SHOCK CARDIOGENIC

Bag. Anestesiologi dan Therapy Intensive Care

Fakultas Kedokteran Universitas Islam Sumatera Utara
2014
Dr Dody
Firmanda,SpAn

DEFINISI
Gangguan dari perfusi jaringan yang
terjadi akibat adanya
ketidakseimbangan antara suplai
oksigen ke sel dengan kebutuhan
oksigen dari sel tersebut.
Semua jenis shock mengakibatkan
gangguan pada perfusi jaringan yang
selanjutnya berkembang menjadi
gagal IT
sirkulasi
akut
atau
disebut
juga
IS NOT LOW BLOOD
sindroma shock
PRESSURE !!!
IT IS HYPOPERFUSION..

Shock adalah kondisi saat transport oksigen

(DO2, delivery O2) ke jaringan gagal memenuhi
kebutuhan metabolik di jaringan tersebut.

Shock
Always a symptom of primary cause
Inadequate blood flow to meet tissue oxygen demand
May be associated with hypotension
Associated with signs of hypoperfusion: mental status
change, oliguria, acidosis

Classification of shock states

Type of shock

Primary mechanism

Clinical causes

Hypovolemic

Volume loss

Exogenous
Blood loss due to hemorrhage
Plasma loss due to burn, inflammation
Fluid and electrolyte loss due to vomiting, diarrhea,
dehydration, osmolal diuresis [diabetes]
Endogenous
Extravasation due to inflammation, trauma, anaphylaxis,
snake venom, pheochromocytoma

Cardiogenic

Pump failure

Myocardial infarction
Heart failure
Arrhythmia
Intracardiac obstruction

Distributive [vasomotor
dysfunction]
. High or normal
resistance

Expanded venous capacitance

[pooling], CO normal or low

Hypodynamic septic shock due to gram-negative enteric bacillary

Spinal shock, Narcotic over dose, barbiturate intoxication

Arteriovenous shunting
CO normal or high
Extracardiac obstruction of
main channel of blood flow

Pneumonia, peritonitis, abscess, reactive hyperemia

. Low resistance
Obstructive

Vena caval obstruction, pericarditis [cardiac tamponade]

pulmonary embolism, aorta dissecting aneurysm
Weil, MH et al : Cardiovascular System failure. In Principles and practice of
emergency medicine. Schwartz. GR [ed] WB. Saunders 1986

6/17/16

Approach to various etiologic types of shock

Hemorrhagic

Cardiogenic

Traumatic

Septic

Sign & Symptoms

Sign & Symptoms

Sign & Symptoms

Pallor, fainting
Skin clammy, cold
Tachycardia
Oliguria
Collapse

Pallor, fainting
Skin clammy, cold
Arrhythmias
Oliguria
Collapse

Sign & Symptoms

History & Physical

evidence of injury
Oliguria
Tachycardia
Collapse

Fever, chills
Skin warm
Tachycardia
Oliguria
Altered mental status
Collapse

Laboratory

Laboratory

Laboratory

Laboratory

X-Rays, CT-scan

[+] smears & culture

Pathophysiology

Pathophysiology

Hct, Hb
Pathophysiology

Blood volume

Cardiac enzymes
ECG
Pathophysiology

Cardiac output

Direct injury to organ

Peripheral resistance

Therapy

Therapy

Therapy

Therapy

1. Fluids
2. Blood
3. Control Bleeding

1. Antiarrhythmic
2. Vasopressors
3. Vasodilators

1. Repair injury
2. Fluids
3. Blood

1. Antibiotics
2. Fluids
3. Drain abscess

Shoemaker, Textbook of Critical Care, third ed. 1995

6/17/16

PATHOPHYSIO, CONTN

Cellular hypoxia /
anaerobic
metabolism

Survival / delayed
morbidity / mortality

ATP production / lactic acidosis

Intervention / stabilization

Cellular function
impaired
Continued volume loss
Membrane porosity

Irreversibl
e shock
intervention
No. intervention

6/17/16

DEATH

Movement of
fluid from
intravascular to
interstitial
spaces

Lysozymal
leakage
Cellular autodigestion

PRE-LOAD

CONTRACTILITY

STROKE VOLUME

CARDIAC OUTPUT

HEART-RATE

TOTAL
PERIPHERAL
RESISTANCE

BLOOD PRESSURE
6/17/16

AFTER-LOAD

CARDIAC OUTPUT
Cardiac output = stroke volume X heart rate
Stroke volume preload, contractility & afterload
Venous return (preload) blood volume,posture &venous tone
Venous tone control of the sympatheticnervous system

CARDIAC OUTPUT
FrankStarling relationship between the left
ventricularend-diastolic pressure (LVEDP) and
stroke volume (SV)
The FrankStarling curve mechanism allows a
ventricle to match its output (stroke volume)to
the volume of blood that enters it (the preload)

OXYGEN TRANSPORT
DO2 = CAO2 X CO
VO2 = [CAO2-CVO2] X CO
CAO2 = SAO2 X HB X 1.34
CVO2 = SVO2 X HB X 1.34
SHOCK,
6/17/16

DO2 < VO2

CARDIOGENIC SHOCK

Decreased contractility

Increased filling pressures, decreased LV stroke work,

decreased cardiac output

Increased systemic
vascular resistance compensatory

PATOFISIOLOGI DARI RESPON

TUBUH TERHADAP SHOCK

Respon Neuroendokrin
Respon Hemodinamik
Respon Metabolik

FEAR

Neuroendocrine Respons

Stimulation of limbic
area of brain
Increased:
hypothalamic,
adrenomedullary
adrenocortical activity

R atrium

low-pressure stretch
receptors
HYPOVOLEMIA

Aorta/carotids

Adrenal cortex
Cortisol release

Renal
Renin release
LOSS OF TONIC
INHIBITION OF
CENTRAL AND
SYMPATHETIC
NERVOUS SYSTEMS

High-pressure
baroreceptors

Pituitary gland
ACTH, ADH and GH release
Adrenal gland (medulla)
Epinephrine/norepinephrine
release

Angiotensin II
Decreased renal
perfusion
Adrenal cortex

Aldosterone release

RESPON HEMODINAMIK

Mekanisme untuk memperbaiki keseimbangan

kardiovaskular

Redistribusi aliran darah

Peningkatan cardiac output
Memperbaiki volume intravaskular

RESPON HEMODiNAMiK
REDISTRIBUSI ALIRAN DARAH

HYPOTENSION
STIMULASI NEUROENDOKRIN

BLOOD FLOW PROTECTED

Heart
Brain
Adrenal/pituitary gland

BLOOD FLOW DECREASED

Skin
Muscle
Splanchnic circulation

Limited to 180 beats/min

before decreased CO due to
decreased diastolic filling
time

CARDIAC OUTPUT = HR X SV

Increased
contractility
Sympathetic n. system
Catecholamine
release

Increase EDV via:

Venoconstriction
Arteriolar constriction
Renal reabsorption

 Transcapillary refill phase

1. Decreased capillary pressure caused by hypotension

2. Sympathetic increase in precapillary arteriolar constriction

Decrease capillary hydrostatic pressure promotes passage of fluid

from interstitium to intravascular space

Plasma protein restitution phase

Increased plasma osmolarity due to mainly hepatic release of

glucose, pyruvate, amino acids, etc.
Increased interstitial osmolarity
Increased interstitial volume and pressure
Transcapillary movement of albumin into intravascular space

HAEMODYNAMIC RESPONSES
Venoconstriction

Sympathetic n. system (SNS)

Catecholamines (CA)
Angiotensin II (ATII)
ADH

Reduced venous
capacitance

Arteriolar constriction
SNS, CA, ATII, ADH

Increased
ventricular
filling P

Decreased capillary P
Fluid shift from interstitium into
vascular compartment

Restoration of
blood volume

SV

Increased distal tubular

reabsorption
Aldosterone, ADH
Increased proximal tubular
reabsorption
SNS, CA, ATII
Increased myocardial
contractility
SNS, CA
Increased heart rate
SNS, CA
Increased SVR due to
arteriolar construction
SNS, CA, ATII, ADH

CO
Increased ventricular
ejection fraction

BP
SVR

RESPON METABOLIK
Hyperglikemia
Mobilisasi lemak
Katabolisme/pemecahan Protein
Peningkatan sintesis urea
Peningkatan asam amino aromatik

Penurunan sintesis reactan fase akut

Peningkatan osmolalitas ekstrasel

RESPON METABOLIK
Release of:
Catecholamines
Cortisol
Glucagon
Growth hormone

HYPERGLYCEMIA
Impaired
peripheral
glucose uptake

Glycogen
breakdown
Conversion
of a.a. to
glucose

Breakdown of
skeletal muscle
into a.a.

EFEK SHOCK PADA TINGKATAN SEL

LOW-FLOW,
POOR PERFUSION

HYPOXIA
ACIDOSIS

ANAEROBIC
METABOLISM

DECREASED CELLULAR
ENERGY EFFICIENCY

EFEK SHOCK PADA TINGKATAN SEL

CELL MEMBRANE FAILURE:
DIRECT
Endotoxin
Complement
INDIRECT
Failure to maintain normal Na+, K+ or Ca2+ gradient
Decreased oxidative phosphorylation

L
CELTH
DEA

OSMOTIC
GRADIENT

Na+ entry
into cell

Water entry
into cell

CELLULAR
EDEMA

IMPAIRED
INTRACELLULAR
METABOLISM

EFEK SHOCK PADA TINGKATAN

ORGAN
Kidney

Oliguric renal failure

High output renal failure

Liver

Liver failure

GI tract

Failure of intestinal barrier (sepsis, bleeding)

Lung

Capillary leak associated with or caused by sepsis and

infection

PRINSIP RESUSITASI

Mempertahankan ventilasi
Meningkatkan perfusi
Terapi penyebab

MAINTAIN VENTILATION
Especially in:

Increased oxygen
demand

Sepsis
Hypovolemia
Trauma

Hyperventilation

Respiratory fatigue

Respiratory failure
Respiratory acidosis, lethargy-coma, hypoxia

Diversi blood flow from

vital organ

Organ injury

TREATMENT OF RESPIRATORY FAILURE

Hypovolemia (blood loss)

Decreased CO

Decreased oxygen delivery, increased

oxygen requirement

Metabolic acidosis, hypoxemia tachypnea

TREATMENT:

Primary resuscitation
Oxygen
Mechanical ventilation if needed

TREATMENT CONCEPT OF SHOCK

ENHANCING PERFUSION / OXYGEN DELIVERY

DO2 = CO x CaO2
Arterial O2
content

Cardiac
output

Oxygen delivery/DO2 = HR X SV X Hb X S02 X 1.34 + Hb X paO2

Inotropes

Fluids

Transfuse

Partially
dependent on
FIO2 and
pulmonary
status

THERAPEUTIC GOALS IN SHOCK

Increase O2 delivery

Optimize O2 content of blood

Improve cardiac output and

blood pressure
Match systemic O2 needs with O2 delivery

Reverse/prevent organ hypoperfusion

CARDIOGENIC SHOCK
MANAGEMENT

Treat arrhythmias

Diastolic dysfunction may

require increased filling
pressures

Vasodilators if not hypotensive

Inotrope administration

CARDIOGENIC SHOCK
MANAGEMENT

Vasopressor agent needed if

hypotension present to raise
aortic diastolic pressure

Consultation for mechanical

assist device

Preload and afterload reduction

to improve hypoxemia if blood
pressure adequate

FLUID THERAPY

Crystalloids

Lactated Ringers solution

Normal saline

Colloids

Hetastarch

Albumin

Gelatins

Packed red blood cells

Infuse to physiologic endpoints

FLUID THERAPY

Correct hypotension first

Decrease heart rate

Correct hypoperfusion abnormalities

Monitor for deterioration of oxygenation

INOTROPIC / VASOPRESSOR AGENTS

Dopamine

Low dose (2-3 g/kg/min) mild inotrope

plus renal effect

Intermediate dose (4-10 g/kg/min)

inotropic effect

High dose ( >10 g/kg/min) vasoconstriction

Chronotropic effect

INOTROPIC AGENTS

Dobutamine

5-20 g/kg/min

Inotropic and variable chronotropic

effects

Decrease in systemic vascular

resistance

INOTROPIC / VASOPRESSOR
AGENTS

Norepinephrine

0.05 g/kg/min and titrate to

effect

Inotropic and vasopressor

effects

Potent vasopressor at high

doses

INOTROPIC / VASOPRESSOR AGENTS

Epinephrine

Both and actions for inotropic

and vasopressor effects
0.1 g/kg/min and titrate
Increases myocardial O2
consumption

HOW MUCH FLUID TO GIVE?

Some measure of intravascular filling

Pressure (CVP or PAOP)

Some assessment of risk of pulmonary oedema and capillary leak

Pulmonary gas exchange (PaO2:FiO2)
Requirement for positive pressure (PEEP)
Chest X-ray

Some assessment of response to treatment

Changes in acid base balance, lactate
Measurement of cardiac output

WHAT DO YOU NEED TO KNOW WHEN

YOU RESUSCITATE A PATIENT IN
Arterial blood pressure
SHOCK?

Urine output
Systemic acidbase balance (pH, SBE, lactate)
Some clinical assessment of tissue perfusion

warm and well perfused or cold and shut down

Some measurement of global blood flow and tissue

perfusion

Cardiac output or cardiac index

Arterial oxygen delivery, oxygen uptake index
Mixed venous saturation and PvO2

Cardiogenic
Shock

Distributive
Shock

Inotropes
(Dob,Dop,Adr,Amr)

Pump =
Heart

Pipe = Vascular

Release
tamponade,etc

Vasopressor ( NE,PE,Adr,Dop)

Blood Pressure

Cardiac Output x SVR

Obstructive
Shock
Volume =
Blood

Fluids

Hypovolemic
Shock

SUMMARY
Shock is an altered state of tissue perfusion severe enough
to induce derangements in normal cellular function
Neuroendocrine, hemodynamic and metabolic changes work
together to restore perfusion
Shock has many causes and often may be diagnosed using
simple clinical indicators
Treatment of shock is primarily focused on restoring tissue
perfusion and oxygen delivery while eliminating the cause