For Bsc clinical medicine, MBBS, mbchb, MD students

1. Shock
IBRAHIM KIMANI WAINAINA

2. definition
This is a physiological state in which there is reduction in tissue perfusion,
therefore, resulting into decreased tissue oxygen delivery.
can also be defined as a condition in which the circulation fails to meet the
metabolic needs of the tissue and at the same time fails to effectively remove
the metabolic waste products.

3. Epidemiology
 shock lead to thousands of children being admitted to intensive care setting per year
 it is estimated that septic shock affects more than 30 million people globally/year
 3 million newborns and 1.2 million children suffer from sepsis three out of every 10 deaths
due to neonatal sepsis are thought to be caused by persistent pathogens

4. pathophysiology
 Tissue perfusion is entirely dependent on the mean arterial pressure(cardiac
output)
 MAP = cardiac output * stroke volume
 The initial response is driven by : hypoperfusion and cellular energy deficit
 Demand-supply mismatch
 The specific responses depends on etiology of shock
Cellular level- compensation/dysfunction/death
Decreased concentration of oxygen in the cells, decreased oxidative phosphorylation,
decreased ATP synthesis, shift from aerobic to anaerobic glycolysis, pyruvate is
converted to lactate( instead of glucose; leading to increase of lactic acid),
accumulation of lactate and other inorganic phosphates therefore decreasing the P.H,
lactate and other metabolic wastes exists the cells leading to a systemic metabolic
acidosis

5. Microvascular pathophysiology
 There is both activation of the alpha and the beta receptors
 Alpha: vasoconstriction activated by norepinephrine and epinephrine from the
adrenal medulla(alpha 1), others: angiotensin converting enzyme 2,
vasopressin, endothelial 1
 Vasodilators such as adenosine
Therefore;
There is hypoxia and increased acidosis that leads to the activation of the
complement and neutrophil activation, Free radicals and cytokines are released ,
there is injury to the capillary endothelial cells, there is further activation of the
immune and the coagulation system, there is damage of the endothelium with
loss of integrity leading to leaking of the capillary endothelium, resulting into
tissue edema and cellular hypoxia

6. Cardiovascular level;
 In the heart: there is decreased preload and hence decreased afterload
 The sympathetic system is activated
 Catecholamine are released from the adrenal medulla
 There is increased heart rate and contractility; venous and arterial
vasoconstriction
 Arterial vasoconstriction has regional variations; there is shunting of blood
away from the less essential organ beds such as, intestines, kidneys and the
skin.
 Brain and the heart: increased supply
Pulmonary level
Tachypnea, increased ventilation and increased carbon dioxide excretion
(compensatory respiratory alkalosis). Non-cardiogenic pulmonary edema

7. Renal level:
 Decreased renal blood flow, rennin angiotensin system is activated: decrease in glomerulus
filtration rate, increase in aldosterone and vasopressin resulting into oliguria. Further
vasoconstriction leads to increased sodium and water retention hence oedema
 Resulting into a toxic tubular injury and tubular obstruction
Metabolic derangements:
Disruption of the metabolism resulting into, anaerobic metabolism: lactic acid
There is increased hepatic gluconeogenesis, increased hepatic gluconeogenesis, increased
proteins catabolism leading to muscle wastion

8. stages of shock
Compensated /non-progressive shock
Homeostasis is able to reverse the shock, when the underlying
cause is corrected, the patient will recover with little or no
residual effects. If the body fails to achieve homeostasis then the
shock enters the uncompensated(progressive shock)
Uncompensated/progressive
Aggressive interventions are needed to prevent MODS( multiple
organ dysfunction syndrome)
Irreversible/ refractory shock
Final stage, when there is complete failure of homeostasis

9. EVALUATION: Regardless of the cause
 ABC
 Early signs of shock: sinus tachycardia, delayed capillary refill irritable,
 late signs of shock: bradycardia, altered mental status, hypotonic, chyne-
strokes breathing
 hypotension is a very late sigh

10. General laboratory studies:
 Arterial blood gases
 Blood sugars
 Electrolytes
 Complete blood count
 Prothrombin time
 cultures

11. Types of shock
Hypovolemic shock
Loss of redistribution of blood, plasma or any thither body fluids; leading into decreased circulatory volume.
Causes/history: hemorrhagic shock, intra-abdominal bleeding, significant vaginal bleeding gastrointestinal
bleeding, vomiting, diarrhea etc.
In hypovolemic shock there is: increased heart rate, decreased pulse pressure and decreased blood pressure
CLINICAL FEATURES
Cardiovascular: decreased preload and stroke volume, decreased capillary refill
Pulmonary: tachypnea or bradypnoea (is a late sign)
Renal: decreased urine output
Skin: pallor, cold and clammy

12.  Neurologic: anxiety, confusion, agitation
 Gastrointestinal : absent bowel sounds
 Lad diagnosis: decreased hematocrit, decreased hemoglobin, increased
lactate, increased urine gravity, changes is electrolytes.
Treatment
Shout for help
ABC
Administer oxygen
Establish intravenous access

13. CONT…
 replace the circulating blood volume rapidly: start with crystalloids
 blood products for hemorrhagic shock
 treat the underlying cause

14. Cont..
 Fluid bolus of isotonic fluid 20ml/kg (maximum of three times), until
perfusion improves or hepatomegaly develops
 Transfuse whole blood or its products
 Supportive
 Monitor vitals every five minutes until out of shock

15. Cardiogenic shock
 There is impaired ability of the left ventricle, leading to inadequate emptying of the left
ventricle, :increased left ventricle filling pressure, increased left atrial pressure, decreased
stroke volume and decreased cardiac output.
 Increased pulmonary capillary pressure, leading to pulmonary interstitial and intra-alveolar
pressure.
Causes
Myocarditis, dysrhythmias , drugs with myocardial depressant activity, acidosis, congenital heart
lesions, infections,

16. CONT…
 Clinical features: tachycardia, low volume pulse, cold and clammy extremities,
pulmonary edema, jugular venous distension, hepatomegaly, hypotension, oliguria,
changes in mental status
 Differentiation from other types of shock: physical exam-enlarged liver, gallop
rhythm, murmur, rales. Chest x-ray-enlarged heart, pulmonary venous congestion.

17. treatment
 Goal: increase cardiac output, treat the reversible causes, decrease
myocardial workload.
 Improve cardiac output: correct, dysthymias, optimize pre-load, improve
contractility, reduce afterload
 Minimize cardiac work: maintain normal temperature, sedation,
intubation and mechanical ventilation, correct anemias

18. Obstructive shock
 Pathology: There is decreased cardiac output secondary to restriction of all cardiac
chambers. There is physical obstruction to blood flow, leading to decreased cardiac output,
decreased tissue perfusion, compensatory mechanisms, leading to systemic vascular
resistance.
CAUSES: tension pneumothorax, pericardial tamponade, pulmonary embolism, anterior
mediastinal masses, coarctation of aorta, pulmonary hypertension
clinical presentation
 Pericardial Effusion: muffled heart sounds, distended neck veins, pulsus paradoxus
(increased systolic blood pressure on inspiration)
 Pulmonary embolism: Signs of right sided heart failure plus cyanosis , tachycardia and
hypotension

19. Cont..
 History; excessive respiratory effort, prolonged feeding time, poor weight gain,
excessive sweating, frequent respiratory tract infections
 physical exam: gallop, cold extremities, weak peripheral pulses, dyspnea, cyanosis,
hepatomegaly, peripheral edema, hypotension

20. Treatment
 Pericardial drainage: incase of pericardial effusion
 Tension pneumothorax: immediate thorax decompression, then thoracostomy
for chest tube.
 Anticoagulants: or embolectomy for pulmonary embolism

21. Distributive shock
Pathology:
 Maldistribution of blood flow;
 Some tissues are inadequately perfused (splanchnic circulation)
 Some tissues are over perfused (skeletal muscles and skin)
CLINICAL PRESENTATION
Tachypnea without increased work of breathing, hypotension/normal tension
,warm flushed skin or cold pale skin
Causes: anaphylaxis, drug toxicity, neurologic injury(neurogenic), early sepsis, spinal
anesthesia

22. TREATMENT
 1. ANAPHYLACTIC SHOCK
airways, intravenous epinephrine, antihistamines, corticosteroids, withdrawal of the
antigen, vasopressors, inotropes, continuous fluid administration.
2. NEUROGENIC SHOCK
Continuous fluid administration, vasopressors, inotropes, correct hypothermia, treat
bradycardia with atropine, observe and prevent DVT (due to peripheral pooling of blood)

23. Septic shock
 Pathology: bacterial products and components enter the body, activation of
coagulation and the complement system, tissue factors release fibrinolytic
activity, endothelial damage, tissue injury , organ dysfunction
Stages: sirs, sepsis, severe sepsis, septic shock
SIRS: temperatures>38 degrees Celsius or ,35 degrees Celsius, respiratory
rate >24 or < 18 breaths per minute, heartrate: >90b/m , WBC >12000 or <
4000, PCo2 <32mmhg.
Sepsis: SIRS plus confirmed or/and suspected locus of infection
Severe sepsis: sepsis plus signs of end organ damage. Hypotension
(systolic blood pressure) <90, lactate >4mmol
Septic shock: severe sepsis with persistent: hypotension, end organ
damage, lactate >4mmol

24. Mods :Multi-organ damage syndrome: more than two systems has been affected(organ damage).
Hemostasis cannot be achieved without medical intervention
Treatment of septic shock
Antibiotics: administered within the first hour of diagnosis (empherically), must be broad
spectrum, covering: gram positive and negatives and the anaerobes
Regimen of shock of unknown etiology (empherically) is: gentamycin, third generation
cephalosporin, if pseudomonas is suspected, ceftazidime be used

25. Differential diagnosis of shock
Hypovolemic
 Hemorrhage
 Fluid loss
 Drugs
 Distributive
 Anaphylactic
 neurogenic
 septic
 Cardiogenic
 Myocardial dysfunction
 Dysrhythmias
 Congenital heart disease

26. Cont.….
Obstructive
 Pneumothorax
 Cardiac tamponade
 Aortic dissection
Dissociative
 Heat
 Carbon monoxide
 Cyanide
 Endocrine causes

27. Neonates in shock: rule out
 Congenital adrenal hyperplasia
 Inborn errors of metabolism
 Obstructive left sided cardiac lesions: aortic stenosis, hypo
plastic left heart syndrome, coarctation of aorta, interrupted
aortic arch