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N332 > Emerg Week 3 (textbook) > Flashcards

Emerg Week 3 (textbook) Flashcards

1
Q

What is shock?

A

Shock is characterized by inadequate perfusion that results in poor delivery of 02 and nutrients, cellular hypoxia, and cell death that can lead to organ dysfx and death
• Shock affects all body systems

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2
Q

What kind of physiological responses typically ocur with shock, regardless of cause?

A

Hypoperfusion
Hypermetabolism
Activation of inflm response
(last two d/t mountain sympathetic response)

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3
Q

What cellular changes occur in shock?

A

• In shock cells must metb anaerobically, resulting in low energy yield and acidotic intracellular environment causing usual cell fx to cease. Na-K pump is impaired causing K to leave the cell and Na and water to enter The cell swells and becomes permeable; Mitochondria and lysosomes are damaged and the cell dies.

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4
Q

How do glucose levels r/t shock and the stress response?

A

• In stress states catecholamines, cortisol, glucagons, and inflm cytokines and mediators are releasedhyperglycemia and insulin resistance to mobilize glucose for cellular metb. These substancesgluconeogenesis from proteins and fats. Glycogenolysis occurs in liverhyperglycemia.
All this Eventually depleting glycogen stores and protein storesorgan failure

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5
Q

Vascular response during sepsis?

A

• Sepsis leads to an overactivation and release of biochemical mediators (cytokines)vasodilation, inc cap permb, inc clot formation, dec fibrinolysis.

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6
Q

Formula for MAP? What is adequate/inadequate values for this? What does it indicate?

A
  • MAP=cardiac output x peripheral resistance
  • MAP indicates the sufficiency of 02 to vital body organs.
  • Normal=70-105mm Hg
  • Less than 65mmHg is inadequate perfusion
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7
Q

BP is regulated in what parts of the heart?

A

baroreceptors in the carotid sinus and aortic arch

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8
Q

How are E and NE effective in regulating BP?

A

• When BP drops catecholamines (epinephrine and NE) are released from adrenal medullainc HR and vasoconstriction

Aortic arch and carotid arteries have pressure receptors but also chemoreceptors which regulate BP and resp rate from C02 levels in blood and somewhat to 02 levels (can have moment to moment changes in BP)

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9
Q

Mechanism by which kidneys are a part of BP regulation?

A

• Kidneys regulate BP by renin release, the enzyme to convert Angiotensin IA II a potent vasoconstrictor. Indirectly leading to release of aldosteroneretention of sodium and water. ADH is released to retain water more and inc blood volume and BP. The secondary processes can take days

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10
Q

Stages of shock?

When does it need to be treated for survival?

A
  • Can be early or late, depending on the signs and symptoms and overall severity of organ dysfx
  • Can be divided Stage 1: compensatory Stage 2: progressive Stage 3 irreversible

• The ideal window of opportunity for survival of shock involves aggressive therapy within 6hrs of identifying a shock state, especially septic shock, with some aspects of therapy (antimicrobial therapy) to be started in first hr

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11
Q

What occurs in the compensatory stage of shock?

A

• BP remains within expected limits but are many signs of inadequate perfusion to organs
• Vasoconstriction and inc contractility maint adequate CO
(caused by SNS stimulation)
• Body shunts blood from skin, kidneys, GI to brain, heart and lungscool, clammy skin, hypoactive BS, dec urine output (d/t ADH and aldosterone)

BP Normal
HR >100
RR >20
PaC02

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12
Q

What will you see in progressive shock?

A

Systolic 150
Rapid shallow resps; crackles
PaC02 >45mm Hg
Pa02

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13
Q

What will you see in irreversible shock?

A

Requires mechanical or pharmacological support
HR: Erratic or asystole
Requires intubation and mechanical ventilation and oxygenation
Jaundice
Anuric, requires, dialysis
Unconsciousness
Profound acidosis

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14
Q

WHy do you see resp alkalosis + changes in mentation with compensated shock?

A

• The inadequate perfusionmetb acidosisinc resps to remove the C02 but this inc the blood pH and often causes compensatory resp alkalosis. This alkalosismental status changes eg confusion and combativeness and arteriolar dilation

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15
Q

Recognizing shock in older pts

A
  • Inc risk of shock (can recover if caught early) and multi organ dysfx.
  • Meds like metoprolol may mask tachycardia
  • Aging immune sys might not inc temp significantly but look at the trend. Pt may report fatigue/malaise
  • May become dysrhythmic d/t hypoxemia
  • Older pt decompensates respiratorily more quickly. Dec resp muscle strength, dec max ventilation etc
  • Changes in mentation can be mistaken for dementia. If change, Tx for organ hypoperfusion and infect
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16
Q

Medical management of compensated shock?

A
  • ID the cause, correct, support
  • As compensation cant continue indefinitely, fluid replacement and med therapy must be started to maint adequate BP and MAP
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17
Q

What is a nurse assessing in potential compensated shock?

A

• Assess for changes in LOC, VS (including pulse pressure), urinary output, skin, lab values (eg lactic acid levels, ABGs)

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18
Q

How are serum sodium + sugars seen in compensated shock and why?

A

• In compensatory stage of shock serum sodium and BG levels are inc in response to the release of aldosterone and catecholamines

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19
Q

At what BP should a nurse report suspected shock?

At this stage, has damage occurred?

A

• Nurse should report systolic

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20
Q

How does pulse pressure r/t shock?

Normal pp?

A
  • Pulse pressure correlates well with stroke volume systolic BP – Diastolic BP=pulse pressure
  • Narrowing or dec pulse pressure is an earlier indicator of shock than a drop in systolic BP and indicates arterial vasoconstriction

• Usual pulse pressure is 40mm Hg. An eg of narrowing pulse pressure is 20mm Hg

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21
Q

How do we support inc O2 needs in shock?

A
  • Interventions to dec 02 requirements include: sedatives, IV opioids, shivering prevention
  • Supplemental 02 and mechanical ventilation may be nec to inc the delivery of 02 in the blood. IV fluids nd meds support BP and CO and packed RBCs inc 02 transport
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22
Q

How should families be supported during pt in shock?

A
  • Families have needs during crisis for: honest, consistent, thorough communication; psyical and emotional closeness to the pt; sensing the HCP cares about pt; seeing the pt frequently; knowing exactly whats been done
  • Nurse should advocate that family members be present during procedures and while pt care is being provided
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23
Q

Risk of disorientation of patients in shock? How to manage this?

A
  • High anxiety and alt menta status impair pt judgement. Pt may now disrupt Iv lines and catheters and complicate their condition.
  • Reorient and monitor closely
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24
Q

What characterizes the progressive stage of shock?

A
  • The mechanisms that reg BP cant compensate anymore and MAP falls
  • Pts gen hypotensive (systolic
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25
Q

Patho of progressive shock

What perpetruates the shock syndrome?

A

• All organ systems suffer from hypoperfusion t this stage
• Several events perpetuate the shock syndrome:
1. the overworked heart gets dysfx (inadequate 02ischemia and biochemical mediatorsmyocardial depression)
2. the autoregulatory fx of microcirculation fails in response to the biochemical mediators released by cellsinc cap pemb with areas of arteriolar and venous constriction further compromising perfusion.
• Precapillary sphincters relax and fluid leaks from capsinterstitial edema and dec VR.
• Also, inflm response activates coagulation system activated. Body mobilizes energy stores and inc oxygen consumption to meet the inc metb needs of the underperfused tissues and cells
• Even if cause is reversed the sequence of compensatory responses to the dec in tissue perfusion perpetuates the shock state and a viious cycle ensues

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26
Q

Mnfsts of progressive stage of shock?

A

• Chnces of survival depend on pts gen health and amount of time it takes to restore tissue perfusion
Resp effects
• Resps rapid and shallow
• Crackles
• Hypoxemia and cytokinesinflm response–>vasoconstrictionl/o surfactantcollapse
• Leaky pulm capspulm edema, diffusion abn, additional alveolar collapse. Called acute lung injury which can lead to ARDS
Cardiovascular effects pg 340
• Dysrhythmias and ischemia
• Rapid HR, sometimes >150
• Chest pain
• May have MI
• Inc cardiac enzymes
• Myocardial depression and ventricular dilation
• BNP is inc when the ventricle is overdistended and can be used to assess ventricular fx in septic and shock pts. Inc levels prompt earlier Tx
- Neurologic effects=subtle then lethargy then begins to lose consciousness

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27
Q

Renal effects of progressive shock?

A

• When MAP below 70mm Hg the GFR of kidneys cant be maint and drastic changes in renal fx occur. May ARF

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28
Q

Hepatic effects of progressive shock?

A
  • Dec blood flow to liver impairs med metb and metabolism of metb wastes
  • More susceptible to infect as pt no longer filtering bact from blood
  • Inc liver enzymes and bilirubinjaundice
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29
Q

GI effects of progressive shock?

A
  • Ischemiastress ulcers in stomach (inc risk of GI bleed)
  • Bloody diarrhea from sloughing
  • Bact toxins may enter circulation via lymph
  • Enteral feeding in shock states is recommended
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30
Q

Hematologic effects of progressive shock?

A
  • Microthrombi deposited in multiple places in body and clotting factors are consumed all d/t overactivation of inflm response. Disseminated intravascular coagulation may occur
  • Pt may need platelets and clotting factor replacements
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31
Q

Medical management of progressive shock?

A
  • Interventions common to all types=supporting resp system, optimizing the intravascular volume, supporting heart, improving competence of vascular system
  • May have some of the following: Early enteral nutrition support, Aggressive hyperglycaemic control w IV insulin, Antacids, Histamine 2 blockers or antipeptic agents to dec GI bleed, DVT prophylaxis
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32
Q

Nursing management of progressive shock

A

• Suspecting a pt is in shock and reporting subtle changes imperative
• Cared for in ICU for hemodynamic monitoring, ECG, ABG, serum lytes, etc)
Preventing complications
• Blood levels of meds, lines, prevent ventilator pneumonia (freq oral care with subglottic suctioning, oral decontamination) skin integrity
- Promoting rest and comfort—to dec cardiac workload, only perform essential acitivities to let pt sleep, treat pain and anxiety, protect pts temp but don’t use warming blankets as it could cause vasodilation
Supporting family members—they may not want to distract or get in way. Keep informed

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33
Q

What occurs at the irreversible stage of shock?

A
  • Despite tx BP remains low. Renal and liver failure –> overwhelming acidosis + lactic acid
  • Resp failure prevents adequate oxygenation despite mechanical ventilation
  • Multiple organ dysfx can occur as a progression along the shock continuum or as a syndrome unto itself
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34
Q

Medical tx for irreversible shock? Does a doctor know it’s irreversible?

A
  • Same as for progressive stage in gen

* The judgement that shock is irreversible can only be made retrospectively

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35
Q

Nursing management of pt in irreversible stage of shock?

A
  • As evidence that pt wont survive mounts the family must be informed of prognosis and likely outcomes. Let family see, talk, touch pt
  • When possible approach family about living will, advance directives
  • Pts may misinterpret the team saying survival is unlikely and yet team works feverishly on pt. They may think this means theres chance of recovery and may get angry when pt dies
  • Important to suggest in a family conference that the equipment is for pt comfort and doesn’t mean pt will live
36
Q

4 important general management strategies in shock?

A

• Resp support- o2, ventilation
• Fluid replacement to restore vasomotor tone and improve cardiac function
- Vasoactive meds to restore vasomotor tone + improve cardiac fx
• Nutrtitional support to address the metabolic requirements that are often dramatically inc in shock

37
Q

Why might crystalloids be used in shock?

Effect of RL in shock?

A

o Crystalloids are electrolyte solutions that move freely between the intravascular compartment and the IS.

**istonic crystalloid solutions are often selected because they contain the same conc o electrolutes as the extracellular fluid and ca be given without altering plasma electrolytes
o Examples: NS and RL
o In RL- lactate ion (not lactic acid) converts to bicarbonate and buffers the acidosis that occurs in shock.

38
Q

Disadvantage of using crystalloids?

A

some is lost in the interstitial compartment d/t cellular permeability from the shock. More fluid will need to be administered.

39
Q

Too much fluid can cause/lead to what conditions?

A

cause pulmonary edema and progress to ARDS, abdominal compartment syndrome (ACS) and multiple organ dysfunction syndrome (MODS)

40
Q

Why would a hypertonic crystalloid solution be used in shock?

A

o A hypetonic crystalloid solution such as 3% sodium chlordide is sometimes administered in shock- exerts a large osmotic force that pulls fluid from the intracellular space to the extracellular space to achieve a fluid balance.

41
Q

Effect of colloids? Advantages?

A

o Colloidal solutions- contain molecules that are too large to pass through capillary membranes and they expand the intravascular volume by exerting oncotic pressure and pull fluid into the intravascular space. Longer duration and less volume of fluid is required. Albumin is the greatest agent prescribed in this case- but expensive.

42
Q

Abdominal compartment syndrome

What is it?

A

o ACS is a serious complication of excess fluid: fluid leaks into the intra-abdominal cavity, inc pressure that is displaced on surrounding vessels and organs. VR, CO, and preload are compromised. Pressure also elevates diaphragm- difficulty breathing. Renal and GI system begin to losf cuntion. Interventions for this might be surgical decompression, arterial pressure lines.

43
Q

What kind of meds will be given for shock?

What effects do they have on what receptors?

How often are vitals monitored when using vasoactive meds? What kind of lines should be established?

A

• Vasoactive Medication therapy-action on receptors of SNS. Alpha and beta. Inc HR, reduce myocardial resistance and initiate vasoconstriction.
o Alpha- constriction on GI systems, skin and kidneys
o Beta 1- HR, contraction
o Beta 2- vasodilation in heart and skeletal muscles and bronchodilation
(also other meds mentiobed before)

With vasoactive meds:
o Vitals must be monitored q15
o Should have arterial line (for ongoing BP monitoring)
o Administer through CVC because extravasation. Never stopped abruptly.
**ALways wean slowly from these meds

44
Q

What sort of nutritional support is needed and why for pts with shock?

A

o May require 3000 cal.
o Release of ctecholamines early in shock continuum cause depletion of glycogen stores in 8-10 hours.
o Breaks down lean body mass and skeletal muscle mass is broken done even if has large fat stores.
o TPN or enteral nutrition should be started. Enteral preferred to benefit gut mucosa and prevent bacterial translocation and dec risk of organ dysfnction
o Stress ulcers freq occur bc of compromised blood supply to GI
♣ Antacids, H2 blockers, and proton pump inhibitors often prescribed to prevent formation of gastric acid sec.

45
Q

What is the most common kind of shock?

A

Hypovolemic

46
Q

How is body water stored (how much in what compartments)?

A
  • Intracellular -2/3 of body water

* Extracelluar- intravascular, interstitial (4x of intravascular)

47
Q

Risks/causes of external fluid loss and internal fluid shifts leading to hypovolemia?

A 
o	External (fluid loss)- trauma, sx, vomiting, diarrhea, diuresis, Diabetes insibipidus
o	Internal (fluid shift): haemorrhage, burns, ascites, peritonitis, dehydration
48
Q

Medical management of hypovolemic shock

A
  • Fluid + blood replacement
  • Pharmacologic tx: if fluid admin not enough, give vasoactive meds to prevent heart failure. + Meds to reverse cause = insulin (if cause of hypovol is hyperglycemia), anti-diarrheals, etc.
49
Q

WHy have 2 IV’s?

A

So can administer fluids, blood and/or meds simultaneously if needed

50
Q

Important considerations for giving fluids to restore vascular vol…what is typically useD?

A

o Want to expand blood volume without it all shifting into intercellular compartment – commonly use NS, RL as need large volumes quickly to restore vascular volume
o May also use hypertonic saline, or colloids

51
Q

How much fluid is given to compensate for loss as gen rule?

A

o Gen every 1L fluid lost requires 3L to replace it

52
Q

How might patient be positoned when giving fluids for hypovol shock?

A

Want proper Fluids redistribution: pt put into modified trendelenberg (supine but legs elevated)

53
Q

Nursing Management of hypovolemic shock

A
  • Admin fluids + blood safely: monitoring for complications, ensure blood is matched, labs (arterial blood gases, lactate levels, Hb + Hct), vitals, I&O, temp (ensure does not cause hypothermia), JVD, heart + resp fx
  • O2 admin
54
Q

What is cardiogenic shock? Causes?

A
  • = heart’s ability to contract impaired + blood supply to heart + tissues is inadequate
  • Cause can be coronary or non-coronary
  • Conory causes more common – most often MI leading to left V dysfx
  • Noncoronary causes: conditions that stress the myocardium (hypoxemia, acidosis, hypoglycemia tension pneumothorax) or those that cause innefective myocardial fx (cardiomyopathies, valvular damage, dysrhythmias)
55
Q

Patho of cardiogenic shock

A
  • SV + HR decrease BP dec tissue hypoperfusion

* Heart does not get adequate perfusion –weakening - incomplete emptying of V – fluid accum in lungs

56
Q

Mnfsts of cardiogenic shock

A

• angina, dysrhythmias, fatigue, signs of hemodynamic instability

57
Q

Medical management of cardiogenic shock - what are the goals?

A

o Goals are to limit further myocardial damage, improve cardiac fx by inc contractility + reducing afterload, inc O2 to heart while reducing O2 demands

+ Correction of cause - Might require thrombolytic therapy, a percutaneous coronary intervention (PCI), coronary artery bypass gradt, surgery, etc. (if cononary cause) or Correct dyryhytmias, acidosis and el- imbalances, or treatment of tension pneumothorax (if non-coronary cause)

58
Q

Components of medical management of cardiogenic shock? (in text described as first line of treatment)

A
  • Oxygenation
  • Pain control for angina. Ie) morphine
  • Hemodynamic monitoring- initiated to assess the pt response to treatment (w arterial line)
  • Labs: ECG, CK-MB, BNP
  • Fluid therapy
  • Pharmacologic therapy- vasoactive medication
59
Q

How does morphine benefit a pt with cardiogenic shock other than pain managment?

A

also dilates the blood vessels, reducing workload on the heart by reducing preload

60
Q

How is fluid therapy of cardiogenic shock differnt than other forms of shock?

A

never give bolus to these pt’s as many cause acute pulm edema

61
Q

Goals of vasoactive meds for cardiogenic shock?

What two classifications of meds might be used here? Benefits of each?

A

in coronary cardiogenic shock, aim is to improve contractility, dec preload and afterload and stabilized heart rate and rhythm.

• Two types of meds: inotropic agents and vasodilators.
o Inotropic: inc CO by mimicking SNS- inc contractility and HR
o Vasodilator: dec afterload, reducing the workload of the heart and the o2 demand

62
Q

Specific meds that may be used in treating cardiogenic shock?

A

o Dobutamine- inotropic effects
o Nitroglycerin- acts as a vasodilator and reduces preload
o Dopamine- vasoactive effects highly dependent on dose – titrate carefully!. Doses 2-8 improve contractility (inotropic action), slightly increase the HR (chronotropic action), and may increase the heart rate and CO
o Other vasoactive medications: managing cardiogenic shock include norepinephrine and epineiphrine, milrinone, vasopressin, and phenylephrine. Each of these medications stimulates different recpetors
o Antiarryhtmic medications
o Mechanical assistive devices

63
Q

Nursing management of cardiogenic shock?

A
  • cardiac workload can prevent cardiogenic shock. Preserve pt energy, promptly relieving angina nad administering supplemental oxygen
  • Monitoring Hemodynamic Status: Maintain arterial lines and ECG monitoring equipment
  • IV fluids, medications
  • Monitoring pulm status
  • Administering Medications and IV Fluids
  • Maintaining Intra- aortic balloon counterpulsation
  • The nurse makes ongoing timing adjustments of the balloon pump to maximize its effectiveness by synchornizing it with the cardiac cycle
  • Enhancing safety and comfort
  • Admin medication to relieve chest pain, preventing infection, protecting the skin and monitoring respiratory and renal function, proper positioning of the paitent to improve breathing
64
Q

3 types of circulatory shock?

A

septic, neurogenic + anaphylactic

65
Q

What is circulatory shock?

A
  • Occurs when blood vol pools in peripheral vessels CO decreases inadequate tissue perfusion
  • Can be caused by either loss of sympathetic tone or release of biochemical mediators by cells (as vascular tone is regulated by both central + local regulatory mechanisms)
  • In all types have massive venous + arterial dilation
  • Dec venous return - dec Stroke vol - dec CO - dec BP - dec tissue perfusion
66
Q

Most common kind of circulatory shock?

A

Septic

67
Q

risk factors for septic shock?

A
  • Risk factors: immunosuppression, extremes of age, malnourishment, chronic illness, invasive procedures
  • Pneumonia is common cause
68
Q

S&S of severe sepsis (in addition to obvious ones of infection)

A

lactic acidosis, oliguria, altered LOC, Thrombocytopenia + coagulation disorders, altered hepatic fx

69
Q

Causes of sepsis?

Basic outline of patho?

A
  • Caused by bacteria, viruses, fungi (bact most common)
  • Up to 1/3 of cases have no identifiable cause
  • Immune resonse –> inflm response–> inc cap perm + vasodilation
  • Coagulation system also activated
70
Q

Earlier signs of septic shock:

A

BP remains normal at first, tachycardia begins, hyperthermia, flushing, tachypnea, bounding pulses, possible GI upset (N+V+D+ dec bowel sounds), inc serum glucose + insulin resistance (hypermetabolism), confusion + agitation, inc lactate levels, WBC’s high or low

71
Q

Late signs of septic shock?

A

organ dysfx, BP stops responding to fluid resuscitation + vasoactive agents

BP drops, skin cool, pale + mottled, temp normal or low, HR + RR remain high, oliguria, MODS + possible death

72
Q

What is SIRS?

A

Systemic Inflammatory Response Syndrome (SIRS):
• presents similar to sepsis + is part of initial continuum of sepsis
o Results from severe clinical insult that triggers overwhelming inflammatory immunologic + hormonal response – not infection (but may be on abx anyway in case)
o May progress to sepsis w/o early recognition + tx

73
Q

Medical Tx of septic shock

A
  • Identify + treat source of infection
  • Want to tx those in early sepsis w/in first hour – cultures taken as long as does not delay abx by more than 45 mins
  • Blood, sputum, urine, wound drainage + catheter tip samples taken (routes of infection must be identified + treated)
  • IV lives removed + reinserted; foleys taken out if possible
  • Any abscesses drained, wound debrided
  • Fluid replacement essential: crystalloids + possible albumin
  • Nutritional therapy: nutritional supplementation critical, given enteral feeds within 48hrs + may need TPN or glucose infusions in first 7 days
  • Insulin infusions to keep gluose control
74
Q

Nursing mngt of septic shock?

A
  • Monitor for infection Older, immunocompromised, extensive trauma + burns, diabetics all at particular risk – may show atypical signs
  • Hyperthermia common – is body’s normal response to fighting infection so may not treat right away, but important to help with comfort
  • Watch for shivering – increases metb + O2 demand
  • Give Abx + vasoactive agents, fluids important to ensure dec in kidney + liver fx doesn’t allow toxic builup of abx
  • Monitor hemodynamic status, I/O, nutritional status (daily weight + albumin levels)
75
Q

What is neurogenic shock?

A

• Vasodilation resulting from loss of balance btwn parasympathetic + sympathetic stimulation –> predominant parasympathetic –> bradycardia + drop in BP

76
Q

Causes of neurogenic shock?

A

spinal cord injury, spinal anesthesia, depressant action of meds, glucose deficiency (insulin reaction or shock)

• May have prolonged course (spinal cord injury) or short (syncope)

77
Q

WHat is different about neuogenic shock in terms of symptoms?

A

• No sympathetic response can’t respond to stress see symptoms of parasympathetic response (dry, warm skin, HoTN with bradycardia)

78
Q

Tx of neurogenic shock?

A
  • Depends on cause…
  • Restore sympathetic tone by stabilization of spinal cord injury
  • Glucose given if insulin shock
79
Q

Important nursing interventions for prevention of neurogenic shock?

A

after spinal or epidural analgesia, important to elevate HOB to 30 degrees (prevents spead of anesthetic spinal cord); immobilize spine if injury suspected

80
Q

Nursing management in neurogenic shock?

A

• Interventions aimed as cardiovascular + neurologic support antiembolism stockings + elevating feet of bed prevents lower pooling, monitor for signs of DVT (big risk), passive ROM for extremities, anticoags

81
Q

S&S of anaphylactic shock

A
  • Mast cells release vasoactive substances (bradykinins + histamine)
  • Common present with resp distress (wheezing, stridor), HoTN, tachycardia, prolonged cap refill, neurological compromise, + possible pruritis, abdominal cramping
82
Q

Medical management of anaphylactic shock?

A

epinephrine, Benadryl, albuterol via neb, CPR, intubation, IV insert

83
Q

What is MODS?

A

MULTIPLE ORGAN DYSFUNCTION SYNDROME

  • Develops with acute illnesses that compromise perfusion
84
Q

Typical path of MODS?

A
  • Usual pattern of failure occurs (though varies based on kind of illness):
    o Lungs first –> dyspnea, resp failure requiring intubation
    o At first, hemodymically stable, requires inc amounts of fluids + vasoactive agents
    o Signs of hyper-metb: hyperglycemia, hyperlactic academia, inc BUN – see severeskeletal muscle mass loss to meet high energy demands (makes for long rehab process
    o 7-10days: hepatic & renal issues appear
    o Immunologic – becomes immunocompromised + bleeding risk inc
    o Cardiovasular instability as no longer reacts to tx
    o CNS follow – unresponsive, coma
85
Q

WHo is at increased risk of MODS?

A
  • Advanced age, malnutrition + coexisting illness inc risk of MODS
    o Old = immunocompromised + comorbidities
86
Q

Does MODS presentation have rapid onset?

A

Presentation is insidious

87
Q

S&S of MODS? Tx?

A
  • HoTN, hypoxemia, hypercarbia, adventitious breath sounds, inc creatinine, dec urine output, thrombocytopenia, coagulation abnormalities, lactic acidemia, metb acidosis, altered LOC, elevated LFT’s, hyperbiliirubenemia
  • Management very similar to septic shock

N332 (8 decks)

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