This document discusses different types of shock, including their causes, signs and symptoms, and treatment approaches. It defines shock as a syndrome characterized by decreased tissue perfusion and impaired cellular metabolism due to an imbalance between the supply and demand of oxygen and nutrients. The main types of shock covered are cardiogenic, hypovolemic, neurogenic, anaphylactic, and septic shock. For each type, the document details precipitating causes, physical exam findings, and collaborative care involving fluid resuscitation, vasopressor drugs, antibiotics, and other interventions to restore perfusion and prevent multiple organ dysfunction.
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Types and Treatment of Shock
1. ShockArun M. Boban
Dharanidharan Jeyaseelan
W.P. Rivindu H. Wickramanayake
Tbilisi State Medical University, Georgia
3rd Year 2nd Semester – Group no. 04a
2017 November
2. Shock
Syndrome characterized by decreased tissue perfusion and
impaired cellular metabolism.
Imbalance between the supply and demand for O2 and
nutrients
7. Physical examination
Tachypnea, pulmonary congestion
Pallor; cool, clammy skin
Decreased capillary refill time
Anxiety, confusion, agitation
↑ in pulmonary artery wedge pressure
Decreased renal perfusion and UO
Continued ;
8. Hypovolemic Shock
Absolute hypovolemia:
- Loss of intravascular fluid volume
Hemorrhage
GI loss (e.g., vomiting, diarrhea)
Fistula drainage
Diabetes insipidus
Hyperglycemia
Diuresis
Next ;
9. - Results when fluid volume moves out of
the vascular space into extravascular space
(e.g., interstitial or intra-cavitary space)
Termed third spacing
Relative hypovolemia
Next ;
Continued ;
10. Response to acute volume loss depends on
- Extent of injury or insult
- Age
- General state of health
- Anxiety
- Tachypnea
- Increase in CO, heart rate
- Decrease in stroke volume, PAWP, UO
If loss is >30%, blood volume is replaced
Clinical manifestations
Continued ;
11. Mal-distribution of Blood Flow
Neurogenic Shock
Hemodynamic phenomenon that can occur
within 30 minutes of a spinal cord injury at
the fifth thoracic (T5) vertebra or above and
can last up to 6 weeks
Can be in response to spinal anesthesia
Results in massive vasodilation leading to
pooling of blood in vessels Next ;
12. Hypotension
Bradycardia
Temperature dysregulation
(resulting in heat loss)
Dry skin
Poikilothermia (taking on the
temperature of the environment
Clinical manifestations
Continued ;
13. Anaphylactic Shock
Massive vasodilation
Release of mediators
↑ Capillary permeability
Acute, life-threatening hypersensitivity reaction
Next ;
14. Anxiety, confusion, dizziness
Sense of impeding doom
Chest pain
Incontinence
Swelling of the lips and tongue, angioedema
Wheezing, stridor
Flushing, pruritus, urticarial
Respiratory distress and circulatory failure
Clinical manifestations
Continued ;
15. Septic Shock
Sepsis: Systemic inflammatory response to documented or
suspected infection
Severe sepsis = Sepsis + Organ dysfunction
Septic shock = Presence of sepsis with hypotension despite
fluid resuscitation + Presence of tissue perfusion abnormalities
Mortality rates as high as 50%
Primary causative organisms
- Gram-negative and gram-positive bacteria
- Endotoxin stimulates inflammatory response
Next ;
16. ↑ Coagulation and inflammation
↓ Fibrinolysis
Formation of microthrombi
Obstruction of microvasculature
Hyperdynamic state: Increased CO and
decreased SVR
Clinical manifestations
Next ;
Continued ;
18. Stages of Shock
Initial Stage
Usually not clinically apparent
Metabolism changes from aerobic to anaerobic
- Lactic acid accumulates and must be
removed by blood and broken down by liver
- Process requires unavailable O2
19. Compensatory Stage
Clinically apparent
- Neural
- Hormonal
- Biochemical compensatory mechanisms
Attempts are aimed at overcoming consequences of
anaerobic metabolism and maintaining homeostasis
Impaired GI motility
- Risk for paralytic ileus
Cool, clammy skin from blood
- Except septic patient who is warm and flushed
20. Progressive Stage
Begins when compensatory mechanisms fail
Aggressive interventions to prevent multiple organ
dysfunction syndrome (MODS)
Movement of fluid from pulmonary vasculature to
interstitium
Pulmonary edema
Bronchoconstriction
↓ Residual capacity
Next ;
21. Fluid moves into alveoli
Edema
Decreased surfactant
Worsening V/Q mismatch
Tachypnea
Crackles
Increased work of breathing
Next ;
Continued ;
22. Myocardial dysfunction results in
Dysrhythmias
Ischemia
Myocardial infarction
End result: Complete deterioration of
cardiovascular system
Next ;
Continued ;
23. Ulcers
Bleeding
Risk of translocation of bacteria
Decreased ability to absorb nutrients
Mucosal barrier of GI system becomes ischemic
Next ;
Continued ;
24. Liver fails to metabolize drugs and wastes
Jaundice
Elevated enzymes
Loss of immune function
Risk for DIC and significant bleeding
Acute tubular necrosis/acute renal failure
Continued ;
25. Refractory Stage
Exacerbation of anaerobic metabolism
Accumulation of lactic acid
↑ Capillary permeability
Profound hypotension and hypoxemia
Tachycardia worsens
Decreased coronary blood flow
Cerebral ischemia
Failure of one organ system affects others
Recovery unlikely
26. Diagnostic Studies
Thorough history and physical examination
No single study to determine shock
Blood studies
- Elevation of lactate
- Base deficit
12-lead ECG
Chest x-ray
Hemodynamic monitoring
27. Collaborative Care
Cardiogenic Shock
Restore blood flow to the myocardium by restoring the balance
between O2 supply and demand
Thrombolytic therapy
Angioplasty with stenting
Emergency revascularization
Valve replacement
Hemodynamic monitoring
Drug therapy (e.g., diuretics to reduce preload)
Circulatory assist devices (e.g., intra-aortic balloon pump,
ventricular assist device)
28. Hypovolemic Shock
Management focuses on stopping the loss of fluid and
restoring the circulating volume
Fluid replacement is calculated using a 3:1 rule (3 ml of
isotonic crystalloid for every 1 ml of estimated blood loss)
29. Septic Shock
Fluid replacement (e.g., 6 to 10 L of isotonic crystalloids
and 2 to 4 L of colloids) to restore perfusion
Hemodynamic monitoring
Vasopressor drug therapy; vasopressin for patients
refractory to vasopressor therapy
Intravenous corticosteroids for patients who require
vasopressor therapy, despite fluid resuscitation, to maintain
adequate BP
Next ;
30. Antibiotics after obtaining cultures
(e.g., blood, wound exudate, urine, stool, sputum)
Drotrecogin alfa (Xigris)
- Major side effect: Bleeding
Glucose levels <150 mg/dl
Stress ulcer prophylaxis with histamine (H2)-receptor
blockers
Deep vein thrombosis prophylaxis with low-dose
unfractionated heparin or low-molecular-weight heparin
Continued ;
31. Neurogenic Shock
In spinal cord injury: Spinal stability
Treatment of the hypotension and bradycardia
with vasopressors and atropine
Fluids used cautiously as hypotension is
generally not related to fluid loss
Monitor for hypothermia
32. Anaphylactic Shock
Epinephrine, diphenhydramine
Maintaining a patent airway
Nebulized bronchodilators
Endotracheal intubation or cricothyroidotomy
may be necessary
Aggressive fluid replacement
Intravenous corticosteroids if significant
hypotension persists after 1 to 2 hours of
aggressive therapy
33. FIRST AID
If you suspect a person is in shock, call 911.
Then immediately take the following steps:
Lay the person down and elevate the legs and
feet slightly, unless you think this may cause
pain or further injury.
Keep the person still and don't move him or her
unless necessary.
Begin CPR if the person shows no signs of life,
such as breathing, coughing or movement. Next ;
34. Loosen tight clothing and, if needed, cover
the person with a blanket to prevent chilling.
Don't let the person eat or drink anything.
If the person vomits or begins bleeding from
the mouth, turn him or her onto a side to
prevent choking, unless you suspect a spinal
injury
Continued ;