CCRN Review Part 2 (of 2)

CCRN REVIEW PART 2

“Education is a progressive
discovery of our own
ignorance”
- Will Durant -

Sherry L. Knowles, RN, CCRN, CRNI

CCRN REVIEW PART 2
 TOPICS
 Renal Alterations  Metabolic Alterations
– Acute Renal Failure – DKA & HNNK
– Electrolytes – DI & SIADH
– IV Fluid Therapy – DIC
 Neurological Alterations – Shock States
– AVM’s & Cerebral – Sepsis
Aneurysms
– Intracranial Hemorrhage
– Stroke

CCRN REVIEW PART 2
 OBJECTIVES
1. List the main functions of the kidney.
2. List the common diagnostic tests associated with renal function.
3. List the complications associated with acute renal failure.
4. Describe the common treatments of acute renal failure.
5. List the major signs & symptoms associated with electrolyte disturbances of
sodium, potassium magnesium and calcium and phosphorus.
6. Define serum osmolality.
7. List the intracellular & extracellular fluid compartments of the body.
8. Describe the effects of hypotonic, isotonic and hypertonic IV fluids.
9. Describe the different treatments for intravascular depletion verses cellular
dehydration.
10. Identify the risk factors and signs & symptoms of brain aneurysms and
AVM’s.
11. Explain the current treatments available for brain aneurysms and AVM’s.
12. Describe the different types of intracranial hemorrhage and their associated
signs & symptoms.

CCRN REVIEW PART 2
 OBJECTIVES
13. List the potential complications of associated with intracranial hemorrhages,
brain aneurysms and AVM repairs.
14. List the types of CVA’s, their risk factors and related pathophysiology.
15. Identify the recommended treatments for CVA’s.
16. Differentiate between the signs and symptoms of DKA and HHNK.
17. Describe the treatment of DKA and HHNK.
18. Differentiate between the signs and symptoms of DI and SIADH.
19. Describe the treatment of DI and SIADH.
20. List the signs & symptoms of Disseminated Intravascular Coagulation.
21. Explain the treatments for disseminated intravascular coagulation.
22. Understand the different stages of shock.
23. Differentiate between different types of shock.
24. Identify the different treatments used for the different types of shock.
25. Describe the stages of the sepsis syndrome.
26. Explain the treatment of septic shock.

Renal Alterations

 Acute Renal Failure

 Electrolytes

 IV Fluid Therapy

Acute Renal Failure
 WHAT DO THE KIDNEYS DO?
– Filter blood
 Regulates electrolytes

– Regulate blood pressure
 Renin-angiotensin system (RAS)

– Maintain acid/base balance
 Removes wastes, detoxifies blood

Acute Renal Failure
 WHAT ELSE DO THE KIDNEYS DO?
– Stimulate RBC production
 Make erythopoietin

– Make corticosteroids
 Regulate kidney function

– Increase calcium absorption
 Convert Vitamin D to its active form Calcitriol

The Nephron
 Glomerulus
– Network of capillaries
 Bowman’s capsule
– Membrane that surrounds
the glomerulus
 Renal Tubules
– Travel from cortex to
medulla and back to cortex
 Collecting duct
– Within the medulla

The Kidney
 The Renal Cortex Contains
– Bowman's Capsules
– Glomerulus
– Proximal Tubules
– Distal Convoluted Tubules
 The Renal Medulla Contains
– The Pyramids
 Loop of Henle
 Collecting Duct
 Blood Vessels

The Juxtaglomerular Apparatus

 Lies within Cortex

 Controls the activity of
the nephron

 Plays major role in the
renin-angiontension-
aldosterone system

Acute Renal Failure
 DEFINITIONS
– Sudden interruption of kidney function resulting
from obstruction, reduced circulation, or disease of
the renal tissue

– Rapid deterioration of renal function
 increase of creatinine of >0.5 mg/dl in <72hrs
 “azotemia” (accumulation of nitrogenous wastes)
 elevated BUN and Creatinine levels
 decreased urine output (usually but not always)

Acute Renal Failure
 TERMINOLOGY
– Anuria: No UOP (or <100mL/24hrs)
– Oliguria: UOP<400-500 mL/24hrs
– Azotemia: (Increased BUN, Cr, Urea)
 May be prerenal, renal, postrenal
 Does not require any clinical findings
– Chronic Renal Insufficiency
 Deterioration over months-years
 GFR 10-20 mL/min, or 20-50% of normal
– ESRD: GFR <5% of mL/min

Acute Renal Failure
 PERSONS AT RISK
– Major surgery
– Major trauma
– Receiving nephrotoxic medications
– Hypovolemia > 40 minutes
– Elderly

Acute Renal Failure
 SIGNS & SYMPTOMS
– Azotemia – Oliguria - anuria
– Hyperkalemia – HTN
– Electrolyte Disturbances – Hypovolemia
⇑ K+ ⇑ phosphate – Pulmonary edema
⇓ Na+ ⇓ calcium – Ascites
– Metabolic acidosis
⇑ Cr ⇑ BUN
– Asterixis
– Metabolic acidosis
– Encephalopathy
– Nausea/Vomiting

Acute Renal Failure
 COMPLICATIONS
– Results in retention of toxins, fluids, and end
products of metabolism

– May be reversible with medical treatment

Acute Renal Failure
 DIAGNOSTIC TESTS
– H&P
– BUN, creatinine, sodium, potassium, pH,
bicarb, Hgb and Hct
– Urine studies
– US of kidneys
– 24 hour urine for protein and creatinine
– Urine eosinophils

Acute Renal Failure
 OTHER DIAGNOSTIC TESTS
– Albumin, glucose, prealbumin
– KUB
– ABD and renal CT/MRI
– Retrograde pyloegram
– Renal biopsy
– Post-void residual or catheterization

Acute Renal Failure
 PHASES
– Onset
 1-3 days with ⇑ BUN and ⇑ creatinine and
possible decreased UOP
– Oliguric
 UOP < 400/day, ⇑ BUN, ⇑ Cr, ⇑ P04, ⇑ K, may
last up to 14 days
– Diuretic
 UOP ⇑ to as much as 4000 mL/day but without
waste products, may begin to see improvement at
end of this stage
– Recovery
 things go back to normal or may remain
insufficient and become chronic

Acute Renal Failure
 CAUSES

– Pre-renal (hypoperfusion)

– Renal (intrinsic)

– Post-renal (obstructive)

Acute Renal Failure
 SPECIFIC CAUSES
– Prerenal
 Hypovolemia, shock, blood loss, embolism,
pooling of fluid due to ascites or burns,
cardiovascular disorders, sepsis
– Intrarenal
 ATN, nephrotoxic agents, infections, ischemia
acute tubular necrosis, acute nephritis, polycystic
kidney disease
– Postrenal
 Stones, blood clots, BPH, urethral edema from
invasive procedures, renal calculi

Pre-Renal or Intra-Renal?

Pre-renal Intra-renal
BUN/Cr > 20 < 20
UNa (mEq/L) < 20 > 40
Specific gravity high low
BUN/CR Ratio > 20:1 10-15:1

Acute Renal Failure
 TREATMENT
– Make/consider the diagnosis
– Treat life threatening conditions
– Identify the cause if possible
Hypovolemia
Toxic agents (drugs, myoglobin)

Obstruction

– Treat reversible elements
Hydrate
Remove drug

Relieve obstruction

Acute Renal Failure
 NURSING CARE
– Fluid and dietary restrictions
 Protein, potassium & phosphate restriction
– Maintain electrolytes
– D/C or reduce causative agent
– Adjust medication doses
– May need dialysis to jump start renal function
– May need to stimulate production of urine with
IV fluids, Dopamine, diuretics, etc.

Acute Renal Failure
 DIALYSIS
– Hemodialysis

– Peritoneal Dialysis

– Continuous Renal Replacement Therapy (CRRT)

Chronic Renal Failure
 TREATMENT
– Strict I&O – Watch for
hyper/hypoglycemia
– Daily weights
– Watch for heart failure – Maintain nutrition
– Monitor lab results – Mouth care
– Watch for hyperkalemia – Monitor skin

– S & S of Hyperkalemia: Malaise, anorexia,
parenthesia, muscle weakness,EKG changes

CCRN REVIEW PART 2

BREAK

K+ HCO3-
PO4
Ca++

Mg+

Cu Na+

Electrolyte
Disturbances NaCl

Cl- NH3

Potassium (K+)
 Dominant intracellular electrolyte

 Primary buffer in the cell

K+

Normal serum K+ level: 3.5-5.5 mEq/L

Potassium (K+)
 INVOLVED IN
– Muscle contraction
– Nerve impulses
– Cell membrane function
– Attracting water into the ICF
– Imbalances interfere with neuromuscular function
and may cause cardiac rhythm disturbances

Hyperkalemia
– Weakness, malaise, lethargy
– Anorexia
– Muscle cramps
– Paresthesias
– Dysrhythmias

Hyperkalemia
 K > 5.5 -6
 Tall, peaked T’s
 Wide QRS
 Prolong PR
 Diminished P
 Prolonged QT
 QRS-T wave
merge = “sine wave”

Hyperkalemia
 CAUSES
– Chronic or acute renal failure
– Burns
– Crush injuries
– Excessive use of Potassium salts

Hyperkalemia
 TREATMENT
– Calcium Gluconate (carbonate)
– Calcium Chloride
– Sodium Bicarbonate
– Insulin/glucose
– Kayexalate
– Lasix
– Albuterol
– Hemodialysis

Hypokalemia
–Malaise
–Skeletal muscle weakness
–Decreased reflexes
–Hypotension
–Vomiting
–Excessive thirst
–Cardiac arrhythmias and cardiac arrest
–Flattened T wave
–U wave

Hypokalemia
 CAUSES
– Reduced dietary intake
– Poor absorption by the body
– Vomiting and/or diarrhea
– Renal disease
– Medications (typically diuretics)

Hypoglycemia
– Cold, clammy, pale skin
– Nervousness
– Shakiness, lack of coordination, staggering gait
– Irritability, hostility, and strange behavior
– Difficulty concentrating
– Fatigue
– Excessive hunger
– Headache
– Blurred vision and dizziness
– Abdominal pain or nausea
– Fainting and unconsciousness

Acute Hypoglycemia
SIGNS & SYMPTOMS
Cardiovascular Signs Neurological Signs
Palpitations Agitation

Tachycardia Confusion
Slurred Speech
Anxiety
Staggering Gait
Irritability
Paraplegia
Diaphoresis
Seizures
Pale, cool skin
Coma
Tachypnea

Hyperglycemia
– Thirst
– Polyuria
– Dehydration
– Nausea, vomiting
– DKA
– HNNK

Normal serum Glu level: 70 - 110 mg/dL

Sodium (Na+)
 Dominant extracellur electrolyte

 Chief determinant of osmolality

NaCl

Normal serum Na+ level: 135-145 mEq/L

Hyponatremia
– Deficiency of sodium in the blood
– Hypotension
– Tachycardia
– Muscle weakness
– Mental Confusion

Hypernatremia
– Excess sodium in the blood
– Hypertension
– Muscle twitching
– Mental confusion
– Coma

Magnesium (Mg+)
 Activates many enzymes
 50% is insoluble in bone
Mg+
 45% is intracellular
 5% is extracellular

Normal serum Mg+ level: 1.5 - 2.5 mg/dL

Hypomagnesemia
– Tremors
– Positive Chvostek & Trousseau
– Nystagmus
– Dysrhythmias
– Confusion/Hallucinations– ECG Changes
– Diarrhea  Flat T wave

– Hyperactive deep reflexes  ST interval depression
– Seizures  Prolonged QT interval

– May lead to
Torsade de
Pointes

Hypomagnesemia
 CAUSES
–Alcoholism
–Malabsorption
–Starvation
–Diarrhea
–Diuresis

Hypermagnesemia
– Peaked T wave
– Bradycardia
– CNS Depression
– Areflexia
– Sedation
– Respiratory paralysis

Hypermagnesemia
 CAUSES
– Not common
– Occurs with chronic renal insufficiency
– Treatment is hemodialysis

Calcium (Ca++)
– ESSENTIAL FOR
– Neuromuscular transmission
– Growth and ossification of bones

Ca++

Normal serum Ca++ level: 8 - 11 mg/dL

Calcium (Ca++)
– INVOLVED IN
– Blood clotting
– Nerve impulse

Excreted through urine, feces, and perspiration

Ca++

Hypocalcemia
– Tetany (cramps/convulsions in wrists and ankles)
– Weak heart muscle
– Increased clotting time
– Prolonged QT interval
 May lead to Torsade de Pointes
– Abnormal behavior
– Chvostek's sign (facial twitching)
– Paresthesia

Hypocalcemia
 CAUSES
– Renal insufficiency

– Decreased intake or malabsorption of Calcium

– Deficiency in or inability to activate Vitamin D

Hypercalcemia
– Kidney stones
– Bone pain
– Hypotonicity of muscles (decreased tone)
– Altered mental status
– Cardiac arrhythmias
– Shortened QT interval

Hypercalcemia
 CAUSES
– Neoplasms (tumors)
– Excessive administration of Vitamin D

 TREATMENT
– Usually aimed at underlying disease and
hydration
– Severe hypercalcemia may be treated with
forced diuresis

Phosphorus (P, PO4)
 INVOLVED IN
–Energy metabolism PO4

–Genetic coding
–Cell function
–Bone formation

Normal serum PO4 level: 2.5-4.5 mg/dL

Hypophosphatemia
– Respiratory difficulty
– Confusion
– Irritability
– Coma

Hypophosphatemia
 CAUSES
– Severe infections
– Kidney failure
– Thyroid failure
– Parathyroid Failure
– Often associated with hypercalcemia or
hypomagnesemia or too much Vitamin D
– Cell destruction - from chemotherapy, when the
tumor cells die at a fast rate
 Can cause tumor lysis syndrome

Hyperphosphatemia


– Elevated blood phosphate level

– There are no symptoms of hyperphosphatemia

Hyperphosphatemia

 TREATMENT
– Calcium Carbonate tablets

– Aluminum hydroxide
 Can cause aluminum toxicity

IV Fluid Therapy

 OSMOLALITY
– Concentration of a solution
– The higher the osmolality the greater
its pulling power for water

Normal serum osmolality is 275 to 295 mOsm/L

Serum Osmolality
 Sodium = major solute in plasma
– Estimated serum osmolality = 2 X serum Na

 Urea (BUN) and glucose are large molecules
that ↑ serum osmolality
– When either or both are elevated, the serum osmolality
will be higher than 2 times the sodium level, so the
following formula is more accurate:

Serum osmolality = 2 X serum Na + BUN + glucose
3 18

Major Mediators of
Sodium and Water Balance

 Angiotensin II

 Aldosterone

 Antidiuretic hormone (ADH)

Renin-Angiotensin-Aldosterone

Angiotensin II  1. Stimulates production of aldosterone
2. Acts directly on arterioles to cause vasoconstriction
3. Stimulates Na+/H+ exchange in the proximal tubule
Aldosterone  1. Stimulates reabsorption of Na+ and excretion of K+ in
the late distal tubule
2. Stimulates activity of H+ ATPase pumps in the late
distal tubule

Antidiuretic Hormone (ADH)
 Synthesized in the hypothalamus and stored in the
posterior pituitary
 Released in response to plasma hyperosmolality
and decreased circulating volume
 Actions of ADH
– Increases the water permeability of the collecting tubule
(makes kidneys reabsorb more water)
– Mildly increases vascular resistance

IV Fluid Therapy

Isotonic – same osmolality as serum

Hypotonic – lower osmolality than serum

Hypertonic – higher osmolality than serum

IV Solutions
D5W Isotonic 3% NaCl Hypertonic
D10W Hypertonic LR Isotonic
D50W Hypertonic D5LR Hypertonic
½ NS Hypotonic Albumin Hypertonic
NS Isotonic Dextran Hypertonic
D51/2 NS Hypertonic Hetastarch Hypertonic
D5NS Hypertonic PRBC’s Hypertonic

D5W Hypotonic in the body

IV Solutions

D5W Hypotonic in the body

Hypotonic Used for cellular dehydration
Solutions Not used with head injuries

Isotonic
Hydrates extracellular compartment
Solutions

Hypertonic
Pulls fluid into vascular space
Solutions

Daily Fluid Balance
Intake:
1-1.5 L

Insensible Loss
- Lungs 0.3 L
- Sweat 0.1 L

Urine: 1.0 to 1.5 L

Solids 40% of Wt

Intracellular Extracellular
(2/3) (1/3)

H2O H2O
Na

E.C.F. COMPARTMENTS

Interstitial (3/4) Intra-
vascular
(1/4)
H2O H2O

Na Na
Colloids
& RBC’s

“Third Space”
 Third space refers to collection of fluids (usually
isotonic) that is sequestered in potential spaces.

 This situation is not normal and the fluid is derived
from extracellular fluid.

Principles of Treatment
 How much volume?
– Need to estimate fluid deficit

 Which fluid?
– Which fluid compartment is predominantly affected?
– Must evaluate other acid/base, electrolyte &
nutrition needs

Fluid Replacement Products

Crystalloids – able to pass through semi permeable membranes
–Isotonic solutions
–Hypotonic solutions
–Hypertonic solutions
 Colloids – do not cross the semi permeable membrane and remain
in the intravascular space for several days (pulling fluid
out of the intracellular and interstitial space)
–Albumin
–Dextran
–Hetastarch

1 liter 5% Albumin

Total body water

ECF

Intravascular
=1 liter

1 Liter 0.9% saline

Total body water

ECF=1 liter ICF=0

Interstitial=3/4
of ECF=750ml

Intravascular
=1/4 ECF=250 ml

1 liter 5% Dextrose

Total body water

ECF=1/3 = 300ml ICF=2/3 = 700ml

Intravascular
=1/4 of ECF~75ml

Ringers Lactate
 Infusion of Ringer Lactate solution may lead to metabolic
alkalosis because of the presence of lactate ions

 Lactated Ringer’s should be used with great care with
patients with hyperkalemia, severe renal failure, and
hepatic insufficiency

 Solutions containing lactate are not for use in the
treatment of lactic acidosis

Neurological Alterations

 Brain Aneurysms & AVM’s

 Intracranial Hemorrhage

 Stroke

Cerebral Spinal Fluid

The serum-like fluid that circulates through the ventricles of the
brain, the cavity of the spinal cord, and the subarachnoid space

Brain Aneurysms & AVM’s
 Brain Aneurysm
– An intracranial aneurysm is a weak or thin spot on a blood
vessel in the brain that balloons out and fills with blood

 AV Malformation (AVM)
– Arteriovenous malformation (AVM) of the brain is a "short
circuit“ between the arteries and veins

Intracranial Aneurysms
 Usually occur at bifurcations and branches of the
large arteries located in the Circle of Willis

 The most common sites include the:
– Anterior Communicating artery (30 - 35%)
– Bifurcation of the Internal Carotid and Posterior
Communicating artery (30 - 35%)
– Bifurcation of Middle cerebral (20%)
– Basilar artery bifurcation (5%)
– Remaining posterior circulation arteries (5%)

Types of Aneurysms
 Saccular aneurysm
– Occurs at bifurcations
 Fusiform aneurysm
– Often in basilar artery
 Dissecting aneurysm
 Ruptured aneurysm

Arterial Circulation in the Brain

 RISK FACTORS
– Smoking
– Hypertension
– Coarctation of the aorta
– Dissections/trauma
– Intracranial neoplasm
– Polycystic kidney disease
– Abnormal vessels or High-flow states (eg, vascular
malformations, fistulae)
– Hypercholesterolemia
– Connective tissue disorders (eg, Marfan, Ehlers-Danlos)

– Usually asymptomatic until rupture
Cranial Nerve Palsy
Dilated Pupils

Double Vision

Pain Above and Behind Eye

Localized Headache

– Warning signs prior rupture
Localized Headache
Nausea & Vomiting

Stiff Neck

Blurred or Double Vision

Sensitivity to Light (photophobia)

Loss of Sensation

Treatment of Brain Aneurysms
 Surgery
– Craniotomy and clipping

 Endovascular coiling

Aneurysm Post-Op Risks
 Rebleeding
– Most frequently within the first 24 hours
– Up to 20% of patients rebleed within 14 days
– Main preventative measure is control of blood pressure
(preferably beta blockers)
 Vasospasm
– Usually occurs before 3 days or after 10 days (post bleed)
– May require hypervolemic therapy
 Hydrocephalus
 Hyponatremia
 Fluids / Electrolytes

Arterio-Venous Malformation
 The arteries and veins have a direct connection,
bypassing the capillary network

 Presents with ongoing headaches, seizures,
hemorrhage, or progressive neurological
dysfunction

– Seizures
– Headaches
– “Whooshing" Sound (Bruit)
– Other Signs
 Subtle behavioral changes
 Communication or thinking disturbances
 Loss of coordination and balance
 Paralysis or weakness in one part of the body
 Visual disturbances
 Abnormal sensations


 COMPLICATIONS
– Hemorrhage (into surrounding tissue)
– Ischemia
– Seizures
– Brain Cell Death


 DIAGNOSIS
– MRI (including MR Angiography) as well as CT
Angiography help identify AVM’s
– Cerebral Angiography is a prerequisite to
treatment
 To identify the precise anatomy and configuration
of both the lesion and the feeding and draining
vessels


 TREATMENT
– Surgery
 Usually delayed

Open ligation and/or resection of the AVM
– Radiosurgery
– Embolization
 Usually as adjunct to surgery
– Observation


 RADIOSURGERY
– Believed to "work" by initiating an "inflammatory"
response in the pathological blood vessels
ultimately resulting in their progressive narrowing
and ultimate closure

– The risk for hemorrhage is not reduced during this
lag time

– There is the added risk of radiation necrosis of
adjacent healthy brain tissue or brain cyst formation

Brain Radiosurgery
 ADVANTAGES
– Noninvasive
– Can access all anatomic locations of the brain

 DISADVANTAGES
– Can only treat smaller lesions
(<3 cm in diameter)
– Requires 2 or more years to complete

AVM Post-Op Risks

 Perfusion-breakthrough bleeding

 Endovascular occlusion

Intracranial Hemorrhage

Sudden onset of “the worst headache of my life”

 Epidural
 Subdural
 Subarachnoid
 Intraparencymal
 Intraventricular
 Cerebellar

 ICH is a dynamic, not a static process
 Hemorrhage volume can increase over time
 CT scan is the most important diagnostic tool
 Managing blood pressure is extremely important
 Must aggressively manage fever and seizures
 Consider hyperventilation and paralytics in setting
of increased ICP and deterioration

Treatment of ICH
 KEY CONCEPTS
1) Intracranial Pressure
– Elevated when ICP >20 mm Hg
2) Cerebral Perfusion Pressure
– CPP = MAP - ICP
– Must maintain CPP > 70 mm Hg
– Example: MAP = 100, ICP = 20
CPP = 80 mmHg

Subarachnoid Hemorrhage (SAH)

 DEFINITION
–When a blood vessel just outside the brain ruptures, the
area of the skull surrounding the brain (the subarachnoid
space) rapidly fills with blood


–Sudden, intense headache
–Neck pain
–Nausea or vomiting
–Neck stiffness
–Photophobia

Sudden onset of “the worst headache of my life”


 SAH may be spontaneous or traumatic
 Spontaneous SAH causes
–Cerebral aneurysms
–AV malformations
–Trauma
 Uncommon causes
–Neoplasms, venous angiomas, infections

Subarachnoid Hemorrhage
 Warning bleeds” are relatively common

 Sentinel headache 30-50%

 Early diagnosis prior to rupture will improve outcomes

 50% of patients die within 48 hours irrespective of
therapy

Subarachnoid Hemorrhage
 Often accompanied by a period of unconsciousness
(50% never wake up)

 Common signs include neck stiffness, photophobia,
headache

 20% have ECG evidence of myocardial ischemia

Complications of SAH
 Hydrocephalus may develop within the first 24
hours because of obstruction of CSF outflow in the
ventricular system by clotted blood

 Rebleeding of SAH occurs in 20% of patients in the
first 2 weeks. Peak incidence of rebleeding occurs the day
after SAH and may be from lysis of the aneurysmal clot

 Vasospasm from arterial smooth muscle contraction
(symptomatic in 36% of patients)

Re-bleeding After SAH
 Re-bleeding occurs most frequently within the first 24 hrs

 Up to 20% of patients rebleed within 14 days

 The main preventative measure is to control the blood
pressure – preferably beta blockers

 Early clipping of the aneurysm allows hypertensive and
hypervolemic therapy to prevent vasospasm

Vasospasm After SAH
 Worst time is day 7 to day 10 (most frequent time for
vasospasms)

 Diagnosed by neurologic exam, transcranial doppler and
angiography

 May use calcium channel blockers
– Reduces vasospasm, neurological deficit, cerebral infarction
and mortality

 May use some antispasmodics

Vasospasm & HHH Therapy
 Hemodilution
–Hct 30-35%

 Hypertension
–Phenylephrine / Norepinephrine
–BP titration to CPP/exam

 Hypervolemia
–Colloids/crystalloids

Other Vasospasm Therapy
 Angioplasty
–BP management during procedure
–Reperfusion issues
–Timing

 Papaverine Infusion
–Side effects
–Repeated trips

Other Complications of SAH
 Neurologic deficits from cerebral ischemia, peaks at days 4-12

 Hypothalamic dysfunction causes excessive sympathetic
stimulation, which may lead to myocardial ischemia or labile BP

 Hyponatremia may result from cerebral salt wasting / SIADH

 Nosocomial pneumonia and other such complications

 Pulmonary edema neurogenic & non-neurogenic

Treatment of SAH

1) Identify and treat the causative lesion
– Thus preventing re-bleeding

1) Treat hydrocephalus

2) Treating and prevent vasospasm

Treatment of SAH

 Maintain systolic BP >130mmHg
– Use vasopressors if necessary to maintain CPP
and reduce ischemic complications from vasospasm

– Generally avoid vasodilators (except calcium
channel blockers)

Stroke
 RISK FACTORS
 TIA  Excessive alcohol
 CAD  Family History
 High Blood Pressure  Age
 High Cholesterol  Sex
 Smoking  Race
 Heart Disease  Obesity
 Diabetes

Annual risk of stroke: Increases with age

Stroke Tests
 Computed Tomography (CT)
 Magnetic Resonance Imaging (MRI)
 Cerebral Angiography: identify responsible vessel
 Carotid Ultrasound: carotid artery stenosis
 Echocardiogram: identify blood clot from heart
 Electrocardiogram (ECG): underlying heart conditions
 Heart monitors, blood work and more tests!!

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Treatment of Ischemic CVA
 Tissue plasminogen activator (tPA) can be given
within three hours from the onset of symptoms
 Heparin
 Intra-arterial thrombolysis
 Hemicraniectomy
 In addition to being used to treat strokes, the
following can also be used as preventative
measures
–Anticoagulants/Antiplatelets
–Carotid Endarterectomy
–Angioplasty/Stents

Treatment of Hemorrhagic CVA

 Surgery is often required to remove pooled blood
from the brain and to repair damaged blood vessels

 Prevention:
– An obstruction is introduced to prevent rupture and
bleeding of aneurysms and AVM’s
– Surgical Intervention
– Endovascular Procedures

Prevention of CVA
 Control high Blood Pressure
 Lower cholesterol
 Quit smoking
 Control diabetes
 Maintain healthy weight
 Exercise
 Manage stress
 Eat a healthy diet

Metabolic Alterations
 DKA & HHNK
 DI & SIADH
 DIC
 Shock States
 Sepsis

Diabetic Ketoacidosis

 What is DKA?
– Diabetic Ketoacidosis

– A life-threatening complication seen with
Diabetes Mellitus Type 1

Diabetic Ketoacidosis
– Serum Glucose 300-800
– Ketoacidosis Present
– Large Serum And Urine Ketones
– Fruity Breath
– Kussmaul Respirations
– Serum pH < 7.3
– Dehydration

HHNK

 What is HHNK?
– Hyperglycemic Hyperosmolar Nonketonic Coma

– A life threatening complication seen with
Diabetes Mellitus Type 2

HHNK
– Serum Glucose 600-2000
– Ketoacidosis Not Present
– Absent Or Slight Serum And Urine Ketones
– Normal Breath
– Shallow Respirations
– Serum pH Normal
– Severe Dehydration

DKA vs HHNK

DKA HHNK
 Faster Onset  Slower Onset
 Glucose 300-800  Glucose 600-2000
 Acidosis  No Acidosis
 Fruity Breath  Normal Breath
 Kussmaul Respirations  Shallow Respirations

Treatment of DKA & HHNK

 Reverse Dehydration
NS, then ½ NS
 Restore Glucose Levels
D5 ½ NS When Glu 250
 Restore Electrolytes

Diabetes Insipitus

 What is Diabetes Insipitus?
– A Condition resulting from too little ADH

 Why is it called Diabetes Insipitus?
– The term Diabetes refers to polyuria

Diabetes Insipitus
– Polyuria
– Severe Hypovolemia
– Severe Dehydration
– Elevated Serum Osmolality
– Elevated Serum Sodium
– Shock

Diabetes Insipitus

 CAUSES
– Decreased ADH
– Neurological Surgery
– Head Trauma
– Dilantin or Lithium

Diabetes Insipitus

 TREATMENT
– Fluid Resuscitation
– ADH Replacement
 Vasopressin, Pitressin, DDAVP

– Treat The Cause

SIADH

 What is SIADH?

– Syndrome of Inappropriate ADH

– Too much ADH

SIADH
 SIGNS & SYMPTOMS
– Hyponatremia – Elevated ADH Level
– Low Serum Sodium – Weight Gain Without Edema
 Serum NA < 135 – Elevated CVP, PAP, PAWP
– Low Serum Osmolality – Hypertension
– High Urine Osmolality – Concentrated And  UOP
– Elevated Specific Gravity – Headache
 Urine specific gravity
> 1.030
– Altered LOC
– Elevated Urine Osmolality – Seizures

SIADH

 CAUSES
– Head Trauma – Medications
– Oat Cell Carcinoma – Stress
– Other Cancers – Mechanical Ventilation

– Viral Pneumonia

SIADH
 TREATMENT
– Monitor Fluid Balance, Monitor I & O
– Restrict Fluids
– Replace Na+ loss when necessary
– May Give 3% (Hypertonic) Saline
– May Give Dilantin or Lithium
– May require PA Catheter For Monitoring
– May Give Diuretics

DI vs SIADH
DI SIADH
 Too Little ADH  Too Much ADH
 Dehydration  Water Intoxication
 High Serum Sodium  Low Serum Sodium
 High Serum Osmolality  Low Serum Osmolality
 Low Urine Osmolality  High Urine Osmolality

DI vs SIADH Treatment

DI SIADH
 Lots of Fluids  Fluid Restriction
 Hold Dilantin  May Give Dilantin
 Hold Lithium  May Give Lithium
 Give ADH  3% Saline

DIC

 What is DIC?
– Disseminate Intravascular Coagulation

– A clotting disorder that ultimately causes
bleeding

DIC
 Caused by over-activation of the clotting pathways

 Causes widespread fibrin deposits

 Bleeding and renal failure are most common manifestations

 Treating the underlying disease is the most important step

Disseminated Intravascular
Coagulation
Systemic activation
of coagulation

Intravascular Depletion of platelets
deposition of and coagulation
fibrin factors

Thrombosis of small
and midsize vessels BLEEDING
with organ failure

DIC
–Bleeding

–Thrombosis

–Organ Failure

DIC
 CAUSES
– Massive Tissue Injuries
– Obstetric Emergencies
– Septicemia
– Cancers
– Vascular Disorders
– Systemic Disorders
– Many More Causes

DIC Lab Results
 CLOTTING TESTS ELEVATED
– PT ↑
– aPTT ↑
– Fibrin degradation products (D-dimer) ↑

 CLOTTING FACTORS DEPLETED
– Platelets ↓
– Fibrinogen ↓
– Protein C ↓
– Antithrombin ↓

DIC
 TREATMENT
–Treat the Cause

–Replace Clotting Factors

–Anticoagulation Therapy (Heparin)

CCRN REVIEW

THE END
PART 2

CCRN REVIEW PART 2

THANK YOU!

References
 American Stroke Association. (2007). Acute and Preventative
Treatments. Retrieved March 4, 2007 from
http://www.strokeassociation.org/presenter.jhtml?identifier=2532.
 Block, C., and Manning, H. (2002). Prevention of acute renal failure in
the critically ill. American Journal of Respiratory and Critical Care
Medicine; (165)320-324.
 Brenner, B. M., and Rector, F.C. (2000). The kidney (6th ed), Vol I.
Philadelphia: W.B. Saunders Company; (1)399-416.
 Brettler S. (2005). Endovascular coiling for cerebral aneurysms. AACN
Clinical Issues; (16)515-525.
 Britz, G. W. (2005). ISAT trial: Coiling or clipping for intracranial
aneurysms? Lancet; (366)783-785.
 Campbell, D. (2003). How acute renal failure puts the breaks on kidney
function. Nursing 2003; (33)59-63.

References Continued
 Campbell, D. (2003). How acute renal failure puts the breaks on kidney
function. Nursing 2003; (33)59-63.
 Carlson, K. (2009) Advanced Critical Care Nursing. Philadelphia, Pa:
Saunders/Elsevier.
 Guyton, A. C., and Hall, J. E. (2000). Unit V: The kidneys and body fluids. In
A. C. Guyton & J. E. Hall. Textbook of medical physiology (10th ed.).
Philadelphia: W.B. Saunders Company; pg. 264-379.
 Impact of Stroke. (2007). American Stroke Association. Retrieved March 4,
2007 from http://www.strokeassociation.org/presenter.jhtml?identifier=1033.
 Lynn-Mchale Wiegand, D. J. (ed.). (2011). AACN Procedure Manual for
Critical Care. 6th ed. St. Louis, MO: Saunders.
 Pagana, K. D. & Pagana, T. J. (2008). Mosby’s Diagnostic and Laboratory
Test Reference. 9th ed. St. Louis, MO: Mosby/Elsevier.
 Stillwell, S. (2006). Mosby’s Critical Care Nursing Reference. 4th ed. St.
Louis, MO: Mosby/Elsevier.: Diagnosis and Management (5th ed).

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