3. PCCN 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.
4. PCCN REVIEW
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.
6. 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
7. 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
10. 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
11. 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
12. The Juxtaglomerular Apparatus
Lies within Cortex
Controls the activity of
the nephron
Plays major role in the
renin-angiontension-
aldosterone system
14. 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)
15. 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
16. Acute Renal Failure
PERSONS AT RISK
– Major surgery
– Major trauma
– Receiving nephrotoxic medications
– Hypovolemia > 40 minutes
– Elderly
18. Acute Renal Failure
COMPLICATIONS
– Results in retention of toxins, fluids, and end
products of metabolism
– May be reversible with medical treatment
19. 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
20. Acute Renal Failure
OTHER DIAGNOSTIC TESTS
– Albumin, glucose, prealbumin
– KUB
– ABD and renal CT/MRI
– Retrograde pyloegram
– Renal biopsy
– Post-void residual or catheterization
21. 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
23. 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
24. 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
25. 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
26. 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.
31. Potassium (K+)
Dominant intracellular electrolyte
Primary buffer in the cell
K+
Normal serum K+ level: 3.5-5.5 mEq/L
32. 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
43. Sodium (Na+)
Dominant extracellur electrolyte
Chief determinant of osmolality
NaCl
Normal serum Na+ level: 135-145 mEq/L
44. Hyponatremia
SIGNS & SYMPTOMS
– Deficiency of sodium in the blood
– Hypotension
– Tachycardia
– Muscle weakness
– Mental Confusion
45. Hypernatremia
SIGNS & SYMPTOMS
– Excess sodium in the blood
– Hypertension
– Muscle twitching
– Mental confusion
– Coma
46. 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
47. Hypomagnesemia
SIGNS & SYMPTOMS
– 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
50. Hypermagnesemia
CAUSES
– Not common
– Occurs with chronic renal insufficiency
– Treatment is hemodialysis
51. Calcium (Ca++)
– ESSENTIAL FOR
– Neuromuscular transmission
– Growth and ossification of bones
– Muscle contraction
Ca++
Normal serum Ca++ level: 8 - 11 mg/dL
52. Calcium (Ca++)
– INVOLVED IN
– Blood clotting
– Nerve impulse
– Muscle contraction
Excreted through urine, feces, and perspiration
Ca++
53. Hypocalcemia
SIGNS & SYMPTOMS
– 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
54. Hypocalcemia
CAUSES
– Renal insufficiency
– Decreased intake or malabsorption of Calcium
– Deficiency in or inability to activate Vitamin D
55. Hypercalcemia
SIGNS & SYMPTOMS
– Kidney stones
– Bone pain
– Hypotonicity of muscles (decreased tone)
– Altered mental status
– Cardiac arrhythmias
– Shortened QT interval
56. 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
57. Phosphorus (P, PO4)
INVOLVED IN
–Energy metabolism
PO4
–Genetic coding
–Cell function
–Bone formation
Normal serum PO4 level: 2.5-4.5 mg/dL
59. 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
60. Hyperphosphatemia
SIGNS & SYMPTOMS
– Elevated blood phosphate level
– There are no symptoms of hyperphosphatemia
61. Hyperphosphatemia
TREATMENT
– Calcium Carbonate tablets
– Aluminum hydroxide
Can cause aluminum toxicity
62. 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
63. 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
64. Major Mediators of
Sodium and Water Balance
Angiotensin II
Aldosterone
Antidiuretic hormone (ADH)
65. 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
66. 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
67. IV Fluid Therapy
Isotonic – same osmolality as serum
Hypotonic – lower osmolality than serum
Hypertonic – higher osmolality than serum
69. 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
70. 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
71. 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
72. Solids 40% of Wt
Intracellular Extracellular
(2/3) (1/3)
H2O H2O
Na
74. “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.
75. 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
76. 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
77. 1 liter 5% Albumin
Total body water
ECF
Intravascular
=1 liter
78. 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
79. 1 liter 5% Dextrose
Total body water
ECF=1/3 = 300ml ICF=2/3 = 700ml
Intravascular
=1/4 of ECF~75ml
80. 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
84. 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
85. 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
86. 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%)
87. Types of Aneurysms
Saccular aneurysm
– Occurs at bifurcations
Fusiform aneurysm
– Often in basilar artery
Dissecting aneurysm
Ruptured aneurysm
91. Intracranial Aneurysms
SIGNS & SYMPTOMS
– 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
92. Treatment of Brain Aneurysms
Surgery
– Craniotomy and clipping
Endovascular coiling
93. 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
95. 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
96. Arterio-Venous Malformation
SIGNS & SYMPTOMS
– 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
98. Arterio-Venous Malformation
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
99. Arterio-Venous Malformation
TREATMENT
– Surgery
Usually delayed
Open ligation and/or resection of the AVM
– Radiosurgery
– Embolization
Usually as adjunct to surgery
– Observation
100. Arterio-Venous Malformation
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
101. 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
105. Intracranial Hemorrhage
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
106. 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
107. 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
108. Subarachnoid Hemorrhage (SAH)
SIGNS & SYMPTOMS
–Sudden, intense headache
–Neck pain
–Nausea or vomiting
–Neck stiffness
–Photophobia
Sudden onset of “the worst headache of my life”
109. Subarachnoid Hemorrhage (SAH)
SAH may be spontaneous or traumatic
Spontaneous SAH causes
–Cerebral aneurysms
–AV malformations
–Trauma
Uncommon causes
–Neoplasms, venous angiomas, infections
110. 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
111. 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
112. 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)
113. 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
114. 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
116. Other Vasospasm Therapy
Angioplasty
–BP management during procedure
–Reperfusion issues
–Timing
Papaverine Infusion
–Side effects
–Repeated trips
117. 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
118. Treatment of SAH
1) Identify and treat the causative lesion
– Thus preventing re-bleeding
1) Treat hydrocephalus
2) Treating and prevent vasospasm
119. 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)
123. 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
124. 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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126. 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
127. 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
128. Prevention of CVA
Control high Blood Pressure
Lower cholesterol
Quit smoking
Control diabetes
Maintain healthy weight
Exercise
Manage stress
Eat a healthy diet
136. Treatment of DKA & HHNK
Reverse Dehydration
NS, then ½ NS
Restore Glucose Levels
D5 ½ NS When Glu 250
Restore Electrolytes
137. 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
144. 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
145. 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
146. 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
147. DIC
What is DIC?
– Disseminate Intravascular Coagulation
– A clotting disorder that ultimately causes
bleeding
148. 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
149. 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
154. DIC
TREATMENT
–Treat the Cause
–Replace Clotting Factors
–Anticoagulation Therapy (Heparin)
155. Shock
DEFINITION
–Inadequate perfusion to body tissues
156. Shock
COMPENSATORY MECHANISMS
–Tachycardia
Attempts to deliver more blood to the tissues
–Vasoconstriction
Attempts to maintain adequate BP in order to
adequately perfuse the body tissues
–Increased ADH Secretion
ADH makes the body hold onto water in an effort to
maintain volume and thus enough blood pressure to
perfuse the body tissues
157. Types of Shock
Hypovolemic Shock
– Inadequate perfusion to the tissues due to insufficient intravascular
volume
Cardiogenic Shock
– Inadequate perfusion to the tissues due to heart failure
Distributive Shock
– Inadequate perfusion to the tissues due to blood flow out of the
intravascular space causing insufficient intravascular volume
– Anaphylactic, Septic, and Spinal Shock
Obstructive Shock
– Inadequate perfusion to the tissues due to obstruction of blood flow
164. Septic Shock
EARLY STAGE (Hyperdynamic)
Normal BP Tachycardia
Confusion Agitation (or listless)
↑ Respiratory Rate Temperature
Normal Color Normal or ↑ UOP
Normal PAWP ↑ CO ↓ SVR
LATE STAGE (Hypodynamic)
Low BP Tachycardia
Orthostatic Hypotension Restlessness
Confusion Agitation (or listless)
Thirst Pallor
Cool, Clammy Skin ↓ UOP
↓ CO ↓ PAWP
↓ CVP ↑ SVR
↑ Lactate Levels
165. Septic Shock
TREATMENT
– IVF (150cc/hr or wide open)
– Treat Cause (Pan culture, antibiotics)
– Vasoconstrictors in warm phase
– Treat Temp as needed
166. Obstructive Shock
CAUSES
Pulmonary Embolus Tamponade
Tension Pneumothorax Aortic Aneurysm
TREATMENT
Treat the Cause
167. Sepsis Syndrome
SIRS Sepsis Severe Septic MODS Death
Infection Sepsis Shock
168. Sepsis Syndrome
Sepsis
– SIRS’ response with presumed/confirmed infection
Severe Sepsis
– Sepsis associated with organ dysfunction, hypoperfusion
(lactic acidosis, oliguria, altered mental status etc.), or
hypotension (SBP < 90 mmHg or ↓ SBP > 40 mmHg)
Septic Shock
– Sepsis with perfusion abnormalities and hypotension
despite adequate fluid resuscitation
171. Treatment for Sepsis
1. Stabilize The Patient
– Fluids (lots of fluids)
– Vasoconstrictors
2. Treat The Cause
– Seek primary site of infection
– Direct therapy to primary cause
3. Improve Perfusion
– Prevent organ dysfunction
175. Resources
American Stroke Association. (2007). Acute and Preventative Treatments. Retrieved
March 4, 2007 from http://www.strokeassociation.org/presenter.jhtml?identifier
=2532
Anderson, L. (July 2001). Abdominal Aortic Aneurysm, Journal of Cardiovascular
Nursing:15(4):1–14, July 2001.
Balk, R. A. (2000). Severe sepsis and septic shock. Critical Care Clinics; (2)179-92.
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.
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Editor's Notes
Detoxify harmful substances (e.g., free radicals, drugs) Increase the absorption of calcium by producing calcitriol (form of vitamin D) Produce erythropoietin (hormone that stimulates red blood cell production in the bone marrow) Secrete renin (hormone that regulates blood pressure and electrolyte balance)
Detoxify harmful substances (e.g., free radicals, drugs) Increase the absorption of calcium by producing calcitriol (form of vitamin D) Produce erythropoietin (hormone that stimulates red blood cell production in the bone marrow) Secrete renin (hormone that regulates blood pressure and electrolyte balance)
Kidney - has 3 main sections 1. Renal Cortex - outer region (most of the nephron is located here) 2. Renal Medulla - inner region a. columns - contains blood vessels b. pyramids - contain loops of henle and collection ducts 3. Renal Pelvis
Network of Tubes Each kidney has approximately 1 million nephrons Most parts of the Nephron are in the renal cortex
Proximal Convoluted Tubule Leads away from Bowman’s capsule to the Loop of Henle Removes waste products (ammonia, nicotine) Reabsorbs useful substances (glucose, soduim, chloride, potassium, amino acids, vitamins, water and more) Loop of Henle a U-shaped extension of the proximal convoluted tubule The descending loop is highly permeable to water and impermeable to substances in the urine (e.g., salt, ammonia), The ascending loop is impermeable to water and permeable to other substances Distal Convoluted Tubule Leads away from the Loop of Henle to the collecting tubule substances are directly transferred from the surrounding capillaries into the renal tubule Secretes & collects potassium and bicarbonate (hydrogen ions) Collecting Tubule Concentrates urine in the medulla The channels are controlled by ADH Aldosterone receptors regulate Na uptake and K excretion
July 2004November 2002 COMMON CRITICAL CONDITIONS Part One
BUN / Cr ratio normally 12:1-20:1
If caused by meds, must stop meds If caused by obstruction, must remove obstruction If caused by blockage of artery, must open artery Dietary restrictions may include : low K+, adequate carbs, also may give TPN Fluids : calculate closley I/O Hyperkalemia is life threatening Lower K+ with Kayexalate, glucose, insulin, NaBicarb, caalcium carbonate
Neurological signs due to sympathetic nervous system stimulation
Osmolality = the concentration of solute (particles) per kilogram of water, which creates the pulling power of that solution for water Osmolarity – concentration of solute (particles) per liter of solution, which creates the pulling power of that solution for water Because body fluid solvent is water and one liter of water weighs one kilogram, the terms can be used interchangeably in discussing human fluid physiology
July 2004November 2002 COMMON CRITICAL CONDITIONS Part One
July 2004November 2002 COMMON CRITICAL CONDITIONS Part One
To begin this discussion, one needs to know what the volume of distribution of water is. Water accounts for 50% of total body weight in females and up to 60% in males. Thus if one administers 1 liter of water to a 70 kg female, it will be diluted 1 in 35 liters (total body water= 0.5 x body weight in females).
Total body water is divided in to 2 basic compartments: Intracellular (2/3) and extracellular (1/3). The cell membrane is freely permeable to water but dissolved electrolytes do not share the same permeability. Examples 1. 5% Dextrose in water (D5W) is handled just as free water is (since dextrose is metabolized). 2. Intravenous 0.9% saline (isotonic) does not diffuse through all compartments since the cell membrane is impermeable to sodium. 3. If 1 liter 0.45% saline is administered, ½ behaves as free water and ½ as saline.
Extracellular water is further divided into intravascular and extravascular (interstitial) compartments. The distribution of IV fluids may be further restricted by the capillary membrane, thus: 5% albumin is restricted to the intravascular space Isotonic saline can easily cross the capillary membrane and disperse throughout the extravascular (interstitial) space.
Since this fluid accumulates under conditions when patients are ill and thereby are not able to take in enough fluids, IV replacement frequently becomes necessary to prevent/treat extracellular volume depletion.
July 2004November 2002 COMMON CRITICAL CONDITIONS Part One
5% Albumin will remain in the intravascular space, at least acutely. It is the most efficient way to treat shock. However, this effect is not permanent and, paradoxically in patients who are hypoalbuminemic (cirrhosis, nephrotic syndrome), albumin eventually enters the interstitial space because the integrity of the capillary barrier is not intact.
Isotonic (normal, 0.9%) saline is distributed in extracellular fluid since the cell membrane is not permeable to sodium. Thus, of 1 liter of NS in our hypothetical 70 kg male: 250ml will remain in the intravascular space and the remainder 750ml will exit into the interstitial space. In a patient with shock from fluid depletion, 1 liter of intravascular saline = 4 liters total saline may be required to restore hemodynamics
Solutions containing dextrose in water are handled like free water (although dextrose enters cells, it is metabolized). Thus 1 liter of D5W in a 70kg male will diffuse throughout body water 60ml will remain in the intravascular space, 240 will be in interstitial fluid and, 700ml will enter cells Dextrose in water is obviously not an efficient method to treat someone with shock.
CSF is produced in the choroid plexus. CSF is absorbed into the blood stream through the arachnoid villi. Protection : the CSF protects the brain from damage by "buffering" the brain. In other words, the CSF acts to cushion a blow to the head and lessen the impact. Buoyancy : because the brain is immersed in fluid, the net weight of the brain is reduced from about 1,400 gm to about 50 gm. Therefore, pressure at the base of the brain is reduced. Excretion of waste products : the one-way flow from the CSF to the blood takes potentially harmful metabolites, drugs and other substances away from the brain. Endocrine medium for the brain : the CSF serves to transport hormones to other areas of the brain. Hormones released into the CSF can be carried to remote sites of the brain where they may act.
Pheochromocytoma Cocaine
Pheochromocytoma Cocaine
AVM = defect of the circulatory system consisting of an abnormal connection between the arterial system (which normally has a higher intravascular pressure) and the lower pressure venous pathways.
Normally the connection between arteries and veins is through a network of smaller vessels (capillaries) which slow the blood down and permit the exchange of food, oxygen and nutrients into the tissues.
20% have ECG evidence of myocardial ischemia • ST segment elevation, T wave changes ( Due to high levels of circulating catecholamines)
Papaverine is an opium alkaloid with vasodilatory action.
Stroke is the third leading cause of death in the United States. Every year 600,000 people will suffer a new or recurrent stroke, and of those, 160,000 will die. That’s one in 20 people that will suffer a stroke or TIA in their lifetime. Types of Ischemic strokes: Thrombotic Stroke Embolic Stroke
July 2004November 2002 COMMON CRITICAL CONDITIONS Part One High BP : weakens and damages blood vessels High cholesterol : increase risks of arthrosclerosis and plaque buildup in arteries.
July 2004November 2002 COMMON CRITICAL CONDITIONS Part One
July 2004November 2002 COMMON CRITICAL CONDITIONS Part One A 60-year-old woman was brought to the Emergency 3 hours after developing left hemiparesis. 1. A CT scan taken after being admitted. 2. An MRI scan performed the next day.
July 2004November 2002 COMMON CRITICAL CONDITIONS Part One
July 2004November 2002 COMMON CRITICAL CONDITIONS Part One
July 2004November 2002 COMMON CRITICAL CONDITIONS Part One
Metabolizes fats for energy resulting in buildup of fatty acids. Kussmaul = Rapid and deep respirations Polyuria Unconsciousness
Similar Symptoms include: Hypotension, LOC Changes, N/V, Polyuria, Thirst, Dry Mouth, Dry Skin, Weakness,
Severe Dehydration With HHNK NS X 1 Hours, then ½ NS with DKA NS X 2 Hours, then ½ NS with HHNK Continue NS as needed. Give insulin Watch for dilutional electrolyte lows
Decreased ADH Causes Inability To Concentrate Urine, Thereby Losing Water (Polyuria) Severe Hypovolemia
Watch for chest pain or abdominal cramps. Watch for for ST depressions.
Seizures due to cerebral edema
Holding onto water Water Intoxication
Activation of intrinsic or extrinsic pathways
Fibrin deposition in organs, leading to organ failure
Replacement Therapy FFP Platelets Cryoprecipitate Packed Red Blood Cells Anticoagulation Therapy Heparin Antithrombin III Recombinant tissue plasminogen activator Activated protein C
Orthostatic Hypotension
Orthostatic Hypotension
Toxins and bradykinins cause massive vasodilatation, a positive inotropic effect and stimulate the respiratory rate. May cause release of myocardial depressant factor in late phase. May stimulate the clotting cascade. Often leads to ARDS or/and DIC.
MODS = Multiple Organ Dysfunction Syndrome
Definitions – ACCP/SCCM Consensus Conference Definition Bone et al.1992. Chest 101:1644-1655. Sepsis: a systemic inflammatory response to infection Severe Sepsis: systemic inflammation, coagulation and impaired fibinolysis. Septic Shock: severe sepsis defined as sepsis-induced hypotension (systolic blood pressure < 90mmHg or a reduction of=40mmHg from baseline in the absence of other causes for hypotension) despite adequate fluid resuscitation along with the presence of perfusion abnormalities. Patients receiving inotropic or vasopressor agents may no longer be hypotensive by the time that they manifest hypoperfusion abnormalities or organ dysfunction, yet they would be considered having septic shock.
The cumulative effect of the cascades is an unbalanced state, with inflammation dominant over anti-inflammation and coagulation dominant over fibrinolysis. Microvascular thrombosis, hypoperfusion, ischemia, and tissue injury result. Severe sepsis, shock, and multiple organ dysfunction may occur, leading to death.
Optimize intravascular volume Consider Xygris (Activated Protein C)