Chapter 66: Shock

- Syndrome characterized by decreased tissue perfusion and impaired cellular metabolism

- Imbalance in supply/demand for O2 and nutrients
- The exchange of oxygen and nutrients at the cellular level is essential to life.
- When a cell experiences a state of hypoperfusion, the demand for oxygen and nutrients exceeds the supply at the
microcirculatory level.

Types of Shock
• Cardiogenic - systolic or diastolic dysfunction that results in reduced cardiac output (CO).
• Hypovolemic – increased Loss of blood or body fluids
• Distributive – Neurogenic, Anaphylactic, Septic
• Obstructive
• See Table 66-1 for more information.
• Although the cause, initial presentation, and management strategies vary for each type of shock, the physiologic responses
of the cells to hypoperfusion are similar.

I. Cardiogenic Shock
Causes:
- Myocardial infarction
- Cardiomyopathy
- Blunt cardiac injury
- Severe systemic or pulmonary hypertension
- Cardiac tamponade
- Myocardial depression from metabolic problems
- Whether the first event is myocardial dysfunction, a structural problem (e.g., valvular disorder, ventricular septal rupture),
or dysrhythmias, the physiologic responses are similar.
- The patient experiences impaired tissue perfusion and cellular metabolism because of cardiogenic shock.
Manifestations
- Tachycardia
- Hypotension
- Narrowed pulse pressure
- ↑ Myocardial O2 consumption
- The early clinical presentation of a patient with cardiogenic shock is similar to that of a patient with acute decompensated
heart failure.
- The heart’s inability to pump blood forward will result in a low CO (<4 L/min) and cardiac index (<2.5 L/min/m 2).
Assessment
- Tachypnea, pulmonary congestion
- Pallor and cool, clammy skin
- Decreased capillary refill time
- Anxiety, confusion, agitation
- Decreased renal perfusion and urinary output
Care Management
- Overall goal: restore blood flow to myocardium by restoring balance between O 2 supply and demand
- Reperfusion with thrombolytics - within 30minutes – thrombolytics –streptokinase, Urokinase, Altepase
- Angioplasty with stenting – cardiac catheterization, balloon angioplasty – within 90minutes
- Emergency revascularization – CABG – bypass graft
- Valve replacement
- Cardiac catheterization is performed as soon as possible after the initial insult.
- Specific measures to restore blood flow include angioplasty with stenting, emergency revascularization, and valve
replacement (see Chapter 33).
- Until these interventions are performed, the heart must be supported to optimize stroke volume and CO to achieve optimal
perfusion.
- ABC then treat cause
- Hemodynamic monitoring
- Drug therapy
o Nitrates to dilate coronary arteries
o Diuretics to reduce preload – HF, pulmonary edema
o Vasodilators to reduce afterload - nitroprusside
 o β-adrenergic blockers to reduce HR – if there’s BP
o **Dobutamine to increase myocardial contractility thereby increase CO (Table 66-8)
o Drugs can be used to decrease the workload of the heart by dilating coronary arteries (e.g., nitrates), reducing
preload (e.g., diuretics), reducing afterload (e.g., vasodilators), and reducing heart rate and contractility (e.g., β-
adrenergic blockers).
II. Hypovolemic Shock
- Absolute hypovolemia: loss of blood & body fluids
o Hemorrhage
o GI loss (e.g., vomiting, diarrhea)
o Fistula drainage
o Diabetes insipidus
o Diuresis
- Relative hypovolemia
o Results when fluid volume moves out of the vascular space into extravascular space (e.g., intracavitary space)
o Termed third spacing
o One example of relative volume loss is leakage of fluid from the vascular space to the interstitial space from
increased capillary permeability, as seen in burns.
Manifestations
- Anxiety
- Tachypnea
- Tachycardia
- Decrease in CO
- Decrease in stroke volume, urinary output
- If loss is >30%, blood volume is replaced
- If volume loss is greater than 30%, compensatory mechanisms may fail and immediate replacement with blood products
should be started.
- Loss of autoregulation in the microcirculation and irreversible tissue destruction occur with loss of more than 40% of total
blood volume.
- Common laboratory studies and assessments that are done include serial measurements of hemoglobin and hematocrit
levels, electrolytes, lactate, blood gases, central venous oxygenation (SvO 2), and hourly urine outputs.
Care Management
- Management focuses on stopping loss of fluid and restoring the circulating volume
- Fluid resuscitation is calculated using a 3:1 rule (3 mL of isotonic crystalloid for every 1 mL of estimated blood loss)p. 1601
- If hypotension persists and patient is no longer fluid responsive, vasopressors may be added. First drug of choice is
norepinephrine. p. 1601
- selecting appropriate fluids for replacement
- Table 66-7 delineates the different types of fluid used for volume resuscitation, the mechanisms of action, and specific
nursing implications for each fluid type.
- SIGN CONSENT when giving blood – by physician – positive cannot have negative blood. AB+ universal recipient,

III. Distributive Shock – Neurogenic Shock

- Can occur in response to spinal cord injury at the fifth thoracic (T5) vertebra or above or spinal anesthesia
- Results in massive vasodilation, tissue hypoperfusion, ultimately impaired cellular metabolism
- The injury results in massive vasodilation without compensation due to the loss of SNS vasoconstrictor tone.
- This massive vasodilation leads to a pooling of blood in the blood vessels, tissue hypoperfusion, and ultimately impaired
cellular metabolism (Fig. 66-4).
- Depression of the vasomotor center of the medulla from drugs (e.g., opioids, benzodiazepines) also can lead to decreased
vasoconstrictor tone of the peripheral blood vessels, resulting in neurogenic shock.
Manifestations
- Hypotension and bradycardia
- Inability to regulate body temperature (resulting in heat loss)
- Dry skin
- Initially, the patient’s skin will be warm, owing to the massive dilation.
- As the heat disperses, the patient is at risk for hypothermia.
- Later, the patient’s skin may be cool or warm, depending on the ambient temperature.
- Table 66-3 further describe the clinical presentation of a patient with neurogenic shock.
Care Management
- In spinal cord injury: spinal stability
 - Spinal precautions to promote spinal stability is the initial intervention
- Treatment of hypotension and bradycardia with vasopressors and atropine
- Fluids infused cautiously as hypotension generally is not related to fluid loss
- Monitor for hypothermia
- The specific treatment of neurogenic shock is based on the cause.
- If the cause is spinal cord injury, general measures to promote spinal stability (e.g., spinal precautions, cervical stabilization
with a collar) are initially used.

IV. Distributive Shock - Anaphylactic Shock

- Acute, life-threatening hypersensitivity (allergic) reaction
- Massive vasodilation
- Release of vasoactive mediators
- ↑ Capillary permeability
- Hypoperfusion
- Impaired cellular metabolism
- Anaphylactic shock is a hypersensitivity reaction to a sensitizing substance (e.g., drug, chemical, vaccine, food, insect
venom).
- As capillary permeability increases, fluid leaks from the vascular space into the interstitial space.
- Anaphylactic shock can lead to respiratory distress, due to laryngeal edema or severe bronchospasm, and circulatory failure
from the massive vasodilation.
- A patient can develop a severe allergic reaction, possibly leading to anaphylactic shock, after contact, inhalation, ingestion,
or injection with an antigen (allergen) to which the person has previously been sensitized.
Manifestations
- Swelling of lips and tongue, angioedema
- Wheezing, stridor due to laryngeal edema
- Flushing, pruritus, urticaria
- Respiratory distress and circulatory failure
- Anxiety, confusion, dizziness
- Incontinence
- A patient can have a severe allergic reaction, possibly leading to anaphylactic shock, after contact, inhalation, ingestion, or
injection with an antigen (allergen) to which the individual has previously been sensitized.
- Parenteral administration of the antigen (allergen) is the route most likely to cause anaphylaxis. However, oral, topical, and
inhalation routes can also cause anaphylactic reactions.
Care Management
- Epinephrine, diphenhydramine, ranitidine
- Maintain a patent airway
o Nebulized bronchodilators – d/t edema
o Aerosolized epinephrine
o Endotracheal intubation or cricothyroidotomy may be necessary
- The first strategy in managing patients at risk for anaphylactic shock is prevention.
- A thorough history is key in avoiding the risk factors for anaphylaxis.
- IM epinephrine is the first drug of choice to treat anaphylactic shock. It causes peripheral vasoconstriction and
bronchodilation and opposes the effect of histamine.
- Aerosolized epinephrine can also be used to treat laryngeal edema.
- Diphenhydramine (Benadryl) along with ranitidine (Zantac) are given as adjunctive therapies to block the ongoing release of
histamine from the allergic reaction.
- Aggressive fluid replacement
o Usually crystalloids
- IV corticosteroids if significant hypotension persists after 1–2 hours of aggressive therapy
- Hypotension results from leakage of fluid out of the intravascular space into the interstitial space as a result of increased
vascular permeability and vasodilation.

V. Distributive Shock – Septic Shock

- Sepsis: systemic inflammatory response to documented or suspected infection
- Severe sepsis: sepsis complicated by organ dysfunction
- Vasodilation causes Hypotension despite fluid resuscitation
- Presence of inadequate tissue perfusion resulting in hypoxia
- In as many as 10% to 30% of patients with sepsis, the causative organism is not identified.
 - Severe sepsis is diagnosed in more than 750,000 patients per year with mortality rates as high as 28% to 50%.
Manifestations
- Tachypnea/hyperventilation
o Results in respiratory alkalosis
o Respiratory failure develops in 85% of patients
- ↓ Urine output
- Altered neurologic status
- GI dysfunction, GI bleeding, paralytic ileus
- The patient will initially hyperventilate as a compensatory mechanism, resulting in respiratory alkalosis.
- Once the patient can no longer compensate, respiratory acidosis will develop.
- Respiratory failure will develop in 85% of patients with sepsis, and 40% will develop acute respiratory distress syndrome
(ARDS) (see Chapter 67).
- These patients may need to be intubated and mechanically ventilated.
- Table 66-3 gives the clinical presentation of a patient with septic shock.
Care Management
- Fluid replacement to restore perfusion
o Hemodynamic monitoring
o urine output
- Vasopressor drug therapy
- IV corticosteroids for patients who cannot maintain an adequate BP with vasopressor therapy despite fluid resuscitation
- Antibiotics should be started within first hour
o After cultures are obtained (e.g., blood, wound exudate, urine, stool, sputum)
- Patients in septic shock require large amounts of fluid replacement. Volume resuscitation of 30 to 50 mL/kg is usually done
with isotonic crystalloids to achieve adequate fluid resuscitation. Albumin 4%-5% may be added when patients require
substantial volumes.
- A fluid challenge technique (e.g., to achieve a minimum of 30 mL/kg of crystalloids) is used and repeated until
hemodynamic improvement (e.g., increase in MAP and/or CVP, change in SVV) is noted.
- If the patient remains hypotensive after initial volume resuscitation with minimally 30 ml/kg, vasopressors may be added.
The first drug of choice is norepinephrine. Vasodilation and low CO, or vasodilation alone, can cause low BP in spite of
adequate fluid resuscitation. Vasopressin (Pitressin) may be added for patients refractory to initial vasopressor therapy.
Exogenous vasopressin is used to replace the stores of physiologic vasopressin that are often depleted in septic shock.
- Glucose levels <180 mg/dL
- Stress ulcer prophylaxis with proton pump inhibitors (e.g., pantoprazole [Protonix])
- Deep vein thrombosis prophylaxis (e.g., heparin, enoxaparin [Lovenox])
- Intensive glucose control (81 to 108 mg/dL) actually increases mortality.
- Frequent monitoring of glucose levels of all patients in septic shock is necessary.

VI. Obstructive Shock

- Develops when physical obstruction to blood flow occurs with decreased CO
o Caused by restricted diastolic filling of right ventricle from compression
o Abdominal compartment syndrome- abdominal pressure compresses inferior vena cava
- Rapid assessment and immediate treatment are important
- Other causes include abdominal compartment syndrome in which increased abdominal pressures compress the inferior
vena cava, thus decreasing venous return to the heart
- Pulmonary embolism and right ventricular thrombi cause an outflow obstruction as blood leaves the right ventricle through
the pulmonary artery.
- This leads to decreased blood flow to the lungs, as well as decreased blood return to the left atrium.
Care Management
- Primary strategy is early recognition and treatment to relieve obstruction
o Mechanical decompression in pneumothorax
o Thrombolytic therapy in pulmonary embolism
o Radiation or removal of mass
o Decompressive laparotomy
- Mechanical decompression for pericardial tamponade, tension pneumothorax, and hemopneumothorax may be done by
needle or tube insertion.
- Obstructive shock from a pulmonary embolism may require thrombolytic therapy.
- Superior vena cava syndrome, a compression or obstruction of the outflow tract of the mediastinum, may be treated by
radiation, debulking, or removing the mass or cause.
 - A decompressive laparotomy may be indicated for abdominal compartment syndrome for patients with high
intraabdominal pressure and hemodynamic instability.

Stages of Shock
- Initial
o Usually not clinically apparent
o Metabolism changes at cellular level from aerobic to anaerobic
 Lactic acid builds up and must be removed by liver
 Process requires O2, unavailable due to decreased tissue perfusion
- Compensatory
o Attempt to overcome consequences of anaerobic metabolism and maintain homeostasis
o body’s responses to the imbalance in oxygen supply and demand
o The patient’s clinical presentation begins to reflect the body’s responses to the imbalance in oxygen supply and
demand.
o Impaired GI motility
 Risk for paralytic ileus
o Cool, clammy skin
 Except septic patient who is warm and flushed
o ↓ Blood to kidneys activates renin–angiotensin system causes vasoconstriction
o The decrease in blood flow to the GI tract results in impaired motility and a slowing of peristalsis. This increases
the risk for the development of a paralytic ileus.
o Decreased blood flow to the skin results in the patient feeling cool and clammy. The exception is the patient in
early septic shock who may feel warm and flushed due to a hyperdynamic state.
o Body is able to compensate for changes in tissue perfusion
o If cause of shock is corrected, patient recovers with little or no residual effects
o If cause of shock is not corrected, patient enters progressive stage
o Distinguishing features of ↓ cellular perfusion and altered capillary permeability
 Leakage of protein into interstitial space
 ↑ Systemic interstitial edema
o The cardiovascular system is profoundly affected in the progressive stage of shock.
o CO begins to fall, resulting in hypoperfusion and myocardial dysfunction
o ↓ Blood flow to pulmonary capillaries
o The cardiovascular system is profoundly affected in the progressive stage of shock.
o CO begins to fall, resulting in a decrease in BP and coronary artery, cerebral, and peripheral perfusion.
- Progressive
o Movement of fluid from pulmonary vasculature to interstitium
 Pulmonary edema
 Bronchoconstriction
 ↓ Functional residual capacity
 Tachypnea, dyspnea, crackles
o Respiratory failure, Ac kidney injury
o Liver failure
o Another key response in the lungs is the movement of fluid from the pulmonary vasculature into the interstitial
space.
o As capillary permeability increases, the movement of fluid to the interstitial spaces results in interstitial edema,
bronchoconstriction, and a decrease in functional residual capacity.
- Refractory
o Exacerbation of anaerobic metabolism
o Accumulation of lactic acid
o ↑ Capillary permeability
o Profound hypotension and hypoxemia
o Tachycardia worsens
o Failure of one organ system affects others
o Recovery unlikely
o In the final stage of shock, the refractory stage, decreased perfusion from peripheral vasoconstriction and
decreased CO exacerbate anaerobic metabolism.
o Increased capillary permeability allows fluid and plasma proteins to leave the vascular space and move to the
interstitial space.
 o Blood pools in the capillary beds secondary to the constricted venules and dilated arterioles.
o Loss of intravascular volume worsens hypotension and tachycardia and decreases coronary blood flow.
o Decreased coronary blood flow leads to worsening myocardial depression and a further decline in CO.
o See next slide for figure.

Diagnostics
- Thorough history and physical examination
- No single study to determine shock
o Blood studies
 Elevation of lactate
 Base deficit
- 12-lead ECG, continuous ECG monitoring
- Chest x-ray
- Hemodynamic monitoring
- Obtaining a thorough medical and surgical history, and a history of recent events (e.g., surgery, chest pain, trauma)
provides valuable data.
- Table 66-2 summarizes laboratory findings seen in shock.
- Additional diagnostic studies include a 12-lead electrocardiogram (ECG), continuous ECG monitoring, chest x-ray,
continuous pulse oximetry, and invasive and noninvasive hemodynamic monitoring.

Care Management
- Successful management
o Identification of patients at risk for developing shock p. 1602
o Interventions to control or eliminate cause of decreased perfusion
o Protection of target and distal organs from dysfunction
o Provision of multisystem supportive care
- General management strategies
o Ensure a patent airway
o Maximize oxygen delivery, mechanical ventilation as needed
o Optimize CO with fluid replacement or drugs
o Increase hemoglobin by transfusion
o Table 66-6 provides an overview of initial assessment findings and interventions for the emergency care of patients
in shock.
o Supplemental oxygen and mechanical ventilation may be necessary to maintain an arterial oxygen saturation of
90% (PaO2 >60 mm Hg) to avoid hypoxemia.
- Cornerstone of therapy for septic, hypovolemic, and anaphylactic shock = volume expansion via fluid resuscitation
o One or two large-bore IV catheters , intraosseous access device, or central venous catheter
o Isotonic crystalloids (e.g., normal saline, lactated Ringers) and colloids (e.g., albumin)
o Before beginning fluid resuscitation, the nurse should insert two large-bore (e.g., 14- to 16-gauge) IV catheters, an
intraosseous (IO) access device; or a central venous catheter.
o Both crystalloids (e.g., normal saline, lactated ringers) and colloids (e.g., albumin) have a role in fluid resuscitation.
p. 1596 (Table 66-; see Table 16-17).
- Volume expansion
o Fluid responsiveness is determined by clinical assessment
 Vital signs
 Capillary refill
 Skin temperature
 Urine output – 30 – 50mL/hr
 Cardiac and respiratory assessment
o Hemodynamic parameters, such as SVV or CO, are also used.
o Monitor trends in BP with an automatic BP cuff or an arterial catheter to assess the patient's response.
o Use an indwelling bladder catheter to monitor urine output during resuscitation.
o Two major complications of large volumes
o Hypothermia - Warm crystalloid and colloid solution
o Coagulopathy - Replace clotting factors
o Persistent hypotension after adequate fluids
o Vasopressor may be added
 o When large amounts of fluids are required, you must protect the patient against two major complications:
hypothermia and coagulopathy.
o If the patient has persistent hypotension after adequate fluid resuscitation, a vasopressor (e.g., norepinephrine
[Levophed], dopamine [Intropin]) and/or an inotrope (e.g., dobutamine [Dobutrex]) may be added. The goal for
fluid resuscitation is restoration of tissue perfusion.
- Primary goal of drug therapy = correction of decreased tissue perfusion
- Vasopressor drugs (e.g., norepinephrine)
o Achieve/maintain MAP >60 to 65 mm Hg
o Reserved for patients unresponsive to fluid resuscitation
o Continuously monitor end-organ perfusion
o Vasodilator therapy (e.g., nitroglycerin, nitroprusside, dobutamine – cardiogenic shock to  BP) may be needed in
cardiogenic shock to Decrease afterload
o Drugs used to improve perfusion in shock are given intravenously via an infusion pump and a central venous line.
o Drugs that mimic the action of the SNS are termed sympathomimetic. The effects of these drugs are mediated
through their binding to α-adrenergic or β-adrenergic receptors.
o These drugs have the potential to cause severe peripheral vasoconstriction and an increase in SVR. These further
risks tissue perfusion. The increased SVR increases the workload of the heart. This can harm a patient in
cardiogenic shock by causing further myocardial damage.
- Nutrition is vital to decreasing morbidity from shock
o Start enteral nutrition within first 24 hours - PEG or NG tube,
o Parenteral nutrition used only if enteral feedings contraindicated
 TPN – total parenteral nutrition – 2 RNs need to check. only 24hrs
 sometimes need to add insulin – BLOOD GLUCOSE q6h
o Weigh patient daily
o Monitor serum protein, total albumin, prealbumin, BUN, glucose, electrolytes: CBC and BMP
o Protein-calorie malnutrition is one of the main manifestations of hypermetabolism in shock.
o Enteral nutrition should be started within the first 24 hours. However, full calorie replacement is not
recommended for previously well-nourished adults early on in critical illness.
o Generally, parenteral nutrition is used only if enteral feedings are contraindicated.

Nursing Assessment
- ABCs
o Airway
o Breathing
o Circulation
- Focused assessment of tissue perfusion
o Vital signs
o Peripheral pulses
o Level of consciousness
o Capillary refill
o Skin (e.g., temperature, color, moisture)
o Urine output
- As shock progresses, the patient’s skin becomes cooler and mottled, urine output will decrease, peripheral pulses will
diminish, and neurologic status will decline.
- Brief history
o Events leading to shock
o Onset and duration of symptoms
- Health history
o Medications
o Allergies
o Vaccinations, recent travel
- Diagnoses
o Ineffective peripheral tissue perfusion and risk for decreased cardiac tissue perfusion, ineffective cerebral tissue
perfusion, ineffective renal perfusion, impaired liver function, and ineffective GI perfusion related to low blood
flow or maldistribution of blood
o Anxiety related to severity of condition and hypoxemia
- Shock Planning
o Goals
  Evidence of adequate tissue perfusion
 Restoration of normal or baseline BP
 Recovery of organ function
 Avoidance of complications from prolonged states of hypoperfusion
 Also included may be prevention of health care–acquired complications of disease management and care.
- Health Promotion
o Identify patients at risk
 Older patients
 Those who are immunocompromised
 Those with chronic illness
 Surgery or trauma patients
o In general, patients who are older, are immunocompromised, or have chronic illnesses are at an increased risk.
o Any person who has surgery or trauma is at risk for shock resulting from hemorrhage, spinal cord injury, sepsis, or
other conditions.
o Planning to prevent shock
 Monitoring fluid balance to prevent hypovolemic shock
 Maintenance of hand washing to prevent spread of infection
o For example, a person with an acute anterior wall MI is at high risk for cardiogenic shock.
o The primary goal for this patient is to limit the infarct size.
o This is done by restoring coronary blood flow through percutaneous coronary intervention, thrombolytic therapy,
or surgical revascularization.
o Rest, analgesics, and sedation can reduce the myocardial demand for oxygen.
o Acute Care
 Plan and implement nursing interventions and therapy
o Monitor patient’s ongoing physical and emotional status
o Identify trends to detect changes in patient’s condition
o Evaluate patient’s response to therapy
o Provide emotional support to patient and caregiver
o Collaborate with other members of interprofessional team to coordinate care
o Neurologic Status
 Assess orientation and level of consciousness, clinical manifestations
 Orient to person, place, time, events
o Cardiovascular status
 Continuous ECG monitoring
 Monitor for dysrhythmias
o Assess the patient’s neurologic status, using a valid tool, at least every 1 to 2 hours.
o The patient’s neurologic status is the best indicator of cerebral blood flow. Be aware of the clinical manifestations
that may indicate neurologic involvement (e.g., changes in behavior, restlessness, hyperalertness, blurred vision,
confusion, paresthesia).
o Respiratory status
 Respiratory rate, depth, and rhythm
 Breath sounds
 Continuous pulse oximetry
 Arterial blood gases
 Many patients will be intubated and on mechanical ventilation
o Initially monitor the rate, depth, and rhythm of respirations as frequently as every 15 to 30 minutes. Increased rate
and depth provide information regarding the patient’s attempts to correct metabolic acidosis.
o Pulse oximetry using a patient’s finger may not be accurate in a shock state because of poor peripheral circulation.
Instead, attach the probe to the ear, nose, or forehead (according to the manufacturer’s guidelines) to increase
accuracy.
o Arterial blood gases (ABGs) provide definitive information on ventilation and oxygenation status and acid-base
balance. Initial interpretation of ABGs is often your responsibility. A PaO 2 below 60 mm Hg (in the absence of
chronic lung disease) indicates hypoxemia and the need for higher oxygen concentrations or for a different mode
of oxygen administration. Low PaCO2 with a low pH and low bicarbonate level may indicate that the patient is
attempting to compensate for metabolic acidosis from increasing lactate levels.
o A rising PaCO2 with a persistently low pH and PaO2 indicates the need for advanced pulmonary management.
Many patients in shock are intubated and on mechanical ventilation. Maintaining a patent airway and monitoring
for ventilator-related complications are critical.
 o Renal status
 Urine output
 Serum creatinine
o Body temperature and skin changes
 Core temperature
 Skin: temperature, pallor, flushing, cyanosis, diaphoresis, piloerection
o Urine output of <0.5 mL/kg/hr may indicate inadequate perfusion of the kidneys.
o Also use trends in serum creatinine values to assess renal function.
o Monitor temperature every 4 hours if normal. In the presence of an elevated or subnormal temperature, obtain
hourly core temperatures (e.g., urinary, central line, PA catheter).
o Monitor the patient's skin (e.g., upper and lower extremities) for signs of adequate perfusion. Changes in
temperature, pallor, flushing, cyanosis, diaphoresis, and piloerection may indicate hypoperfusion.
o Gastrointestinal status
 Auscultate bowel sounds
 NG drainage/stools for occult blood
o Personal hygiene
 Perform bathing, nursing measures carefully
 Turn every 1 to 2 hours
 Passive/active range of motion
o Auscultate bowel sounds at least every 4 hours, and monitor for abdominal distention. If a nasogastric tube is
present, measure drainage and check for occult blood. Similarly, check all stools for occult blood.
o Hygiene is especially important for the patient in shock because impaired tissue perfusion predisposes the patient
to skin breakdown and infection. Perform bathing and other nursing measures carefully because a patient in shock
is experiencing problems with oxygen delivery to tissues.
o Monitor trends in oxygen consumption (e.g., SpO 2, ScvO2/SvO2) during all nursing interventions to assess the
patient's tolerance of activity.
o Emotional support and comfort
 Assess level of anxiety, fear, pain
 Drugs PRN
 Talk to patient
 Give simple explanations of all procedures
 Visit from clergy
 Caregiver involvement
 Privacy
 Call light within reach
o Fear, anxiety, and pain may aggravate respiratory distress and promote the release of catecholamines.
o Provide drugs to decrease anxiety and pain as appropriate. Continuous infusions of a benzodiazepine (e.g.,
lorazepam [Ativan]) and an opioid or sedative (e.g., morphine, propofol [Diprivan]) are extremely helpful in
decreasing anxiety and pain.
o Talk to the patient and encourage the caregiver to talk to the patient, even if the patient is intubated, is sedated,
or appears comatose. Hearing is often the last sense to decrease.
o Give the patient simple explanations of all procedures before you carry them out, as well as information regarding
the current plan of care.
o Do not overlook the patient's spiritual needs. Patients may desire a visit from a chaplain, priest, rabbi, or minister.
Ambulatory Care
- Rehabilitation of patient requires
o Correction of precipitating cause
o Prevention or early treatment of complications
o Teaching focused on disease management or prevention of recurrence
- Continue to monitor the patient for indications of complications throughout the recovery period. These may include
decreased range of motion, muscle weakness, decreased physical endurance, acute kidney injury (acute tubular necrosis)
(see Chapter 46), and fibrotic lung disease (from ARDS) (see Chapter 67).
- Patients recovering from shock often require diverse services after discharge. These can include admission to transitional
care units (e.g., for mechanical ventilation weaning), rehabilitation centers (inpatient or outpatient), or home health care
agencies. Start planning for a safe transition from hospital to home as soon as the patient is admitted to the hospital.
-