Shock

School of Nursing & Midwifery
Department of Adult Health Nursing
1P.by: Habtemariam Mulugeta
College of Medicine &
Health Sciences

Presentation Outline
1. Objectives
2. Introduction
3. Definition
4. Incidence/Prevalence Rate
5. Etiology
6. Risk Factors
7. Pathophysiology
8. Stages of shock
9. Clinical presentation
10. Diagnosis
10. Investigation
11. Effect of shock
12. Metabolic Changes In
Shock
13. Classification of shock
14. Differential Diagnosis
15. prognosis
16. Nursing Process
17. Summery
18. Reference
19. Acknowledgment 2

Objectives
At the end of the session, you will be able to:
 Define Shock
 Explain the sign and symptom of Shock
 Differentiate the diagnostic modalities of Shock
 Discuss the management of Shock 3

INTRODUCTION
 Term “choc” – French for “push” or impact was
first published in 1743 by the physician LeDran
 shock is a condition in which circulation fails to
meet the nutritional needs of cells and at the same
time fails to remove metabolic waste products.
4
ATLS - Student Course Manual (10 ed.). 2018. pp. 43–52, 135.

Definition
 Shock is the state of insufficient blood flow to the
tissues of the body as a result of problems with the
circulatory system.1
 Shock also known as Circulatory Failure/ Circulatory
Collapse/ circulatory shock / Hypovolemic Shock/
blood poisoning - septic shock.2
5
1. International Trauma Life Support for Emergency Care Providers (8 ed.)
2018. pp. 172–173.
2. Tintinalli, Judith E. (2010). p. 168.

Cont.
 Shock is a life threatening situation due to poor tissue
perfusion with impaired cellular metabolism, manifested
in turn by serious pathophysiological abnormalities.1
 Shock is a term used to describe the clinical syndrome
that develops when there is critical impairment of tissue
perfusion due to some form of acute circulatory failure.2
6
1. Bailey and love
2. Davidson’s

Cont.
 Shock may be defined as inadequate delivery of oxygen
and nutrients to maintain normal tissue and cellular
function.1
 The state in which profound and widespread reduction of
effective tissue perfusion leads first to reversible, and
then if prolonged, to irreversible cellular injury.2
71. Schwartz’s
2. Kumar and Parrillo ,1995

Incidence/Prevalence Rate
 Shock from blood loss occurs in about 1–2% of trauma
cases.1
 Up to 1/3 of people admitted to the ICU are in circulatory
shock.2
 Of these, cardiogenic shock accounts for approximately
20%, hypovolemic about 20%, and septic shock about 60%
of cases.3
8
1. Cherkas, David (Nov 2011). PMID 22164397
2. Vincent JL, De Backer D (October 2013. 369 (18): 1726–34.
3. Cecconi M, et al (December 2014). 40 (12): 1795–815.

Etiology
 Heart conditions (heart attack, heart failure)
 Heavy internal or external bleeding, such as from a
serious injury or rupture of a blood vessel
 Dehydration, especially when severe or related to heat
illness.
 Infection (septic shock)
 Severe allergic reaction (anaphylactic shock)
 Spinal injuries (neurogenic shock)
 Burns
 Persistent vomiting or diarrhea 9
Elbers PW, Ince C (2006). 10 (4): 221.

Cont.
10
Elbers PW, Ince C (2006). PMC 1750971

Risk Factors
 Heart failure,
 Old age,
 Hypertension,
11
"Cardiogenic shock - Mayo Clinic. Retrieved 22 May 2020.

Stages of shock
 Deterioration of circulation in shock is a progressive
& continuous phenomenon & compensatory
mechanisms become progressively less effective
1) Non-progressive (initial, compensated, reversible)
shock
2) Progressive decompensated shock
3) Decompensated (irreversible) shock
14
Armstrong, D.J. (2004). The Adult.(2nd edition)

17
Progressive decompensated shock

19
Armstrong, D.J.
(2004). The
Adult.(2nd edition)

Clinical Presentations
 Hypotension - Systolic BP<100mmHg and
tachycardia - >100/min are the key signs of shock.
 Symptoms of all types of shock include:
• Rapid, shallow breathing
• Cold, clammy skin
• Rapid, weak pulse
• Dizziness or fainting
• Weakness
20
International Trauma Life Support for Emergency Care Providers (8 ed.). 2018.
pp. 172–173

Cont.
 Depending on the type of shock the following symptoms may
also be observed:
 Eyes appear to stare
 Anxiety or agitation
 Seizures, Confusion or unresponsiveness
 Low or no urine output (Urine Output<30ml/hour)
 Bluish lips and fingernails
 Sweating
 Chest pain
 Elevated or Reduced central venous pressure
 Multi-Organ Failure
21

Diagnosis
Initial Assessment – ABC
 Airway:
Does patient have mental status to protect airway?
GCS less than “eight” means “intubate” (E4 V5 M6)
Airway is compromised in anaphylaxis
 Breathing:
 If patient is conversing, A& B are fine Place patient on oxygen
 Circulation:
 Vitals (HR, BP)
 IV, start fluids, put on continuous monitor
24
ATLS - (10 ed.). 2018. pp. 43–52, 135.

Cont.
 In a trauma, perform ABCDE, not just ABC
 Deficit or Disability
 Assess for obvious neurologic deficit
 Movement of all four extremities? Pupils?
 Glasgow Coma Scale (V5, M6, E4)
 Exposure
 Loosening of clothing on trauma patients.
25

ATLS - Student Course Manual (10 ed.). 2018. pp. 43–52, 135.

29
• In management of trauma patients, understanding the
patterns of injury of the patient in shock will help
direct the evaluation and management.
• Blood loss sufficient to cause shock is generally of a
large volume (e.g. external, intrathoracic, intra-
abdominal, retroperitoneal, and long bone fractures).
Cont.
ATLS - (10 ed.). 2018. pp. 43–52, 135.

30
• Diagnostic and therapeutic tube thoracotomy may be
indicated in unstable patients based on clinical findings
and clinical suspicion.
• Chest radiographs, pelvic radiography,
diagnostic ultrasound or diagnostic peritoneal
lavage.
Cont.
ATLS - (10 ed.). 2018. pp. 43–52, 135.

Investigation
 CXR - consolidation
 FBC – WCC elevated or low
 CBC,
 ABG - hypoxia, acidosis, raised lactate
 ECG - low voltage, ST elevation, True Posterior MI
 Urgent Echo - LV dysfunction
 CT/MRI - to exclude constructive pericarditis
 Blood and urine culture
31
ATLS - (10 ed.). 2018. pp. 43–52, 135.

Effect of shock
 CARDIOVASCULAR
 decrease of preload and afterload
 Baroreceptor response
 Release of catechol amines
 Tachycardia and vasoconstriction.
 RESPIRATORY
 Metabolic acidosis
 Inc. respiratory rate and excretion of carbon dioxide
 Results in compensatory resp. alkalosis.
32Tintinalli, Judith E. (2010). pp. 174–175.

Cont.
 RENAL AND ENDOCRINE
 decreased urine output
 stimulation of renin angiotensin and aldosterone
axis
 release of vasopressin from hypothalamus
 resulting vasoconstriction and increase Na+ and
water reabsorption.
33

Cont.
 MICROVASCULAR
 Activation of immune and coagulation systems
hypoxia and acidosis, activate complement and
prime neutrophils oxygen free radicles and
cytokine release damaged and endothelium fluids
leak out and edema ensues.
34Tintinalli, Judith E. (2010). pp. 174–175.

Cont.
 CELLULAR
1. Cells switch from aerobic to anaerobic metabolism
2. Decreased ATP production
3. lactic acidosis
4. Glucose exhausts and aerobic respiration ceases
5. Na+/ K+ pump impaired
6. Lysosomes release autodigestive enzymes
7. mitochondria damage
8. cell death. 35

Metabolic Changes In Shock
 CARBOHYDRATE METABOLISM
 Compensated shock : Hyperglycemia due to
increased hepatic glycogenolysis.
 Decompensated shock : Hypoglycemia due to
hepatic glycogen depletion & increased
consumption of glucose by tissue.
 Anaerobic glycolysis occurs as assessed by high
blood levels of lactate & pyruvate. 36

Cont.
 PROTEIN METABOLISM
 Increased intracellular protein catabolism
 Conversion of amino acids to urea.
 Increased blood non-nitrogen protein.
 FAT METABOLISM
 Increased endogenous fat metabolism.
 Rise of fatty acid level in blood.
37
Kumar, Vinay; et al. (2007). pp. 102–103

Cont.
 WATER & ELECTROLYTE DISTURBANCES
 Failure of sodium pumppotassium leaves the cell
(hyponatremia)causes cellular swelling.
 Shock due to loss of plasma only (in
burns)hemoconcentration
38

Cont.
 METABOLIC ACIDOSIS
 Hypoxia of kidney, renal function is impaired blood levels of acids
like lactate, pyruvate, phosphate & sulfate rise causing metabolic
acidosis.
 MORPHOLOGIC COMPLICATIONS
 Morphologic changes in shock are due to Hypoxia. resulting in
degeneration & necrosis in various organ.
 Organs affected are : Brain, Heart, Lungs, Kidneys, Adrenals
and GIT. 39

Cont.
 HYPOXIC ENCEPHALOPATHY
 Compensated shock results in cerebral ischemia which
produce altered state of consciousness. However, if
blood pressure falls below 50 mmHg as in systemic
hypotension in prolonged shock & cardiac arrest, Brain
suffers from serious ischemic damage with loss of
cortical functions, coma,& vegetative state.
40

Cont.
 HEART IN SHOCK
 Two types of morphologic changes in Heart
1. Hemorrhage's & Necrosis: Located in
subepicardial & subendocardial region.
2. Zonal Lesion: Opaque transverse contraction
bands in a myocyte near an intercalated disc.
41

Cont.
 SHOCK LUNG
 Lungs have Dual blood supply & generally not affected by
hypovolemic shock
 But in Septic shock  SHOCK LUNG seen as symptoms of
ARDS including: congestion, interstitial & alveolar edema,
interstitial lymphocytic infiltrate, alveolar hyaline membrane,
Thickening & fibrosis of alveolar septa, fibrin & platelet thrombi in
pulmonary microvasculature.
42

Cont.
 SHOCK KIDNEY
 Irreversible renal injury  Important
complication of Shock.
 Renal ischemia following systemic
hypotension is considered responsible for
renal changes in Shock  End result is
generally anuria & death. 43

Cont.
 ADRENALS IN SHOCK
 Adrenals show stress response in SHOCK. It includes
1. Release of aldosterone in response to hypoxic kidney.
2. Release of glucocorticoids from adrenal cortex
& catecholamine like adrenaline from adrenal
medulla.
“SEVERE SHOCK RESULTS IN ADRENAL
HAEMORRHAGES”
44

Cont.
 HYPOXIC ENCEPHALOPATHY
 Compensated shock results in cerebral ischemia which
produce altered state of consciousness. However, if
blood pressure falls below 50 mmHg as in systemic
hypotension in prolonged shock & cardiac arrest, Brain
suffers from serious ischemic damage with loss of
cortical functions, coma,& vegetative state.
45

Cont.
 GIT
 Hypo perfusion of Alimentary tract  Mucosal & Mural
infarction called “HAEMORRHAGIC GASTROENTEROPATHY”
 In Shock due to burns, acute stress  ulcers of
stomach/duodenum  “CURLING’S ULCERS”
 LIVER
 Hypoxia, VDM is released  Vasodilatation
 Others include focal necrosis, fatty change, impaired
liver function.
46

ISCHEMIC REPERFUSION
SYNDROME
 It is the injury that occurs once the normal circulation is restored
to the tissues
 Reasons:
 Acidand potassium load built up leads to myocardial
depression, vascular dilatation and hypotension.
 Neutrophils are flushed back into the circulation; causes further
injury to the endothelial cells of lungs and kidneys.
 Results:
 Acute lung and renal injury
 Multiple organ failure
 Death
48

Classification of SHOCK
 Primary (INITIAL SHOCK)
 Secondary (TRUE SHOCK)
 Anaphylactic (Type I immunologic reaction)
49
Guyton, Arthur; Hall, John (2006). Textbook of Medical Physiology (11th
ed.).. pp. 278–288.

Cont.
 Initial shock is a transient and usually benign vasovagal
attack resulting from sudden reduction of venous return to
the heart caused by neurogenic vasodilatation and
consequent peripheral pooling of the blood.
 It can occur immediately following:
 Trauma
 Severe pain
 Emotional overreaction due to:
 Fear
 Sorrow and surprise
 Sight of blood
50

Cont.
 Primary shock can be labeled as a severe form of
syncope because Clinically Patient develops, signs and
symptoms similar to that of syncope:
 Unconsciousness
 Weakness
 Sinking Sensation
 Pale and Clammy limbs
 Weak and rapid pulse and
 Low Blood Pressure
51

Cont.
 True shock is circulatory imbalance between
oxygen supply and oxygen requirements at cellular
level; hence name CIRCULATORY SHOCK.
 occurs due to hemodynamic derangements with
hypo perfusion of the cells.
52
Guyton, Arthur; Hall, John (2006). Textbook of Medical Physiology (11th
ed.).. pp. 278–288.

Cont.
 Anaphylaxis is a serious allergic reaction that is rapid
in onset and may cause death.
 It typically causes : an itchy rash, throat or tongue
swelling, SOB, vomiting, lightheadedness, and low
blood pressure.
 These symptoms typically come on over minutes to
hours.
53

Classification Based on Etiology
 HYPOVOLEMIC SHOCK
 CARDIOGENIC SHOCK
 SEPTIC SHOCK
 OTHER TYPES :
 TRAUMATIC
 NEUROGENIC
 HYPOADRENAL
54
Harsh Mohan 4th ed

Cont.
 Due to low flow(reduced stroke volume)
 hypovolemic
 cardiogenic
 obstructive
 Due to low peripheral arteriolar resistance
(vasodilatation)
 septic
 anaphylactic
 neurogenic
Davidson’s 21st ed 55

Cont.
56
• Vasovagal
• Psychogenic
• Neurogenic
• Hypovolemic
• Traumatic
• Burns
• Cardiogenic
• Septic (endotoxin):
• Anaphylactic
hyper dynamic /warm
hypovolemic hypo dynamic /cold
(Bailey & Love’s short practice of surgery)

Proposed by HINSHAW and COX (1972)
1. Hypovolemic shock
2. Cardiogenic shock
3. Extra cardiac obstructive shock
4. Distributive shock
Septic shock
Anaphylactic shock
Neurogenic shock 57

58
• Shock due to reduced blood volume (Hypovolemic
shock or cold shock)
 Traumatic shock
 Hemorrhagic shock
 Surgical shock
 Burn shock
 Dehydration shock

• SHOCK due to increased vascular capacity (Blood volume
normal; occurs because of inadequate blood supply to the tissues
due to increased vascular capacity):
 Neurogenic shock
 Anaphylactic shock
 Septic shock
• SHOCK due to diseases of the Heart (cardiogenic shock)
• SHOCK due to obstruction of blood flow.
59

HYPOVOLEMIC SHOCK
61
• Occurs from inadequate circulating blood
volume
• Major effects are due to decreased cardiac
output and low intra cardiac pressure
• Severity of clinical features depends on degree
of blood volume lost
ATLS - (10 ed.). 2018. pp. 43–52, 135.

PATHOPHYSIOLOGY
64
Hemorrhage from small venules & veins (50%)
↓
Decreased filling of right heart
↓
Decreased filling of pulmonary vasculature
↓
Decreased filling of left atrium & ventricle
↓
Left ventricular stroke volume decreases (Frank Starling )
↓
Drop in arterial blood pressure & tachycardia
↓
Poor perfusion to pulmonary arteries
↓
Cardiac depression & pump failure

CLASSSIFICATION OF
HYPOVOLEMIC SHOCK
HEMORRHAGIC
 TRAUMA
 GASTROINTESTINAL
BLEEDING
NON-HEMORRHAGIC
 EXTERNAL FLUID LOSS
 DIARRHOEA
 VOMITING
 POLYUREA
 FLUID REDISTRIBUTION
 BURNS
 ANAPHYLAXS 65

CLASSIFICATION OF
ACUTE BLOOD LOSS
66
 Class I: blood loss up to 15% (≤1000ml)  mild clinical symptoms
(compensated)
 Class II: blood loss 15-30% (1000-1500ml)  mild tachycardia,
tachypnea, weak peripheral pulses and anxiety (mild)
 Class III: blood loss 30-40% (1500-2000ml)  Hypotension,
marked tachycardia [pulse >110 to 120 bpm], and confusion
(moderate)
 Class IV: blood loss >40% (>2000ml)  significant depression in
systolic BP, very narrow pulse pressure (severe)

Class I Class II Class III Class IV
Blood loss
(mL)
Up to 750 mL 750 – 1500 mL 1500- 2000mL >2000 mL
Pulse rate
& pulse
pressure
<100 normal
or decreased
>100
decreased
>120
decreased
>140
Decreased
Blood
pressure
Normal Normal Decreased Decreased
Respiratory
rate
14 – 20 20 -30 30 - 40 > 35
Urine output
mL/hr
> 30 20 -30 5 -15 Negligible
Fluid
replacement
Crystalloid Crystalloid
& blood
Crystalloid
& blood
Crystalloid
43

Signs & Symptoms
72
 Anxiety, restlessness, altered mental state
 Hypotension
 A rapid, weak, thready pulse
 Cool, clammy skin
 Rapid and shallow respirations
 Hypothermia
 Thirst and dry mouth
 Distracted look in the eyes

Compensatory Mechanisms
73
1. Adrenergic discharge
2. Hyperventilation
3. Vasoactive hormones
Angiotensin ,Vasopressin, Epinephrine
4. Collapse
5. Re-absorption of fluid from interstitial tissue
6. Resorption of fluid from intracellular to extracellular space
7. Renal conservation of body water & electrolyte.

Clinical Monitoring
74
 Blood pressure
 Respiration
 Urine output
 Central venous pressure
 ECG
 Swan-Ganz catheter
* cardiac output
* mixed venous oxygen level
* vascular pressure
 Pulmonary artery wedge pressure

General Principles In Management
 Patients should be treated in ICUs preferably
 Continuous electrocardiographic monitoring
 Pulse oximetry
 A reduction of elevated serum lactate levels is one
good indicator of successful resuscitation and is
often used as a therapeutic goal
76

Medical & Surgical Management
77
OBJECTIVES
a. Increase Cardiac Output
b. Increase Tissue Perfusion
The plan of action should be based on
a. Primary problem
b. Adequate fluid replacement
c. Improving myocardial contractility
d. Correcting acid base disturbances
ATLS - (10 ed.). 2018. pp. 43–52, 135.

• Resuscitation
• Immediate control of bleeding: Rest, Pressure Packing,
Operative Methods
• Extracellular fluid replacement:
- Infusion of fluid is the fundamental treatment
- Crystalloids, for initial resuscitation for most forms of
hypovolemic shock.
- After the initial resuscitation, with up to several liters of
crystalloid fluid, use of colloids.
• Drugs
1. Sedatives
2. Chronotropic agents
3. Inotropic agents
78
Cont.
ATLS - (10 ed.). 2018. pp. 43–52, 135.

MAST  Crystalloid
 Colloid
 Blood

DISTRIBUTIVE SHOCK
80
• 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
• Examples of this form of shock :
 Septic shock
 Anaphylactic shock
 Neurogenic shock
ATLS - (10 ed.). 2018. pp. 43–52, 135.

TRAUMATIC SHOCK
81
• Primarily due to hypovolemia from :
 Bleeding externally eg: open wounds, fractures
 Bleeding internally eg: ruptured liver, spleen
• Clinical features :
 Presence of peripheral & pulmonary edema.
 Infusion of large amount of fluid which is adequate in
hypovolemic shock is inadequate here.
ATLS - (10 ed.). 2018. pp. 43–52, 135.

PATHOPHYSIOLOGY
82
Traumatic tissue activates the coagulation system
↓
Release of micro-thrombi into circulation
↓
Obstruction parts of pulmonary micro vasculature
↓
Increased pulmonary vascular resistance
↓
Increased right ventricular diastolic & right atrial pressure
↓
Humoral products of thrombi induce increase in capillary permeability
↓
Loss of plasma into interstitial tissue
↓
Depletion of Vascular volume

MANAGEMENT
83
1. Resuscitation
2. Local treatment of trauma & control of bleeding ,
surgical debridement of ischemic & dead tissue &
immobilization of fracture.
3. Fluid replacement with Ringers lactate, Ringers
acetate, Normal saline.
4. Anticoagulation with one intravenous dose of
10,000 units of heparin

CARDIOGENIC SHOCK
84
• Primary dysfunction of one ventricle or the other
• Dysfunction may be due to
> Myocardial infarction
> Chronic congestive heart failure
> Cardiac arrhythmias
> Pulmonary embolism
> Systemic arterial hypertension

Dysfunction of right ventricle  right heart unable to pump
blood in adequate amount into lungs, filling of left heart
decreases , so left ventricular out put decreases.
Dysfunction of left ventricle  left ventricle unable to
maintain adequate stroke volume , left ventricular output &
systemic arterial blood pressure decreases ,there is
engorgement of the pulmonary vasculature due to normal
right ventricular output, but failure of left heart
86
Cont.
Schumann, J: et al (29 January 2018).

• Arises when heart is compressed from outside to
decrease cardiac output , the cause may be
*Tension pneumothorax
*Pericardial tamponade
*Diaphragmatic rupture with herniation of
the bowel into the chest.
87
Cardiogenic compressive shock:

CLINICAL FEATURES
88
• Skin is pale & urine out put is low.
• Pulse becomes rapid & the systemic blood pressure is
low.
• Right ventricular dysfunction, neck veins are distended
& liver is enlarged.
• Left ventricular dysfunction , there are bronchial
rales & third heart sound heard.
• Gradually, the heart also becomes enlarged.

MANAGEMENT
90
• Air way must be cleaned
• Initial measures include supplemental oxygen and,
when systolic blood pressure permits, administration
of i.v. nitroglycerin. Insertion of an intra-aortic
balloon pump decreases ventricular after load,
improving myocardial performance
ATLS - (10 ed.). 2018. pp. 43–52, 135.

Cont.
 Revascularization with either angioplasty or
bypass
 surgery have suggested improved survival
 Vasodilators
 Beta-Blockers
91
ATLS - (10 ed.). 2018. pp. 43–52, 135.

• Cardiogenic shock can also occur after prolonged
cardiopulmonary bypass ; the stunned myocardium may
require hrs or days to recover sufficiently to support
circulation. Treatment consists of combination of
inotropic agents
• In case of pulmonary embolus it should be treated with
large doses of heparin, intravenously
92
Cont.

Cont.
 Pain ,if present should be controlled with
sedatives like morphine
 Fulminant pulmonary edema should be
controlled with diuretics.
 Drugs mainly employed are Inotrophicagents
93

EXTRACARDIAC
OBSTRUCTIVE SHOCK
94
• Flow of blood is obstructed, which impedes circulation
and can result in circulatory arrest
• Several conditions result in this form of shock
a. Cardiac tamponade
b. Constrictive pericarditis
c. Tension pneumothorax
d. Massive pulmonary embolism
Cotran, Ramzi S.; et al. (2005).. p. 141.

• Treatment of choice is pericardial drainage via
surgery
• Pulmonary embolism is usually treated with
systemic anticoagulation, but when massive
pulmonary embolism causes right ventricular failure
and shock, thrombolytic therapy should be strongly
considered 102
Management

NEUROGENIC SHOCK
103
• Primarily due to blockade of sympathetic nervous system
 loss of arterial & venous tone with pooling of blood in the
dilated peripheral venous system.
• The heart does not fill  the cardiac output falls.
• Neurogenic shock caused by:
 Paraplegia
 Quadriplegia.
 Trauma to Spinal cord.
 Spinal anesthesia.

syncope
Holtz, Anders; Levi, Richard (6 July 2010). Spi).. p. 63–4.

CLINICAL FEATURES:
 Warm skin, pink & well perfused
 Heart rate is rapid
 Blood pressure is low
 Urine output may be normal
106

Pathophysiology
107
Dilatation of the systemic vasculature
↓
Decreased systemic arterial pressure
↓
Pooling of blood in systemic venules & small veins
↓
The right heart filling & stroke volume decreases
↓
Decreased pulmonary blood volume & left heart filling
↓
Discharge of angiotensin & vasopressin though they fail to
restore the cardiac output to normal

MANAGEMENT
108
1. Assuming Trendelenburg position - displaces blood
from systemic venules into right heart & increases
cardiac output.
2. Administration of fluids.
3. Vasoconstrictor drugs.
Phenylephrine & Metaraminol
• Only type of shock safely treated with vasoconstrictor.
• Its prompt action saves patient from immediate damage
to important organs like brain, heart & kidney.

VASOVAGAL / VASOGENIC SHOCK
110
• Part of neurogenic shock
• Pathophysiology: pooling of blood due
to dilatation of peripheral vascular
system particularly in the limb muscle &
in splanchnic bed.

Cont.
 This causes reduced venous return to the heart leading
to low cardiac output & bradycardia, blood flow to
brain is reduced causing cerebral hypoxia &
unconsciousness.
 Management: Trendelenberg position -
increases cerebral flow & consciousness is
restored
111

PSYCHOGENIC SHOCK
112
Part of Neurogenic shock.
 Occurs following sudden fright from unexpected
bad news or at the sight of horrible accident.
 Effect may vary in intensity from
temporary unconsciousness to even
sudden death.

SEPTIC SHOCK
113
• Most often due to gram-negative & gram-positive
septicemia.
• It occurs in cases of,
-Severe septicemia
-Cholangitis
-Peritonitis
-Meningitis etc.
• The common organisms that are concerned with septic shock are
E.coli, klebsiella, aerobactor, proteus, pseudomonas, bacteroides, etc
Singer M, et al. (February 2016). JAMA. 315 (8): 801–10.




Clinical features
Hypotension – correct with pressors
Elevated serum lactate
Initially heart rate increase then decrease

GRAM POSITIVE SEPSIS AND SHOCK
117
• It is usually caused by dissemination of a potent
exotoxin liberated from gram positive bacteria without
evidence of bacteremia.
• It is usually seen in Clostridium Tetany or
Clostridium Perfringes infection.
• It is basically caused due to massive fluid losses.
• Arterial resistance falls but there is no fall in
cardiac output.
• Urine output usually remains normal.

GRAM NEGATIVE SEPSIS AND
SHOCK
118
• The most common cause of this infection is genito-
urinary infection.
• Persons who have had operations of the genito-urinary tract
are also susceptible.
• It may also be seen in patients who have undergone
tracheostomy or those with gasterointestinal system
infections.

• The severity may vary from mild hypotension to
fulminating septic shock which has a poor
prognosis.
• The prognosis is more favorable when the infection
is accessible to surgical drainage.
• The clinical manifestations of septic shock may be
fulminating and rapidly fatal. It is recognized initially
by the development of chills & fever of over 100
degrees.
• Two types are clearly defined
-Early warm shock.
-Late cold shock. 119
Cont.

EARLY WARM SHOCK
120
• In this type there is cutaneous vasodilatation.
• Toxins increase the body temperature. To bring this
down vasculature of the skin dilates. This increases the
systemic vascular resistance.
• Arterial blood pressure falls but the cardiac
output increases, because the left ventricle has
minimal resistance to pump against.

Cont.
 Adrenergic discharge further Increases the
cardiac output. The skin remains pink,
warm & well perfused.
 The pulse is high & the blood pressure low.
 There are intermittent spikes of fever with
bouts of chills.
121

LATE COLD SHOCK
122
• There is increased vascular resistance due to release of
toxic products.
• This leads to hypovolemia with decrease in right heart filling.
• There is decreased flow to pulmonary vasculature so the
left heart filling & the cardiac output decreases.
• The knowledge of existence of a septic focus is the only factor
that differentiates septic shock from traumatic & hypovolemic
shock.

123
• The only way to reduce mortality in septic shock
is by prompt diagnosis & treatment.
• It can be divided into two groups.
 Treatment of the infection.
Treatment of the shock.
Management

• Therapy of septic shock has 3 main components
• 1st, the nidus of infection must be identified and
eliminated
• 2nd, adequate organ system perfusion and function must
be maintained, guided by cardiovascular monitoring.
76
Cont.

• Maintenance of blood Hb level, O2 saturation
are imp therapeutic guidelines.
• 3rd therapeutic goal is to interrupt the pathogenic
sequence leading to septic shock, achieved by
inhibiting toxic mediators such as endotoxin, TNF, and
IL-1.
76
Cont.

• It consists of:
 Fluid replacement.
 Debridement & drainage of the infection.
 Administration of the antibiotics.
 Mechanical ventilation.
 Steroids.
 Vasoactive drugs.
 Specific gamma globulins to bind the endotoxins.
 The antibiotic polymixin E also absorbs some of
the endotoxin. 126
Cont.

ANAPHYLACTIC SHOCK
128
 Etiology :
• The most common cause of anaphylaxis is the
administration of penicillin.
• The other causes include anesthesia, dextrans, serum
injections, stings, consumption of shell fish.
 Pathophysiology:
• The antigen combines with Ig E on the mast cell &
basophils releasing large amounts of histamine and slow
releasing substances of anaphylaxis.

 Clinical features:
• It manifests as bronchospasm, laryngeal edema,
respiratory distress, hypoxia, massive vasodilatation,
hypotension and shock.
• The mortality rate is 10%.
• In the dental office this reaction can occur during or
immediately following the administration of penicillin or
LA to a previously sensitized patient.
129
Cont.
Tintinalli, Judith E. (2010). pp. 174–175.

Management
134
• Immediate & aggressive management is imperative if
the patient is to survive.
Step 1: Position the patient
Place the patient in a supine position with the
legs slightly elevated.
Step 2: A-B-C
Open the airway by tilting the head. Breathing &
circulation should be established carrying BLS
as needed.
Step 3: Definitive care
As soon as a systemic allergy is suspected
emergency medical help is sought.

(A) Administration of epinephrinesubcutaneously
• 0.3ml of 1:1000 for adults, 0.15 for children,0.075ml forinfants.
• With decreased perfusion the absorption of epinephrine willbe
delayed.
• In such situations it can be administered sublinguallyor
intralingually.
• If the respiratory or cardiovascular regions fail to improve within 5
minutes of administration, a 2nd dose should begiven.
• Subsequent doses can be given away 5-10 minutes as needed
provided the patient is properly monitored.
(B) Administration of oxygen
• Deliver oxygen at a flow of 5-6 liters per minute by nasal hood or
full face mask at any time during the episode.
135
Cont.

(C) Monitoring of vital signs
• Monitoring the patients cardiovascular & respiratory
status continuously.
• Record blood pressure & carotid heart rate at least
every 5minutes & start closed chest compression if
cardiac arrest occurs.
(D) Additional drug therapy
• After the administration of epinephrine, the other drugs
to be administered are : Antihistamines, Corticosteroids.
• These drugs are administered only after clinical
improvement is noted & are not be given during the acute
phase as they are too slow in onset.
Cont.

Prevention
 AvoidTrigger
 Desensatization

Nursing Management of Shock
 Check for a response.
 Give Rescue Breaths or CPR as needed.
 Lay the person flat, face-up, but do not move him or
her if you suspect a head, back, or neck injury.
 Raise the person's feet about 12 inches. Use a box,
etc. If raising the legs will cause pain or further
injury, keep him or her flat. Keep the person still.
139
Sharma Asha, pp 1722- 1750

Cont.
 Do not raise the feet or move the legs if hip or leg
bones are broken. Keep the person lying flat.
 Check for signs of circulation. If absent, begin CPR.
 Keep the person warm and comfortable. Loosen belt
(s) and tight clothing and cover the person with a
blanket.
140

Cont.
 NPO: Even if the person complains of thirst, give
nothing by mouth. If the person wants water, moisten
the lips.
 Reassure the person. Make him or her as comfortable.
 Fluid and blood replacement: Open IV line on both
hands with two wide bore cannulas and start fluid
rapidly as advised.
141

Cont.
 Administer oxygen via face mask.
 Identify the cause and treat accordingly.
 Vasoactive medications to improve cardiac
contractility, i.e. Dopamine, Dobutamine,
Noradrenaline.
142

Self-Care at Home
 Call for help and Stay with the person until help
arrives,
 check the person's airway, breathing and circulation
(the ABCs).
 Administer CPR if you are trained. If the person is
breathing on his or her own, continue to check
breathing every 2 minutes until help arrives.
143
Sharon Mantik 3rd Ed pp. 740-757

Cont.
 Do NOT move a person who has a known or suspected
spinal injury (unless they are in imminent danger of
further injury).
 Have the person lie down on his or her back with the
feet elevated above the head (if raising the legs causes
pain or injury, keep the person flat) to increase blood
flow to vital organs. Do not raise the head.
144

Cont.
 Keep the person warm and comfortable.
 Loosen tight clothing and cover them with a blanket.
 Do not give fluids by mouth, even if the person complains
of thirst. There is a choking risk in the event of sudden
loss of consciousness.
 Give appropriate first aid for any injuries.
 Direct pressure should be applied to any wounds that are
bleeding significantly. 145

Differential Diagnosis
 Systemic inflammatory response syndrome (SIRS)
 Acute coronary syndrome (ACS)
 Aortic regurgitation
 Dilated cardiomyopathy
 Restrictive cardiomyopathy
 Congestive heart failure (CHF) and pulmonary
edema 146
Alonso DR, et al . 1973 Sep. 48 (3):588-96.

Cont.
 Mitral regurgitation
 Pericarditis and cardiac tamponade
 Hypovolemic shock
 Papillary muscle rupture
 Acute valvular dysfunction
147
Alonso DR, et al . 1973 Sep. 48 (3):588-96.

Prognosis
 The prognosis varies with the origin of shock and its
duration.
 Low volume, anaphylactic, and neurogenic shock
are readily treatable and respond well to medical
therapy.
 80%-90% of young patients survive hypovolemic
shock with appropriate management.
148

Cont.
 Cardiogenic shock associated with extensive
myocardial infraction : (mortality rate up to
75%)
 Septic shock, however has a mortality rate between
30% and 80% while cardiogenic shock has a
mortality rate between 70% and 90%.
149

Cont.
 Hypovolemic, anaphylactic and neurogenic shock
are readily treatable and respond well to medical
therapy.
 Perfusion of the brain may be the greatest danger
during shock.
 Therefore urgent treatment is essential for a good
prognosis
150

NURSING PROCESS
ASSESSMENT
1. Health Perception and Management
Subjective Data
 c/c: SOB/chest pain/dizziness
etc
 HPI: Mr. X is a 25yr old male
married pt, presented with sob,
weakness, fainting /2day…
 Hx Past: pt has Hx of HTN Rx
in the past months….
 Life style changes: sport, avoid
salt, avoid smoking…
 Non/prescribed: penicillin
 He has visit to hospital in the
past
Objective Data
 Blood Pressure: 90/60
mmHg
 Heart Rate: 120bpm
 2 appointment missed by the
pt in the past Rx
151

2. ACTIVITY AND EXERCISE
2.1 Mobility & Self Care
Subjective Data
 Appropriate bathing,
toileting, dressing,
grooming, feeding.
 Good motor activities like
sitting, standing, walking,
and , opening doors.
 Good home maintenance
skill
 Restriction of rigorous
physical activity
Objective Data
 Good balance, coordination,
abnormal movements
 Good muscle tone, strength,
bulk
 Good body position
152

2.2 Respiration functioning
Subjective Data
 Smoking cigarette
 Shortness of breath
Objective Data
 Increased respiratory rate
 Decreased SpO2
 Crackles in lungs
 No asymmetric expansion
 Tactile fremitus present
 No wheezing, rales,
crackling, rhonchus sound
153

2.3 Cardio vascular functioning
Subjective Data
 Hx of smoking
 Hx Hypertension
 Fainting
 Dizziness
Objective Data
 Blood Pressure: 90/60
mmHg (decreased bp)
 Heart Rate: 120bpm
(increased heart rate)
 Heart sounds muffled
 S3, S4 present
 JVD
154

3. Nutrition & Metabolism
Subjective Data
 Decreased food and fluid
intake
 Nausea
 Vomiting
 Salty food intake restriction
Objective Data
 BMI: with in normal range
 No edema
 No scars, stretch
marks, lesions, dilated
veins, or rashes.
 No organomegaly
155

4. ELIMINATION
4.1 Urinary elimination
Subjective Data
 Small amount of urine
 Less frequent urination
Objective Data
 Normal color of urine
 No bladder distension,
tenderness
156

4. ELIMINATION
4.2 Bowel Elimination
Subjective Data
 Recent change in bowl
movement
 Normal color of stool
 Hx of Bowel Surgery
Objective Data
 No hemorrhoids, wart, sores
or masses
 No masses or tenderness
 No enlargement of prostate
157

5. Sleep & Rest Pattern
Subjective Data
 Normal Hour of sleep: <8hr
 Nap during the day: present
 Satisfaction with sleep
pattern: NO
Objective Data
 Frequently yawning
 Decreased attention span.
 Dark circles or puffiness
around the eyes.
 Continual dozing
158

6. Cognition & Perception
Subjective Data
 Orientation to place, person
and time: absent
 Pain
 Fluid imbalance
 Decreased oxygen supply
 Inadequate blood flow
 Neurological impairment
 Systemic infection
 Medication toxicity
Objective Data
 Shallow or rapid respiration/
SOB
 Abnormal cardiovascular
function/ Hypotension
 History of HTN
159

7. Self- Perception & Self- Concept
Subjective Data
 The pt describe him self as
good person
 Pt consider his illness as his
weakness
 Pt. feels good most of the
time
Objective Data
 Good eye contact
 Personal grooming and
appearance is good
 Posture and body
movements is normal
 Mood and emotions are
good
 Voice and speech pattern
are normal
160

8. Roles & Relationship
Subjective Data
 Good financial status of the
pt family
 The husband & the wife
makes the decision of the
house
 Family members support
each others well
 No financial problem in the
family
Objective Data
 Good family interactions
 No behavioural signs of
dysfunction like labile
emotions, withdrawal,
irritability, poor sleeping
and eating, inability to
concentrate, and
dependency
 No indicators of physical
abuse
161

9. Coping & Stress Tolerance
Subjective Data
 Praying relieve pt stress
 Pt talk when he is worried
 Little bad effect on the pt
feeling due to illness
Objective Data
 Pt has sympathetic
stimulation for sudden
stressors.
162

10. SEXUALITY AND
REPRODUCTION PATTERN
Subjective Data
 No STI
 No change in sexuality
Objective Data
 No abnormal findings in
Examination of reproductive
organs
163

11. Values & Beliefs Pattern
Subjective Data
 Praying, fasting are among
the Religious practices that
are important to the pt
 Significance of religion to
the person is high
 No Impact of illness on the
patient’s belief
Objective Data
 Pt. Visit clergy
 Pt. seen praying
164

Nursing Diagnosis
 Ineffective breathing patter related to the disease
process as evidenced by change in respiratory rate
 Anxiety related to the disease process as evidenced
by dizziness and light headedness
 Risk of infection related to hospitalization
165

Nursing Plan
 Goal
 Return the Client breathing pattern to normal level
 Remove the Client anxiety completely
 Avoid the Client infection risk completely
166

Cont.
 Expected Outcome
 Client breathing pattern improved in 50% after
15min oxygenation
 Client anxiety decrease by half after 10 min health
education
 Client risk of infection decrease by 75% after
giving prophylactic ordered medication and CASH
167

Intervention
 Giving ordered medication and oxygenation
 Health Education And Reassurance
 Performing CASH
 Monitoring the client changes and treat
accordingly
168

Evaluation
 Client condition Improved
 Proposed goal met
169

 Shock is a life-threatening medical condition and is a
medical emergency.
 Symptoms of septic shock include fever, nausea, vomiting,
and dizziness or fainting.
 There are several types of shock: septic shock caused by
bacteria, anaphylactic shock caused by hypersensitivity or
allergic reaction, cardiogenic shock from heart damage,
hypovolemic shock from blood or fluid loss, and neurogenic
shock from spinal cord trauma.
 Treatment for shock depends on the cause. Tests will
determine the cause and severity. Usually IV fluids are
administered in addition to medications that raise blood
pressure. 170
Summary

Cont.
 Septic shock is treated with antibiotics and fluids.
 Anaphylactic shock is treated with diphenhydramine (Benadryl),
epinephrine (an "Epi-pen"), and steroid medications (solu-medrol).
 Cardiogenic shock is treated by identifying and treating the
underlying cause.
 Hypovolemic shock is treated with fluids (saline) in minor cases, and
blood transfusions in severe cases.
 Neurogenic shock is the most difficult to treat as spinal cord damage
is often irreversible. Immobilization, anti-inflammatories such as
steroids and surgery are the main treatments.
 Shock prevention includes learning ways to prevent heart disease,
injuries, dehydration and other causes of shock.
171

Reference
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2018. pp. 43–52, 135. ISBN 978-78-0-9968267
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(Tintinalli)). New York: McGraw-Hill Companies. p. 168. ISBN 978-0-07-148480-0.
4) Cherkas, David (Nov 2011). "Traumatic Hemorrhagic Shock: Advances In Fluid Management“
(https://web.archive.org/web/20120118152838/http://www.ebmedicine.net/store.php?paction=showProduct
&catid=8&pid=244). Emergency Medicine Practice. 13 (11). PMID 22164397
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(https://semanticscholar.org/paper/f8eb49085615fe6fac11777ae1f36786d161dfbe). The New England
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Teboul JL, Vincent JL, Rhodes A (December 2014). "Consensus on circulatory shock and hemodynamic
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doi:10.1007/s00134-014-3525-z (https://doi.org/10.1007%2Fs00134-014-3525-z). PMC 4239778
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Cont.
6) Davidson’s Principles And Practice Of Medicine – 22nd ed.
7) Schwartz’s Principles Of Surgery – 8th ed.
8) Bailey & Love’s short practice of surgery
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(https://www.mayoclinic.org/diseases-conditions/cardiogenic-
shock/symptoms-causes/syc-20366739). Mayo Clinic. Retrieved 22 May
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10) Alonso DR, Scheidt S, Post M, Killip T. Pathophysiology of cardiogenic
shock. Quantification of myocardial necrosis, clinical, pathologic and
electrocardiographic correlations. Circulation. 1973 Sep. 48 (3):588-96.
11) Elbers PW, Ince C (2006). "Mechanisms of critical illness--classifying
microcirculatory flow abnormalities in distributive shock"
(https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1750971).Critical Care. 10
(4): 221. doi:10.1186/cc4969 (https://doi.org/10.1186%2Fcc4969).PMC
1750971 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC1750971). PMID
16879732 (https://pubmed.ncbi.nlm.nih.gov/16879732).
173

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11) Armstrong, D.J. (2004). Shock. In: Alexander, M.F., Fawcett, J.N., Runciman, P.J. Nursing
Schumann, J; Henrich, EC; Strobl, H; Prondzinsky, R; Weiche, S; Thiele, H; Werdan, K; Frantz,
S; Unverzagt, S (29 January 2018). "Inotropic agents and vasodilator strategies for the
treatment of cardiogenic shock or low cardiac output syndrome" (https://www.ncbi.nlm.nih.gov/p
mc/articles/PMC6491099). The Cochrane Database of Systematic Reviews. 1: CD009669.
doi:10.1002/14651858.CD009669.pub3 (https://doi.org/10.1002%2F14651858.CD009669.pub
3). PMC 6491099 (https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6491099). PMID 29376560
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doi:10.1001/jama.2016.0287 (https://doi.org/10.1001%2Fjama.2016.0287). PMC 4968574 (http
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13) Sharma Asha, Lewis medical surgical nursing, Elsevier publication,page no 1722-
1750
14) Sharon Mantik Lewis Medical Surgical Nursing, Mosby's year book publication3rdEdition page
no 740-757
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16) Practice. Hospital and Home. The Adult.(2nd edition): Edinburgh: Churchill Livingstone.
17) Tintinalli, Judith E. (2010). Emergency Medicine: A Comprehensive Study Guide
(Emergency
Medicine (Tintinalli)). New York: McGraw-Hill Companies. pp. 174–175. ISBN 978-0-07-
18) Kumar, Vinay; Abbas, Abul K.; Fausto, Nelson; & Mitchell, Richard N. (2007). Robbins
Basic
Pathology (8th ed.). Saunders Elsevier. pp. 102–103 ISBN 978-1-4160-2973-1
19) Guyton, Arthur; Hall, John (2006). "Chapter 24: Circulatory Shock and Physiology of Its
Treatment". In Gruliow, Rebecca (ed.). Textbook of Medical Physiology (11th ed.).
Philadelphia,
Pennsylvania: Elsevier Inc. pp. 278–288. ISBN 978-0-7216-0240-0.
20) Holtz, Anders; Levi, Richard (6 July 2010). Spinal Cord Injury
(https://books.google.com/books?
id=ZvCqdwWwGRsC&pg=PA63). Oxford University Press. p. 63–4. ISBN 978-0-19-
970681-5.
21) Cotran, Ramzi S.; Kumar, Vinay; Fausto, Nelson; Nelso Fausto; Robbins, Stanley L.;
Abbas,
Abul K. (2005). Robbins and Cotran pathologic basis of disease. St. Louis, Mo: Elsevier
Saunders. p. 141. ISBN 0-7216-0187-1. 175

ACKNOWLEDGMENT
 First I would like to express my heartfelt gratitude
to WU CMHS for giving me this chance to
enhance my knowledge and skill.
 Secondly I would like to thank my instructor Mr.
Wondwossen Yimam for sharing me his deep
knowledge, experience and expertise.
 Last but not least I would like to thank my family
and friends in helping me in ideas and material
during my entire work.
176

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