SHOCK

kontraktilitas
Definition
A state of acute circulatory failure leading to decreased
organ perfusion, with inadequate delivery of oxygenated
blood to tissues and resultant end organ dysfunction.
Stages
1. Initial
Hypoperfusion hypoxia increased anaerobic
metabolism lactic acid is building metabolic
acidosis.
2. Compensatory
Compensation of metabolic acidosis hyperventilate
The baroreceptors (aortic and carotid sinus) detect
the hypotension release catecholamines
(epinephrine & norepinephrine) vasoconstriction,
increase HR & contractility of the heart
maintaining adequate CO blood pressure
Renal hypoperfusion Renin-angiotensin system
vasoconstriction and stimulation of aldosterone.
Aldosterone Na reabsorbtion and water
conservation.
The body shunts blood from non vital organ to ensure
adequate blood supply to vital organs (heart & brain)
patients skin is cold, bowel sounds are hypoactive,
urine output decreases.
Sign&Symptoms :
Weakness & lightheadedness caused by decreased blood volume
Thirst caused by hypovolemia loss of extracellular fluid
Tachycardia caused by the effects of catecholamines on the heart as
the brain increases the activity of the sympathetic nervous system
Diaphoresis caused by the effects of catecholamines on sweat glands
Tachypnea caused by brain elevating the respiratory rate under the
influence of stress, catecholamines, acidosis, and hypoxia
Decreased urinary output caused by hypovolemia, hypoxia, and
circulating catecholamines
Weakened peripheral pulse
3. Progressive
The overworked heart dysfunctional ischemia.
Biochemical mediators myocardial depression
failure of the cardiac pump
The autoregulatory function of the microcirculation
fails in response to numerous biochemical
mediators increased capillary permeability, with
areas of arteriolar and venous constriction fluid
to leak from the capillaries, creating interstitial
edema and return of less fluid to the heart.
Sign and symptoms:
Pulmonary capillaries begin to leak their
contents pulmonary edema
Dysrhythmias and ischemia. The patient has a
rapid heart rate, sometimes exceeding 150 bpm
Confusion lethargy lose consciousness.
The pupils dilate and are only sluggishly
reactive to light
When the MAP falls below 80 mm Hg, the GFR
of the kidneys cannot be maintained. Acute
renal failure (ARF) can develop.
4. Refractory (Irreversible)
Organ damage is so severe that the patient does not
respond to treatment BP remains low.
Complete renal and liver failure release of necrotic
tissue toxins overwhelming metabolic acidosis.
Reserves of ATP are almost totally depleted, and
mechanisms for storing new supplies of energy have
been destroyed.
Multiple organ dysfunction progressing complete
organ failure death
Sign & Symptoms
Hypotension caused by hypovolemia, either
relative or absolute, and/or by diminished cardiac
output seen in mechanical shock
Altered Mental Status (confusion, restlessness,
combativeness, unconsciousness) caused by
decreased cerebral perfusion, acidosis, hypoxia, and
catecholamine stimulation
Cardiac Arrest caused by critical organ failure
secondary to blood / fluid loss, hypoxia, and
occasionally dysrhythmias caused by catecholamines
and/or low perfusion
Classification
Weil and Subin :
the vascular reservoir
(hypovolaemic shock)
the pump (cardiogenic
shock)
the conduits (obstructive
shock)
distribution of blood flow
among and within the organs
(distributive shock)
septic shock, anaphylactic
shock, neurogenic shock.
Hypovolemic Shock
Rapid fluid loss inadequate circulatory volume
decrease tissue perfusion multiple organ failure
Etiology :
- Hemorrhagic (penetrating trauma, severe GI bleeding)
- Non-hemorrhagic (gastroenteritis, extensive burns)
Cardiogenic Shock
A condition when the hearts ability to contract and to
pump blood is impaired and the supply of oxygen is
inadequate for the heart and tissues.
The causes of cardiogenic shock are either coronary or
noncoronary.
Clinical presentation
Clinical evidence of hypoperfusion (low cardiac output),
which is manifested by sinus tachycardia, low urine
output, and cool extremities.
Systemic hypotension: systolic blood pressure below 90
mm Hg or a decrease in mean blood pressure by 30 mm
Hg.
Most patients who develop acute MI present with an
abrupt onset of squeezing or heavy substernal chest
pain; the pain may radiate to the left arm or the neck.
The pain quality may be burning, sharp, or stabbing.
Distributive Shock
Distributive shock results from excessive vasodilation and the
impaired distribution of blood flow.
The reduction in systemic vascular resistance results in inadequate
cardiac output and tissue hypoperfusion despite normal circulatory
volume
Characterized by an abnormal distribution of intravascular volume
as a result of decreased sympathetic tone, increased vascular
permeability, and pooling of blood in venous and capillary bed.
Three categories: septic, anaphylactic, and neurogenic shock.
Septic Shock
Sepsis is defined as life-threatening organ dysfunction
due to dysregulated host response to infection, and
organ dysfunction is defined as an acute change in total
Sequential Organ Failure Assessment (SOFA) score >2
points secondary to the infection cause.
Septic shock is defined by persisting hypotension
requiring vasopressors to maintain a mean arterial
pressure of 65 mm Hg or higher and a serum lactate
level greater than 2 mmol/L (18 mg/dL) despite adequate
volume resuscitation.
Pathophysiology
Clinical Presentation
Fever is a common symptom, though it may be absent in
elderly or immunosuppressed patients.
Chills are a secondary symptom associated with fever,
developing as a consequence of increased muscular
activity that produces heat and raises the body
temperature.
Mental function is often altered.
Hyperventilation with respiratory alkalosis is a common
feature of patients with sepsis. This feature results from
stimulation of the medullary respiratory center by
endotoxins and other inflammatory mediators.
Tachycardia. An increased heart rate often persists in
sepsis despite adequate fluid repletion.
 Patient's skin color Pallor or grayish or mottled skin
are signs of poor tissue perfusion seen in septic shock.
Early stages: the vasodilation warm skin, warm
extremities, and normal capillary refill (warm shock).
Late stage: stroke volume and cardiac output fall poor
perfusion cool skin, cool extremities, and delayed
capillary refill (cold shock).
 Anaphylactic Shock
Anaphylaxis is an acute, potentially fatal,
multiorgan system reaction caused by the
release of chemical mediators from mast
cells and basophils.
The classic form involves prior sensitization
to an allergen with later reexposure,
producing symptoms via an immunologic
mechanism.
Neurogenic Shock
Neurogenic shock describes the sudden loss of
autonomic tone due to spinal cord injury (SCI)
Disruption of the descending sympathetic pathways
unopposed vagal tone in the vascular smooth muscle
decreased systemic vascular resistance and vasodilation.
Clinical Presentation
Hypotension and bradycardia.
The skin is often warm and flushed initially.
Hypothermia may develop because of profound
vasodilation and heat loss.
Often the central venous pressure is low due to
decreased systemic vascular resistance.
Obstructive Shock
Obstructive shock occurs when adequate oxygen and
nutrient delivery to the organs and tissues of the body is
compromised as a direct result of an obstruction to flow
into or out of the heart.
The most common causes of obstructive shock in
children aretension pneumothorax, pulmonary
embolism, and cardiac tamponade.
 Bibliography
Belinda Hammonds, Polly Gerbers. 2012. Sheehy's
Manual of Emergency Care. Elsevier.
Brunner and Suddarth. 2009. Textbook of Canadian
Medical-Surgery Nursing.
Carl Waldman, Neil Soni, Andrew Rhodes. 2008. Oxford
Desk Reference: Critical Care.
Kolecki, Paul. 2016. Hypovolemic Shock. Medscape.
http://emedicine.medscape.com/ article/760145-
overview#a6
Patient Care Protocols: Shock.
http://www.summahealth.org/~/media/files/summahe
alth/ems/ems-protocols/patient-care-protocols/shock.pdf