (C.I < 2.2 L/min)
High PCW-pressure (>18 mmHg)
High systemic vascular resistence
Pulmonary congestion/oedema
A severity scoring system for risk assessment of patients with
cardiogenic shock: A report from the SHOCK Trial and Registry

Sleeper et al. Am Heart J 2010;160:443-50

 Diuresis monitoring
• Diuresis monitoring (urine output on a given time frame) provide
relevant information on the renal function and hydration status of
the patient, helping to guide fluid and diuretic therapy
• A normal urine output ranges between 0.5–1 mL/kg/h, while the
presence of oliguria, a diuresis of <500 mL over a 24-hour period,
might indicate a decreased renal perfusion
• The presence of oliguria in critically ill subjects with AMI is a sensitive
marker of acute kidney injury, and it has been shown to be linked to
higher mortality rates in these patients

Barcan et al. Journal of Cardiovascular Emergencies 2017;3(2):61-71

 Diuresis monitoring
• A mean arterial pressure (MAP) of over 65 mmHg is required to avoid
organ failures, including renal dysfunction
• Additional cause of reduced diuresis is contrast-induced
nephropathy, a complication of contrast media administration during
coronary angiography and the third most common cause of hospital-
acquired acute renal injury

Barcan et al. Journal of Cardiovascular Emergencies 2017;3(2):61-71

 Evaluation of Body Temperature
• Fever is a negative prognostic factor that can indicate elevated
systemic inflammation or infection, while a decreased peripheral
temperature is a sign of decreased tissue perfusion.
• Body temperature is assessed through peripheral (tympanic
membrane, temporal artery, axillary, or oral), or central (pulmonary
artery catheter, urinary bladder, esophageal, or rectal) methods.
• However, a meta-analysis on 75 studies stated that peripheral
thermometers should not be used if the body temperature will
influence the therapeutic management, as they do not present an
acceptable clinical accuracy
Barcan et al. Journal of Cardiovascular Emergencies 2017;3(2):61-71
 Pulse oximetry
• The evaluation of arterial oxygen saturation with the use of pulse
oximetry is used for noninvasively detecting the ventilatory status of
the patients in the CCU
• Pulse wave in the fingernail, requiring a systolic blood pressure of
more than 85 mmHg
• Clinical situations in which the patients present hypovolemia, low
blood pressure, CS, or other types of shock associated with decreased
tissular perfusion, can impair the evaluation of ventilatory status
using this method

Barcan et al. Journal of Cardiovascular Emergencies 2017;3(2):61-71

 ECG Monitor
• Early identification of arrhythmias and conduction disturbance as
well as ST-segment and T-wave changes
• More than three ischemic events or one hour repeated ischemic
event on the continuous ECG tracing records indicate a three-vessel
coronary artery disease or severe coronary atherosclerosis

Barcan et al. Journal of Cardiovascular Emergencies 2017;3(2):61-71

 Echocardiography
Echocardiography should be performed immediately after presentation
• Rule out mechanical complications
• Evaluate the etiology of CS
o Evaluate myocardial segment, ventricular septal rupture, severe
MR, tamponade/free wall rupture, aortic dissection
• Assess cardiac function
o Evaluate LV and RV function, stroke volume, cardiac output
Repetitive echocardiography should be used to monitor
hemodynamic evolution
Menon V and Hochman J. Heart 2002;88:531–537
 Stroke volume = End diastolic volume – End systolic volume
LV volumes estimated by Simpson’s method, which is the summation of the volume of stacked
cylinders within the LV at end- diastole and end-systole

150 ml - 52 ml= 98 ml
 Flow (stroke volume) = Area * Velocity
Doppler Method CO=Stroke volume * Heart rate
CI=Cardiac output / BSA
Area of left ventricular outflow tract
Obtain LVOT dimension in parasternal long axis view

Flow Velocity at LVOT

Pulsed wave Doppler at LVOT
in apical 5 chamber view

Velocity time integral 25 cm

D=2.1 cm

Simplified formula= (2.1cm)2 * 0.785

3.46cm X 25cm = 87 cm3

2
Assessment of fluid status

ESC textbook of intensive and acute cardiovascular care.

 Laboratory Investigation

Van Diepen et al. Circulation. 2017;136:e232–e268

 Invasive arterial blood pressure monitoring
• The inherent hemodynamic instability and high prevalence of
vasopressor use in CS merit invasive arterial blood pressure
monitoring to guide drug titration
• A mean arterial pressure (MAP) of over 65 mmHg is required to avoid
organ failures, including renal dysfunction
• Arterial catheters also allow repetitive blood gas analyses to monitor
respiratory support therapy
• In addition, repeated serum lactate measurements, which are
required to assess improving or worsening organ hypo-perfusion, can
be obtained through arterial catheter.
Mebazaa et al. Intensive Care Med (2016) 42:147–163
 Invasive arterial blood pressure monitoring
• The invasive evaluation of blood pressure is achieved by placing a
catheter in a superficial artery (radial, femoral, or pedis artery),
which is connected to a transducer that transforms the mechanical
pulse wave into a pressure curve.
• Analysis of the invasive arterial pressure waveform allows the
estimation of CO and ventricular ejection fraction, and the invasive
measurements are performed simultaneously with the noninvasive
evaluation of blood pressure.

Barcan et al. Journal of Cardiovascular Emergencies 2017;3(2):61-71

Asian Intensive Care International. (2009) Intensive Care Conference, Hong Kong
 *Liljestrand and Zander Formula

Predictive of LV Function

Koenig, et al. Biomed Sci Instrum. 2015 ; 51: 85–90

S.A. Esper, M.R. Pinsky / Best Practice & Research Clinical Anaesthesiology 28 (2014) 363e380
 Central venous catheter
• Can be considered to support the administration of vasoactive
medications and to facilitate monitoring of CVP & mixed central
venous oxygen saturation, which may be helpful in determining the
adequacy of tissue oxygen delivery
• An increased CVP is suggestive of decreased ventricular function,
increased venous return, increased systemic vascular resistance or
elevated intrathoracic pressures.

Mebazaa et al. Intensive Care Med (2016) 42:147–163

 Central venous catheter

• A marked rise in CVP with fluid challenge indicates a failing ventricle

Peter McCanny. European society of invasive care monitoring. 2013

Fluid challenge
responsiveness
 Pulmonary artery catheter
• Although clinical trials have shown no benefit with the routine use of PAC
hemodynamic monitoring, observational studies in CS populations have
been mixed, and the PAC remains a potentially important diagnostic and
management tool for these individuals
• Hemodynamic data provided by a PAC can confirm the presence and
severity of CS, involvement of the RV, pulmonary artery pressures and
transpulmonary gradient, and vascular resistance of the pulmonary and
systemic arterial beds
• In addition, a PAC may provide CS prognostic information such as CI and
cardiac power and enables clinicians to monitor responses to therapeutic
interventions
• Although noninvasive devices may be used, their reliability in this setting
has not been well studied
Mebazaa et al. Intensive Care Med (2016) 42:147–163
 Pulmonary artery catheter
• These hemodynamic data in turn can guide the therapeutic choices
through volume optimization, vasodilators, vasopressors, and
inotropes as appropriate and the critical decision regarding whether
to provide mechanical circulatory support (MCS).

Mebazaa et al. Intensive Care Med (2016) 42:147–163

Hemodynamic parameters in PAC
Swan-Ganz Catheter: Differentiating Types of Shock