College of Medicine &

Health Sciences

School of Nursing & Midwifery

Department of Adult Health Nursing

[Link]: Habtemariam Mulugeta 1

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

ATLS - Student Course Manual (10 ed.). 2018. pp. 43–52, 135.
4
 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
1. International Trauma Life Support for Emergency Care Providers (8 ed.)
2018. pp. 172–173. 5
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

1. Bailey and love

2. Davidson’s 6
 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

1. Schwartz’s 7
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
1. Cherkas, David (Nov 2011). PMID 22164397
2. Vincent JL, De Backer D (October 2013. 369 (18): 1726–34.
8
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,

"Cardiogenic shock - Mayo Clinic. Retrieved 22 May 2020.

11
Pathophysiology

12
 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)

15
Non progressive
shock
16
Progressive decompensated shock

17
Decompensated shock

18
 Armstrong, D.J.
(2004). The
Adult.(2nd edition)

19
 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
International Trauma Life Support for Emergency Care Providers (8 ed.). 2018.
pp. 172–173
20
 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
22
 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.
 Cont.
• 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).

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

29
 Cont.
• 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.
ATLS - (10 ed.). 2018. pp. 43–52, 135.
30
 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

ATLS - (10 ed.). 2018. pp. 43–52, 135. 31

 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.
Tintinalli, Judith E. (2010). pp. 174–175. 32
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.

Tintinalli, Judith E. (2010). pp. 174–175. 34

 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
35
8. cell death.
 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.

Kumar, Vinay; et al. (2007). pp. 102–103
37
 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

Kumar, Vinay; et al. (2007). pp. 102–103

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.
Kumar, Vinay; et al. (2007). pp. 102–103
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
44

HAEMORRHAGES”
 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.
Kumar, Vinay; et al. (2007). pp. 102–103
46
47
 ISCHEMIC REPERFUSION
SYNDROME
 It is the injury that occurs once the normal circulation is restored
to the tissues
 Reasons:
 Acid and 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

Kumar, Vinay; et al. (2007). pp. 102–103

48
Classification of SHOCK
 Primary (INITIAL SHOCK)

 Secondary (TRUE SHOCK)

 Anaphylactic (Type I immunologic reaction)

Guyton, Arthur; Hall, John (2006). Textbook of Medical Physiology (11th

ed.).. pp. 278–288.
49
 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.

Guyton, Arthur; Hall, John (2006). Textbook of Medical Physiology (11th

ed.).. pp. 278–288. 52
 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.
• Vasovagal
• Psychogenic
• Neurogenic
• Hypovolemic
• Traumatic
• Burns
• Cardiogenic hyper dynamic /warm
• Septic (endotoxin): hypovolemic hypo dynamic /cold
• Anaphylactic
56
(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
Proposed by HINSHAW and COX (1972)

• Shock due to reduced blood volume (Hypovolemic

shock or cold shock)
 Traumatic shock

 Hemorrhagic shock

 Surgical shock

 Burn shock

 Dehydration shock 58
Proposed by HINSHAW and COX (1972)

• 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

• 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. 61
HYPOVOLEMIC SHOCK
PATHOPHYSIOLOGY
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
64
 CLASSSIFICATION OF
HYPOVOLEMIC SHOCK
HEMORRHAGIC NON-HEMORRHAGIC
 TRAUMA  EXTERNAL FLUID LOSS

 GASTROINTESTINAL  DIARRHOEA
BLEEDING  VOMITING

 POLYUREA

 FLUID REDISTRIBUTION

 BURNS

 ANAPHYLAXS 65
 CLASSIFICATION OF
ACUTE BLOOD LOSS
 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)
66
 Class I Class II Class III Class IV

Blood loss Up to 750 mL 750 – 1500 mL 1500- 2000mL >2000 mL

(mL)

Pulse rate <100 normal >100 >120 >140

& pulse or decreased decreased decreased Decreased
pressure

Blood Normal Normal Decreased Decreased

pressure

Respiratory 14 – 20 20 -30 30 - 40 > 35

rate

Urine output > 30 20 -30 5 -15 Negligible

mL/hr

Fluid Crystalloid Crystalloid Crystalloid Crystalloid

43
replacement & blood & blood
Burns
 Third Spacing
.
Signs & Symptoms
 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 72

Compensatory Mechanisms
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. 73

Clinical Monitoring
 Blood pressure
 Respiration
 Urine output
 Central venous pressure
 ECG
 Swan-Ganz catheter
* cardiac output
* mixed venous oxygen level
* vascular pressure
 Pulmonary artery wedge pressure
74
75
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
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. 77
 Cont.
• 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
ATLS - (10 ed.). 2018. pp. 43–52, 135. 78
MAST  Crystalloid
 Colloid
 Blood
 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

• Examples of this form of shock :

 Septic shock

 Anaphylactic shock

 Neurogenic shock
ATLS - (10 ed.). 2018. pp. 43–52, 135. 80
TRAUMATIC SHOCK
• 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. 81

PATHOPHYSIOLOGY
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
↓ 82
Depletion of Vascular volume
MANAGEMENT
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
83
CARDIOGENIC SHOCK
• 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 84

Cont.
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
Schumann, J: et al (29 January 2018). 86
Cardiogenic compressive shock:

• 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
 CLINICAL FEATURES
• 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. 88
89
 MANAGEMENT
• 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. 90

 Cont.
 Revascularization with either angioplasty or
bypass

 surgery have suggested improved survival

 Vasodilators

 Beta-Blockers

91
ATLS - (10 ed.). 2018. pp. 43–52, 135.
Cont.
• 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.
 Pain ,if present should be controlled with
sedatives like morphine

 Fulminant pulmonary edema should be

controlled with diuretics.

 Drugs mainly employed are Inotrophic agents

93
 EXTRACARDIAC
OBSTRUCTIVE SHOCK
• 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. 94
Tension Pneumothorax
Constrictive pericarditis
 CardiacTamponade
Pulmonary embolism
Aortic stenosis
 Management
• 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
NEUROGENIC SHOCK
• 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. 103
 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

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

106
 Pathophysiology
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
107
 MANAGEMENT
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.
Holtz, Anders; Levi, Richard (6 July 2010). Spi).. p. 63–4.
108
 VASOVAGAL / VASOGENIC SHOCK

• Part of neurogenic shock

• Pathophysiology: pooling of blood due
to dilatation of peripheral vascular
system particularly in the limb muscle &
in splanchnic bed.
Holtz, Anders; Levi, Richard (6 July 2010). Spi).. p. 63–4.
110
 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

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.
112
 SEPTIC SHOCK
• 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
[Link], klebsiella, aerobactor, proteus, pseudomonas, bacteroides, etc
Singer M, et al. (February 2016). JAMA. 315 (8): 801–10. 113
 Clinical features

 Hypotension – correct with pressors

 Elevated serum lactate
 Initially heart rate increase then decrease
 GRAM POSITIVE SEPSIS AND SHOCK

• 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.

117
Singer M, et al. (February 2016). JAMA. 315 (8): 801–10.
 GRAM NEGATIVE SEPSIS AND
SHOCK
• 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.

118
Cont.
• 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
EARLY WARM SHOCK
• 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.
120
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
• 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.
122
 Management
• 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.

123
Singer M, et al. (February 2016). JAMA. 315 (8): 801–10.
Cont.
• 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
ANAPHYLACTIC SHOCK
 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
128
releasing substances of anaphylaxis.
Cont.
 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
Tintinalli, Judith E. (2010). pp. 174–175.
132
Management
• 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.
134
Tintinalli, Judith E. (2010). pp. 174–175.
Cont.
(A) Administration of epinephrinesubcutaneously
• 0.3ml of 1:1000 for adults, 0.15 for children,0.075ml for infants.
• With decreased perfusion the absorption of epinephrine will be
delayed.
• In such situations it can be administered sublingually or
intralingually.
• If the respiratory or cardiovascular regions fail to improve within 5
minutes of administration, a 2nd dose should be given.
• 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
Tintinalli, Judith E. (2010). pp. 174–175.
 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.
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
Sharma Asha, pp 1722- 1750
 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

Sharma Asha, pp 1722- 1750

 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 Alonso DR, et al . 1973 Sep. 48 (3):588-96. 146
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 Objective Data
 c/c: SOB/chest pain/dizziness  Blood Pressure: 90/60
etc mmHg
 HPI: Mr. X is a 25yr old male  Heart Rate: 120bpm
married pt, presented with sob,
 2 appointment missed by the
weakness, fainting /2day…
pt in the past Rx
 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
151
past
2. ACTIVITY AND EXERCISE
2.1 Mobility & Self Care
Subjective Data Objective Data
 Appropriate bathing,  Good balance, coordination,
toileting, dressing, abnormal movements
grooming, feeding.  Good muscle tone, strength,
 Good motor activities like bulk
sitting, standing, walking,  Good body position
and , opening doors.
 Good home maintenance
skill
 Restriction of rigorous
physical activity
152
2. ACTIVITY AND EXERCISE
2.2 Respiration functioning
Subjective Data Objective Data
 Smoking cigarette  Increased respiratory rate
 Shortness of breath  Decreased SpO2
 Crackles in lungs
 No asymmetric expansion
 Tactile fremitus present
 No wheezing, rales,
crackling, rhonchus sound

153
2. ACTIVITY AND EXERCISE
2.3 Cardio vascular functioning
Subjective Data Objective Data
 Hx of smoking  Blood Pressure: 90/60
 Hx Hypertension mmHg (decreased bp)
 Fainting  Heart Rate: 120bpm
(increased heart rate)
 Dizziness
 Heart sounds muffled
 S3, S4 present
 JVD

154
3. Nutrition & Metabolism
Subjective Data Objective Data
 Decreased food and fluid  BMI: with in normal range
intake  No edema
 Nausea  No scars, stretch
 Vomiting marks, lesions, dilated
 Salty food intake restriction veins, or rashes.
 No organomegaly

155
4. ELIMINATION
4.1 Urinary elimination
Subjective Data Objective Data
 Small amount of urine  Normal color of urine
 Less frequent urination  No bladder distension,
tenderness

156
4. ELIMINATION
4.2 Bowel Elimination
Subjective Data Objective Data
 Recent change in bowl  No hemorrhoids, wart, sores
movement or masses
 Normal color of stool  No masses or tenderness
 Hx of Bowel Surgery  No enlargement of prostate

157
5. Sleep & Rest Pattern
Subjective Data Objective Data
 Normal Hour of sleep: <8hr  Frequently yawning
 Nap during the day: present  Decreased attention span.
 Satisfaction with sleep  Dark circles or puffiness
pattern: NO around the eyes.
 Continual dozing

158
6. Cognition & Perception
Subjective Data Objective Data
 Orientation to place, person  Shallow or rapid respiration/
and time: absent SOB
 Pain  Abnormal cardiovascular
 Fluid imbalance function/ Hypotension
 Decreased oxygen supply  History of HTN
 Inadequate blood flow
 Neurological impairment
 Systemic infection
 Medication toxicity
159
7. Self- Perception & Self- Concept
Subjective Data Objective Data
 Good eye contact
 The pt describe him self as  Personal grooming and
good person appearance is good
 Pt consider his illness as his  Posture and body
weakness movements is normal
 Pt. feels good most of the  Mood and emotions are
time good
 Voice and speech pattern
are normal

160
8. Roles & Relationship
Subjective Data Objective Data
 Good financial status of the  Good family interactions
pt family  No behavioural signs of
 The husband & the wife dysfunction like labile
makes the decision of the emotions, withdrawal,
house irritability, poor sleeping
 Family members support and eating, inability to
each others well concentrate, and
dependency
 No financial problem in the
family  No indicators of physical
abuse
161
9. Coping & Stress Tolerance
Subjective Data Objective Data
 Praying relieve pt stress  Pt has sympathetic
 Pt talk when he is worried stimulation for sudden
stressors.
 Little bad effect on the pt
feeling due to illness

162
 10. SEXUALITY AND
REPRODUCTION PATTERN
Subjective Data Objective Data
 No abnormal findings in
 No STI Examination of reproductive
organs
 No change in sexuality

163
11. Values & Beliefs Pattern
Subjective Data Objective Data
 Praying, fasting are among  Pt. Visit clergy
the Religious practices that  Pt. seen praying
are important to the pt
 Significance of religion to
the person is high
 No Impact of illness on the
patient’s belief

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
 Summary
 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
170
pressure.
 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
1) ATLS - Advanced Trauma Life Support - Student Course Manual (10 ed.). American College of Surgeons.
2018. pp. 43–52, 135. ISBN 978-78-0-9968267
2) International Trauma Life Support for Emergency Care Providers (8 ed.). Pearson Education Limited. 2018.
pp. 172–173. ISBN 978-1292-17084-8.
3) Tintinalli, Judith E. (2010). Emergency Medicine: A Comprehensive Study Guide (Emergency Medicine
(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“
([Link]
&catid=8&pid=244). Emergency Medicine Practice. 13 (11). PMID 22164397
([Link] Archived from the original
([Link] on 2012-01-18.
5) Vincent JL, De Backer D (October 2013). "Circulatory shock"
([Link] The New England
Journal of Medicine. 369 (18): 1726–34. doi:10.1056/NEJMra1208943
([Link] PMID 24171518
([Link]
6) Cecconi M, De Backer D, Antonelli M, Beale R, Bakker J, Hofer C, Jaeschke R, Mebazaa A, Pinsky MR,
Teboul JL, Vincent JL, Rhodes A (December 2014). "Consensus on circulatory shock and hemodynamic
monitoring. Task force of the European Society of Intensive Care Medicine"
([Link] Intensive Care Medicine. 40 (12): 1795–815.
doi:10.1007/s00134-014-3525-z ([Link] PMC 4239778 172
([Link] PMID 25392034
([Link]
 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
9) "Cardiogenic shock - Symptoms and causes"
([Link]
shock/symptoms-causes/syc-20366739). Mayo Clinic. Retrieved 22 May
2020.
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"
([Link] Care. 10
(4): 221. doi:10.1186/cc4969 ([Link]
1750971 ([Link] PMID 173

16879732 ([Link]
 Cont.
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" ([Link]
mc/articles/PMC6491099). The Cochrane Database of Systematic Reviews. 1: CD009669.
doi:10.1002/14651858.CD009669.pub3 ([Link]
3). PMC 6491099 ([Link] PMID 29376560
([Link]
12) Singer M, Deutschman CS, Seymour CW, Shankar-Hari M, Annane D, Bauer M, et al.
(February 2016). "The Third International Consensus Definitions for Sepsis and Septic Shock
(Sepsis-3)" ([Link] JAMA. 315 (8): 801–10.
doi:10.1001/jama.2016.0287 ([Link] PMC 4968574 (http
s://[Link]/pmc/articles/PMC4968574). PMID 26903338 ([Link]
[Link]/26903338).
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

174
Cont.
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
([Link]
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
Thank You

177