1. Management and Resuscitation of the Critical Patient
Chapter 40
Management and Resuscitation of the Critical Patient

2. National EMS Education Standard Competencies
Shock and Resuscitation
Integrates a comprehensive knowledge of the causes and pathophysiology into the management of shock, respiratory failure or arrest with an emphasis on early intervention to prevent arrest.

3. Introduction When working with a critical patient:
Conduct a rapid assessment
Provide life saving treatment
Develop a differential field diagnosis.

4. Introduction
If a patient is in critical condition, you must be well prepared to:
Make the right decision
Use time appropriately
Provide care

5. Developing Critical Thinking and Decision-Making Abilities
Excellent decision making comes with experience.
Acquired through training and internships
State and national certification/registration/ licensure follows.

6. Critical Patients
While caring for critical patients you will come across:
Premorbid conditions
Major trauma
Patients in the periarrest period

7. Critical Patients
Many adult patients have preexisting conditions putting them in the critical patient category.
© Mark C. Ide

8. The EMS Approach to Diagnosis
Follow a standard approach when determining a field diagnosis.

9. The EMS Approach to Diagnosis
To consider differential diagnosis for an altered mental status, use:
M-T SHIP
For chest pain, consider:
Ischemic chest pain
GI system causes
Musculoskeletal problems
Respiratory causes
Panic attack
Shingles
Cancer in the chest

10. The Role of Intuition in Critical Decision Making
Intuition: pattern recognition and matching based on previous experience
Can be used to “up-triage” the patient
Don’t make decisions based on intuition that draws on incorrect experiences.

11. The Role of Intuition in Critical Decision Making
Karl Weick’s process for communicating intuitive decisions:
Here is what I think we are dealing with.
Here is what I think we should do.
Here is why.
Here is what we should keep our eyes on.
Are there any other concerns?

12. Bias to Decision Making
Confrontation bias: tendency to gather and rely on information that confirms your views
Anchoring bias: allowing an initial reference point to distort your estimates

13. A Snapshot of Critical Decision Making
You have been dispatched to the home of a 62-year-old woman with chest pressure.
Accompanied by nausea and tingling in right arm
She is put on oxygen, vital signs are obtained.
You give her four baby aspirin to chew.
You go through the OPQRST mnemonic.

14. A Snapshot of Critical Decision Making
She is tachycardic and slightly hypertensive.
A12-lead ECG is obtained and transmitted to a hospital with a coronary catheterization lab.
The patient has ST-segment elevations in three contiguous leads (II, III, AVF).

15. A Snapshot of Critical Decision Making
When the patient is lifted from the couch, she passes out.
ECG changes to ventricular fibrillation.
You begin chest compressions.
An oropharyngeal airway is inserted.
A shock at 200 joules is delivered.

16. A Snapshot of Critical Decision Making
You make sure personnel perform specific tasks at the right time.
After a third shock, there is rhythm but no pulse.
CPR continues.
An antidysrhythmic is administered.

17. A Snapshot of Critical Decision Making
You consider causes of cardiac arrest.
After the fourth shock, the patient wakes up.
Once en route, you update the ED.
The patient is admitted directly to the catheterization lab.

18. Shock: The Critical Patient Evolving in Front of You
Shock: state of collapse and failure of the cardiovascular system
Leads to insufficient perfusion of organs/tissues
Normal compensatory mechanism
Untreated shock will lead to death.

19. Anatomy and Physiology of Perfusion
Perfusion: circulation of blood in adequate amounts to meet the cells’ needs
Requires working cardiovascular system
Requires adequate gas exchange, glucose, and waste removal

20. Anatomy and Physiology of Perfusion
Cardiovascular system requires three components:
Functioning pump
Adequate fluid
Intact system of tubing

21. Anatomy and Physiology of Perfusion
The heart’s contractility allows it to increase or decrease the volume of blood pumped
Cardiac output (CO): volume of blood that the heart can pump per minutes
Heart must have adequate strength.
Heart must receive adequate blood.

22. Anatomy and Physiology of Perfusion
Blood pressure is generated by:
Contractions of the heart
Dilation and constrictions of blood vessels
Blood pressure varies directly with cardiac output, systemic vascular resistance, and blood volume.

23. Anatomy and Physiology of Perfusion
Cardiac output = Heart rate × Stroke volume
Blood pressure = Cardiac output × systemic vascular resistance
Mean arterial pressure: blood pressure.
MAP = DBP + 1/3 (SBP – DBP)

24. Anatomy and Physiology of Perfusion
The body is perfused via the cardiovascular system.
Controlled by the autonomic nervous system

25. Anatomy and Physiology of Perfusion

26. Respiration and Oxygenation
Alveoli receive oxygen-rich air from breath.
Oxygen and carbon dioxide pass across tissue layers through diffusion.
Molecules move from area of higher concentration to area of lower concentration

27. Respiration and Oxygenation
Carbon dioxide is dissolved in plasma and attaches to the blood’s hemoglobin.
Combines with water to create carbonic acid.
Breaks down at the lungs and carbon dioxide is exhaled.

28. Regulation of Blood Flow
Blood flow through capillary beds is regulated by the capillary sphincters.
Under control of the autonomic nervous system
Regulation is determined by cellular need.

29. Pathophysiology of Shock
Shock results from:
Inadequate CO
Decreased SVR
Inability of RBCs to deliver oxygen
The body shunts blood flow to vital organs.

30. Pathophysiology of Shock
The cardiovascular system consists of the “perfusion triangle.”
Shock means one part is not working properly.

31. Pathophysiology of Shock
Blood carries oxygen and nutrients through vessels to the capillary beds to tissue cells.
Blood clots control blood loss.
Form depending on:
Retention of blood because of blockage
Changes in a vessel wall
Blood’s ability to clot

32. Pathophysiology of Shock
When pressure is failing, neural and hormonal mechanisms are triggered.
Epinephrine and norepinephrine causes changes in pulse rate, cardiac contractions, and vasoconstriction.
Body fluids shift to maintain pressure.

33. Compensation for Decreased Perfusion
The body responds to any event that leads to decreased profusion.
Baroreceptors activate vasomotor center to begin constriction of the vessels.
Chemoreceptors measure shifts in carbon dioxide in the arterial blood

34. Compensation for Decreased Perfusion
Stimulation normally occurs when the systolic pressure is between 60–80 mm Hg.
Drop in pressure causes baroreceptor stimulation to decrease.
Sympathetic nervous system is stimulated.
The renin-angiotensin-aldosterone system is activated and antidiuretic hormone is released.

35. Compensation for Decreased Perfusion
The overall response is to increase preload, stroke volume, and pulse rate.
Myocardial oxygen demand increases if hypoperfusion persists.
Cells switch to anaerobic metabolism.

36. Compensation for Decreased Perfusion
The release of epinephrine and norepinephrine improves cardiac output.

37. Compensation for Decreased Perfusion
Failure to preserve perfusion leads to decreases in preload and cardiac output.
Myocardial blood supply decreases.
Coronary artery perfusion decreases.
Liver and pancreas functions are impacted.
Gastrointestinal motility is decreased.
Urine production decreases.

38. Shock-Related Events at the Capillary and Microcirculatory Levels
Decreased perfusion leads to cellular ischemia.
The body can tolerate anaerobic metabolism for only a short time.
Leads to systemic acidosis
Ischemia stimulates increased carbon dioxide.

39. Shock-Related Events at the Capillary and Microcirculatory Levels
Sodium-potassium pump normally sends sodium back out against the concentration gradient.
Reduced ATP results in dysfunctional pump
Excessive sodium diffuses into the cells.

40. Shock-Related Events at the Capillary and Microcirculatory Levels
Intracellular enzymes are usually bound in an impermeable membrane.
Cellular flooding explodes the membrane.
Leads to last phase of shock
Decreases venous return and diminishes blood flow.

41. Shock-Related Events at the Capillary and Microcirculatory Levels
Reduced blood supply results in slowing of sympathetic nervous system activity.
The buildup of lactic acid and carbon dioxide acts as a potent vasodilators.
Accumulation washes into the venous circulation

42. Shock-Related Events at the Capillary and Microcirculatory Levels
White blood cells and blood clotting systems are impaired.
May lead to:
Decreased resistance to infection
Disseminated intravascular coagulation (DIC)

43. Multiple-Organ Dysfunction Syndrome
Progressive condition characterized by failure of two or more organs that were initially unharmed
Each tissue has its own warm ischemic time.
Patients have a mortality rate of 60-90%
Classified as primary or secondary

44. Multiple-Organ Dysfunction Syndrome
Occurs when injury or infection triggers a massive systemic response.
Results in the release of inflammatory mediators and activation of the:
Complement system
Coagulation system
Kallikren-kinnin system

45. Multiple-Organ Dysfunction Syndrome
Overactivity results in a maldistribution of systemic and organ blood flow.
Body accelerates tissue metabolism.
Progression causes organs to malfunction.

46. Multiple-Organ Dysfunction Syndrome
Typically develops within hours or days after resuscitation.
Affects specific organs and organ systems:
Heart
Lungs
Central nervous system
Kidneys
Liver
GI tract

47. Causes of Shock
Normal tissue perfusion requires an intact heart, fluid volume, and tubing.
Damage to any one disrupts tissue perfusion.
Shock results from many conditions.
Have a high index of suspicion in emergency medical situations.

48. Causes of Shock Three basic causes of shock:
Pump failure
Low fluid volume
Poor vessel function
Certain patients are more at risk.

49. The Progression of Shock
Shock occurs in three phases: compensated, decompensated, and irreversible.
Also called four grades of hemorrhage or four classes of shock
Class I and II = compensated shock
Class III = decompensated shock
Class IV = irreversible shock

50. The Progression of Shock
Recognize signs and symptoms early on.
Begin immediate treatment before damage occurs.

51. Compensated Shock Earliest stage of shock
The body can still compensate for blood loss.
Level of responsiveness is the best indication of tissue perfusion.
Blood pressure is maintained.

52. Decompensated Shock Blood volume drops more than 30%
Compensatory mechanisms begin to fail
Signs and symptoms become obvious.
Sometimes treatment will result in recovery.

53. Decompensated Shock
Once blood pressure drop is detected, shock is well developed.
Consider an emergency and start transport in less than 10 minutes.

54. Irreversible (Terminal) Shock
Last phase of shock
Life-threatening reductions in cardiac output, blood pressure, tissue perfusion
Cells begin to die and vital organ damage cannot be repaired.

55. Scene Size-Up Size up the scene for hazards.
Follow standard precautions.
Determine the number of patients and the need for additional resources.
Quickly assess the MOI or nature of illness.

56. Primary Assessment Form a general impression
How does the patient look?
Assess mental status using AVPU
Introduce yourself and ask their name, location and day of the week.

57. Primary Assessment Airway and breathing
If you suspect cardiac arrest, use CAB approach.
Otherwise, asses the ABCs.
Manage immediate threats.
If difficulty breathing, examine the chest.
Assess the adequacy of the patient’s ventilation.

58. Primary Assessment Circulation
Take CAB approach if you suspect the patient does not have a pulse.
In patients with a pulse, determine if it is adequate.
In conscious patients, assess the radial pulse.
In unconscious patients, check the carotid pulse.

59. Primary Assessment Circulation (cont’d)
If you know the patient is hypotensive, provide immediate transport to the ED.
Also note the patient’s skin color, temperature, and condition.

60. Primary Assessment Transport decision
All patients need to be prioritized
If shock is from a medical problem, fast-track to an assessment based on body systems.
If shock is from trauma, let the MOI guide your assessment.

61. History Taking
Can be done en route to the ED in a high-priority patient
Unless patient is pinned, and you suspect a delay in extrication, delay establishing IV/IO access.

62. Courtesy of EKF Diagnostics www.ekfdiagnostics.com
Secondary Assessment
Drop in systolic blood pressure or altered mental status indicates the body can no longer compensate.
Other indicators include end-tidal carbon dioxide and lactic acid buildup.
Portable lactate monitors can be used.
Courtesy of EKF Diagnostics

63. Reassessment
Re-visit the primary assessment, vital signs, chief complaint, and treatment performed.
Determine what interventions are needed.
Patients in decompensated shock will need rapid intervention.

64. Special Considerations for Assessing Shock
Healthy, fit, young adults are equipped to combat life-threatening blood loss.
Resilient cardiovascular system
Not smoking increases oxygenation

65. Pediatric Considerations
Pediatric patients can compensate until a 30–35% blood loss.
Treat aggressively and early with significant MOI or indication of shock.
Never wait to see a drop in blood pressure.

66. Geriatric Considerations
Ability to manage blood loss is diminished
Manage fluid therapy carefully.
Cardiovascular disorders or diabetes affect ability to compensate.
Medications may prevent clot formations.

67. Emergency Medical Care of a Patient With Suspected Shock
Airway and ventilatory support take priority when treating a patient with shock.
Maintain an open airway and suction as needed.
Administer high-flow supplemental oxygen.

68. Emergency Medical Care of a Patient With Suspected Shock
IV therapy can be helpful in supplementing initial therapies.
Administer IV volume expanders.
Maintain perfusion without increasing internal or uncontrollable external hemorrhage.

69. Emergency Medical Care of a Patient With Suspected Shock
If signs of tension pneumothorax, perform the needle chest decompression.
With suspected cardiac tamponade, recognize the need for pericardiocentesis.

70. Emergency Medical Care of a Patient With Suspected Shock
Nonpharmacologic interventions include:
Proper positioning of the patient
Prevention of hypothermia
Rapid transport

71. IV Therapy IV lines are inserted to provide:
Immediate replacement of fluids
Potential replacement
Administration of medication
All patients in (or who are likely to develop) hypovolemic shock need fluid replacement.

72. IV Therapy
IV lines should be inserted to keep a vein open for emergency administration of drugs.
Patients who need a vein kept open include:
Those at risk of cardiac arrest
Those needing parenteral medication
IV flow rate is determined by local protocol.

73. Volume Expanders and Plasma Substitutes
Hypovolemic shock should be treated with volume expanders.
A variety of solutions have properties similar to those of plasma.
Used to maintain circulatory volume

74. Volume Expanders and Plasma Substitutes
Plasma substitutes and volume expanders include:
Dextran
Plasma protein fraction (Plasmanate)
Polygeline, hetastarch, and other starch solutions

75. Crystalloids
Solutions that do not contain proteins or other large molecules
Rapidly equilibrates into tissues
Fluids of choice when only salt and water have been lost

76. Crystalloids Commonly used crystalloids are:
Normal saline
Lactated Ringer’s solution
Most ALS protocols limit the number of liters administered to the patient.

77. Pathophysiology, Assessment, and Management of Specific Types of Shock
Three classifications of shock: cardiogenic, distributive, hypovolemic
Cardiogenic shock results from a weakening pumping action of the heart.
Distributive shock is broken down into:
Septic shock
Neurogenic shock

78. Pathophysiology, Assessment, and Management of Specific Types of Shock
Other conditions decrease tissue perfusion:
Conditions that obstruct the flow of oxygen into the bloodstream and tissue
Leads to obstructive shock
Nonhemorrhagic causes of hypovolemic shock are grouped by how they reduce perfusion.

79. Pathophysiology, Assessment, and Management of Specific Types of Shock
Initial management of shock:
Manage the airway.
Administer supplemental oxygen.
Put the patient in a position of comfort.
Obtain vital signs and IV access.
Maintain body heat.

80. Cardiogenic Shock
Occurs when the heart cannot circulate sufficient blood to maintain adequate peripheral oxygen delivery
Most commonly caused by an AMI accompanied by dysfunction of left ventricle

81. Cardiogenic Shock
Manifests with poor contractility, decreased cardiac output, impaired ventricular filling
Populations at the greatest risk include:
Elderly
Patients with a history of diabetes mellitus
Patients with a history of AMI with an ejection fraction of less than 35%

82. Cardiogenic Shock
Prolonged efforts to stabilize the patient is not recommended.
Expedite transport as quickly as possible.
Secure the airway and administer oxygen.
Obtain a 12-lead ECG.
Administer crystalloid solution.
Auscultate the lungs.

83. Cardiogenic Shock
Some EMS systems use dopamine at low doses if the patient has a MAP of less than 60 mm Hg.
Combination drug therapy is often needed at the hospital.

84. Obstructive Shock
Causes are not directly associated with loss of fluid, pump failure, or vessel dilation.
Occurs when blood flow in the heart or great vessels becomes blocked

85. Obstructive Shock Tension pneumothorax
Caused by damage to the lung tissue
Air accumulates within the chest cavity and applies pressure to the mediastinum.
Life-threatening condition

86. Obstructive Shock Cardiac tamponade
Caused by blunt or penetrating trauma, tumors, or pericarditis
Occurs when blood leaks into the pericardium
Leads to compression of the heart

87. Obstructive Shock Cardiac tamponade (cont’d)
The ultimate treatment is pericardiocentesis.
Signs include:
Muffled heart sounds
Systolic and diastolic blood pressure merging

88. Distributive Shock
Occurs when there is widespread dilation of the resistance vessels, the capacitance vessels, or both
Circulating blood volume pools in vascular beds.

89. Distributive Shock Septic shock Occurs from a widespread infection
Usually caused by gram-negative bacterial organisms
Activates inflammatory-immune response
An uncontrolled response results in hypoperfusion.

90. Distributive Shock Septic shock (cont’d) Septic shock is complex.
Insufficient volume of fluid in the container
Fluid leaks out and collects in respiratory system.
Larger-than-normal vascular bed must contain the smaller-than-normal volume of fluid.

91. Distributive Shock Septic shock (cont’d)
Presents similarly to hemorrhagic shock
But patients usually have warm or hot skin.
Treatment requires complex hospital management.
Transport as quickly as possible.

92. Distributive Shock Septic shock (cont’d)
Give normotensive patients dopamine.
Give norepinephrine for “warm” shock.
Give epinephrine for “cold” shock.

93. Distributive Shock Neurogenic shock
Usually results from spinal cord injury
Results in loss of normal sympathetic nervous system tone and vasodilation
Muscles in blood vessels are cut off from nerve impulses that cause them to contract.

94. Distributive Shock Neurogenic shock (cont’d)
Spinal shock: occurs after a spinal injury produces motor and sensory losses
Characterized by flaccid paralysis, flaccid sphincters, and absent reflexes
Level of injury is related to severity of shock.

95. Distributive Shock Neurogenic shock (cont’d)
Care is similar to general management.
The patient should also be immobilized.
Determine the necessity for IV fluids.
With pure neurogenic shock, vagal blockers and vasopressor agents may be used.

96. Distributive Shock Anaphylactic shock
Occurs when a person reacts violently to a substance to which he or she has been sensitized
Patient experiences widespread vascular dilation.
While the container is larger, the blood volume is less.

97. © SPL/Photo Researchers, Inc.
Distributive Shock
Anaphylactic shock (cont’d)
Fluid leaks out of the blood vessels and into interstitial space, resulting in:
Hypovolemia
Significant swelling
© SPL/Photo Researchers, Inc.

98. Distributive Shock Anaphylactic shock (cont’d)
Management needs to occur quickly.
Remove the inciting cause and resolve life threats.
Evaluate the patient’s ventilatory status.
Provide cardiovascular support.
Administer epinephrine or vasopressor.

99. Distributive Shock Psychogenic shock
Sudden reaction of the nervous system that produces a temporary vascular dilation, resulting in syncope
Life-threatening causes include:
Irregular heartbeat
Brain aneurysm

100. Distributive Shock Psychogenic shock (cont’d)
If the patient has fallen, check for injuries.
Assess the patient for any other abnormality.
Record your initial observations.
Obtain an ECG.

101. Hypovolemic Shock Occurs because of inadequate blood volume
Hemorrhagic and nonhemorrhagic causes
Nonhemorrhagic hypovolemic shock occurs when the fluid loss is contained within the body.
Early signs are restlessness and anxiety.

102. Hypovolemic Shock Physical exam reveals: Symptoms of dehydration:
Poor skin turgor
Shrunken tongue
Sunken eyes
Weak, rapid pulse
Symptoms of dehydration:
Loss of appetite
Nausea
Vomiting
Fainting when standing up

103. Hypovolemic Shock
Give a dehydrated patient an IV infusion of normal saline or lactated Ringer’s solution.
Establish and maintain an open airway.
Do not administer anything orally.
If patient vomits, administer an antiemetic.

104. Hypovolemic Shock Monitor patient’s:
ECG rhythm
Mental status
Pulse rate
Blood pressure
SpO2
ETCO2
The goal is to save the brain, lungs, and kidneys.
Rely on state of consciousness to tell you how well the vital organs are being perfused.

105. Respiratory Insufficiency
The inability to breathe in adequate amounts of oxygen affects the ventilation process.
Insufficient amounts of oxygen in the blood can produce shock.
Some poisoning may affect the ability of cells to metabolize or carry oxygen.

106. Respiratory Insufficiency
An abnormally low amount of RBCs causes anemia.
Tissues may become hypoxic.
Pulse oximeter may still indicate adequate saturation.
Hypoxemic hypoxia

107. Respiratory Insufficiency
When treating a patient in shock from poor respiration, you must:
Seal the hole and stabilize impaled objects.
Secure and maintain the airway.
Assess SpO2, ETCO2, and vital signs.
Determine need for assisted ventilations.
Determine most appropriate destination.

108. Transportation of Shock Patients
Ask yourself when, where, and how.
Limit scene time to 10 minutes or less.
Know how to access aeromedical transportation.

109. Transportation of Shock Patients
Consider the priority of the patient and availability of a regional trauma center.
Transport to a facility with appropriate capabilities.
If not available, medical control will help make the transport decision.

110. Prevention Strategies
Prevention begins with your assessment of the MOI, findings, and the clinical picture.
Be alert and search for early signs of shock.
Don’t rationalize irregularities.

111. Summary
Develop expertise in quickly developing a differential field diagnosis of patients found in periarrest condition or period.
Work with an experienced paramedic to develop skills in intuition and become comfortable in making critical decisions.

112. Summary
Hypoperfusion occurs when the level of tissue perfusion decreases below normal. Shock refers to a state of failure of the cardiovascular system.
The body is perfused via the cardiovascular system.
Tissue perfusion requires a pump (heart), fluid volume (blood and body fluids), and tubing capable of reflex adjustments (constriction and dilation).

113. Summary
Shock occurs in three successive phases (compensated, decompensated, and irreversible). This is also referred to as the four grades of hemorrhage or four classes of shock.
Airway and ventilatory support are top priority when treating a patient with shock.
If a patient is in shock, transport is inevitable.

114. Summary Don’t wait for blood pressure to drop.
Nonhemorrhagic causes of hypovolemic shock are grouped by how they reduce perfusion.
Prevention of shock and its effects begins with your assessment of the MOI, primary assessment findings, and the patient’s clinical picture.

115. Credits Chapter opener: © Mark C. Ide
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Unless otherwise indicated, all photographs and illustrations are under copyright of Jones & Bartlett Learning, courtesy of Maryland Institute for Emergency Medical Services Systems, or have been provided by the American Academy of Orthopaedic Surgeons.