SHOCK

PRESENTED BY-
RIT JHALAK
INTRODUCTION

 Shock is a serious, life-threatening medical emergency and one of the most the blood carries death for
critically ill people.
 Shock leads to insufficient blood flow which reaches the body tissues. As the blood carries oxygen and
nutrients people the body, reduced flow hinders the delivery of these components to the tips and stop
the tissues from functioning properly. The process of blood entering the tissues is called perfusion. So,
when perfusion is not occurring properly, this is called hypoperfusion.
DEFINITION

 Shock is a syndrome characterized by decreased tissue-perfusion and impaired cellular metabolism.

This results in an imbalance between the supply of and demand for oxygen and nutrients. The
exchange of oxygen and nutrients at the cellular level is essential to life. When a cell experiences a
state of hypoperfusion, the demand for oxygen and nutrients exceeds the supply and this leads to
shock.
INCIDENCE

 Shock is common in both sexes

 Children and old age-group more prone to shock
 80% of mortality rate is caused by shock.
ETIOLOGY
 Hemorrhage
 Burns
 Dehydration
 Myocardial infarction
 Anaphylaxis
 Neurogenic condition
 Sepsis
 Vascular insufficiency and cardiac dysfunction
 Obstructive condition
 Diarrhea and dysentery
STAGES OF SHOCK
INITIAL STAGE

During this stage, the hypoperfusion state causes hypoxia leading to the mitochondria being unable to
produce adenosine triphosphate (ATP).
Due to this lack of oxygen, the cell membranes become damaged, they become leaky to extracellular
fluid, and the cells perform anerobic respiration.
This causes a build-up of lactic and pyruvic acid, which results in systemic metabolic acidosis. The
process of removing these compounds from the cells by the liver requires oxygen, which is absent.
COMPENSATORY (COMPENSATING) STAGE
This stage is characterized by the body employing physiological mechanisms, including neural,
hormonal and bio-chemical mechanisms in an attempt to reverse the condition. As a result of acidosis, the
person will begin to hyperventilate in order to raise the pH of the blood.
 The Baroreceptors in the arteries detect the resulting by removing it the body is attempting adrenaline
and noradrenaline.
Noradrenaline causes predominately vasoconstriction with a mild increase in heart rate, whereas
adrenaline predominately causes an increase in heart rate with a small effect on the vascular tone; the
combined effect results in an increase in blood pressure.
Renin-angiotensin axis is activated and arginine vasopressin is released to conserve fluid via the kidneys.
 Also, these hormones cause the vasoconstriction of the kidneys, gastrointestinal tract, and other organs
to divert blood to the heart, lungs and brain.
 The lack of blood to the renal system causes the characteristic low urine production.
PROGRESSIVE (DECOMPENSATING)
Should the cause of the crisis not be successfully treated, the shock will proceed to the progressive stage
and the compensatory mechanisms begin to fail. Due to the decreased perfusion of the cells, sodium ions
build up within while potassium ions leak out.
As anerobic metabolism continues, increasing the body's metabolic acidosis, the arteriolar and
precapillary sphincters constrict such that blood remains in the capillaries.
Due to this, the Hydrostatic pressure will increase and, combined with histamine release, this will lead
to leakage of fluid and protein into the surrounding tissues.
As this fluid is lost, the blood concentration and viscosity increase, causing sludging of the
microcirculation. The prolonged vasoconstriction will also cause the vital organs to be compromised due
to reduced perfusion.
REFRACTORY (IRREVERSIBLE)

At this stage, the vital organs have failed and the shock can no longer be reversed. Brain damage and
cell death have occurred. Death will occur immediately.
TYPES OF SHOCK
HYPOVOLEMIC SHOCK

This is the most common type of shock and based on insufficient circulating volume
Its primary cause is loss of fluid from the circulation from either an internal or external source. An
internal source may be hemorrhage. External causes may include extensive bleeding, high output fistulae
or severe burns.
SIGNS AND SYMPTOMS

 Anxiety, restlessness, altered mental state due to decreased cerebral perfusion and subsequent hypoxia
 Hypotension due to decrease in circulatory volume
 A rapid, weak-thready pulse due to decreased blood flow combined with tachycardia
 Cool, clammy skin due to vasoconstriction and stimulation of vasoconstriction
 Rapid and shallow respirations due to sympathetic nervous system stimulation and acidosis
 Hypothermia due to decreased perfusion and evaporation of sweat
 Thirst and dry mouth, due to fluid depletion
 Fatigue due to inadequate oxygenation
 Cold and mottled skin (cutis marmorata), especially extremities, due to insufficient perfusion of the
skin
 Distracted look in the eyes or staring into space, often with pupils dilated.
EMERGENCY CARE

Fluid Replacement
CARDIOGENIC SHOCK

This type of shock is caused by the failure of the heart to pump effectively. This can be due to damage
to the heart muscle, most often from a large myocardial infraction. Other causes of cardiogenic shock
include arrhythmias, cardiomyopathy, congestive heart failure (CHF) or cardiac valve problem.
PATHOPHYSIOLOGY
SIGNS AND SYMPTOMS

 Distended jugular veins due to increased jugular venous pressure

 Absent pulse due to tachyarrhythmia.
EMERGENCY MANAGEMENT

 Initial drug therapy for myocardial infarction

 Replace Fluids.
SPECIAL MEASURES

Definitive measures to restore blood flow include thrombolytic therapy, angioplasty with stenting,
emergency revascularization, and value replacement.
Cardiac catheterization should be performed as soon as possible after the initial insult. Coronary
angioplasty with or without stenting may be performed during the cardiac catheterization.
Drugs can be used to decrease the workload of the heart by dilating coronary arteries (e.g. nitrates),
reducing preload (e.g. diuretics), reducing afterload (e.g. vasodilators), and reducing heart rate and
contractility (e.g. beta-adrenergic blockers).
The patient may also benefit from a circulatory assist device as an intra-aortic balloon pump (IABP) or
a ventricular assist device (VAD).
The IABP is a circulatory assist device that is inserted into the femoral artery and placed in the aorta just
distal to the aortic arch.
DISTRIBUTIVE SHOCK

As in hypovolemic shock, there is an insufficient intravascular volume of blood. This form of 'relative'
hypovolemia is the result of dilation of blood vessels which diminishes systemic vascular resistance.
SEPTIC SHOCK

This is caused by an overwhelming infection leading to vasodilation, such as by Gram negative bacteria,
i.e. Escherichia coli, Proteus species, Klebsiella pneumoniae which release an endotoxin which produces
adverse biochemical, immunological and occasionally neurological effects which are harmful to the body.
Gram-positive cocci, such as pneumococci and streptococci, and certain fungi as well as Gram-positive
bacterial toxins produce a similar syndrome.
CONT.…..

 In the early stages of septic shock, the body experiences massive vasodilation.
 Warm, dry, flushed skin is apparent during this hyperdynamic stage of septic shock.
 The compensatory increase in cardiac output and resultant increased perfusion of the skin gives this
stage the name 'warm shock. During the later stages, when compensatory mechanism fails, the release
of MDF and decreased venous return result in decreased perfusion and ‘cold shock’ or the
hypodynamic stage.
 At this stage the skin becomes cool, clammy and mottled. Body temperature drops to subnormal
levels. Auscultation of the lungs reveals crackles and wheezes. There is change in the level of
consciousness, and may include drowsiness and stupor progressing to coma.
TYPES OF SEPTIC SHOCK

Early (Warm)
 Decreased peripheral vascular resistance
 Increased cardiac output.
Late (Cold)
 Increased peripheral vascular resistance
 Decreased cardiac output.
PATHOPHYSIOLOGY
SIGNS AND SYMPTOMS

 Hot, dry, flushed skin

 Hypotension
 Increased heart rate
 Pyrexia and fever, or hyperthermia, due to overwhelming bacterial infection. Vasodilation and
increased cardiac output.
EMERGENCY CARE

 Locate the source of infection and treat with broad spectrum antibiotic
 Replace fluids.
ANAPHYLACTIC SHOCK

Caused by a severe anaphylactic reaction to an allergen, antigen, drug or foreign protein causing the
release of histamine which Causes widespread vasodilation, leading to hypotension and increased
capillary permeability.
PATHOPHYSIOLOGY
SIGNS AND SYMPTOMS

 Throat edema
 In congestion with increasing breathing difficulty
 Hypotension
 Increased heart rate
 Skin eruptions and large welts
 Localized edema, especially around the face
 Weak and rapid pulse
 Breathlessness and cough due to narrowing of airways and swelling of the throat.
EMERGENCY CARE

 Manage ABC
 Administer (adrenaline) epinephrine
 Administer diphenhydramine hydrochloride (Benadryl).
NEUROGENIC SHOCK

Neurogenic shock is caused by trauma to the spinal cord resulting in the sudden loss of autonomic and
motor reflexes below the injury level. Without stimulation by sympathetic nervous system, the vessel
walls relax uncontrolled, resulting in a sudden decrease in peripheral vascular resistance, leading to
vasodilation and hypotension.
PATHOPHYSIOLOGY
SIGNS AND SYMPTOMS

 Slowed heart rate

 Hypotension
 Skin is warm and dry
EMERGENCY CARE

 Replace fluids
 Administer drugs to increase blood pressure and heart rate.
OBSTRUCTIVE SHOCK

In this situation, the flow of blood is obstructed, which impedes circulation and can result in circulatory
arrest. Several conditions result in this form of shock:
Cardiac tamponade: In which blood in the pericardium prevents inflow of blood into the heart (venous
return). Constrictive pericarditis, in which the pericardium shrinks and hardens, is similar in presentation.
Tension pneumothorax: Through increased intrathoracic pressure, blood flow to the heart is prevented
(venous return).
Massive pulmonary embolism: It is the result of a thromboembolic incident in the blood vessels of the
lungs and hinders the return of blood to the heart.
Aortic stenosis hinders circulation by obstructing the ventricular outflow tract.
SIGNS AND SYMPTOMS

 Distended jugular veins due to increased jugular venous pressure

 Pulsus paradoxus in case of tamponade.
ENDOCRINE SHOCK BASED ON ENDOCRINE
DISTURBANCES

 Hypothyroidism, in critically ill patients, reduces cardiac output and can lead to hypotension and
respiratory insufficiency
 Thyrotoxicosis may induce a reversible cardiomyopathy
 Acute adrenal insufficiency is frequently the result of discontinuing corticosteroid treatment without
tapering the dosage. However, surgery and intercurrent disease in patients on corticosteroid therapy
without adjusting the dosage to accommodate for increased requirements may also result in this
condition.
COMPENSATORY MECHANISMS
 Initial stage of shock, the body hemostasis mechanism are trigged and attempt to return the body to
steady state. Sympathetic nerves are stimulated by the fall in arterial blood pressure and fall in PO2
 They act to pressure blood supply to the vital organs, i.e. the heart and the brain by vasoconstriction
and by increasing heart rate, throughout stroke volume.
 The volume pumped by each contraction diminishes. This may be felt as a rapid weak pulse
 The skin becomes cold as blood is dilated to the vital organs and the patient may become confused and
disoriented because blood supply to the brain is reduced
 The fall in PO2 level triggers up deep and rapid breathing (air hunger) but this will only rectify the
situation if sufficient. Blood is passing through the system for adequate oxygenation to occur
 In early stage of shock, intestinal fluid is returned to the circulation through capillary wall in an
attempt to raise the circulatory blood volume
 But once the cell damage begins this mechanism also fails. Sodium and water are presented in the
body by the production of ADH and aldosterone and this further helps to rise blood volume. Urine
output falls as a result of this.
DIAGNOSTIC EVALUATION

 History collection
 ECG 12 leads
 X-Ray chart
 Continuous pulse oximetry.
 Physical examination
 Continuous cardiac monitoring
 Hemodynamic monitoring
COMPLICATION OF SHOCK
Multiple Organ Dysfunction Syndrome (MODS)
Multiple organ dysfunction syndrome (MODS): The combination of direct and reperfusion injury may cause MODS-
the progressive dysfunction of 2 or more organs consequent to life-threatening illness. MODS can follow any type of
shock but most common when infection is involved; organ failure is one of the defining features of septic shock.
Any organ system can be affected but the most frequent target organ is the lung, in which increased membrane
permeability leads to flooding of alveoli due to capillary leaks. Progressive hypoxia may be increasingly resistant to
supplemental oxygen therapy. This condition is termed 'Acute Lung Injury' or, if severe, acute respiratory distress
syndrome (ARDS).
The kidneys are injured when renal perfusion is critically reduced, leading to acute tubular necrosis and renal
insufficiency manifested by oliguria and progressive rise in serum creatinine.
In the heart, reduced coronary perfusion and mediators may depress contractility, worsen myocardial compliance and
down-regulate beta receptors. These factors decrease cardiac output, further worsening the myocardial and systemic
perfusion and causing a vicious circle often culminating in death.
The GI tract can develop ileus and submucosal hemorrhage. Liver hypoperfusion can produce focal or extensive
hepatocellular necrosis, transaminase elevation and decreased production of clotting factors.
TREATMENT

 Oxygen and ventilation

 Drug therapy
 Fluid therapy in shock
 Nutrition therapy
OXYGEN AND VENTILATION
Oxygen delivery is dependent upon CO, available hemoglobin, and arterial oxygen saturation (SaO₂).
Methods to optimize oxygen delivery are directed at increasing supply and decreasing demand. Supply
can be increased by
 (1) optimizing the CO with drug therapy or fluid replacement,
 (2) increasing the hemoglobin by the transfusion of blood or packed red blood cells,
(3) increasing the arterial oxygen saturation with supplemental oxygen and mechanical ventilation.
Activities that increase oxygen consumption (e.g. endotracheal suctioning, position changes) should be
appropriately spaced for oxygen conservation.
NUTRITION THERAPY
Protein-calorie malnutrition is one of the primary manifestations of hypermetabolism in shock.
Nutrition is vital to decreasing morbidity. Essential nutrition should be initiated within the first 24 hours.
The patient is started on a continuous drip of very small amounts of enteral feedings. Early enteral
feedings are thought to enhance perfusion of the G.l tract and help maintain the integrity of gut mucosa. A
patient in shock should be weighed daily on the same scale at the same time of the day. If the patient
experiences a significant weight loss, dehydration should be ruled out before additional calories are
provided. Large weight gains are common because of third spacing fluids. Therefore, daily weights may
function between indicator of fluid status than caloric needs and balance. Serum protein, nitrogen balance,
BUN, serum glucose, and serum electrolytes are all used to assess nutritional status.
NURSING DIAGNOSIS
 Fluid volume deficit related to loss of circulatory volume
 Decreased cardiac output related to decreased central venous pressure
 Ineffective breathing pattern related to inadequate oxygenation Impaired systemic tissue perfusion
related to hypovolemic shock
 Impaired skin integrity related to edema
 Fear and anxiety related to severity of the disease condition
 Nutritional pattern less than body requirement related to anorexia nervosa
 Sleep pattern disturbance related to hospitalization
 Impaired sensory and perceptual activities related to dilated pupils.
HEALTH EDUCATION

 Give printed notes to the client and family members regarding shock, its causes, stage and its types,
and signs and symptoms
 Taught all initial treatment measures to the family members to avoid shock
 Asked the client not to worry about the disease condition, because it may lead to stress that may still
worsen the condition
 Advised the client to take good nutritious food to improve nutritious status
 Encouraged the client to take medication regularly and come for regular check-ups.
SUMMARY
BIBLIOGRAPHY
 1. Suddarth's & Brunner. TEXTBOOK OF MEDICAL- SURGICAL NURSING. Wolters Kluwer pvt. ltd. volume-2.
Twelfth edition. New Delhi. 2011. Page no: 2161-2163. 2. Brar Navdeep Kaur. Rawat HC. TEXTBOOK OF
ADVANCED NURSING PRACTICE. First edition. New Delhi. Jaypee Brothers medical publishers (p) ltd. 2015.
Page no: 405- 413.
 3. Basher P. Shabeer and Khan. A CONCISE TEXTBOOK OF ADVANCED NURSING PRACTICE. first edition.
Bangalore. Emeses medical publishers. 2015. Page no: 233- 237.
 4. Clement I. The textbook of first aid and emergency nursing. 6th edition. New Delhi. Jaypee brothers'
medical publishers (p) ltd. 2014. Page no: 120-163.
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