shock

4th stage

Medicine
Lec-
د.جاسم

1/3/2016

SHOCK

Shock :- is a syndrome of impaired tissue oxygenation and perfusion which fails to meet the metabolic requirement due to a variety of etiologies.
Pathophysiology :-
1-Cells switch from aerobic to anaerobic metabolism
2-lactic acid production
3-Cell function ceases & swells
4-membrane becomes more permeable
5-electrolytes & fluids seep in & out of cell
6-Na+/K+ pump impaired
7-mitochondria damage
8-cell death


COMPENSATORY MECHANISMS: 1- Sympathetic Nervous System (SNS)-Adrenal Response
2- SNS - Neurohormonal response Stimulated by baroreceptors
Increased heart rate
Increased contractility
Vasoconstriction (Afterload)
Increased Preload
3- Hormonal: Renin-angiotension system
Releases renin angiotension II angiotension I Decrease renal perfusion potent vasoconstriction & releases aldosterone adrenal cortex sodium & water retention ( intravascular volume )

4-Antidiuretic Hormone

Osmoreceptors in hypothalamus stimulatedADH released by Posterior pituitary gland Vasopressor effect to increase BP-Acts on renal tubules to retain water
Stages 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 signs :-
Hypotensive: (may be WNL or due to compensatory mechanism) < 90 mmHg
MAP < 60 mmHg
Tachycardia: Weak and Thready pulse
Tachypneic : blow off CO2 , Respiratory alkalosis
Mental status: (LOC) restless, irritable, apprehensive and unresponsive
Decreased Urine output


Shock Syndromes(Types) :-
1-Hypovolemic Shock
blood VOLUME problem
2-Cardiogenic Shock
blood PUMP problem
3-Distributive Shock [septic ; anaphylactic ; neurogenic]
blood VESSEL problem

Hypovolemic shock

Loss of circulating volume decrease tissue perfusion
Etiology :
External fluid or blood loss.
1-Fluid loss: Dehydration Nausea & vomiting, diarrhea, massive diuresis, extensive burns
2-Blood loss: trauma: blunt and penetrating
BLOOD YOU SEE
BLOOD YOU DON’T SEE

Internal fluid loss -pancreatitis

Clinical Presentation :
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 & UOP
30-40% [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 hemorrhage
Restore circulating volume crystalloids(NS),colloids(dextran)
Optimize oxygen delivery
Vasoconstrictor if BP still low after volume loading

Cardiogenic shock

The impaired ability of the heart to pump blood
Pump failure of the right or left ventricle
Mortality rate of 80 % or MORE
Etiology:
Most 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:
Cardiomyopathies
Tamponade
Arrhythmias
valve disease
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 !!!!
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 !!!!


Clinical Presentation :Features of shock (Hypotension + Hypoperfusion) with features of pulmonary congestion.
Features of cause VSD , Tamponade

MANAGEMENT :

Goals 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
Steps :
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

Distributive shock

Inadequate perfusion of tissues through maldistribution of blood flow and volume because of alterations in blood vesselsCardiac pump & blood volume are normal but blood is not reaching the tissues
Etiology
Septic 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
Etiology
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
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
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 T6

Causes 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 ASSESSMENT
Hypotension
Bradycardia
Hypothermia
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
Age
Malnutrition
General debilitation
Use of invasive catheters
Traumatic wounds
Drug Therapy


Pathophysiology :
Initiated 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 :

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
Crackles
Late -- hypodynamic state -- decompansation:
Vasoconistriction
Skin is pale & cold
Tachycardia
Decrease BP
Change LOC
Decrease UOP
Decrease CO
Metabolic & 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 Support
Comfort & Emotional support

SH.J