Diagnosis and Management of Shock

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

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 sirkulasi akut atau disebut juga sindroma shock IT IS NOT LOW BLOOD PRESSURE !!! IT IS HYPOPERFUSION..

Shock Categories

Cardiogenic
Hypovolemic Distributive Obstructive

Cardiogenic Shock

Decreased contractility
Increased filling pressures, decreased LV stroke work, decreased cardiac output Increased systemic vascular resistance compensatory

Hypovolemic Shock

Decreased cardiac output

Decreased filling pressures Compensatory increase in systemic vascular resistance

Distributive Shock

Normal or increased cardiac output

Low systemic vascular resistance Low to normal filling pressures

Sepsis, anaphylaxis, neurogenic, and acute adrenal insufficiency

Obstructive Shock

Decreased cardiac output Increased systemic vascular resistance Variable filling pressures dependent on etiology Cardiac tamponade, tension pneumothorax, massive pulmonary embolus

CARDIOGENIC
OBSTRUCTIVE O2 O2 SEPTIC

O2
HYPOVOLEMIK

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

Hypovolemic Shock Management

Volume resuscitation crystalloid, colloid Initial crystalloid choices Lactated Ringers solution Normal saline (high chloride may produce hyperchloremic acidosis) Match fluid given to fluid lost Blood, crystalloid, colloid

Distributive Shock Therapy

Restore intravascular volume

Hypotension despite volume therapy

Inotropes

and/or vasopressors

Vasopressors for MAP < 60 mm Hg

Adjunctive interventions dependent on etiology

Obstructive Shock Treatment

Relieve obstruction

Pericardiocentesis
Tube thoracostomy Treat pulmonary embolus

Temporary benefit from fluid or inotrope administration

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 and variable chronotropic effects in systemic vascular resistance

Inotropic Decrease

Inotropic / Vasopressor Agents

Norepinephrine
0.05

g/kg/min and titrate to effect

Inotropic
Potent

and vasopressor effects

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

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

Pediatric Considerations

BP not good indication of hypoperfusion Capillary refill, extremity temperature better signs of poor systemic perfusion Epinephrine preferable to norepinephrine due to more chronotropic benefit Fluid boluses of 20 mL/kg titrated to BP or total 60 mL/kg, before inotropes or vasopressors

Pediatric Considerations

Neonates consider congenital obstructive left heart syndrome as cause of obstructive shock Oliguria <2 yrs old, urine volume <2 mL/kg/hr Older children, urine volume <1 mL/kg/hr

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 Shock?

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

warm and well perfused or cold and shut down

Cardiac output or cardiac index

Some measurement of global blood flow and tissue perfusion

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

Cardiogenic Shock
Inotropes (Dob,Dop,Adr,Amr) Release tamponade,etc

Distributive Shock
Vasopressor ( NE,PE,Adr,Dop)

Pump = Heart

Pipe = Vascular

Blood Pressure

Obstructive Shock
Volume = Blood

Cardiac Output x SVR

Fluids

Hypovolemic Shock

PATOFISIOLOGI DARI RESPON TUBUH TERHADAP SHOCK

Respon Neuroendokrin Respon Hemodinamik Respon Metabolik

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

Neuroendocrine Respons
Adrenal cortex
Cortisol release

R atrium
low-pressure stretch receptors HYPOVOLEMIA LOSS OF TONIC INHIBITION OF CENTRAL AND SYMPATHETIC NERVOUS SYSTEMS

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

Aorta/carotids
High-pressure baroreceptors

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

Increase EDV via:

Venoconstriction Arteriolar constriction Renal reabsorption

Sympathetic n. system Catecholamine release

Memperbaiki volume darah

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

Decreased capillary P Fluid shift from interstitium into vascular compartment Increased distal tubular reabsorption Aldosterone, ADH Increased proximal tubular reabsorption SNS, CA, ATII

Increased ventricular filling P Restoration of blood volume

SV CO
Increased ventricular ejection fraction

Increased myocardial contractility SNS, CA

Increased heart rate SNS, CA Increased SVR due to arteriolar construction SNS, CA, ATII, ADH

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

Glycogen breakdown

HYPERGLYCEMIA

Conversion of a.a. to glucose

Impaired peripheral glucose uptake

Breakdown of skeletal muscle into a.a.

METABOLIC RESPONS
Decreased blood volume

Decreased CO

Cellular hypoperfusion and hypoxia

Anaerobic glycolysis Pyruvate converted to lactic acid

METABOLIC ACIDOSIS

METABOLIC RESPONS
Release of: Catecholamines Cortisol Glucagon

LIPOLYSIS

INCREASE IN PLASMA FREE FATTY ACIDS

EFEK SHOCK PADA TINGKATAN SEL

LOW-FLOW, POOR PERFUSION

HYPOXIA
ACIDOSIS

ANAEROBIC METABOLISM

DECREASED CELLULAR ENERGY EFFICIENCY

Glucose breakdown. (A) Stage one, glycolysis, is anaerobic (does not require oxygen). It yields pyruvic acid, with toxic by-products such as lactic acid, and very little energy. (B) Stage two is aerobic (requires oxygen). In a process called the Krebs or citric acid cycle, pyruvic acid is degraded into carbon dioxide and water, which produces a much higher yield of energy.

EFEK SHOCK PADA TINGKATAN SEL

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

TENSION PNEUMOTHORAX

PRINSIP RESUSITASI

Mempertahankan ventilasi
Meningkatkan perfusi Terapi penyebab

MAINTAIN VENTILATION
Especially in: Sepsis Hypovolemia Trauma

Increased oxygen demand

Hyperventilation Diversi blood flow from vital organ

Respiratory fatigue

Respiratory failure Respiratory acidosis, lethargy-coma, hypoxia

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
Cardiac output
Arterial O2 content

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

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