SHOCK

INTRODUCTION
Shock is a life threating condition, in which the tissue become hypo perfused due to which
circulatory collapse occurs.
It is reversible, treatable & resusitable only if detected in early stage or otherwise it may
cause multi organ defect & ultimately death.
Septic shock has the highest mortality prevalence (40%-60%) as compare to other.
DEFINITION
A clinical syndrome that results from inadequate tissue perfusion creating an imbalance
between the delivery of & requirements for oxygen & nutrients that support cellular func-
tion.
ETIOLOGY
Hypovolemic shock
 Bleeding/ Haemorrhage (internal/external) (Most Common)
 dehydration (sever vomiting, severe diarrhoea, excess sweating)
 plasma loss (as in burns, trauma) à low blood volume
Lead to: Reduced venous return (preload)à loss of 15-25% of CO / 1-2 L hypotension

Distributive shock
 infection
 spinal cord injury
 allergy
 stress, pain
Cardiogenic shock
 myocardial infarction (Most common), heart failure, cardiac dysrhythmias
 Myocarditis, cardiomyopathy, cardiac tamponade, congestive heart failure
 Acute valvular dysfunction (e.g., rapture of papillary muscles post MI)
 Sustained arrhythmias (e.g., heart block, ventricular tachycardia)
 pulmonary embolism
Obstructive shock
 Obstruction of venous return: like Vena Cava syndrome (usually neoplasms)
 Compression of heart: like haemorrhagic pericarditis > cardiac tamponade
 Obstruction of outflow: like aortic dissection*, massive pulmonary embolism, pneumo-
thorax.
PATHOPHISIOLOGY
 Shock is a state of circulatory insufficiency creating imbalance between oxygen delivery
and demand to the tissues, resulting in end-organ dysfunction.
 At the cellular level, shock first affects the mitochondria.
 Majority of the aerobic energy comes from combustion of substrates (carbohydrates and
fats) along with oxygen, forming carbon dioxide and water.

 But in shock there is cellular hypoxemia; the tissues enter in anaerobic state and accumu-
late lactic acid. Lactate starts building up in the blood and acidosis develops.

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 reduce capillary inadequate tissue shift to anaerobic
perfussion oxygen metabolism

release of free radical& oxidative stress metabolic acidosis

tissue damage apoptosis

ANY INSULT LEADS

OXYGENATION &TISSUE PERFUSSION

HOMEOSTATIC RESPONCE

SYMPATHETIC RESPONSE RESPIRATORY RATE TO

(H.R, B.P, CARDIAC OUTPUT) OXYGEN SATURATION & DELIV-
ERY

RENIN – ANGIOTENSIN ACTIVATION CATECHOLAMINES & CORTISOL TO PRO-

Na &H2O REABSORPTION VIDE GLUCOSE FOR METABOLISM

RESTORATION OF TISSUE PERFUSION &

OXYGENATION

COMPENSATORY MECHANISM

STAGES OF SHOCK

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CLASSIFICATION
Haemorrhagic shock (or hypovolemic shock)
Non-haemorrhagic shock includes:
 Septic shock
 Cardiogenic shock
 Obstructive shock (tension pneumothorax, pericardial tamponade)
 Neurogenic shock
 Anaphylactic shock

A. HAEMORRHAGIC SHOCK

 There is loss in intravascular volume which decreases preload and diminishes the
cardiac output.
 Due to rapid drop in the blood volume, there is activation of the baro receptors
causing peripheral vasoconstriction and increased cardiac contractility and heart
Shock rate.
 Initially, as a response to the blood loss, the body tries to compensate by increas-
ing the pulse rate and diastolic pressure, causing the pulse pressure (difference
between systolic and diastolic pressure) to narrow.
 As the volume deficit continues, the cardiac output drops followed by reduction in
the blood pressure. Simultaneously there is renal vasoconstriction too, leading to
tubular necrosis.

 There is impaired fuel delivery to all the vital organs including the brain, due to
impaired hepatic glucose output and peripheral lipolysis.

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STAGES
STAGES STUDY DEFINITION
Stage A: At Risk No hypo htn, tachycardia, hypoperfusion
Stage B: Beginning Hypo htn &tachycardia without hypoperfusion
Stage C: Classic Hypoperfusion without deterioration
Stage D: Deteriorat- Hypoperfusion with deterioration without refractory shock
ing
stage: Extremis Hypoperfusion with deterioration with refractory shock

MANAGEMENT
 PRINCIPLE- The main treatment is to stop bleeding and restore volume by ad-
ministering fluids, including blood.
 Establish a secure patent airway and optimize breathing.
 Establish intravenous access for fluid resuscitation.
 Determine the level of conscious (by evaluating the eye, verbal, and best motor
response) (Glasgow Coma score, GCS).
 Expose the patient from head to toe to look for injuries or deformities, bearing in
mind avoid hypothermia.
 Patient may need to have orogastric tube in place to relieve gastric distension and
urinary catheter to monitor output.
 Patient may need central venous access for measuring central venous pressure,
fluid resuscitation, and blood sampling.
 Imaging studies would aid to the diagnosis of the source of haemorrhage. Initial
resuscitation should start with 1–2 L of fluid bolus in adults and 20 ml/kg in pae-
diatric patients.
 Blood transfusion might be needed too.

B. SEPTIC SHOCK
 It is the most common form of distributive shock. The body’s defense system is
overwhelmed by infection leading to life-threatening organ dysfunction.
 In resuscitating septic shock, few effects should be considered: hypovolemia, car-
diovascular depression, and systemic inflammation. Besides, there is capillary
leak, which causes intravascular volume loss.
 The combined interaction of chemical mediators, inflammation, and disturbed
metabolism causes heart injury during septic shock. There is also capillary leak in
the lungs, presenting as acute respiratory distress syndrome (ARDS).
 Common causative organisms are pneumococcus, methicillin-resistant Staphylo-
coccus aureus (MRSA), Klebsiella pneumoniae, Pseudomonas aeruginosa, etc.
 Thus, the early use of antibiotics is advised. Ensuring good oxygenation and vent-
ilation, the use of fluids and vasopressors is the main pillar of treatment in septic
shock
 The use of parenteral steroids is controversial and can only be considered in pa-
tients who are on chronic steroid therapy.

Definitions and criteria for septic shock:

 Systemic inflammatory response syndrome (SIRS) includes Two or more of the
following:
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  Temperature > 38°C or < 36°C.
 Heart rate > 90 beats/min.
 Respiratory rate > 20 breaths/min or paCO2 < 32 mmHg.
 White blood cell count >12,000 or < 4000 or > 10% band neutrophilia

MANAGEMENT
 The latest Surviving Sepsis Campaign Bundles are as follows:
 To be completed 3 hr of time of presentation:
1. Measure lactate level.
2. Obtain blood cultures prior to administration of antibiotics.
3. Administer broad spectrum antibiotics.
4. Administer 30 ml/kg crystalloid for hypotension or lactate ≥4 mmol/L.
 To be completed within 6 hr of time of presentation:
5. Apply vasopressors (for hypotension that does not respond to initial fluid resuscita-
tion) to maintain a mean arterial pressure (MAP) ≥65 mmHg.
6. In the event of persistent hypotension after initial fluid administration (MAP <65
mm Hg) or if initial lactate was ≥4 mmol/L, reassess volume status, tissue perfu-
sion, and document findings.
7 Remeasure lactate if initial lactate is elevated.
 Document reassessment of volume status and tissue perfusion with either:
Repeat focused exam (after initial fluid resuscitation) including vital signs, cardi-
opulmonary examination, and skin findings. Or any two of the following:
• Measure CVP.
• Measure ScvO2
• Bedside cardiovascular ultrasound.
• Dynamic assessment of fluid responsiveness with passive leg raises or fluid chal-
lenge.

C. CARDIOGENIC SHOCK
 Cardiogenic shock results when more than 40% of the myocardium is damaged
by necrosis from ischemia, inflammation, and toxins.
 There is decreased cardiac output due to pump failure such as cardiomyopathy,
myocardial infarction, valvular insufficiency, and arrhythmias
Symptoms-
 look ill, drowsy, sweaty, and pale
 can have tachycardia with weak pulse and hypotensive.
 The urine output would be deceased to less than 0.5 ml/kg/h,
 serum lactic acid would be as high as 4 mmol/L, indicating circulatory insuf-
ficiency.
 Left ventricular dysfunction can be detected by echo early in the course of cardio-
genic shock.
 Patients with severe left ventricle dysfunction are more liable to develop shock than
those with mild to moderate dysfunction.
 Serial cardiac markers and bedside echo for such cases are worth doing as they can
aid in diagnosis and effective management.

 Patient needs to be monitored closely and vital signs recorded frequently. It is

worth to have an arterial line in place for accurate blood pressure readings.

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  Monitoring urine output, base deficit, and serum lactic acid is important for the as-
sessment of resuscitation in all patients who are in shock

MANAGEMENT
 Improve the work of breathing by adequate oxygenation and ventilation.
 Initiation of vasopressors or inotropes, e.g., norepinephrine (0.5 μg/min or
dobutamine (5μg/kg/min). Treating arrhythmias.
 Aspirin and heparin (if indicated).
 Treatment of the cause, e.g., thrombolysis or angioplasty (e.g., myocardial infarc-
tion)
 In refractory cases of cardiogenic shock, intra-aortic balloon pump can be used.
 Emergency reperfusion procedure (thrombolysis/PTCA) is not superior to medical
management in cardiogenic shock, secondary to myocardial infarction.
 There is no reduction in the mortality rate

D.OBSTRUCTIVE SHOCK
 Obstructive shock refers to the anatomical obstruction of the great vessels of the
heart (e.g., superior vena cava, inferior vena cava, and pulmonary vessels) that
leads to decreased venous return and/or excessive afterload (i.e., the force that the
left ventricle has to overcome to eject blood through the aortic valve), resulting in
decreased cardiac output.
 It is usually due to extra cardiac etiologies which result in poor right ventricle out-
put.
 Pulmonary: right ventricular failure from pulmonary embolism or severe pulmon-
ary hypertension, as the heart cannot generate enough pressure to overcome the
high pulmonary vascular resistance.
 Mechanical: there is a reduction in venous return to the right atrium and inad-
equate right
ventricle filling. Causes: tension pneumothorax, tamponade, constrictive peri-
carditis, and restrictive cardiomyopathy.

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 DIAGNOSIS
 Individual’s medical history and physical examination.
 A detailed respiratory and cardiovascular examination is necessary in order to dis-
tinguish the underlying cause of obstructive shock.
 Arterial saturation may also be assessed, using a pulse oximeter, and can be de-
creased in cases of tension pneumothorax.
 Lab studies, such as a metabolic panel, lactic acid, arterial blood gas, or electrocar-
diogram (ECG) are often performed.
 Imaging studies, such as point of care ultrasound or CT scan.

MANAGEMENT
 Judicious use of IV crystalloids.
 If shock persists, early initiation of vasopressors-norepinephrine is the first choice
and add vasopressin if refractory.
 If acute massive pulmonary embolism -thrombolysis. Judicious use of IV fluids has
a paradoxical worsening of hypotension; it may develop due to severe right
ventricular dilatation and septal bowing compromising left ventricle filling.
 If tension pneumothorax - needle thoracotomy followed by tube thoracotomy. If
cardiac tamponade-pericardiocentesis, significant clinical improvement is possible,
even with minimal fluid removal).

E. NEUROGENIC SHOCK
 Neurogenic shock is a devastating consequence of spinal cord injury (SCI).
 It manifests as hypotension, bradyarrhythmia, and temperature dysregulation due to
peripheral vasodilatation following an injury to the spinal cord. This occurs due to
the sudden loss of sympathetic tone, with preserved parasympathetic function, lead-
ing to autonomic instability.
 It is mostly associated with cervical and high thoracic spine injury.

MANAGEMENT
 Initial management of neurogenic shock is focused on hemodynamic stabilization.
 Hypotension should be treated first to prevent secondary injury.
 The first-line treatment for hypotension is intravenous fluid resuscitation.
 If hypotension persists despite euvolemia, vasopressors and inotropes are the second
lines.
 Treatment for bradycardia is atropine and glycopyrrolate to oppose vagal tone, espe-
cially before suctioning.

F. ANAPHYLACTIC SHOCK
 Anaphylactic shock is a systemic, type I hypersensitivity reaction that often has fatal
consequences.
 Anaphylaxis causes the immune system to release a flood of chemicals that can
cause a person to go into shock.

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 PATHOPHYSIOLOGY
Anaphylaxis occurs in an individual after re-exposure to an antigen to which that per-
son has produced a specific IgE antibody.
 Re-exposure. Upon re-exposure to the sensitized allergen, the allergen may cross-link
the mast cell or basophil surface-bound allergen-specific IgE resulting in cellular de-
granulation as well as de novo synthesis of mediators.
 Binding. Immunoglobulin E (IgE) binds to the antigen (the foreign material that pro-
vokes the allergic reaction).
 Activation. Antigen-bound IgE then activates FcεRI receptors on mast cells and baso-
phils.
 Inflammatory mediators release. This leads to the release of inflammatory mediators
such as histamine.
 Histamine release. Many of the signs and symptoms of anaphylaxis are attributable to
binding of histamine to its receptors; binding to H1 receptors mediates pruritus,
rhinorrhoea, tachycardia, and bronchospasm.
 Prostaglandin D2. Prostaglandin D2 mediates bronchospasm and vascular dilatation,
principle manifestations of anaphylaxis.
 Leukotriene C4. Leukotriene C4 is converted into LTD4 and LTE4, mediators of hy-
potension, bronchospasm, and mucous secretion during anaphylaxis in addition to act-
ing as chemotactic

Clinical Manifestations
 Anxiety. The first symptoms usually include a feeling of impending doom or fright.
 Skin reactions. Skin reactions such as hives, itching, and flushed or pale skin follow.
 Shortness of breath. Constriction of the airways and a swollen tongue or throat could
cause wheezing and troubled breathing.
 Hypotension. A low blood pressure occurs as one of the major symptoms of shock.
 Tachycardia. The heart compensates through pumping faster and trying to deliver
blood to all body systems.
 Dizziness. The patient may feel dizzy which could lead to fainting.

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 MANAGEMENT

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ADVANCED HEMODYNAMIC MONITORING
The measurement and interpretation of biological systems that describe performance of the
cardiovascular system.

GOALS
 To assure the adequacy of perfusion.
 Early detection of an inadequacy of perfusion - decision making: is monitoring
sufficient, or does the patient need active intervention?
 To titrate therapy to specific hemodynamic endpoints in unstable patients.
 To differentiate among various organ system dysfunctions.

DETERMINANTS
 Preload
 Estimated by end-diastolic volume (pressure)
 CVP for RVEDV, PAOP (wedge) for LVEDV
 Afterload
 SVR = [MAP-CVP]/CO x 80
 Contractility

METHODS
 Arterial Blood Pressure
 Non-invasive
 Direct arterial pressure measurement
 Central Venous Pressure
 The Pulmonary Artery Catheter
 Cardiac Output Measurement
 Tissue Oxygenation
 Biomarkers
 Arterial blood gas
 Arterial Pulse Wave Analysis
 Thoracic impedance

Non-invasive Blood Pressure measurement

 Manual or automated devices
 Method of measurement
 Oscillometric (most common)
 MAP most accurate, DP least accurate
 Auscultatory (Korotkoff sounds)
 MAP is calculated

LIMITATIONS
 CUFF must be placed correctly and must be appropriately sized
 Auscultatory method is very inaccurate

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Direct Arterial Blood Pressure Measurement
 Arterial canulization
 Need for continuous blood gas monitoring
 Need for continuous blood pressure measurement
 Central venous pressure
 Need for continuous CVP monitoring
 Continuous administration of iv medication

Pulmonary Artery Catheter (PA)

 The pulmonary artery catheter offers several advantages over central venous pressure
monitoring. When the balloon tip of a Swan Ganz catheter is properly wedged in a
branch of the pulmonary artery, the pressure sensed by the catheter tip represents that
in the left atrium, taking aside a specific problem of pulmonary capillary wedge pres-
sure monitoring in the septic patient.
 PA catheters may be used for both diagnosis and therapy. Clinical indications include:
 Post myocardial infarction: to assess hemodynamic status and monitor and guide
therapy.
 Cardiac surgery: to monitor cardiac function.
 Major surgery: in the presence of myocardial dysfunction or for preoperative op-
timization of hemodynamic.
 Resuscitation: in case of hemodynamic instability during fluid replacement: to as-
sess left ventricular function.
 Septic shock: assessment of LV function and fluid status.
 Diagnosis of high- and low-pressure pulmonary edema.
 Measurement of oxygen transport, enabling optimization of ventilation and perfu-
sion.
 Pre-eclampsia and eclampsia: to monitor fluid status and assess intravascular
volume.

Cardiac Output Measurement

Multiple techniques
 Thermodilution – most common
 Transpulmonary
 Pulse contour analysis
 Esophageal doppler

Tissue Oxygenation
 Despite advances, our ability to monitor the microcirculation and tissue perfusion is
limited
 Laboratory tests for metabolic acidosis are global and insensitive
 Newer technology on the horizon
 Gastric tonometry
 Sublingual capnometry

Biomarkers
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There has been considerable interest in developing biomarkers that can be used to diagnose,
monitor and predict outcome in shock

 C-reactive protein (CRP) is an acute phase protein synthesized by the liver and in-
creases 4-6 hours (hrs) after onset of inflammation or injury and peaks at 36-50 hrs
 Procalcitonin (PCT) is produced by the thyroid gland as a precursor to calcitonin, but
other tissues can also produce procalcitonin during inflammation or sepsis.
 Ferritin is an iron storage protein that plays a significant role in regulation of iron
metabolism, it is also an acute phase reactant, and its elevation induces a reduction in
available serum iron.
Arterial Pulse Wave Analysis
One of the many techniques used for non-invasive cardiac output monitoring is arterial
pulse wave analysis. It is a common bedside tool used by many intensivists for the estima-
tion of cardiac preload by assessing the variation in the arterial line waveform.
Thoracic impedance
Some monitors measure the bioreactance (phase shift) in voltage across the thorax between
electrodes placed on the chest. It determines the CO measurement signal from each side of
the body and averages the two signals. In adults it has been shown to highly correlate with
CO measured by thermodilution and pulse contour analysis, unlike the other two non-in-
vasive methods for measuring CO.
Arterial blood gas
Blood gas analysis is a commonly used
diagnostic tool to evaluate the partial pressures
of gas in blood and acid-base content. Under-
standing and use of blood gas analysis enable
providers to interpret respiratory, circulatory,
and metabolic disorders
An arterial blood gas (ABG) tests explicitly
blood taken from an artery. ABG analysis as-
sesses a patient's partial pressure of oxygen
(PaO2) and carbon dioxide (PaCO2). PaO2
provides information on the oxygenation status,
and PaCO2 offers information on the ventilation
status (chronic or acute respiratory failure).
PaCO2 is affected by hyperventilation (rapid or
deep breathing), hypoventilation (slow or shal-
low breathing), and acid-base status. Although
oxygenation and ventilation can be assessed
non-invasively via pulse oximetry and end-tidal
carbon dioxide monitoring, respectively, ABG
analysis is the standard. 

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INTRA-AORTIC BALLOON PUMP

The IABP consists of a balloon catheter and a pump console to control the timing of
balloon inflation and deflation. The catheter is a double-lumen, 7.5- to 8.0 French (F)
catheter with a polyethylene balloon attached at its distal end, with one lumen of the
catheter attached to the pump and used to inflate the balloon with gas.
Helium is used because its low viscosity facilitates rapid transfer in and out of the bal-
loon, and because it absorbs very rapidly in blood if the balloon ruptures.
Timing of balloon inflation and deflation is based on electrocardiogram (ECG) or
pressure triggers. The balloon inflates with the onset of diastole, the balloon rapidly
deflates at the onset of LV systole.

Objectives:
 Review the anatomic and physiologic effects of the
intra-aortic balloon pump.
 Review the indications for the intra-aortic balloon
pump procedure.
 Review the technique of intraaortic balloon pump
placement.
 Outline strategies for interprofessional
communication to help make timely decisions
about escalation or deescalation of care consistent
with the patient's goals of care and the long-term
prognosis with an intra-aortic balloon pump.

Indications:
 Acute congestive heart failure exacerbation with hypotension
 As prophylaxis or adjunct treatment in high-risk percutaneous coronary intervention
 Myocardial infarction with decreased left ventricular function leading to hypotension
 Myocardial infarction with mechanical complications causing cardiogenic shock, i.e.,
acute mitral regurgitation due to papillary muscle rupture or ventricular septal rupture
 Low cardiac output state after coronary artery bypass grafting surgery
 As a bridge to definitive treatment in patients with any of the following conditions; in-
tractable angina or myocardial ischemia, refractory heart failure, or intractable
ventricular arrhythmias.
Contraindications:
 Uncontrolled sepsis
 Uncontrolled bleeding diathesis
 Moderate to severe aortic regurgitation
 An aortic aneurysm or aortic dissection
 Severe peripheral artery disease unless pre-treated with stenting.

Preparation
 Before insertion of IABP, informed consent is necessary, with a clear explanation of
the risks and benefits of IABP device insertion, with concise instructions about post-
procedure care.

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  These instructions include not to flex the leg if femoral artery access of that leg was
the entry point for IABP insertion and inability to walk till the device is in place in
case of femoral artery access used for device insertion.
 Before the patient requires a thorough evaluation for any bleeding diathesis,
infection, and presence of severe peripheral arterial disease
 The patient is positioned supine, and adherence to the sterile technique should be prac-
ticed to insert the device.

Nursing role
 Vitals monitoring, If the patient develops a fever, a broad differential diagnosis should
be considered that includes but is not limited to sepsis, thrombosis, or thromboembolic
phenomena related to IABP catheter/balloon, pressure ulcers, pneumonia/atelectasis,
or drug reaction.
 Monitor for haemorrhagic complications.
 Frequent neurological exams to monitor for cerebrovascular complications (stroke)
and to monitor for delirium are needed.
 Helium gas leaks secondary to balloon rupture or malfunction can lead to acute em-
bolic stroke. In case of a suspicion of gas leak from the balloon, the patient should be
placed in a Trendelenburg position, and IABP should be switched off with termination
of gas supply.
 Frequent monitoring of peripheral arterial pulses is imperative to promptly identify the
vascular complications secondary to IABP and manage them accordingly.

MEDICAL MANAGEMENT
 Vasopressors/Inotropes
 Dopamine is an endogenous catecholamine It increases cardiac output, and vascular
smooth muscle relaxation.
 Epinephrine is a hormone produced in the adrenal medulla and stimulates
α-, β1-, β2-receptors. At low infusion rates, the β1- and β2-receptor effects predom-
inate leading to myocardial contraction, increased oxygen consumption along with a
decrease in SVR
 Norepinephrine is a second-line vasopressor after dopamine for warm shock in the
ACCM guideline. Stroke volume increases and cardiac output changes little.
 Vasopressin increases SVR and blood pressure with no inotropy and reduces the
need for catecholamine support in shock patients.
 Corticosteroids
The current recommendations are to use steroids in absolute adrenal insufficiency in
presence of catecholamine resistant shock. As for the recommended dosage, stress-
shock dose has been considered to be 2 - 50 mg/kg/day71.
 Antibiotics current guidelines recommend initiation of antibiotics within one hour of
presentation of severe sepsis and septic shock
 Antipyretics are used to prevent seizures in the patient.

NURSING CARE PLANNING & GOALS

The major goals for the patient are:
 Maintain fluid volume at a functional level.
 Report understanding of the causative factors of fluid volume deficit.
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  Maintain normal blood pressure, temperature, and pulse.
 Maintain elastic skin turgor, most tongue and mucous membranes, and orientation to
person, place, and time.

General Nursing Interventions

Nursing care focuses on assisting with treatment targeted at the cause of the shock and
restoring intravascular volume.

 Safe administration of blood. It is important to acquire blood specimens quickly, to

obtain baseline complete blood count, and to type and crossmatch the blood in anticip-
ation of blood transfusions.
 Safe administration of fluids. The nurse should monitor the patient closely for cardi-
ovascular overload, signs of difficulty of breathing, pulmonary edema, jugular vein
distention, and laboratory results.
 Monitor weight. Monitor daily weight for sudden decreases, especially in the presence
of decreasing urine output or active fluid loss.
 Monitor vital signs. Monitor vital signs of patients with deficient fluid volume every
15 minutes to 1 hour for the unstable patient, and every 4 hours for the stable patient.
 Oxygen administration. Oxygen is administered to increase the amount of oxygen car-
ried by available haemoglobin in the blood.
 Modifications to plan of care.

Nursing Diagnosis
1. Decreased cardiac output related to (specify) blood loss, sepsis, impaired circulation
2. Impaired tissue perfusion related to decreased cardiac output secondary to blood loss,
heart failure,
3. Ineffective gas exchange related to edema in respiratory tract secondary to severe
allergic reaction.
4. Hypothermia related to blood loss
5. Hyperthermia related to altered temperature regulation secondary to sepsis
Evaluation
Expected outcomes for the patient include:
 Maintained fluid volume at a functional level.
 Reported understanding of the causative factors of fluid volume deficit.
 Maintained normal blood pressure, temperature, and pulse.
 Maintained elastic skin turgor, most tongue and mucous membranes, and orientation
to person, place, and time.

Documentation
 Degree of deficit and current sources of fluid intake.
 I&O, fluid balance, changes in weight, presence of edema, urine specific gravity, and
vital signs.
 Results of diagnostic studies.
 Functional level and specifics of limitations.
 Needed resources and adaptive devices.
 Availability and use of community resources.

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  Plan of care.
 Teaching plan.
 Client’s responses to interventions, teachings, and actions performed
 Attainment or progress towards desired outcomes.

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ment and Management of Clinical Problems.3rd Edition - August 20,
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 Howell MD, Davis AM. Management of Sepsis and Septic Shock.
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oring and management of shock. Pediatr Clin North Am. 2013
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A, Rubenfeld G, Kahn JM, Shankar-Hari M, Singer M, Deutschman CS,
Escobar GJ, Angus DC. Assessment of Clinical Criteria for Sepsis: For
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 www.uptodate.com
 https://www.shocksociety.org/
 https://www.heart.org/

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