Module VI – Nursing Care of Clients with

Multisystem Problems

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

1. 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)
- SOFA Score >=2 (or change in SOFA Score by 2 or more points)
- Two-point increase is associated with a mortality increase as much as 20%
 Mortality (based on maximal SOFA Score)
- Mortality <10%: SOFA Score 0 to 6
- Mortality 15-20%: SOFA Score 7 to 9
- Mortality 40-50%: SOFA Score 10 to 12
- Mortality 50-60%: SOFA Score 13 to 14
- Mortality >80%: SOFA Score 15
- Mortality >90%: SOFA Score 15 to 24
 Quick SOFA Score Interpretation
- qSOFA Score 2 consistent with 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
 Test Sensitivity: 70%
 Test Specificity: 80%

Diagnostic Test
Nursing Diagnosis
 Ineffective tissue perfusion: renal, cerebral, cardiopulmonary, gastrointestinal,
hepatic, and peripheral
 Fear
 Potential complication: Organ ischemia/dysfunction
Planning
 Adequate tissue perfusion
 Restoration of normal or baseline BP
 Return/recovery of organ function
 Avoidance of complications from prolonged states of hypoperfusion
MULTISYSTEM PROBLEMS
1. SHOCK
 physiologic state in which there is inadequate blood flow to tissues and cells of the
body.

General Management Strategies in Shock

1. Support of the respiratory system with supplemental oxygen and/or mechanical
ventilation to provide optimal oxygenation
2. Fluid replacement to restore intravascular volume
3. Vasoactive medications to restore vasomotor tone and improve cardiac function
4. Nutritional support to address the metabolic requirements that are often
dramatically increased in shock
When Blood Pressure Drops!!!
5. A drop below 80 mm Hg in systolic blood pressure usually signals inadequate
cardiac output from reduced intravascular volume.
6. Such a drop usually results in inadequate coronary artery blood flow, cardiac
ischemia, arrhythmias, and other complications of low cardiac output.
7. 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.
Fluid Replacement
8. 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
 0.9% Normal saline
 Lactated Ringer
 Hypotonic fluid: shift fluid into intracellular spaces. Useful in preventing cellular
dehydration. They deplete circulatory volume.
 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
 5% Dextrose, Hypertonic
 Saline (7.5%)
9. 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
Blood Products (Natural Colloids)
1. Fresh frozen plasma contains all clotting factors. Used as a blood volume expander
2. Albumin: preferred as volume expander when risk from producing interstitial edema
is great (pulmonary and heart disease)
3. 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
4. Whole blood: can be administered without normal saline, reduces donor exposure
  May require greater amt than packed RBCs to increase oxygen-carrying capacity
of blood
 Not cost effective. Rarely used
Volume replacement with crystalloids
10. Administer 2 ml for each ml lost
11. Pediatric: IV bolus of 20ml/kg of NS or LR
12. IV bolus of 200-300 ml NS in adults
Differentiation of Each Type of Shock
1. 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:
13. correcting underlying cause
14. warm fluids
15. may need supportive therapy withvasopressors
Nursing. Mgt.:
16. ABC, oxygen, patent IV line (large bore needle), V/S q5min (may change very
quickly), meds, fluid resuscitation
17. Place on modified Trendelenburg position
18. If overt bleeding, apply pressure dressing
2. CARDIOGENIC SHOCK
 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
 decreased oxygenation to heart further complicates patient condition
Causes of Cardiogenic Shock include:
 MI, Cardiomyopathy
  Pericardial tamponade
 Dysrhythmias, Trauma
 Structural abnormalities
 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 dysfunction on 2D-echo
Tx:
19. correct dysrhythmias
20. drug therapy: nitrates, inotropes, diuretics, beta blockers
3. OBSTRUCTIVE SHOCK
 It is mostly extracardiac causes of pump failure.
 Often associated with poor right ventricle output
Causes:
 Tension pneumothorax
 Cardiac tamponade
 Pulmonary embolism
S/S:
 Low blood pressure can happen quickly, but the body will be trying to
compensate (unlike neurogenic shock)
 Rapid pulse
 Unequal breath sounds (if caused by a pneumothorax)
 Trouble breathing
Tx.
 Identify & reverse the cause
 Restore tissue perfusion
 Restore organ function
4. 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
S/S: hypotension, bradycardia, inability to regulate temperature
 Cardio: ↑/↓ temperature, bradycardia
 Pulmo: dysfunction r/t level of injury
 Renal: bladder dysfunction
  Skin: ↓ skin perfusion, cool/warm, dry
 Neuro: flaccid paralysis below the level of injury, loss of reflex activity
 Gastro: bowel dysfunction
Dx Findings: history
Tx:
 high dose of steroids: to help decreaseinflammation surrounding\ spinal cord
 treat the symptoms
Nursing. Mgt.:
 elevate and maintain HOB 30 degrees
 support cardiovascular and neurologic function
 prevent blood pooling in lower extremities: apply TED hose, prevent DVTs
5. 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
Nursing. Mgt.:
 assess for allergies
 communication
 knowledgeable about s/s (and how to deal with them should they arise)
 teach about future exposures (and inform the families also so they can help)
6. SEPTIC SHOCK
 The body responds through both hyperinflammatory 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

VASOPRESSORS
a) 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).
b) Epinephrine
 It causes direct stimulation of α 1, ß 1, and ß 2 receptors.
 Main indications for epinephrine are:
 in the management of cardiac arrest,
 severe cardiogenic shock,
 anaphylactic and anaphylactoid reactions.
 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.
c) Norepinephrine
 It is like 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.
d) 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.
e) Dobutamine
21. Dobutamine is mixed ß 1 - and ß 2 -receptor agonist.
22. The primary effect of dobutamine is to increase both heart rate and myocardial
contractility.
23. Dobutamine relaxes vascular smooth muscle via binding at ß 2 - receptors.
24. Dobutamine is typically indicated for the treatment of patients in cardiogenic
shock with high afterload and low cardiac output.
24. Dobutamine is given by continuous infusion only, and the usual dosage range is
between 1 and 20µg/kg/min.
f) Vasopressin
 Vasopressin is a potent vasoconstrictor that does not work via the adrenergic
receptor system.
 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 patients 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 these patients, the dose of vasopressin (0. 1 U/min) is significantly larger than
that used for septic shock.
1. SYSTEMATIC INFLAMATORY RESPONSES SYNDROME (SIRS)
 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.
 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.
 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

2. Multi Organ Dysfunction Syndrome (MODS)

 MODS is a condition that occurs when two or more organs or organ systems are
unable to function in their role of maintaining homeostasis.
 Intervention is necessary to support and maintain organ function.
 MODS isn’t an illness itself; rather, it’s a manifestation of another
progressive underlying condition
 How it happens
 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.
 What to look for
o 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.
o 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
 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
 serial laboratory values
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
 Comfort measures
 Privacy