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SHOCK

Shock is a syndrome of impaired tissue oxygenation and perfusion which fails to meet the metabolic requirement due to a variety of etiologies.


Cardiovascular Diseases

SHOCKPATHOPHYSIOLOGY

Cells switch from aerobic to anaerobic metabolism

lactic acid production

Cell function ceases & swells

membrane becomes more permeable

electrolytes & fluids seep in & out of cell


Na+/K+ pump impaired

mitochondria damage

cell death

PATHOPHYSIOLOGY

COMPENSATORY MECHANISMS: Sympathetic Nervous System (SNS)-Adrenal Response
SNS - Neurohormonal response Stimulated by baroreceptors
Increased heart rate
Increased contractility
Vasoconstriction (Afterload)
Increased Preload

COMPENSATORY MECHANISMS:

Hormonal: Renin-angiotension system
Decrease 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 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

Clinical Presentation: Generalized Shock

- Mental status: (LOC)
restless, irritable, apprehensive
unresponsive
- Decreased Urine output

Shock Syndromes(Types)

-Hypovolemic Shock
blood VOLUME problem
-Cardiogenic Shock
blood PUMP problem
-Distributive Shock [septic ; anaphylactic ; neurogenic]
blood VESSEL problem
Cardiovascular Diseases




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

Cardiovascular Diseases

HYPOVOLEMIC SHOCK

External loss of fluid

Fluid loss: Dehydration

Nausea & vomiting, diarrhea, massive diuresis, extensive burns

Blood loss:

trauma: blunt and penetrating
BLOOD 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 & 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


The impaired ability of the heart to pump blood
Pump failure of the right or left ventricle
Mortality rate of 80 % or MORE

Cardiovascular Diseases


Cardiovascular Diseases

CAROIOGENIC SHOCK

Cardiogenic Shock : Etiologies
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


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
Cardiovascular Diseases



DISTRIBUTIVE SHOCK

Distributive Shock

Etiologies
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

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 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 of Septic shock
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 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

Crackles

Clinical manifestation

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



رفعت المحاضرة من قبل: Abdalmalik Abdullateef
المشاهدات: لقد قام 5 أعضاء و 110 زائراً بقراءة هذه المحاضرة








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