SHOCK
Shock is a syndrome of impaired tissue oxygenation and perfusion which fails to meet the metabolic requirement due to a variety of etiologies.SHOCKPATHOPHYSIOLOGY
Cells switch from aerobic to anaerobic metabolismlactic acid production
Cell function ceases & swellsmembrane becomes more permeable
electrolytes & fluids seep in & out of cellNa+/K+ pump impaired
mitochondria damage
cell deathPATHOPHYSIOLOGY
COMPENSATORY MECHANISMS: Sympathetic Nervous System (SNS)-Adrenal ResponseSNS - Neurohormonal response Stimulated by baroreceptors
Increased heart rate
Increased contractility
Vasoconstriction (Afterload)
Increased Preload
COMPENSATORY MECHANISMS:
Hormonal: Renin-angiotension systemDecrease renal perfusion
Releases renin angiotension I
angiotension II potent vasoconstriction & releases aldosterone adrenal cortex sodium & water retention
( intravascular volume )
COMPENSATORY MECHANISMS:
Antidiuretic Hormone
Osmoreceptors in hypothalamus stimulated
ADH released by Posterior pituitary glandVasopressor effect to increase BP
Acts on renal tubules to retain waterStages of Shock
❇ Initial stage - tissues are under perfused❇Compensatory stage - Reversible.
❇Progressive stage - Failing compensatory
mechanisms , Decompensated.
❇Irreversible or refractory stage - Cellular necrosis and Multiple Organ Dysfunction Syndrome may occur
DEATH IS IMMINENT!!!!
Clinical Presentation: Generalized Shock
Vital signsHypotensive: (may be WNL or due to compensatory mechanism) < 90 mmHg
MAP < 60 mmHg
Tachycardia: Weak and Thready pulse
Tachypneic : blow off CO2 Respiratory alkalosis
Clinical Presentation: Generalized Shock
- Mental status: (LOC)restless, irritable, apprehensive
unresponsive
- Decreased Urine output
Shock Syndromes(Types)
-Hypovolemic Shockblood VOLUME problem
-Cardiogenic Shock
blood PUMP problem
-Distributive Shock [septic ; anaphylactic ; neurogenic]
blood VESSEL problem
Loss of circulating volume decrease tissue perfusion
ETIOLOGY:
External fluid or blood loss.
-Fluid loss:
Nausea & vomiting, diarrhea, extensive burns
-Blood loss Trauma
Internal fluid loss pancreatitis
HYPOVOLEMIC SHOCK
External loss of fluidFluid loss: Dehydration
Nausea & vomiting, diarrhea, massive diuresis, extensive burnsBlood loss:
trauma: blunt and penetratingBLOOD YOU SEE
BLOOD YOU DON’T SEE
Clinical PresentationHypovolemic Shock
Tachycardia and tachypnea
Weak, thready pulses
Hypotension
Skin cool & clammy
Mental status changes
Decreased urine output: dark & concentrated
Assessment & Management
S/S vary depending on severity of fluid loss:15%[750ml]- compensatory mechanism maintains CO
15-30% [750-1500ml- Hypoxemia, decreased BP & UOP30-40% [1500-2000ml] -Impaired compensation & profound shock along with severe acidosis
40-50% - refactory stage:
loss of volume= death
Initial Management Hypovolemic Shock
Early Recognition- Do not relay on BP! (30% fld loss)
Control hemorrhageRestore circulating volume crystalloids(NS),colloids(dextran)
Optimize oxygen delivery
Vasoconstrictor if BP still low after volume loading
The impaired ability of the heart to pump blood
Pump failure of the right or left ventricle
Mortality rate of 80 % or MORE
CAROIOGENIC SHOCK
Cardiogenic Shock : EtiologiesMost common cause is LV MI (Anterior) ,Occurs when > 40% of ventricular mass damage
mechanical complications of MI:
Papillary Muscle Rupture
Ventricular aneurysm
Ventricular septal rupture
Other causes:
Cardiomyopathiestamponade
arrhythmias
valve disease
Cardiogenic Shock: Pathophysiology
Impaired pumping ability of
LV leads to…
Decreased stroke volume leads to…..
Decreased CO leads to …..
Decreased BP leads to…..
Compensatory mechanism which may lead to
Decreased tissue perfusion !!!!
Cardiogenic Shock: Pathophysiology
Impaired pumping ability of LV leads to…Inadequate systolic emptying leads to ...
Left ventricular filling pressures (preload) leads to...
Left atrial pressures leads to ….
Pulmonary capillary pressure leads to …
Pulmonary interstitial & intraalveolar edema !!!!
Cardiogenic Shock : Clinical Presentation
• Features of shock (Hypotension + Hypoperfusion) with features of pulmonary congestion.• Features of cause VSD , Tamponade
MANAGEMENT
Goal of management :
Treat Reversible Causes
The main goal is to improve myocardial function
Arrhythmia should be treated
Reperfusion PCI is the treatment of choice in ACS
Inotropes and vasopressor Dobutamine,Dopamine
Intra-aortic balloon pump
Cautious administration of fluid
Pulmonary artery monitoring is a necessity
Management Cardiogenic Shock
Morphine as needed (Decreases preload, anxiety)Cautious use of diuretics in CHF
Vasodilators as needed for afterload reduction
Short acting beta blocker, for refractory tachycardia
Inadequate perfusion of tissues through maldistribution of blood flow and volume because of alterations in blood vessels
Cardiac pump & blood volume are normal but blood is not reaching the tissues
DISTRIBUTIVE SHOCK
Distributive Shock
EtiologiesSeptic Shock (Most Common)
Anaphylactic Shock
Neurogenic Shock
Anaphylactic Shock
• A type of distributive shock that results from widespread systemic allergic reaction to an antigen• This hypersensitive reaction is LIFE THREATENING
Anaphylactic Shock : Pathophysiology
• Antigen exposure• body stimulated to produce IgE antibodies specific to antigen
• drugs, bites, contrast, blood, foods, vaccines
• Reexposure to antigen
• IgE binds to mast cells and basophils
• Anaphylactic response
Anaphylactic Shock : Clinical Presentation
• Almost immediate response to inciting antigen• Cutaneous manifestations
• urticaria, erythema, pruritis, angioedema
• Respiratory compromise
• stridor, wheezing, bronchorrhea, resp. distress
• Circulatory collapse
• tachycardia, vasodilation, hypotension
Management Anaphylactic Shock
• Early Recognition, treat aggressively
• AIRWAY SUPPORT
• IM EPINEPHRINE
• Antihistamines
• Corticosteroids
• IMMEDIATE WITHDRAWAL OF ANTIGEN IF POSSIBLE
• Judicious crystalloid administration
NEUROGENIC SHOCK
Most common etiology: Spinal cord injury above T6Causes massive vasodilatation in the venous vasculature, venous return to heart, cardiac output.
Neurogenic is the rarest form of shock!
Assessment , Diagnosis and Management of Neurogenic Shock
PATIENT ASSESSMENTHypotension
BradycardiaHypothermia
Warm, dry skin
CO
Flaccid paralysis below level of the spinal lesion
MEDICAL MANAGEMENT
Goals of Therapy are to treat or remove the cause.
Treat Hypovolemia ,hypothermia , hypoxia.
Vasopressors may be needed.
DVT prophylaxsis.
SEPSIS
Systemic Inflammatory Response (SIRS) to INFECTION manifested by : two or > of following:Temp > 38 or < 36 centigrade
HR > 90
RR > 20 or PaCO2 < 32
WBC > 12,000/cu mm or < 4,000
SEPTIC SHOCK
SEPSIS WITH:Hypotension (SBP < 90 or > 40 reduction from baseline) despite adequate fluid resuscitation
Risk Factors Associated with Septic Shock
AgeMalnutrition
General debilitation
Use of invasive catheters
Traumatic woundsDrug Therapy
Pathophysiology of Septic shockInitiated by gram-negative (most common) or gram positive bacteria, fungi, or viruses
Cell walls of organisms contain Endotoxins
Endotoxins release inflammatory mediators (systemic inflammatory response) causes…...
Vasodilation & increase capillary permeability leads to
Shock due to alteration in peripheral circulation & massive dilation
Clinical Presentation Septic Shock
Two phases:“Warm” shock - early phase
hyperdynamic response, VASODILATION
“Cold” shock - late phase
hypodynamic response
Clinical Manifestations
EARLY---HYPERDYNAMIC STATE---COMPENSATION
Pink, warm, flushed skin
Increased Heart Rate
Tachypnea
Massive vasodilation
Increased CO
CracklesClinical manifestation
Late hypodynamic state----- decompansation:
Vasoconistriction
Skin is pale & coldTachycardia
Decrease BP
Change LOC
Decrease UOP
Decrease COMetabolic & respiratory acidosis with hypoxemia
MANAGEMENT
Prevention !!!
Find and kill the source of the infection Antimicrobial
Fluid Resuscitation
Vasoconstrictors
Inotropic drugs
Maximize O2 delivery Support
Nutritional SupportComfort & Emotional support