Critical care exam II notes

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2/2015 4th block Nursing program Spring
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1

BUN

10-20 mg/dL

2

Creatinine:

Female: 0.5-1.1 mg/dL or 44-97umol/L

Male: 0.6-1.2 mg/dL or 53-106 umol/L

*umol/L = SI units

3

Glasgow coma scale: (p. 356)

Total can be 3-15

Positive score (good):

13-15 is a good score to have.

<8 coma!!! ;(

4

Calculation of Cerebral perfusion pressure (CPP)

MAP-ICP= CPP

5

Cerebral perfusion

Optimal cerebral perfusion:

>13 on Glasgow coma scale

<4 NIHSS

<20 ICPmm/Hg

CPP maintained @ 70mm/Hg

- Absence of new neuro deficits

- Vital signs w/in normal limits

6

ICP should be maintained at

< 20 mmg/Hg

7

Cerebral pressure perfusion should be maintained at

70mm/Hg

8

ICP diagnosis concernes

* Still worry about the airway & breathing

9

Skull fracture: Linear

Most common type of fracture. Not serious unless extended to orbit, sinus or across a vessel.

* When there is an extension of fracture, the pt. is admitted for observation for signs of: intracranial bleeding & epidural hematoma.

10

Skull fracture: Basilar fractures

A linear fracture @ the base of the skull. This type of fracture is difficult to determine on x-ray & is diagnosed by clinical presentation to the pt. (raccoon eyes, Battles sign)

* Dural tears are very common w/basilar skull fractures & may lead to meningitis.

* Linear- looks like a line (on the skull)

11

Bruising behind the ear, rhinorrhea

Battle sign

12

Bilateral periorbital edema & bruising, and otorrhea.

Raccoon's eyes

13

Skull fracture: Depressed

Outer table of the skull is depressed inward below the inner table of surrounding intact skull.

* The dura may be intact, bruised or torn

* If dura is torn the brain is open to environment & meningitis can occur

* The compressed & bruised brain beneath the depressed bone or bone lodged in brain parenchyma is the source of focal neuro deficit & may cause seizure

14

Comminuted skill fracture

Occurs from many or multiple linear fractures w/a depressed area at the site of impact @ site of impact.

  • Fracture radiates away from the impact site
  • Referred to as "eggshell fracture"
  • Risks are similar to those occurring w/depressed fracture (torn dura exposing brain to infection like meningitis, or bone lodged in brain, bruised brain).

All the above can lead to seizure or neuro deficit

15

ICP: Symptoms

Early= HTN

Late= Cushing's triad- irreversible

Cushing's triad consists of HTN, w/widening pulse pressure, bradycardia & irregular respirations--> Irreversible

16

ICP: Interventions

A. Monitor pt. w/GCS of 3-8 (coma)- used to monitor response to therapy such as after giving mannitol or to augment neuro assessment.

B. Devices placed in ventricles, parenchyma, or in subarachnoid, epidural & subdural spaces.

C. Ventriculostomy- Most common because it allows for interventions-> drains CSF, remove blood from subarachnoid hemorrhage.

17

Cerebral oxygenation:

Normal 60% to 70% Value <50% suggest cerebral ischemia.

Partial pressure of oxygen w/in brain tissue (PbtO2). Measured by placing monitor probe directly into the brain (damaged or damaged) white matter & attaching to stand alone monitor.

18

Recommended PbtO2

20mm/Hg or device specific

19
  1. ABG's
  2. SpO2
  3. CBC (emphasis on HCT, Hgb & platelets)
  4. Coag profile PT/INR, aPTT- because BI may induce coagulopathy.
  5. Electrolytes, BUN, Cr, Liver function, Serum osmolality.

Diagnostic testing for ICP & TBI

20
  • CT scan (non contrast) to assess for worsening intracranial mass effect
  • MRI anatomical detail to pathology contributing to increased ICP
  • Cerebral blood flow monitoring- transcutaneous Doppler device measures velocity of arterial flow & allows for the indirect monitoring of CBF @ bedside
  • Evoked potential monitoring- noninvasive, applying sensory stimuli & recording the electrical potentials created.
  • EEG - to identify seizure activity or lack of electrical activity which may be consistent w/brain death.

Radiological studies/diagnostic test ICP

21

- Brainstem auditory evoked potentials= evaluation brainstem function, conducted on conscious/unconscious

- Somato sensory evoked potentials- measure peripheral nerve response- helpful in evaluation spinal cord function.

Evoked potential monitoring

22

Stroke assessment: in ED

Witness description of symptoms, ID of exact time symptoms started & a neuro assessment.

23

Stroke assessment:

- Eval mental status (LOC arousal, oritentation)

- Cranial nerve function motor strength, sensory function, nerve function

- Motor strength

- Sensory function

- Coordination

- Deep tendon reflexes

24

NIHSS is use:

To assess severity of presenting signs/symptoms, especially if pt.'s is a candidate for a thrombolytic therapy.

25

Stroke signs/symptoms:

* One side of face or body is weak, limp or numb (or all)

* Slurred speech & Inability to comprehend what's said

* Visual disturbance, transient loss of vision 1 or both eyes

* Double vision or visual field deficit

* Sudden onset of severe HA "worst HA of my life"

26

Stroke monitoring:

  • VS q 15min for first 6 hrs
  • BP elevations is common in stroke pt.

Reducing BP can lower blood flow & O2 to the ischemic brain tissue. A gradual 20% lowering of the BP is recommended to prevent enlargement of infarcted area & worsening the neurological deficit.

27

Spinal cord injury (SCI): Priority intervention

Head in proper alignment, collar placed.

28

Cervical injury affects _____.

airway

29

C1-C3 injury

ventilator dependency

30

C4-C5 injury

Phrenic nerve impairment, tx w/phrenic nerve pacemaker.

* VERY IMPORTANT FOR BREATHING!

31

C5-T6

Intact diaphragmatic breathing, w/varying impairment of intercostal and abdominal muscle function.

32

Spinal cord Injury assessment:

* Respiratory and Neurological are the 1st assessment priority!

- Neuro assessment includes: motor, reflex, sensory responses.

- Assessment of major muscle groups & sensory level is completed to determine level of injury.

- Neuro assessments are done q 15mins & report any change to the doctor

33

SCI alignment:

To prevent further trauma use 3 people to turn and stabilize head and neck when moving them.

34

SCI: GI

Can develop fecal impaction, monitor for BM and supply daily stool softener.

35

Spinal shock:

Electrical silence of the cord below the level of injury that causes complete loss of motor, sensory & reflex activity.

  • Begins minutes after an injury and lasts 4-6wks. Permanence of injury is unknown until spinal shock is resolved.
  • Resolution is signaled by return of the deep tendon reflexes
36

Neurogenic shock:

Disruption of the autonomic pathways, resulting in temporary loss of autonomic function below the level of injury.

Sympathetic input is lost, causing vaso dilation & distributed shock, which manifests as:

  1. Hypotension
  2. Bradycardia- may be sever enough for a temp pacemaker
  3. Hypothermia

Duration varies & resolution is signaled by return of sympathetic tone

37

What type of diuretic is used for head injury?

Mannitol- It is osmotic, pulls water from brain interstitium into plasma.

* Used to treat ICP

* Use inline filter to administer & check for crystals.

38

________ is a priority when looking at vital signs, DO NOT GLOSS OVER!

Hypotension

39

Neuro type pt.'s get ____ instead of saline bolus.

albumin

Why? Albumin is a volume extender.

40

Head injury- which vital sign is more important?

BP is more important than temperature- only if abnormal

41

Dilantin (Phenytoin): Action

Depresses seizure

  • Use separate line
  • Mixed w/NS only
42

Dilantin Dosages for Status epilepticus:

10-20mg/kg, IV in 0.9% NS only!

* Give over 20-30mins

* Do not exceed a total dose of 1.5g or 50mg/min

If doesn't work try another antiepileptic, barbiturate, or anesthesia.

* Don't give w/dextrose- give somewhere else!!

43

Dilantin maintenance dose:

100mg IV over 2mins q 6-8°

44

Seizure Interventions:

  • ENSURE PATENT AIRWAY, MAINTAINS BREATHING & CIRCULATION
  • Padding side rails
  • Bed in low position
  • If pt. in chair- safely lower them onto floor w/pillow under head
  • Remove restrictive clothing & jewelry
45

Dilantin level/range:

Therapeutic Range:: Total: 10 to 20 mcg/ml.

Toxic level: >20-30 mcg/ml

46

1st choice medication for seizures:

Ativan IV

*If it fails to stop seizure in 10mins or if intermittent seizure persists longer than 20mins try-> Phenytoin (Dilantin) or fosphenytoin (Cerebyx)

47

Autonomic dysreflexia (AD)

Medical emergency- can result in stroke, seizure or other complications.

* Occurs w/T6 or above after spinal shock resolved.

* Characterized by- exaggerated response of the sympathetic nervous system.

A. Severe HTN, HA and bradycardia

48

(AD) Interventions:

Assess & remove the cause

  • Kinked urinary catheter
  • Fecal impaction
  • Tight clothing
  • Extreme temps
  • Elevate HOB
  • Remain calm & supportive

For HTN give: Hydralazine, Clonidine or doxazosin, prazosin

49

What to do for admitting diagnosis for meningitis:

Droplet precautions

Assess for fever, cough

Dim light

Private room

Have visitors put on PPE

Mannitol or hypertonic saline given

Ventriculostomy catheter to drain CSF

ABX ASAP

↑ HOB 30-40°

IV corticosteroids

50

Clinical manifestations of Bacterial meningitis:

  1. HA
  2. Fever
  3. Vomiting
  4. Rash
  5. Nuchal rigidity

* Kernig's sign: severe stiffness of the

hamstrings, inability to straighten leg.

* Brudzinski's sign: Sever neck stiffness,

causes him & knees to flex when neck is

flexed.

51

Bacterial meningitis:

Neurological emergency

  • infection of the pia & arachnoid layers
  • CSF
52

Hypoglycemic episode:

Glucose <70 mg/dL

AKA insulin shock or Insulin reaction

1st clinical sign- ↓mental status change

53

Hypoglycemia: Rapid

ANS stimulations: Activates SNS-> release of epinephrine

  • Nervousness, apprehension, tremors
  • Tachycardia, palpitations, tremors
  • Pallor
  • Diaphoretic
  • Dilated pupils
  • Fatigue & weakness
  • HA
  • Hunger
54

Hypoglycemia: Prolonged

  • Headache
  • Restlessness
  • Difficulty speaking/thinking
  • Difficulty walking
  • Visual disturbances (double vision, field deficit
  • Paresthia
  • Altered consciousness (coma, convulsions, seizure
  • Maniacal behavior (acute paranoia or catatonia)
55

DKA- diagnostic labs

  • Blood glucose average 675 & more
  • UA- Ketones, ↑BUN
  • ABG's ↓pH <7.30, ↓bicarb
  • CMP electrolytes: k+, mg & phosphorous
  • CBC: for plasma
56

DKA:

Type 1 DM mostly (can see with DM II)

* Hyperglycemia due to increased glucose production & decreased utilization

* Altered k+ balance (must watch)

* Excess acids result in ↑ anion gap (norm= 8-10mEq/L)

57

Calculating the anion gap

(Na+ + K+) - (Cl + HCO-3 bicarb)= anion gap

58

DKA: Etiology

-Initial presents of type 1 DM

-Infections

-Insufficient insulin relative to need

* Severe stress- trauma, surgery & acute MI

- Missed or reduced insulin

-Pregnancy in type 1 DM

- Medications: glucocorticoids (prednisone, etc)

- Mismanagement of sick days

59

DKA: Clinical presentation

  • Orthostasis
  • 3 P's (poly- uria, dipsia, phagia)
  • Hyperventilation/Kussmaul's respirations
  • Fruity odor breath / Acetone
  • Flushed dry skin
  • Lethargy/ altered consciousness
  • Abd pain/NV
  • Blood glucose ↑250 (much greater)
  • Ketonuria/glucosuria
  • metabolic acidosis
  • Weight loss (may be profuound
60

HHS:

Mainly type II DM

Elerdly w/decreased compensatory mechanisms to maintain homeostasis

Blood glucose >than DKA average 1000mg/dL

More electrolyte imbalances & renal dysfunction

Absent deep tendon reflexes, paresis & Babinski's sign

Profound dehydration

Stress response

61

HHS: Medications that affect glucose levels

  1. Thiazide diuretics
  2. Phenytoin (Dilantin)- anticonvulsant
  3. Glucocorticoids
  4. Beta-blockers
  5. Calcium channel blockers
  6. Enteral & parenteral nutrition
62

HHS vs. DKA

Blood sugar greater, average 1000mg/dL

More "normal" ABG's

More electrolyte imbalances

Higher serum osmolarity

No ketones!

63

DKA & HHS interventions

  1. Manage airway
  2. Fluid replacement 1st- 0.9% NS, then 0.45% NS
  3. Dextrose added when glucose approaches 200mg/dL
  4. Monitor closely for signs of fluid volume overload & cerebral edema
64

DKA & HHS: Dropping blood glucose

Drop slowly 50-75/hr

65

What is the key electrolyte to watch for in DKA & HHS?

Potassium. Osmotic diuresis results in total body k+ depletion ranging from 400-600mEq.

* k+ may be greater in HHS

66

Hyperglycemic: cause & trauma

  • Infection
  • Blood clots
  • Damage to vascular system
  • On alert for drugs that ↑ BG (steroids)
67

Rapid acting insulin's:

Humalog (lispro), Novalog (aspart), Apidra (glulisine)

Onset: 15 mins

Peak: 60-90mins

Duration: 3-4hrs

68

Novalog & Apidra's peak time is__________ & duration time is ___ to ___ hrs.

60-90min / 3 to 4 hrs

69

Insulin: Short acting

Regular (Humalin R, Novolin R, ReliOn R)

Onset: 1/2hr (30min)

Peak: 2-3hrs

Duration: 3-6hrs

70

Humalin R, Novolin R, and ReliOn R have a peak time of ______ & a duration time of ___hrs.

2-3hrs / 3-6hrs

71

Insulin: Intermediate acting

NPH (Humulin N, Novolin N, Relion N

Onset: 2-4hrs

Peak: 4-10hrs

Duration: 10-16hrs

72

Insulin: Long acting

Lantus (glargine) Levemir (detemir)

Onset: 1-2 hrs

Peak: NONE- NO PEAK

Duration: 24°

73

Which insulin has a duration time of a full day?

Lantus & Levemir (Long acting)

74

NPH (Humulin N, Novolin N, Relion N have a peak time of ______ & duration time of _____hrs.

4-10hrs / 10-16hrs

75

Transition from IV insulin to SQ

- Blood glucose is 200mg/dL or less & when 2 of the following have been met:

  1. Venous pH is ↑ 7.30
  2. Serum bicarb level is greater than 15mEq
  3. Calculated anion gap is 12 mEq or less

Weaning: Give SQ, then stop IV drip

76

Adrenal crisis: Primary

- Auto immune disease (Addisons < cortisol)

- Granulomatous: TB, sarcoidosis, histoplasmosis

- Hemorrhagic destruction- anticoag, trauma sepsis

- Infections: meningococcal, staph, pneumonia fungal, AIDS

- Drug: detoconazole, trimetroprim, etomidate, 5-fluorouracil (suppresses adrenals), rifampin

- Irradiation, adrenalectomy & genetic abnormality.

77

Adrenal crisis: Secondary

* Abrupt w/drawl of corticosteroids

* Pituitary - tumors, hemorrhage, radiation, cx

* Systemic inflammation: sepsis, vasculitis, sickle cell anemia

* Trauma- especially head trauma or surgery

* Hypothalamic DO's

78

Manifestations of adrenal insufficiency (AI) result from

Lack of adrenal cortical secretion of glucocosteroids primarily cortisol, mineralocorticoids primarily aldosterone or both.

* Most common cause is abrupt w/drawl of corticosteroids therapy

79

Longer acting agents such as ______________ are more likely to cause suppression than short acting corticosteroids like __________.

Dexamethasone / hydrocortisone

80

AI Laboratory values:

↓ Na+, blood glucose

↑ Ka+, Ca+

Metabolic acidosis

Eosinophilia

Hyperuricemia

* Cortisol levels

* ACTH levels

*Cosyntropin stimulation test

81

AI Assessment:

* Symptoms of hypovolemia

* Fluid / electrolyte imbalances

~Postural hypotension, change LOC, ↑k+

* Fatigue & weakness

* GI complaints

* decreased renal perfusion & ↓ urine output

82

AI interventions

  1. Correct fluid / electrolyte imbalances- NS & dextrose. May need 5L in first 24 hrs.
  2. Hormonal replacement- Hydrocortisone (gluco) & Fludrocortisone (mineral)
  3. Patient and family education
83

Thyroid Storm:

Over production of thyroid hormone

Occurs in mismanagement of pt.'s w/hyperthyroidism

Medical emergency, death w/in 48hrs

Graves' disease (auto immune) most common cause

84

Thyroid storm Precipitating factors:

  1. Stress
  2. General anesthesia
  3. Surgery
  4. Infection
85

Thyroid storm: Presentation

↑ HR, palpitations- presents as sinus tachycardia when pt. is sleeping or A.Fib w/ventricular response.

↑ Irritable, hyper nervous

↑ Temperature, hot w/excessive sweating

↑ Appetite, stools & weight loss

↑ tremors of the tongue & eyelids- muscle wasting and tremors w/ activity

Skin: Thin, fine, fragile hair, soft nails, petechial. * Men ↑ acne & sweating

Eyes: Bulging out (exophthalmos), sight loss, lid lag (delayed movement of eye), Graefe's sign or Ptosis- drooping of upper or lower eyelid.

86

Thyroid storm: Medications/interventions

  • Propylthiouracil (PTU) & methimazole (Tapazole)- they inhibit thyroid synthesis.
  • Iodide agents- retard release of hormones
  • Medication to block effects: beta-blockers, steroids
87

Myexedema

Primary- Hashimoto's or surgical or radioactive tx for Graves' disease

Secondary- Insufficient thyroid stimulation due to hypothalamus or pituitary disease

Most extreme form of hypothyroidism

Life threatening

Mostly common in elderly women- rare in young persons

Occurs more frequently in winter, due to ↑ stress to exposure to cold

88

Myexedema: Precipitating factors

  • Hyperthermia
  • Infection
  • Stroke
  • Trauma & critical illness
89

Myexedema: Assessment

  • Cognitive changes- everything slows down.
  • Activity intolerance- decreased reflexes & slow movements
  • Cardiovascular: bradycardia, hypotension, cardiomegaly
  • ↓ cardiac output
  • Edema
  • Hypoventilation, CO2 retention, pleural effusion
  • Upper airway & tongue edema
  • Hypothermia
90

Myexedema diagnoses: Primary

↓T3 and T4; T3 resin update with ↑ TSH

Hypoglycemia

Hyponatremia ↓Na+- secondary to fluid retention

91

Myexedema diagnoses: Secondary

↓ T3 and T4; ↓ T3 resin update with ↓TSH (all are low)

Hypoglycemia

Hyponatremia ↓Na+: secondary to fluid retention

92

Myexedema interventions:

Treat w/replacement thyroid hormone

Fluid/electrolyte replacement; thyroid replacement usually corrects sodium

Monitor gas exchange & respiratory status

Monitor cardiovascular status

Manage hypothermia

Protect from injury & infection

Educate patient & family

93

Diabetes Insipidus (DI)

Deficiency in synthesis or release of antidiuretic hormone (ADH)

Excessive water loss

Types:

Neurogenic (central) ADH deficiency- primary cause traumatic injury to posterior pituitary or hypothalamus from head injury or surgery.

Nephrogenic Kidneys insensitive to ADH- occurs in genetically predisposed persons, or CRD, drugs, or other conditions that produce permanent kidney damage.

94

DI: Neurogenic etiology

  • Genetically predisposed- familial, auto immune
  • Head trauma
  • ↑ ICP- from meningitis
  • Pituitary surgery
  • Infections: meningitis, encephalitis, syphilis
  • TB, sarcoidosis
  • Tumors: pituitary, metastases to hypothalamus
95

DI: Neurogenic acuity

  • Occurs abruptly with onset of polyuria, as much as 5-40L in 24hrs
  • Urine is pale & dilute, polydipsia, hypotension, ↓ skin turgor, dry mucous membranes, tachycardia, weight loss,
  • Neuro signs are seen with hypovolemia & hypernatremia (↑Na+)
96

DI: Nephrogenic Etiology

  1. Genetically predisposed
  2. Chronic renal disease
  3. Multisystem disorder affecting kidney
  4. Metabolic disturbances: chronic ↓Ka+ and ↑Ca+
  5. Drugs: ethanol, phenytoin (Dilantin), Lithium carbonate, demeclocycline, Amphotericin, Methoxyflurane (inhaled anesthetic)
97

DI: Assessment

↑ urine output

Thirst & polydipsia

Hypotension

↓ skin turgor

Dry mucous membranes

Tachycardia

Weight loss

Neuro changes w/: hypernatremia & hypovolemia

98

DI: Labs for diagnosis

UA- dilute urine w/low specific gravity

↑ serum osmolarity

↑ BUN / Creatinine

Hypokalemia & hyperkalemia

Water deprivation test

Vasopressin test to differentiate

99

DI lab indicators:

Sodium (serum) >145mEq/L

Osmolality (serum) > 295 mOsm/kg H20

Osmolality (urine) <100 mOsm/kg H20

Sodium (urine) 40-200mEq/L = Not affected

100

DI intervention:

  • Volume replacement- monitor for fluid overload & water intoxication.
  • Hormone replacement- vasopressin (desmopressin)
  • Thiazide diuretics (nephrogenic)- monitor neuro status, fluid status, electrolyte status or both.
101

SIADH:

exact opposite of diabetes insipidous

  • Excess ADH
  • Plasma hypotonicity
102

SIADH: Etiology

Central Nervous System disease

  • Trauma
  • Tumor

Malignancy

  • Small-cell lung carcinoma
  • Hodgkin's lymphoma
  • Pancreatic & duodenal carcinoma

Pulmonary disorders

  • TB, lung abscess, pneumonia, COPD

Medications

  • Many medications can result in SIADH
103

SIADH: Assessment

CNS:

  • Confusion
  • HA
  • Seizures
  • Weakness

Pulmonary

  • ↑ respirations, dyspnea & adventitious lung sounds

Cardiovascular

  • HTN
  • ↑ Central venous pressure (CVP) & PA pressure (pulmonary artery)

GI system

  • Anorexia, NV, muscle cramps & ↓ bowel sounds
104

SIADH: Diagnosis

Hyponatremia

Decreased serum osmolality

High urine sodium

Concentrated urine

Decreased BUN (normal 7-20mg/dL) & Creatinine

Decreased albumin

105

SIADH: interventions

  • Fluid restriction 800-1000ml/day
  • If needed hypertonic saline & diuretics
  • I&O's, serum sodium, urine & serum specific gravity and daily weights
  • Loop diuretics
  • Mouth / skin care
  • Patient & family education
106

SIADH: lab indicators

Sodium (serum) <135 mEq/L

Osmolality (serum) <280 mOsm/kg H20

Osmolality (urine) > 100 mOsm/kg H20

Sodium (urine) > 200 mEq/L

107

Cerebral Salt Wasting (CSW)

Result of serious brain injury

Disorder of sodium or fluid balance

Similar to SIADH

Patho is not understood

  • defect in sodium transport
108

CSW Assessment

  • Tachycardia
  • Weight loss
  • Hypotension
  • Dry mucous membranes; poor skin turgor
  • Lethargy & weakness
  • Mental status changes
  • Seizure & coma
109

CSW: Lab indicators

Sodium (serum) <135 mEq/L

Osmolality (serum) <295 mOsm/kg H20

Osmolality (urine) < 100 mOsm/kg H20

Sodium (urine) > 200 mEq/L

110

CSW: interventions

  1. Restore sodium & fluid volume

- Isotonic Saline

- Hypertonic saline

II. Oral or IV fludrocortisone

111

Dolls eyes

Cranial nerve IV:

Oculocephalic response, a neurop reflex that determines brain stem activity.

* Hold eyes open & turn head side to side- If eyes move bilaterally in opposite direction of head movement= means doll's eye reflex is present & cranial nerve is intact.

112

Comatose patient

They can still hear!

You can tell they are stressed or emotional by their VS. ↑VS not good for ICP or stroke pt.

113

Drug of choice for brain & spine injury

Decadon (dexamethasone), & methylpredisone (solumedrol) for spine & brain injury

114

Criteria for rtPa

Less than 3hrs since injury

Ischemic stroke only

Not pregnant

No open wounds

> 18yrs of age

115

SCI: Complete lesion

Total loss of motor, sensory & reflex activity from waist down

116

SCI: Central cord syndrome

Hip to Lower neck- loss of motor function in upper shoulders

ABD- incomplete loss of motor function

117

Brown Sequard syndrome:

Loss of pain, temperature & light touch on opposite side of injury

Loss of motor function, vibration, position & deep touch sensation on same side as cord damage.

*Opposite side to injury site you lose sensation & on same side of injury site you lose motor function.

118

Lab values: AST

0-35 units/L

*In elderly slightly higher

* Females slightly lower

119

Lab values: ALT

4-36 international units/L

* Men, elderly & African Americans are slightly higher

120

pH:

7.35-7.45

↓ 7.35 is acidic

121

Pco2: Respiratory

35-45

↑ 45 is acidic

122

HCO-3:

22-26

↓ metabolic acidosis

123

Respiratory acidosis

Kidneys will retain increases amounts of HCO-3 to ↑ pH

* opposite for alkalosis

124

Metabolic acidosis

Lungs "blow off" CO2 to raise pH

* opposite for alkalosis