Multisystem Problems

By: Isser Jorell L. Yao, RN, MAN, Ed.D.

I. Assessment
- Rapid assessment followed by appropriate interventions influence the
outcome of the patient with multisystem issues. General assessment measures
should be paired with assessment techniques that are specific to the patient’s
condition.
 History Lesson
- Begin your assessment by obtaining the patient’s history, including:
 chief complaint
 present and previous illnesses
 current medications
 family and social history.
- If the patient is unstable, you may need to wait until he has stabilized to
obtain a complete health history.
 Is it life-threatening?
- Assess the patient for life-threatening problems (such as respiratory distress
in the burn victim), and initiate emergency measures such as cardiopulmonary
resuscitation (CPR) as appropriate.
 The once-over
- Your physical examination includes assessment of all body systems, with
particular attention to the body systems involved in the multisystem disorder

- clinical Manifestations and effects

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- Sequential Organ Failure Assessment (SOFA)
 It is a mortality prediction score that is based on the degree of
dysfunction of 6 organ systems.
 The score is calculated at admission and every 24 hours until
discharge, using the worst parameters measured during the prior 24
hours.
 The scores can be used in several ways, including:
 As individual scores for each organ to determine the
progression of organ dysfunction.
 As a sum of scores on a single intensive care unit (ICU) day.
 As a sum of the worst scores during the ICU stay.
 The SOFA score stratifies mortality risk in ICU patients without
restricting the data used to admission values.
 It is not designed to influence medical management.
 It should not be used dynamically or to determine the success or failure
of an intervention in the ICU.
 Interpretation: Total SOFA Score 0 to 24
 Sepsis criteria (in addition to current infection)
o SOFA Score >=2 (or change in SOFA Score by 2 or
more points)
o Two point increase is associated with a mortality increase
as much as 20%
 Mortality (based on maximal SOFA Score)
o Mortality <10%: SOFA Score 0 to 6
o Mortality 15-20%: SOFA Score 7 to 9
o Mortality 40-50%: SOFA Score 10 to 12
o Mortality 50-60%: SOFA Score 13 to 14
o Mortality >80%: SOFA Score 15
o Mortality >90%: SOFA Score 15 to 24

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  Quick SOFA Score Interpretation
 qSOFA Score 2 consistent wth Sepsis (if infectious source)
 qSOFA Score <2 is associated with a mortality of 3%,
compared with 24% mortality for score of 2-3
 Prediction of in-hospital mortality
o Test Sensitivity: 70%
o Test Specificity: 80%

 Diagnostic Assessment

II. Nursing Diagnosis

 Ineffective tissue perfusion: renal, cerebral, cardiopulmonary, gastrointestinal, hepatic,
and peripheral
 Fear
 Potential complication: Organ ischemia/dysfunction

III. Planning
 Adequate tissue perfusion
 Restoration of normal or baseline BP

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  Return/recovery of organ function
 Avoidance of complications from prolonged states of hypoperfusion

IV. Multisystem Problems

 Shock
o physiologic state in which there is inadequate blood flow to tissues and cells of
the body

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o General Management Strategies in Shock
 Support of the respiratory system with supplemental oxygen and/or
mechanical ventilation to provide optimal oxygenation
 Fluid replacement to restore intravascular volume

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  Vasoactive medications to restore vasomotor tone and improve cardiac
function
 Nutritional support to address the metabolic requirements that are often
dramatically increased in shock
o When Blood Pressure Drops!!!
 A drop below 80 mm Hg in systolic blood pressure usually signals
inadequate cardiac output from reduced intravascular volume.
 Such a drop usually results in inadequate coronary artery blood flow,
cardiac ischemia, arrhythmias, and other complications of low cardiac
output.
 If the patient’s systolic blood pressure drops below 80 mm Hg and his
pulse is thready, increase the oxygen flow rate and notify the practitioner
immediately.
o Fluid Replacement
 Crystalloids: increase intravascular volume through actual volume
administered
 Isotonic: similar in composition to body fluid. Provides greater
intravascular volume d/t more fluid staying in the vascular space
o 0.9% Normal saline, Lactated Ringer
 Hypotonic fluid: shift fluid into intracellular spaces. Useful in
preventing cellular dehydration. They deplete circulatory volume.
o 0.45% Normal Saline
 Hypertonic: pulls fluid from interstitial and intracellular spaces into
the vascular space, may be used to replace electrolytes and
promote diuresis
o 5% Dextrose, Hypertonic Saline (7.5%)
 Colloids: pull fluid into the vascular space through osmosis
 Dextran → Rarely used. Used to expand vascular space.
 Hetastarch → Rarely used. Used to expand vascular space.
 Fresh frozen plasma
 Albumin
 Whole blood
 Packed red blood cells
o Blood Products (Natural Colloids)
 Fresh frozen plasma: contains all clotting factors. Used as a blood volume
expander
 Albumin: preferred as volume expander when risk from producing
interstitial edema is great (pulmonary and heart disease)
 Packed Red Blood Cells: Administer with normal saline
 Increases oxygen affinity for hgb, and decrease oxygen delivery to
the tissues
 May cause: hypothermia, hyperkalemia, or hypocalcemia
 Whole blood: can be administered without normal saline, reduces donor
exposure
 May require greater amt than packed RBC’s to increase oxygen-
carrying capacity of blood
 Not cost effective. Rarely used
o Fluid Administration

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  Pediatric fluid guidelines
 Up to 10 kg = 4ml/kg/hr
 11-20kg = 2ml/kg/hr plus 4ml/kg for first 10kg
 >20kg = 1ml/kg/hr plus 2ml/kg for each kg 11 through 20 plus
4ml/kg for first 10 kg
 Volume replacement with crystalloids
 Administer 2 ml for each ml lost
 Pediatric: IV bolus of 20ml/kg of NS or LR
 IV bolus of 200-300 ml NS in adults
o Differentiation of Each Type of Shock
 Hypovolemic Shock
 loss or redistribution of blood, plasma, or other body fluids, which
results in a decreased circulatory volume
 inadequate fluid returning to the heart results in decreased
cardiac output
 Third spacing occurs d/t capillary permeability
 Example: hemorrhagic shock from trauma, intraabdominal
bleeding, significant vaginal bleeding, GI bleeding or vomiting and
diarrhea

 S/S: ↑ HR, narrow PP, ↓ BP
 Cardio: ↓ preload, SV; ↓ capillary refill
 Pulmo: tachypnea ➝ bradypnea (late sign)
 Renal: ↓ urine output
 Skin: pallor; cool, clammy
 Neuro: anxiety, confusion, agitation
 Gastro: absent bowel sounds
 Dx Findings: ↓ hct, ↓ hgb, ↑ lactate, ↑ urine specific gravity,
electrolyte imbalance
 Tx:
o correcting underlying cause
o warm fluids
o may need supportive therapy with vasopressors
 Nsg. Mgt.:
o ABC, oxygen, patent IV line (large bore needle), V/S q5min
(may change very quickly), meds, fluid resuscitation
o Place on modified Trendelenburg position
o If overt bleeding, apply pressure dressing
 Cardiogenic Shock
 occurs when the heart fails as a pump resulting in significant
reduction in ventricular effectiveness
 when pump failure occurs, the myocardium cannot forcibly eject
blood
 stroke volume decreases d/t decreased contractility, which
decreases cardiac output and blood pressure, resulting in
decreased tissue perfusion

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  decreased oxygenation to heart further complicates patient
condition
 Causes of Cardiogenic Shock include:
o MI, Cardiomyopathy
o Pericardial tamponade
o Dysrhythmias, Trauma
o Structural abnormalities
o Valvular abnormality: ventricular septal rupture, tension
pneumothorax
 S/S: ↑ HR, narrow PP, ↓ BP
 Cardio: ↓ capillary refill, chest pain
 Pulmo: tachypnea, cyanosis, crackles, ronchi
 Renal: ↑ Na & H2O retention, ↓ renal blood flow, ↓ urine output
 Skin: pallor; cool, clammy
 Neuro: ↓ cerebral perfusion, anxiety, confusion, agitation
 Gastro: ↓ bowel sounds, N/V
 Dx Findings: ↑ cardiac markers, ↑ blood glucose, ↑ BUN,
dysrhythmias, pulmonary infiltrates on CXR, LV dysfxn on 2D-echo
 Tx:
o correct dysrhythmias
o drug therapy: nitrates, inotropes, diuretics, beta blockers
 Obstructive Shock
 It is mostly extracardiac causes of pump failure.
 Often associated with poor right ventricle output
 Causes:
o Tension pneumothorax
o Cardiac tamponade
o Pulmonary embolism
 S/S:
o Low blood pressure can happen quickly, but the body will
be trying to compensate (unlike neurogenic shock)
o Rapid pulse
o Unequal breath sounds (if caused by a pneumothorax)
o Trouble breathing
 Tx.
o Identify & reverse the cause
o Restore tissue perfusion
o Restore organ function
 Neurogenic Shock
 results from spinal cord trauma (usually T5 or above) or spinal
anesthesia
 injury results in major vasodilation without compensation d/t loss
of sympathetic nervous system vasoconstrictor tone
 major vasodilation leads to pooling of blood in the blood vessels,
tissue hypoperfusion and ultimately impaired cellular metabolism
 spinal anesthesia can block transmission of impulses from the SNS
resulting in neurogenic shock

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 
 S/S: hypotension, bradycardia, inability to regulate temperature
 Cardio: ↑/↓ temperature, bradycardia
 Pulmo: dysfnx r/t level of injury
 Renal: bladder dysfxn
 Skin: ↓ skin perfusion, cool/warm, dry
 Neuro: flaccid paralysis below the level of injury, loss of reflex
activity
 Gastro: bowel dysfxn
 Dx Findings: history
 Tx:
o high dose of steroids: to help decrease inflammation
surrounding\ spinal cord
o treat the symptoms
 Nsg. Mgt.:
o elevate and maintain HOB 30 degrees
o support cardiovascular and neurologic function
o prevent blood pooling in lower extremities: apply TED
hose, prevent DVTs
 Anaphylactic Shock
 acute and life-threatening allergic reaction to a sensitizing
substance
 immediate response causing massive vasodilation, release of
vasoactive mediators, and an increase in capillary permeability
 can lead to respiratory distress d/t laryngeal edema or severe
bronchospasm, and circulatory failure d/t vasodilation

 Sudden S/S: chest pain, dizziness, incontinence, swelling of lips
and tongue, wheezing and stridor, flushing, pruritis, urticaria,
angioedema, anxious & confused
 Cardio: chest pain, 3rd spacing of fluid
 Pulmo: swelling to tongue and lips, shortness of breath, edema of
larynx and epiglottis, wheezing, rhinitis, stridor
 Renal: ↓ urine output
 Skin: flushing, pruritus, urticaria, angioedema
 Neuro: anxiety, ↓ LOC
 Gastro: cramping, abdominal pain, N/V, diarrhea
 Dx Findings: sudden onset, hx of allergens, exposure to contrast
media
 Tx: airway mgt, epinephrine 0.3mg SQ or IM to vastus lateralis,
BLS/ACLS
 Nsg. Mgt.:
o assess for allergies
o communication
o knowledgeable about s/s (and how to deal with them
should they arise)

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 o teach about future exposures (and inform the families also
so they can help)
 Septic Shock
 The body responds through both hyper-inflammatory and anti-
inflammatory means. Endotoxins released by the invading
organisms prompt release of hydrolytic enzymes from weakened
cell lysosomes, which causes cellular destruction of bacteria and
normal cells
 When the body is unable to control the proinflammatory
mediators, it produces a systemic inflammatory response
 As a result, there is widespread cellular dysfunction to the
endothelium, resulting in vasodilation, increased capillary
permeability, and platelet aggregation and adhesions to the
endothelium

 Cardio: ↑/↓ temperature, biventricular dilation, ↓ ejection fraction
 Pulmo: hyperventilation, respi alkalosis then respi acidosis,
hypoxemia, respi failure, ARDS, pulmonary hypertension, crackles
 Renal: ↓ urine output
 Skin: warm and flushed then cool and mottled
 Neuro: alteration in mental status, confusion, agitation, coma
 Gastro: GI bleeding
 Dx Findings: ↑/↓ WBC, ↓ platelets, ↑ lactate, ↑ glucose, ↑ urine
specific gravity, ↓ urine Na, (+) blood cultures
 Tx: fluid administration, monitor V/S, antibiotics: broad spectrum
until source is identified, vasopressors
 Nsg. Mgt.: asepsis and hygiene, culture & sensitivity, parenteral
therapy and medication
o ABCDE
 Airway
 • Determine need for intubation but remember: intubation can worsen
hypotension
 • Sedatives can lower blood pressure
 • Positive pressure ventilation decreases preload
 • May need volume resuscitation prior to intubation to avoid
hemodynamic collapse

 Control Work of Breathing

 • Respiratory muscles consume a significant amount of oxygen
 • Resting ventilatory muscles will permit diversion of cardiac output to
other hypo perfused organs
 • Mechanical ventilation and sedation decrease WOB and improves
survival

 Optimizing Circulation
 • Unless there are signs of intravascular volume overload initial
resuscitation with IV fluids is generally indicated.
 • Isotonic crystalloids

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  • Titrated to:
 • CVP 8-12 mm Hg
 • Urine output 0. 5 ml/kg/hr. (30 ml/hr. )
 • Improving heart rate
 • May require 4-6 L of fluids
 • No outcome benefit from colloids
 • Vasopressor medications should be selected based on the cause of
shock

 Maintaining Oxygen Delivery

 • Decrease oxygen demands
 • Provide analgesia and anxiolytics to relax muscles and avoid
shivering
 • Maintain arterial oxygen saturation/content
 • Give supplemental oxygen
 • Maintain Hemoglobin > 10 g/dL

 End Points of Resuscitation

 • Goal of resuscitation is to maximize survival and minimize morbidity
 • Use objective hemodynamic and physiologic values to guide therapy
 • Goal directed approach
 • MAP: above 65 mm. Hg or
 • Systolic blood pressure: above 90 mmHg
 • Heart rate: between 60-100/min
 • Urine output: > 0. 5 m. L/kg/hr
 • CVP: 8 -12 mm. Hg
 • Central venous oxygen concentration: > 70%
o Vasopressors
 Dopamine
 Clinically, dopamine is regarded as a relatively weak vasopressor
and is useful in mild hypotensive states.
 It is pharmacologic action varies with dose and within individuals
as well.
 With small doses (0 to 5 µg/kg/min) dopamine causes dilatation of
the renal arterioles and promotes diuresis (dopamine-1 receptor
agonist activity).
 At moderate doses (5 to 10 µg/kg/min) dopamine causes an
increase in myocardial contractility, heart rate, and cardiac output
(ß 1 -adrenergic effect).
 At large doses (10 to 20 µg/kg/min) dopamine acts to increase
vascular smooth muscle tone, which increases systemic vascular
resistance (α 1 -agonist effect).
 Epinephrine
 It causes direct stimulation of α 1, ß 1, and ß 2 receptors.
 Main indications for epinephrine are:
o in the management of cardiac arrest,
o severe cardiogenic shock,
o anaphylactic and anaphylactoid reactions.

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  When given as a continuous infusion, the usual range of
epinephrine is between 1 and 20 µg/min.
 However, in patients with refractory, life-threatening shock, it may
be necessary to administer epinephrine at even larger doses.
 Increases in heart rate, myocardial activity, and cardiac output
reflect ß 1 - receptor effects.
 The principal ß 2 - receptor effects are bronchial and vascular
smooth muscle relaxation.
 With larger doses, the α 1 - receptor effects of epinephrine act to
increase systemic vascular resistance and reduce splanchnic and
renal blood flow while maintaining both cerebral and myocardial
perfusion pressure.
 Norepinephrine
 It is similar to epinephrine except that norepinephrine lack the ß 2
- receptor effect of epinephrine and has much stronger α 1 -
receptor activity.
 Norepinephrine can be used for the treatment of septic shock.
 It is ß 1 activity may help offset the myocardial dysfunction
associated with severe sepsis and septic shock.
 Norepinephrine must be given by continuous infusion,
 The typical dose range is between 1 and 20 µg/min.
 Phenylephrine
 Phenylephrine is a direct-acting, highly selective α 1 -receptor
agonist which increases systemic vascular resistance and arterial
blood pressure.
 Phenylephrine is frequently used for the treatment of septic and
other forms of vasodilatory shock to increase systemic blood
pressure.
 Phenylephrine is often administered to brain-injured patients to
improve cerebral perfusion pressure.
 It does not cross the blood-brain barrier,
 It has no effect on the cerebral vasculature.
 The typical dosage range for phenylephrine is up to 200µg/min.
 Larger doses have little therapeutic effect, with only worsening of
splanchnic ischemia.
 Dobutamine
 Dobutamine is mixed ß 1 - and ß 2 - receptor agonist.
 The primary effect of dobutamine is to increase both heart rate
and myocardial contractility.
 Dobutamine relaxes vascular smooth muscle via binding at ß 2 -
receptors.
 Dobutamine is typically indicated for the treatment of patients in
cardiogenic shock with high afterload and low cardiac output.
 Dobutamine is given by continuous infusion only, and the usual
dosage range is between 1 and 20µg/kg/min.
 Vasopressin
 Vasopressin is a potent vasoconstrictor that does not work via the
adrenergic receptor system.

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  Vasopressin binds to peripheral vasopressin receptors to induce
potent vasoconstriction.
 Patients with severe sepsis and septic shock may have a relative
deficiency of vasopressin. This group of patient is remarkably
sensitive to the effects of vasopressin.
 For septic shock, the recommendation is to infuse vasopressin at
0. 04 U/min.
 Vasopressin has been successfully used for cardiogenic shock.
 In this patients, the dose of vasopressin (0. 1 U/min) is
significantly larger than that used for septic shock.

 Systemic Inflammatory Responses syndrome (SIRS)

o Systemic inflammatory response syndrome (SIRS) is a severe systemic response
to a condition that provokes an acute inflammatory reaction. SIRS is nonspecific
and can be caused by ischemia, inflammation, trauma, burns, shock, infection, or
a combination of several insults.
o Local tissue damage or a microorganism invasion causes a local inflammatory
response, which becomes a systemic response impacting the entire body and
resulting in an unregulated inflammatory response with widespread involvement
of endothelial cells. It also causes a generalized activation of inflammation and
coagulation.
o Common Potential Causes of SIRS
 Infectious
 Pneumonia
 Wound Infection
 Endocarditis
 Cellulitis
 Urinary Tract Infection
 Toxic Shock Syndrome
 Gangrene
 Meningitis
 Cholecystitis (gallbladder infection)
 Non-Infectious
 Burns
 Autoimmune Disorders
 Cirrhosis
 Dehydration
 Electrical Injuries
 Hemorrhaging
 Heart Attack
 Surgery
 Transfusion Reaction

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 Multi Organ Dysfunction Syndrome (MODS)
o MODS is a condition that occurs when two or more organs or organ systems are
unable to function in their role of maintaining homeostasis.
o Intervention is necessary to support and maintain organ function.
o MODS isn’t an illness itself; rather, it’s a manifestation of another progressive
underlying condition
o How it happens

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o MODS is classified as primary or secondary:
 Primary MODS involves organ or organ system failure that’s caused by a
direct injury (such as trauma, aspiration, or near drowning) or a primary
disorder (such as pneumonia or pulmonary embolism). Primary MODS
commonly involves the lungs. Patients typically develop acute respiratory
distress syndrome (ARDS), which progresses to encephalopathy and
coagulopathy. As the syndrome continues, other organ systems are
affected.
 Secondary MODS involves organ or organ system failure that’s due to
sepsis. Typically, the infection source isn’t associated with the lungs. The
most common infection sources include intraabdominal sepsis, extensive
blood loss, pancreatitis, or major vascular injuries. ARDS develops sooner
and progressive involvement of other organs and organ systems occurs
more rapidly than in primary MODS.
o What to look for
 Early findings may include:
 fever (temperature usually greater than 101°F [38.3°C])
 tachycardia
 narrowed pulse pressure
 tachypnea
 decreased pulmonary artery pressure (PAP), PAWP, and CVP, and
increased cardiac output.
 As SIRS progresses, findings reflect impaired perfusion of the tissues and
organs, such as:
 decreased LOC
 respiratory depression
 diminished bowel sounds
 jaundice
 oliguria or anuria
 increased PAP and PAWP and decreased cardiac output.
o What tests tell you
 No single test confirms MODS, and test results depend on the cause,
such as trauma, aspiration, pulmonary embolism, or sepsis:
 ABG analysis may reveal hypoxemia with respiratory acidosis or metabolic
acidosis.
 CBC may reveal decreased Hb level and HCT as well as leukocytosis.
 X-rays may reveal fractures, a cervical spine injury, pulmonary infiltrates,
or abnormal air or fluid in the chest or abdominal organs.
 Additional tests that may be performed include MRI, a CT scan, and
angiography.
o How it’s treated
o Treatment focuses on supporting respiratory and circulatory function and
includes:
 mechanical ventilation and supplemental oxygen
 hemodynamic monitoring
 fluid infusion (crystalloids and colloids)
 vasopressors
 measuring intake and output

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  serial laboratory values

V. Implementation
 Collaborative care
 Drug therapy
 Nursing management
o Health Promotion
 Identify patients at risk (e.g., elderly patients, those with debilitating
illnesses or who are immunocompromised, surgical or accidental trauma
patients)
 Planning to prevent shock (e.g., monitoring fluid balance to prevent
hypovolemic shock, maintenance of handwashing to prevent spread of
infection)
o Acute Interventions
 Monitor the patient’s ongoing physical and emotional status to detect
subtle changes in the patient’s condition
 Plan and implement nursing interventions and therapy
 Evaluate the patient’s response to therapy
 Provide emotional support to the patient and family
 Collaborate with other members of the health team when warranted
o Ongoing Monitoring
 Neurologic Status
 Orientation and level of consciousness
 Cardiac status
 Continuous ECG
 VS, capillary refill
 Hemodynamic parameters: central venous pressure, PA pressures, CO,
PAWP
 Ongoing assessment of Cardiac Output
 Respiratory status
 Respiratory rate and rhythm
 Breath sounds
 Continuous pulse oximetry
 Arterial blood gases
 Many patients will be intubated and mechanically ventilated
 Urine output
 Tympanic or pulmonary arterial temperature
 Skin: Temperature, pallor, flushing, cyanosis, diaphoresis, piloerection
 Bowel sounds
 Nasogastric drainage/stools for occult blood
 I&O, fluid and electrolyte balance
 Oral care/hygiene based on O2 requirements
 Passive/active range of motion
 Assess level of anxiety and fear
 Medication PRN
 Talk to patient
 Visit from clergy
 Family involvement

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  Comfort measures
 Privacy

VI. Client Education

VII. Evaluation of the Outcome of Care
o Normal or baseline, ECG, BP, CVP, and PAWP
o Normal temperature
o Warm, dry skin
o Urinary output >0.5 ml/kg/hr
o Normal RR and SaO2 ≥90%
o Verbalization of fears, anxiety

VIII. Reporting and documentation of Care

Bibliography:
 Hargrove-Huttel, R.A. (2005). Medical-surgical nursing (4th. ed.). Hong Kong: Lippincott Williams
& Wilkins.
 Berman, A., Snyder, S., Kozier, B., & Erb, G. (2008). Kozier & Erb’s fundamentals of nursing:
Concepts, process, and practice (8th ed.). Philadelphia: Pearson Education.
 Smeltzer, S.C., Bare, B.G., Hinkle, J.L., & Cheever, K.H. (2010). Brunner & Suddarth's textbook of
medical-surgical nursing (12th. ed.). China: Wolters Kluwer Health / Lippincott Williams &
Wilkins.
 12-lead ECG placement guide with illustrations (n.d.). Retrieved on August 12, 2021 from:
https://www.cablesandsensors.com/pages/12-lead-ecg-placement-guide-with-illustrations
 Sequential Organ Failure Assessment (SOFA) Score (2018). Retrieved on August 29, 2021 from
https://www.ebmedicine.net/media_library/files/Calculated%20Decisions
%20E1018%20Sepsis.pdf

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