SHOCK EXTENDED VERSION
• Universitas Prima Medan
dr. Edlin SpAn
How to Diagnose
Universitas Prima Medan
dr. Edlin SpAn
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
CATEGORIES OF SHOCK
1. CARDIOGENIC
2. HYPOVOLEMIC
3. DISTRIBUTIVE
4. 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,
toxicologic
and adrenal crisis
OBSTRUCTIVE SHOCK
• Decreased cardiac output
• Increased systemic vascular resistance
• Variable filling pressures dependent on
etiology
• Cardiac tamponade, tension
pneumothorax, massive pulmonary
embolus
Shock Made Simple….
Cardiogenic Hypovolemic Obstructive Distributive
Analogy Gas Pump Not Working Not Enough Gas Gas Blockage Broken Gas Hose
Depleted Intravascular Obstructing Tissue Vascular Permeability and
Practical Poor Cardiac Output
Volume Perfusion or/ Dilation
ACS, CHF, Dysrithmia,
Dehydration, Vomiting and Sepsis, Anaphylaxis,
Valvulopathy, Drug PE, Cardiac Tamponade,
Causes Diarrhea, GI, Bleed, Neurogenic, Adrenal
Toxicity, Myocarditis, Pneumothorax
Hemmorrhage Crisis, Toxicologic
Myocardial, Contusion
Blood / Urine Cultures,
EKG, Cardiac Labs, IVC USG, Labs, Cardiac USG, CXR, D-
Diagnostic Workup LActate, Blood Gas, CXR,
Cardiac USG, CXR Coagulation dimer, CT Scan Chest
Labs
PCI, Inotropes, Valvular Fluids, Inopressors, Blood Chest Tube, PCC, Heparin,
Fluids, Antibiotics,
Therapeutic Options Repair, Medical PRoducts, Control Thrombolytics,
Steroids, Vasopressors
Management Bleeding Inopressors
Pathophysiology of Shock
Universitas Prima Medan
dr. Edlin SpAn
Pathophysiology of Body Response to Shock
• Neuroendocrine response
• Hemodynamic response
• Metabolic response
Neuroendocrine Response
R atrium RENAL
low-pressure stretch Renin Release
receptors
Loss of Tonic Inhibition
PITUITARY GLAND
of Central and
ACTH, ADH & GH release
Hypovolemia Symphathetic Nervous
Systems
ADRENAL GLAND
Aorta/carotids (MEDULLA)
high-pressure Epinephrine/norepinephrine
baroreceptors release
Hemodynamic Response
Mekanisme untuk memperbaiki keseimbangan kardiovaskular :
1. Redistribusi aliran darah
2. Peningkatan “cardiac output”
3. Memperbaiki volume intravaskular
Hemodynamic Response
1. REDISTRIBUSI ALIRAN DARAH
HYPOTENSION
HYPOTENSION
STIMULASI
STIMULASI NEUROENDOKRIN
NEUROENDOKRIN
BLOOD
BLOOD FLOW
FLOW PROTECTED
PROTECTED :: BLOOD
BLOOD FLOW
FLOW DECREASED
DECREASED ::
•• Heart
Heart •• Skin
Skin
•• Brain
Brain •• Muscle
Muscle
•• Adrenal
Adrenal // Pituitary
Pituitary Gland
Gland •• Splanchnic
Splanchnic Circulation
Circulation
Hemodynamic Response
2. PENINGKATAN CARDIAC OUTPUT
CARDIAC OUTPUT = HR X SV
Increased contractility
Increased EDV :
Venoconstriction
Sympathetic n. system
Arteriolar constriction
Catecholamine release
Renal reabsorption
Hemodynamic Response
3. MEMPERBAIKI VOLUME INTRAVASKULAR
A. Transcapillary refill phase
• Decreased capillary pressure caused by hypotension
• Sympathetic increase in precapillary arteriolar constriction
Decrease capillary hydrostatic pressure promotes passage of fluid from interstitium to intravascular space
B. 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
Hemodynamic Response
VENOCONSTRICTION
Sympathetic n. system (SNS)
Reduced venous
Catecholamines (CA)
Angiotensin II (ATII) capacitance
ADH
ARTERIOLAR CONSTRICTION Incresed ventricular
SNS, CA, ATII, ADH filling P
Decreased Capillary {P
Fluid shift from interstitium into vascular Restoration of
compartment Blood Volume
Increased distal tubular reabsorption SV
Aldosterone, ADH
Increased proximal tubular reabsorption
SNS, CA, ATII
CO
Increased myocardial contractility Incresed ventricular
SNS, CA ejection fraction BP
Increased Heart Rate
SNS, CA SVR
Increased SVR due to Arteriolar Construction
SNS, CA, ATII, ADH
METABOLIC RESPONSE
● Hyperglikemia
● Mobilisasi lemak
● Katabolisme/pemecahan Protein
1. Peningkatan sintesis urea
2. Peningkatan asam amino aromatik
● Penurunan sintesis reactan fase akut
● Peningkatan osmolalitas ekstrasel
METABOLIC RESPONSE
Release of:
Catecholamines Glycogen
Cortisol breakdown
Glucagon
Growth hormone
Conversion of a.a.
to glucose
HYPERGLYCEMIA
Impaired peripheral Breakdown of
glucose uptake skeletal muscle
into a.a.
METABOLIC RESPONSE
Decreased METABOLIC
blood volume ACIDOSIS
Decreased
Cardiac Output Anaerobic glycolysis
Pyruvate converted to lactic
acid
Cellular hypoperfusion
and hypoxia
METABOLIC RESPONSE
Release of :
CATECHOLAMINES
CORTISOL
GLUCAGON
LIPOLYSYS
INCREASE IN PLASMA
FREE FATTY ACIDS
Shock Therapy Guidelines
Universitas Prima Medan
dr. Edlin SpAn
PRINSIP RESUSITASI
MEMPERTAHANKAN
VENTILASI
MENINGKATKAN
PERFUSI
TERAPI PENYEBAB
TREATMENT CONCEPT OF SHOCK
Enhancing Perfusion / Oxygen Delivery
DO2 = CO x CaO2
Cardiac Arterial O2
output content
Oxygen delivery/DO2 = HR X SV X Hb X SaO2 X 1.34 + Hb X PaO2
Inotropes Partially dependent on
Fluids Transfuse
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
Hypovolemic Shock
• Volume resuscitation – crystalloid, colloid
• Initial crystalloid choices :
• Lactated Ringer’s 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 Ringer’s 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
• Dobutamine
• Epinephrine
• Norepinephrine
DOPAMINE
• An inotropic agent, symphatomimetic amine vasopressor.
• Indications for :
• Corrections for hemodynamic imbalances in shock syndorme due to myocardial
infarction, trauma, sepsis, congestive failure
• Produces positive chronotropic and inotropic effects on the myocardium, resulting in
increased HR and cardiac contractility
DOBUTAMINE
• An inotropic agent, a synthetic catecholamine.
• Indications for :
• inotropic support in short term treatments with cardiac decompensations.
• Produce less increase in HR (less chronotropic) and less increase in peripheral
vascular resistance,
EPINEPHRINE
• A symphatomimetic catecholamine
• Indications for :
• Anaphylaxis, and hypotension associated with septic shock
• In case of anaphylactic shock : Inject adrenalin i.m or s.c in the anterolateral aspect of
thigh. Can be repeated every 5 to 10 minutes (0.3 to 0.5 cc).
• Acts on both alpha and beta-adrenergic receptors. Direct myocardial stimulation that
increases ventricular contraction (inotropic actions), increased HR (chronotropic
actions), and peripheral vasoconstriction.
NOREPINEPHRINE
• Indicated for :
• BP control due to acute hypotensive state, myocardial infarct, septic shock, drug
reactions.
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
