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Chapter 40 Management and Resuscitation of the Critical Patient
Unit Summary
Expertise in critical thinking and decision making are essential tools to use when you are confronted with a critical patient. This process involves conducting a rapid assessment, providing lifesaving treatment, and developing a differential field diagnosis. This chapter discusses the approach that you should take when you are confronted with a critical patient.
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.
Knowledge Objectives
1. List examples of peri-arrest conditions that critical patients can present within the
field. (p 1882)
2. Describe the process of determining a differential diagnosis in the field
assessment of a critical patient. (pp 1882–1883)
3. Discuss the rapid decision making involved in the assessment and management of
a critical patient. (p 1883)
4. List examples of bias that can affect your critical decision making. (pp 1883–
5. Describe the body’s physiologic response to changes in perfusion. (pp 1886–
6. Discuss the pathophysiology of shock and peri-arrest situations. (pp 1889–1895)
7. Describe the effects of decreased perfusion at the capillary level. (pp 1892–1893)
8. Define shock based on aerobic and anaerobic metabolism. (pp 1890–1892)
9. Relate pulse pressure changes to perfusion status. (pp 1886–1889, 1896)
10. Relate orthostatic vital sign changes to perfusion status. (p 1896)
11. Predict shock based on mechanism of injury. (p 1895)
12. Discuss the progression of shock. (pp 1895–1897)
13. Discuss the pathophysiologic changes associated with compensated shock. (p
14. Discuss the assessment findings associated with compensated shock. (pp 1897–
15. Identify the need for intervention and transport of the patient with compensated
shock. (p 1898)
16. Discuss the treatment plan and management of compensated shock. (pp 1900–
17. Discuss the pathophysiologic changes associated with decompensated shock. (p
18. Discuss the assessment findings associated with decompensated shock. (pp 1897–
19. Identify the need for intervention and transport of the patient with decompensated
shock. (p 1898)
20. Discuss the treatment plan and management of the patient with decompensated
shock. (pp 1900–1903)
21. Differentiate between compensated and decompensated shock. (pp 1895–1897)
22. Discuss the assessment findings associated with shock and the peri-arrest
situations. (pp 1897–1899)
23. Identify the need for intervention and transport of the patient with shock or other
peri-arrest situations. (pp 1903–1911)
24. Discuss the treatment plan and management of shock and other peri-arrest
situations. (pp 1903–1911)
25. Describe the pathophysiology, assessment, and management of specific types of
shock, including cardiogenic, obstructive, distributive, and hypovolemic shock.
(pp 1903–1911)
Skills Objectives
1. Defend the importance of teamwork, experience, and practice in preparation to
manage the critical patient. (p 1881)
2. Demonstrate rapid decision making based on differential field diagnosis of the
critical patient with a peri-arrest condition. (pp 1884–1885)
3. Demonstrate the management of shock. (pp 1901–1902, Skill Drill 1)
Readings and Preparation
Review all instructional materials including Chapter 40 of Nancy Caroline’s Emergency Care in the Streets , Seventh Edition, and all related presentation support materials.
Support Materials
- Lecture PowerPoint presentation
- Case Study PowerPoint presentation
Enhancements
- Direct students to visit the companion website to Nancy Caroline’s Emergency Care in the Streets , Seventh Edition, at http://www.paramedic.emszone.com for online activities.
Content connections: Nearly every chapter contains significant information of management of critical patients. Review as many as possible or at a minimum have notes available.
Teaching Tips
Reinforcing the use of the five step process for communicating intutive decision as proposed by Karl Weick will help students in their decision-making process. Use this process during your presentation of this material as much as possible to demonstrate the importance.
Unit Activities
Writing activities: Assign students to prepare a written report on communication bias, to include all items found in this chapter.
Student presentations: Have students present their written reports. Alternatively, have students present the results of their group project.
- Students must acquire entry-level knowledge and skills with guided experience. a. Training is developed to create entry-level paramedics b. Internships help pull together: i. Didactic ii. Lab skills iii. Clinical experiences
- State and national certification/registration/licensure follows.
B. Critical patients
- While caring for critical patients you will be confronted with: a. Premorbid conditions b. Major trauma c. Patients in the periarrest period
- Periarrest period: Period just before or just after cardiac arrest a. Care must be taken to prevent progression or regression into cardiac arrest. b. Examples include: i. Unstable dysrhythmias ii. Shock iii. Syncope iv. Myocardial ischemia v. Heart failure
- Premorbid conditions: Conditions that precede the onset of a disease a. Disease: Life-threatening trauma or medical condition that need to be rapidly identified and managed b. Sorted into: i. Those occurring in presumed to be healthy adults ii. Those occurring in unhealthy adults
- Many adult patients have preexisting conditions putting them in the critical patient category. a. Patients with trauma such as: i. Full-thickness burn over 15-20% of the total body surface area ii. Head, chest, or abdomen involved with hemorrhage leading to shock b. Acute coronary syndrome (ACS) c. Congestive heart failure (CHF) d. Renal failure e. Uncontrolled hypertension f. Uncontrolled diabetes g. Obesity h. Electrolyte imbalance i. Electrocution j. Drowning or submersion k. Hypothermia l. Drug toxicity m. Stroke n. Near-fatal asthma
o. Anaphylaxis p. Pulmonary embolism
C. The EMS approach to diagnosis
- Critical patients often complain about altered mental status, difficulty breathing, severe pain, and chest pain. a. Follow a standard approach to determine a field diagnosis. b. Consider and rule out different conditions. i. Leads to a differential diagnosis
- To consider the differential diagnosis for a patient with an altered mental status, you may use the “M-T SHIP” acronym. a. M: Medication overdose/noncompliance, metabolic causes b. T: Tumor, trauma, toxins c. S: Seizures, stroke d. H: Hypoxia, hyperthermia/hypothermia, hyperglycemia/hypoglycemia, hypertensive crisis, hypovolemia, hyperkalemia/hypokalemia e. I: Infection and uremia f. P: Psychiatric or behavioral disorders
- To consider the differential diagnosis for a patient with chest pain, consider: a. Ischemic chest pain indicating a possible cardiac condition b. Gastrointestinal (GI) system causes i. Heartburn ii. Esophageal spasm iii. Hiatal hernia iv. Gallbladder or pancreas problems c. Musculoskeletal problems i. Costochondritis ii. Sore muscles iii. Injured ribs iv. Pinched nerve d. Respiratory causes i. Pulmonary embolism ii. Pleurisy iii. Pneumothorax iv. Asthma e. Panic attack f. Shingles g. Cancer in the chest
- Your experience will be your guide in determining serious problems.
D. The role of intuition in critical decision making
- Intuition comes with experience and is hard to teach. a. Described as pattern recognition and matching based on previous experience b. Can be used to “up-triage” the patient rather than “down-triage” i. If instinct tells you the patient is more serious than he or she seems, treat as such. ii. If instinct tells you otherwise, investigate the complaint.
i. There is a slight crackling in the bases of her lungs. b. Your partner transmits the results to the nearest hospital with a coronary catheterization lab.
- The patient has ST-segment elevations in three contiguous leads (II, III, AVF).
a. She fits the STEMI protocol for an inferior wall myocardial infarction. b. Criterion for percutaneous coronary intervention is within a 90-minute window. c. Your partner starts an IV line to start morphine sulfate and metoprolol. d. You determine that it is best to take her to the hospital 2 miles beyond closest hospital because it has a coronary catheterization lab.
- When the patient is lifted from the couch to the stairchair, she passes out.
a. The ECG changes from a sinus tachycardia to ventricular fibrillation. b. You and your partner move the patient to the floor. c. You begin chest compressions while the defibrillator pads are placed on the patient. d. An oropharyngeal airway is inserted and bag-mask ventilations are started with supplemental oxygen. e. With the pads in place, compressions are stopped and the first shock at 200 joules is delivered. i. CPR compressions resume.
- You need to make sure personnel perform specific tasks at the right time, which includes:
a. Getting the mechanical CPR device ready to deploy with no interruption for more than 10 seconds b. Ensuring BLS ventilations are effective, and switching to the automatic transport ventilator with the impedance threshold device c. Starting an IV line to administer 1 mg of epinephrine 1:10,000 every 3 minutes until pulse returns. d. Ensuring a fresh person will supply chest compressions for the second 2 minutes e. Drawing up 300 mg of amiodarone because an antidysrhythmic will need to be administered f. Reanalyzing and reshocking the patient at 2-minute intervals
- After the third shock, the patient has rhythm but no pulse.
a. CPR continues b. Antidysrhythmic is administered.
- You take a moment to consider causes of cardiac arrest.
a. You consider reversible causes. i. No signs of trauma or symptoms of GI bleeding ii. Systolic blood pressure was slightly high. (a) Not likely hemorrhaging iii. Not a diabetic and initially was alert (a) Low levels of glucose are unlikely. iv. No signs of respiratory distress and not cold to the touch (a) Pulmonary embolus and hypothermia not likely. v. ST elevation MI (STEMI) and vague presentation in elderly women (a) Likely a massive AMI or coronary thrombosis
- After the fourth shock, the patient wakes up.
a. You assure her all her needs are taken care of b. Crew members are assigned to package and carry the patient.
c. One medic starts an amidarone drop and prepares a mild sedative.
- Once en route, you contact the ED to update staff and another 12-lead ECG is transmitted. a. You reassess vital signs, document the incident, and discuss the situation with the patient.
- Because the ECG was initially transmitted, the patient is admitted directly to the catheterization lab.
IV. Shock: The Critical Patient Evolving in Front of You
A. Shock is a state of collapse and failure of the cardiovascular system where blood
circulation slows and eventually ceases.
- Leads to insufficient perfusion of organs and tissues
- Normal compensatory mechanism to maintain systolic blood pressure and brain perfusion during distress a. Can accompany a broad spectrum of events
- If not treated promptly, shock will injure the body’s vital organs and lead to death.
V. Anatomy and Physiology of Perfusion
A. Perfusion is the circulation of blood within an organ or tissue in adequate
amounts to meet the cells’ needs for oxygen, nutrients, and waste removal.
- Requires having a working cardiovascular system
- Requires adequate gas exchange in the lungs, glucose in the blood, and waste removal
- The cardiovascular system requires three components to keep the blood moving: a. Functioning pump (heart) b. Adequate fluid volume (blood and body fluids) c. Intact system of tubing capable of reflex adjustments in response to changes in pump output and fluid volume (blood vessels)
- The heart’s contractility allows it to increase or decrease the volume of blood pumped with each contraction (stroke volume [SV]). a. The heart can vary the speed at which it contracts by raising or lowering the pulse rate. b. Cardiac output (CO): Volume of blood that the heart can pump per minute i. Heart must have adequate strength (a) Determined by heart muscle’s ability to contract (myocardial contractility) ii. Heart must receive adequate blood to pump (a) As volume of blood increases, precontraction pressure (preload) builds up. (b) Preload: Stretching of the cardiac muscles prior to contraction (1) As preload increases, the heart muscles stretch. (2) When muscles are stretched, myocardial contractility increases and cardiac output increases. iii. The resistance to flow (afterload) must be appropriate.
- Blood pressure is generated by the contractions of the heart and dilation and constrictions of blood vessels. a. Carefully controlled by the body to ensure adequate circulation in various tissues and organs
b. Molecules move from an area of higher concentration of molecules to an area with a lower concentration i. There are more oxygen molecules in alveoli than in the blood. (a) Oxygen moves from the alveoli into the blood. ii. There are more carbon dioxide molecules in the blood than in the inhaled air. (a) Carbon dioxide moves from the blood into alveoli.
- Carbon dioxide is dissolved in plasma and attaches to the blood’s hemoglobin. a. Carbon dioxide combines with water to create carbonic acid. i. Carbonic acid concentrations are high just as the blood is moving toward the lungs. ii. At the lungs, carbonic acid breaks down and carbon dioxide is exhaled.
C. Regulation of blood flow
- Blood flow through the capillary beds is regulated by the capillary sphincters. a. Sphincters constrict and dilate to increase or decrease blood flow. i. Under control of the autonomic nervous system (a) Regulates involuntary functions like sweating and digestion (b) Respond to other stimuli like heat, cold, need for oxygen, and waste removal ii. Not all cells have the same needs at the same time.
- Regulation of blood flow is determined by cellular need. a. Accomplished by vessel constriction or dilation with sphincter constriction or dilation b. Perfusion is accomplished by heart, blood vessels, and blood working together.
VI. Pathophysiology of Shock
A. Shock can result from inadequate cardiac output, decreased SVR, or the
inability of red blood cells (RBCs) to deliver oxygen to tissues.
- Disturbances will create the buildup of dangerous waste products that could lead to death of the organ a. Inadequate perfusion will cause damage to the cells as well as the body b. If shock persists, death will ultimately occur. c. The body compensates by shunting blood flow from organs that are more tolerant of low flow (skin and intestines) to vital organs that cannot tolerate hypoperfusion (heart, brain, lungs).
- The cardiovascular system consists of the heart, blood vessels/arteries, and the fluid/blood. a. Known as the “perfusion triangle” b Shock means one part is not working properly.
- Blood carries oxygen and nutrients through vessels to the capillary beds to tissue cells. a. Supplies are exchanged for waste products created during metabolism. b. Blood contains: i. RBCs: Responsible for transporting oxygen to cells and carbon dioxide away from cells ii. White blood cells: Help the body fight infection iii. Platelets: Responsible for forming clots iv. Plasma
- Blood clots control blood loss. a. Form depending on one of the following: i. Retention of blood because of blockage in circulation (blood stasis) ii. Changes in a vessel wall iii. Blood’s ability to clot b. Injury causes platelets to aggregate at the injury site. i. RBCs become sticky and clump together. ii. Fibrinogen reinforces RBCs. iii. Clots are prone to rupture because blood is always moving due to blood pressure.
- When the body senses that pressure in the system is failing, neural and hormonal mechanisms are triggered. a. Sympathetic nervous system will assume control of the body’s functions during shock b. Parasympathetic system controls involuntary functions by sending signals to the cardiac, smooth, and glandular muscles c. Epinephrine and norepinephrine causes changes in pulse rate, strength of cardiac contractions, and vasoconstriction in nonessential areas. i. Actions maintain pressure in the system, sustaining perfusion of the vital organs.
- Body fluids shift to maintain pressure. a. Response occurs within seconds, causing signs and symptoms of shock.
B. Compensation for decreased perfusion
- The body responds to any event that leads to decreased profusion in order to preserve vital organs a. Baroreceptors located in the aortic arch and carotid sinuses sense decreased blood flow. i. Activate vasomotor center in medulla oblongata to begin constriction of the vessels. (a) Increases blood pressure b. Chemoreceptors measure shifts in carbon dioxide in the arterial blood. i. Regulates respiratory rate ii. Controls acid/base balance in the body
- Stimulation normally occurs when the systolic pressure is between 60-80 mm Hg in adults, or lower in children. a. Vasomotor center increases the arterial pressure by constricting blood vessels b. Drop in pressure causes the artery walls to not stretch as much. i. Baroreceptor stimulation is decreased. c. Normally baroreceptor stimulation prevents vasoconstrictor center from constricting vessels. i. Leads to vasodilatation in the peripheral circulatory system ii. Decreases pulse rate and contractility iii. Causes a concomitant decrease in arterial pressure iv. With dropping pressure, baroreceptors are not stimulated for vasodilation. (a) Vessels constrict to raise blood pressure. d. Sympathetic nervous system is stimulated as the body recognizes a potential catastrophic event. i. Adrenal glands release epinephrine and norepinephrine into the bloodstream. (a) Causes tachycardia and increases contractility of the heart
(a) Placenta (b) Skin (c) Muscles (d) Gut (e) Kidneys (f) Liver (g) Heart (h) Lungs b. Skin and muscles can survive with minimal blood flow for a longer period than major organs. c. If blood supply is inadequate to major organs for more than 60 minutes, they will develop complications. i. Referred to as the “Golden Period”
- Failure of compensatory mechanisms to preserve perfusion leads to decreases in preload and cardiac output. a. Myocardial blood supply and oxygenation decrease, reducing myocardial perfusion. b. Coronary artery perfusion decreases. i. Leads to myocardial ischemia c. Normal functions of liver and pancreas are impacted. i. Inhibits insulin release d. Gastrointestinal motility is decreased. i. Causes stress ulcers to develop e. Diminished kidney perfusion decreases urine production. i. Leads to kidney failure if not reperfused within 45 minutes to 1 hour ii. Normal urine output is 30-40 mL/h iii. An output less than 500 mL per day is considered oliguria and can lead to acute kidney insufficiency.
C. Shock-related events at the capillary and microcirculatory levels
- Decreased perfusion leads to cellular ischemia. a. Minimal blood flow passes through the capillaries. i. Causes cells to switch from aerobic metabolism to anaerobic metabolism b. Decreased circulation leads to blood stagnation in the capillaries. i. The precapillary sphincter relaxes. ii. Postcapillary sphincters remain constricted. (a) Causes capillaries to become engorged with fluid iii. Capillary sphincters regulate blood flow through capillary beds. (a) Under control of autonomic nervous system (b) Blood flow is determined by cellular needs. (c) Blood flow is accomplished by vessel constriction or dilation.
- The body can tolerate anaerobic metabolism for only a short time. a. Leads to systemic acidosis and depletion of the body’s energy reserves b. Incomplete glucose breakdown leads to an accumulation of pyruvic acid. i. Transformed to lactate and other acid by-products ii. Acidosis develops iii. Hydrogen ions and lactic acid accumulate in the body.
- Ischemia stimulates increased carbon dioxide by the tissues. a. Excess carbon dioxide combines with intracellular water to produce carbonic acid.
i. Reacts with other buffers to form more intracellular acidic substances b. Acidosis serves as an indirect measure of tissue perfusion. c. Acidic blood inhibits hemoglobin in the RBCs from binding with and carrying oxygen. i. Adds to cellular oxygen debt
- Sodium is inclined to diffuse into the cells.
a. Sodium-potassium pump normally sends sodium back out against the concentration gradient. i. Involves active transport and an ample supply of ATP ii. Reduced ATP results in dysfunctional sodium-potassium pump. (a) Excessive sodium diffuses into the cells, depleting the interstitial compartment.
- Intracellular enzymes that usually help digest and neutralize bacteria are bound in an impermeable membrane. a. Cellular flooding explodes the membrane and releases the enzymes. i. Auto-digest the cell ii. Leads to last phase of shock (irreversible or terminal shock)
- Accumulating acids and waste products act as potent vasodilators.
a. Decreases venous return and diminishes blood flow to vital organs and tissues b. When aortic pressure falls below MAP of 60 mm Hg: i. Coronary arteries no longer fill. ii. The heart is weakened. iii. Cardiac output falls. c. Myocardial depressant factor is released from ischemic pancreas. i. Further decreases the pumping action of the heart
- Reduced blood supply results in slowing and stopping of sympathetic nervous system activity. a. Metabolic wastes are released into slow-flowing blood. b. Leads to platelet agglutination and formation of microthrombi c. Stretched capillary walls lose their ability to retain large molecules. i. Leak into surrounding interstitial spaces ii. Oxygen transport decreases. (a) Increases cellular hypoxia
- The buildup of lactic acid and carbon dioxide acts as a potent vasodilator.
a. Leads to the relaxation of the postcapillary sphincters b. Accumulation washes into the venous circulation. i. Increases metabolic acidosis ii. Referred to as the capillary washout phase c. Ischemia and necrosis lead to multiple-organ dysfunction syndrome.
- White blood cells and blood clotting systems are impaired.
a. Decreased resistance to infection and disseminated intravascular coagulation (DIC) may occur. b. DIC: Proteins that control clotting become active under abnormal circumstances. i. 97% of patients who die from hemorrhagic shock have evidence of coagulation defects
(a) Release of bradykinin leads to tissue hypoperfusion. b. Overactivity results in a maldistribution of systemic and organ blood flow. c. Body attempts to compensate by accelerating tissue metabolism, which leads to: i. Tissue hypoxia ii. Tissue hypoperfusion iii. Exhaustion of the cells fuel supply (ATP) iv. Metabolic failure v. Lysosome breakdown vi. Anaerobic metabolism vii. Acidosis viii. Impaired cellular function d. Progression causes various organs to malfunction.
- Typically develops within hours or days after resuscitation.
a. Signs and symptoms: i. Hypotension ii. Insufficient tissue perfusion iii. Uncontrollable bleeding iv. Multisystem organ failure v. Possible low-grade fever may from inflammatory response, tachycardia, dyspnea vi. Possible difficulty oxygenating patients due to lung injury and respiratory distress
- From 14-21 days, renal and liver failure can develop.
a. The GI and immune systems may collapse. b. Patient may undergo cardiovascular collapse. c. Death is typical within days to weeks of the insult.
- Affects specific organs and organ systems:
a. Heart i. May result in dysrhythmias, muscle ischemia, infarction, pump failure ii. Peripheral pulses are weak or absent. iii. Extremities are cyanotic and cold. b. Lungs i. Failure is seen by respiratory distress syndrome or noncardiogenic pulmonary edema. ii. Pulmonary arterial pressures increase, producing pulmonary hypertension. iii. Pulmonary capillary blood flow reduction results in: (a) Impaired gas exchange (b) Reduced PaO 2 level (c) Increased PaCO 2 level iv. Alveolar cells are ischemic. v. Interstitial and intra-alveolar edema at low wedge pressures occur. vi. Results are: (a) Respiratory failure (b) Hypoxemia (c) Respiratory acidosis c. Central nervous system i. Decrease in cerebral perfusion pressure and blood flow result in: (a) Confusion
(b) Reduced responses to verbal and painful stimuli (c) Unresponsiveness d. Kidneys i. Reduced renal blood flow results in acute tubular necrosis, which leads to: (a) Oliguria (urine output of greater than 20 mL/h) (b) Retention of toxic waste in the blood (c) Worsened metabolic acidosis e. Liver i. Coagulopathies are produced (clotting and bleeding occur at the same time). ii. Failure to filter bacteria leads to vulnerability to infection. iii. Inability to metabolize waste products leads to increased level of toxins in the blood. iv. Cell death increases enzyme levels in the blood. v. Results in: (a) Ischemic or hypoxic hepatitis (b) Shock liver f. GI tract i. Ischemic gut syndrome occurs. ii. Gut leaks and contributes to progression of shock.
VII Causes of Shock
A. Normal tissue perfusion requires an intact heart, fluid volume, and tubing
capable of reflex adjustments to pump output and fluid volume.
- Damage to any of these mechanisms disrupts tissue perfusion, causing shock to ensue.
- Shock results from many conditions. a. Damage occurs because of insufficient perfusion of organs and tissues. i. Tissues start to die, affecting all local body processes. b. If shock is not promptly arrested or reversed, the patient will die.
- Have a high index of suspicion for shock in emergency medical situations. a. Expect shock to accompany: i. Massive external or internal bleeding ii. Multiple severe fractures iii. Abdominal or chest injury iv. Spinal injury v. Severe infection vi. Major heart attack vii. Anaphylaxis
- There are three basic causes of shock. a. Pump failure b. Low fluid volume c. Poor vessel function
- Certain categories of patients are more at risk to shock. a. Patients with trauma or bleeding b. Patients with massive MI c. Pregnant women
- Last phase of shock when the condition has progressed to a terminal stage a. Arterial blood pressure is abnormally low. b. Rapid, irreversible deterioration of cardiovascular system occurs. c. Life-threatening reductions in cardiac output, blood pressure, and tissue perfusion. d. Blood is shunted away from liver, kidneys, and lungs. e. Cells begin to die. f. Vital organ damage cannot be repaired.
- Aggressive treatment does not usually result in recovery. a. You should still provide aggressive treatment en route to the trauma center.
IX Patient Assessment of Shock
A. Scene size-up
- Size up the scene for hazards.
- Follow standard precautions.
- Determine the number of patients and the need for additional or specialized resources.
- Quickly assess the MOI or nature of illness (NOI). a. Can give you clues about: i. Causes of nonhemorrhagic shock ii. Extent of bleeding
B. Primary assessment
- Form a general impression. a. How does the patient look? i. Some do not pass the look test and will need to be fast tracked based on MOI/NOI. ii. A blue or sweaty pale look will need immediate attention. b. Patients who do not greet you may be concentrating on breathing, injuries, or in severe pain. c. Assess the patients mental status using AVPU. d. Introduce yourself and ask their name, location, and the day of the week.
- Airway and breathing a. If you suspect cardiac arrest, use the CAB approach. i. CAB = circulation/compressions, airway, breathing b. Otherwise, asses the ABCs. i. ABCs = airway, breathing, circulation c. Patients with life-threatening airway problems cannot speak or speak in one- or two- word sentences. d. Manage immediate threats to the patient’s airway or breathing. i. Position the patient’s airway. ii. Clear the airway of secretions, blood, or vomitus. iii. Administer oxygen. e. If difficulty breathing is suspected, examine the chest for: i. Flail segments ii. Impaled objects
iii. Holes that need to be sealed with an occlusive dressing f. Assess the adequacy of the patient’s ventilation in respect to volume and rate. i. Decide if it will be necessary to assist the patient with bag-mask ventilation and high-concentration oxygen.
- Circulation a. Take CAB approach and perform chest compressions if you suspect the patient does not have a pulse. b. In patients with a pulse, determine if it is adequate to sustain life. i. Perform a rapid exam to check for external blood loss that can be controlled. c. In conscious patients, assess the pulse at the radius. i. In unconscious patients, check the carotid pulse in the neck. ii. Is the radial pulse weak and thready, or irregular? (a) If the radial pulse is barely palpable, it is an indicator that systolic blood pressure is dropping fast. d. If you know the patient is hypotensive, provide immediate transport to the ED. e. The rapid exam is meant to detect injuries that are life threatening and need immediate attention. f. Also note the patient’s skin color, temperature, and condition.
- Transport decision a. All patients need to be prioritized. i. If patient has shock from a medical problem, fast track to an assessment based on body systems involved. ii. If patient has shock from trauma, let the MOI guide your assessment of the major body cavities and regions.
C. History taking
- History taking, secondary assessment, and reassessment can be done en route to the ED in a high-priority patient. a. Keep on-scene care to essential items that must be done before moving the patient. b. Unless patient is pinned, and you suspect a delay in extrication, delay establishing IV/IO access until you are en route.
D. Secondary assessment
- Shock is considered hypovolemic or hemorrhagic until proven otherwise. a. Phases of shock relate to percentage of blood loss. i. Compensated ii. Decompensated iii. Terminal/irreversible b. 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. a. Lactate is a sign of metabolic distress and an early indicator of severe sepsis. b. Portable lactate monitors are similar to glucometers. i. Incorporated into sepsis alert programs in some major cities
E. Reassessment
- Revisit the primary assessment, vital signs, chief complaint, and any treatment performed on the patient.
