Exam 3 Flashcards
1
Q
One good sign of an infection
A
Elevated WBC (11,000-25,000) 3,500/5,000-10,000 (normal)
2
Q
Leukemia WBC range
A
WBC 100,000-400,000
3
Q
Eosinophils and basophils
A
Allergies and inflammation
4
Q
Neutrophils
A
Fight infection
5
Q
Lymphocyte
A
A lymphocyte is a type of white blood cell in the vertebrate immune system. Lymphocytes include natural killer cells, T cells, and B cells
6
Q
Serous fluid
A
Watery, like plasma
7
Q
Fibrinous fluid
A
Clotted
8
Q
Serosanguious fluid
A
Clear pink, blood tinged
9
Q
Sanguinous
A
Bloody
10
Q
Shift to the left** of cells
A
*
11
Q
Purulent
A
Pus (suppurative)
12
Q
Serious, fibrinous, serosanguinous, sanguinous, purulent drainage are sisngs of
A
Local manifestations
13
Q
ESR (erythrocyte sedimentation rate)
A
The erythrocyte sedimentation rate is the rate at which red blood cells in anticoagulated whole blood descend in a standardized tube over a period of one hour. It is a common hematology test, and is a non-specific measure of inflammation.
Stimulates angiogenesis
14
Q
Chronic inflammation can cause
A
Cancer
15
Q
Purpose of an inflammatory response
A
To prepare the injured area for healing
16
Q
3 inflammatory responses:
A
- Leukocytes (neutrophils & macrophages) to
remove debris and provide growth factors - Nutrients (proteins, glucose, vitamins) to
provide the building blocks for cells - Clotting factors and platelets to limit damage
17
Q
T/F every disease has some type of inflammation
A
True
18
Q
3 plasma protein systems:
A
- Clotting cascade: prevents further bleeding
- Kinin cascade: produces bradykinin, causing pain, vasodilation, vascular permeability
- Complement cascade: stimulates opsonins,chemotactic factors, and anaphylatoxins which degrade Mast cells to release histamine, a potent vasodilator.
19
Q
Vascular response to inflammation (4 steps)
A
Histamine and bradykinin stimulate vasodilation
and increased permeability, resulting in:
1. Increased blood flow to the area, causing redness
(rubor) and heat (calor)
2. Leakage of protein rich plasma into the
interstitial spaces, causing swelling (tumor)
3. Bradykinin also causes pain (dolor)
4. Cells are unable to function
20
Q
Cellular response of inflammation (4 steps)
A
Chemotactic factors attract neutrophils to:
1. Marginate: move to the capillary walls
2. Emigrate: squeeze through capillary pores
3. Migrate: through chemotaxis to the injury
4. Phagocytosis facilitated by opsonization
(acts to facilitate adherence of WBC’s to
bacteria)
21
Q
5 cardinal signs of inflammation
A
- redness
- swelling
- loss of function
- pain
- heat
22
Q
3 systemic signs of inflammation
A
- Fever: caused by specific cytokines
(endogenous pyrogens) - Leukocytosis: increase in WBC’s (>11,000)
and in infection, a “left shift” ratio - Increase in plasma proteins as measured by ESR (erythrocyte sedimentation rate)
23
Q
3 reasons chronic inflammation occurs and 3 results of it:
A
May occur due to: 1. Chronic infection or contamination 2. Continuous exposure to irritants 3. Immune system abnormalities May result in: 1. Granuloma formation 2. Giant cell formation 3. Cancers in genetically susceptible individuals
24
Q
3 stages of wound healing
A
- Inflammation: usually lasts 1-2 days
- Proliferation and New Tissue Formation:
2-8 weeks until maximum strength achieved.
May involve regeneration and resolution, or
repair with scar tissue but loss of function - Remodeling and Maturation: up to 2 years
25
3 stages of wound healing
Hemostasis is first- wound being closed by clotting
1. Inflammation: usually lasts 1-2 days
2. Proliferation and New Tissue Formation:
2-8 weeks until maximum strength achieved.
May involve regeneration and resolution, or
repair with scar tissue but loss of function
3. Remodeling and Maturation: up to 2 years
26
3 types of wound healing
1. First Intention: must be clean; able to
approximate wound edges; fastest; preferred
2. Second Intention: used in contaminated wounds;
large amount of tissue lost; very slow; large scar
3. Third Intention: rarely used to close large
wounds that are clean enough. Example: skin
grafting
27
3 types of wound healing
1. First Intention: must be clean; able to
approximate wound edges; fastest; preferred
2. Second Intention: used in contaminated wounds;
large amount of tissue lost; very slow; large scar
3. Third Intention: rarely used to close large
wounds that are clean enough. Example: skin grafting
28
Adherence
Wound staying together
29
Wound vacuum
for 2nd intentiton
30
Wound healing process
1. Macrophages: dissolve clots; clear debris; add
a. TGF-B, transforming growth factor-beta to
stimulate collagen precursor procollagen
b. VEGF, vascular endothelial growth factor
stimulates angiogenesis
c. MMPs, Matrix metalloproteinases, remodel collagen and fibrin2. Collagen lattice forms
3. Granulation tissue fills in wound
4. Hypertrophic scar tissue overfills wound
5. Cicatrization (maturation) of wound
may take 1-2 years. Collagen contracts
& scar becomes lighter and smoother
31
Non-union
failure of adherence
32
Dehiscence
wound edges separate, exposing underlying tissues
33
Evisceration
underlying viscera are exposed
34
Abscess
A walled pocket of infection
35
Sinus tract
A narrow tunnel forming
36
Cellulitis
A bacterial infection that enters the skin, affected skin appears swollen and red and may be hot and tender. *edema is a big risk factor with cellulitis*
37
Necrosis
Death of tissues/ cells
38
Gangrene
Type of tissue death caused by a lack of blood supply
39
Fistula
An abnormal connection between two body parts, such as an organ or blood vessel and another structure.
40
Excess fibrin or dysfunctional collagen
synthesis may result in abnormalities such
as: (5)
1. fistula formation
2. adhesions
3. contractures
4. strictures
5. keloids
41
Patients that have the hardest time healing from wounds
Diabetics
42
Systemic markers of vascular inflammation
Homocysteine level: elevated in reduced
levels of folate, B vitamins, and riboflavin.
Inhibits anticoagulation cascade and
increases endothelial damage in arteries.
• C-Reactive Protein: increases to neutralize
inflammatory chemicals
• Infectious agents: often found in plaques
• Endothelial dysfunction: lack of NO
43
Granulation tissue
New connective tissue and microscopic blood vessels that form on the surfaces of a wound during the healing process. Granulation tissue typically grows from the base of a wound and is able to fill wounds of almost any size. Bleeds easily
44
Define CHF and the mortality rate in 5 years
```
A complex syndrome resulting from
any cardiac dysfunction that results
in low cardiac output (CO) and
symptoms of pulmonary or systemic
fluid congestion. In adults, the
mortality rate is 50% within 5 years.
It is considered an end-stage disease.
```
45
Risk factors of CHF
Age: generally seniors
• High cholesterol, HTN, DM, obesity
• Pre-existing heart conditions, CAD, MI
• Valve problem or other mechanical issue
• Fluid overload conditions: renal disease
• Alcoholism, liver disease
46
Cicatrization
scar formation at the site of a healing wound
47
Causes of CHF
1. Coronary Artery Disease/atherosclerosis
2. Hypertension/myocardial hypertrophy
3. Myocardial Infarction
4. Heart Valve Disease
5. Pericardial restriction/pericarditis
6. Fluid overload conditions
48
Hypertrophic cardiomyopathy
Hypertrophic: walls are thickened,
reducing ventricular volume.
• Causes: HTN, CAD, valve stenosis,
remodeling
49
Dilated cardiomyopathy
Dilated: walls are weakened and bulge
out, reducing contractility
• Causes: MI with extensive scar, valve
regurgitation
50
Fluid overload condition
CHF
51
Decrease cardiac output causes: (3 things)
Reduced blood flow to kidneys,
stimulating the RAAS and fluid retention
• Less stimulation to baroreceptors in aortic
arch, stimulating hypothalmus to increase
thirst and ADH production
• Stress response stimulates catecholamines,increasing HR and O2 demand of heart
52
Increase fluid retention in CHF causes
Increase in preload and afterload
53
Increased stress hormones/catecholamines vasoconstrict and...
Increase afterload, HR and O2 demand increase, causing ischemia
54
Ischemia reduces
Compliance, elasticity, and contractility
55
In CHF, wall stress is increased causing CO to
decrease
56
S/S of CHF (8)
```
SOB climbing stairs
• SOB lying flat/orthopnea
• SOB with activities
• Increased abdominal girth
• Lower leg edema
• Cough, white sputum
• Increased weight
• Decreased appetite
```
57
Assessment findings of CHF
```
• SOB on exertion or at rest
• Lungs may have crackles, esp at bases
• Point of maximal impulse (heart) moved
lower and left, indicating enlargement
• X-rays: cardiac enlargement, pulmonary
congestion.
• Ascites & liver congestion, leg edema,
distended jugular veins
• Decreased urinary output
```
58
Left-sided HF s/s
- SOB
- Orthopnea
- Low O2 sat
- Pulmonary crackles
- S1 or S2 gallop
- Weak thready pulse
- Probably low BP
- ***left backs up into the lungs***
59
Right-sided HF s/s
- weight gain
- leg edema
- ascites/liver enlargement
- jugular vein distension
- ***right backs up to the rest of the bpdy***
60
Diagnostic testing of CHF
```
Echocardiogram/Stress Test/Stress Echo
• Chest X-ray: heart and lungs
• Blood tests: BNP and ANP
• Kidney function: BUN, creatinine
• Liver function: LFT’s
• Cardiac Angiography/catheterization
• Right-sided heart catheterization: Swan-
Ganz catheter (ICU only)
```
61
Diagnostic criteria of CHF
1. Ejection fraction less than 40%
2. Atrial Natriuretic Peptide greater than 77 pg/mL
3. Brain Natriuretic Peptide greater than 100 pg/mL
4. S&S of fatigue, SOB, edema, activity intolerance
5. S&S at rest indicate increased disease burden
6. Structural heart disease: decreased wall motion,
coronary artery blockage on angiogram
62
AHA classification system
```
• Stage A: High risk/ no abnormalities
(example: DM/CAD/HTN)
• Stage B: Abnormalities/no S & S
• Stage C: Abnormalities with S & S
• Stage D: advance abnormalities and S
& S at rest on maximum med therapy
```
63
Staging of CHF
```
• Stage 1: SOB with
brisk walk/stairs
• Stage 2: OK at rest.
HR or SOB when
walking or stairs.
• Stage 3: HR up,
tired, daily activity
is an effort.
• Stage 4: HR up,
SOB at rest, fatigue,
anxiety, palpitations
```
64
S/S Pulmonary Edema
Falling O2 sat, confusion, jugular vein distension, infarct, S3 gallop, tachycardia, enlarged spleen and liver, decreased urine output, weak pulse, cool or most skin, skin pale, grey, or cyanotic, dyspnea, orthopnea, crackles, wheeze, cough
65
CHF treatments
CHF medications are used to:
1. Improve cardiac efficiency by strengthening
contractions and slowing rate: glycosides
2. Reduce peripheral vascular resistance:
vasodilators
3. Reduce fluid retention: diuretics
Other treatments include:
1. Exercise: strengthens myocardium & vasodilates
2. Surgery: Bypass or valve repair as needed
66
Mechanical treatments for CHF
```
• Cardiac Resynchronization and
Implantable Cardioverter-Defibrilators
• Balloon Pumps: temporary
• L-VAD: left ventricular assist devices
• Heart transplantation
• LV remodeling surgery
```
67
T/F: CHF is an end-stage disease
True
68
Atrophic scar
A smaller than normal scar that's atrophied
69
Hypertrophic scar
A bigger, thicker hypertrophied scar, not as thick as a keloid
70
Ways to prevent CHF
```
Prevent CHF by controlling risk factors:
• Blood pressure (HTN: meds/diet/exercise)
• Blood sugar (DM: meds/diet/exercise)
• Blood cholesterol (meds/diet/exercise)
• Weight: keep normal
• Exercise: keep it up! Resistance training,
walking, isometrics
• Diet: DASH diet (Dietary Approaches to
Stop Hypertension), Mediterranean diet
```
71
Define renal failure
Renal failure is a condition in which
the kidneys fail to remove metabolic
end products from the blood and
regulate the fluid, electrolyte, and pH
balance of the extracellular fluids. It is
on the list of top 10 causes of mortality
in the United States.
72
Pre-renal failure
Reduced blood flow to the kidneys (CHF, HT, shock, clots, stenosis)
73
Intra-renal failure
damage to the nephrons (meds, infections, DM, cancer, PKD, dyes, metals)
74
Post-renal failure
obstruction of the ureters or urethra (renal calculi, BPH, bladder or prostate cancer that blocks urine)
75
Etiologies of renal failure
Pre-renal failure, intra-renal failure, post-renal failure
76
Acute renal failure
happens suddenly, may resolve
- onset phase
- oliguric (anuric) phase: 8-14 days or more
- diuretic phase
- recovery phase: may take up to a year
77
Chronic renal failure
Happens gradually over a long time, no recovery, 80% damage before s/s may be evident
78
Causes of acute renal failure: prerenal
Prerenal: sudden and severe drop in blood pressure (shock) or interruption of blood flow to the kidneys from severe injury or illness
79
Causes of acute renal failure: intrarenal
direct damage to the kidneys by inflammation or reduced blood supply
80
Causes of acute renal failure: postrenal
sudden obstruction of urine flow due to enlarged prostate. kidney stones, bladder tumor or injury
81
Causes of chronic renal failure
```
Diabetes
HTN
Glomerulonephritis
Cystic disease
Urologic diseases
```
82
Renal failure BUN level
Above 8-20 mg/dL
83
Renal failure creatinine level
above 0.6-1.2 mg/dL
84
Normal calcium level
9 -10.6 mg/ dl (total)
| 4.5 -5.6 mg/dl (ionized)
85
Food sources of calcium
dairy products, green leafy vegetables
86
Where is calcium stored and excreted?
stored in bone, excreted by kidney
87
Hormonal regulation of calcium
parathyroid hormone raises serum levels of calcium by pulling it from bone,- calcitonin (produced by the thyroid gland) lowers serum Ca levels by storing it in bone.
88
Main function of calcium
bone, development, blood clotting, smooth muscular contraction
89
Target organ of calcium
skeletal muscles
90
What vitamin is necessary for calcium absoprtion
Vitamin D
91
What % of calcium is absorbed
About 50%
92
What percentage of calcium serum is bound fo albumin
- 40% in serum bound to albumin. If albumin levels are low, total Ca level will be low, too.
93
What calcium level is more accurate?
Free or ionized
94
Acidosis will ____ serum calcium and alkalosis will ____ it
increase, decrease
95
Excess calcium causes
Paraneoplastic syndrome
96
When phosphates are low, calcium is _____
high
97
Causes of hypocalcemia
```
Impaired ability to mobilize calcium from bone, ie. hypoparathyroidism.
Abnormal calcium binding
- decreased serum albumin
- decreased pH
- increased free fatty acids
- rapid infusion of citrated blood
- acute pancreatitis
Abnormal losses
- renal failure
Inadequate vitamin D
- impaired absorption
- renal failure
- liver disease
```
98
S/S hypocalcemia
```
Laboratory values: below 8.5 mg/dl
Increased nerve excitability
- paresthesias, numbness and tingling
- skeletal muscle cramps
- abdominal spasms and cramps
- hyperactive reflexes
- carpopedal spasm
- ****tetany***
- laryngeal spasm
- positive Chvostek's sign
- positive Trousseau's sign
-
Cardiovascular manifestations
- hypotension
- cardiac insufficiency
- failure to respond to drugs that act via calcium-mediated mechanisms
```
99
Causes of hypercalcemia
```
Excessive gains
- increased intestinal absorption
- excessive vitamin D
- excessive calcium in diet
- milk-alkali syndrome
Increased bone resorption
- immobility
- increased levels of parathyroid hormone
- malignant neoplasms
- thiazide diuretics
Inadequate losses
- hyperthyroidism
```
100
S/S hypercalcemia
```
Signs and Symptoms
Laboratory values: serum Ca above 10.5
Neuromuscular:
- muscle weakness and atrophy
- ataxia, loss of muscle tone
- lethargy
- stupor and coma
- personality and behavioral changes
Bone loss
- deep bone pain
- pathological fractures (without trauma)
Renal
- renal insufficiency
- polyuria
- flank pain
- signs of kidney stones
- increased loss of K and Na
Cardiovascular
- hypertension
- shortened QT interval, AV block
Gastrointestinal
- anorexia
- nausea
- vomiting
- constipation
```
101
Serum calcium of hypercalcemia
Above 10.5 mg/dl
102
Serum calcium of hypocalcemia
Below 8.5 mg/dl
103
Normal magnesium range
1.8-3.0 meq/l
104
Food sources of magnesium
vegetables, nuts
105
What organ regulates magnesium
Kidneys
106
Main function of magnesium
maintains intracellular K. Also functions in enzyme reactions and protein and DNA synthesis.
107
Target organ of magnesium
Heart
108
% of magnesium in bone, cells and serum
50% in bone, 49% in cells, 1% in serum
109
what electrolyte diursese's with water
magnesium
110
Causes of hypomagnesemia
```
Causes of Hypomagnesemia:
Impaired intake or absorption
- Alcoholism
- Malabsorption
- Small-bowel bypass surgery
- Malnutrition or starvation
- Parenteral Hyperalimentation with inadequate Mg
- High dietary intake of calcium without concomitant increase in Mg
Increased losses
- diabetic ketoacidosis
- diuretic therapy
- hyperparathyroidism
- hyperaldosteronism
- magnesium-wasting renal disease
```
111
S/S Hypomagnesemia
```
Laboratory findings: Mg less than 1.8 meq/l
Neuromuscular hyperirritability
- Personality change
- athetoid or choreiform movements
- positive Babinski's sign
- nystagmus
- tetany
- positive Chvostek's or Trousseau's signs
Cardiovascular Manifestations
- tachycardia
- hypertension
- ventricular arrhythmias
```
112
Causes of hypermagnesemia
```
Excess intake, usually in antacid form
Adrenal insufficiency, low aldosterone
Renal failure (most common)
```
113
S/S Hypermagnesemia
```
Laboratory Values: greater than 3.0 meq/l.
Neuromuscular
- skeletal smooth muscle contraction
- excess nerve function
- loss of deep tendon reflexes
- muscular weakness
Gastrointestinal: nausea and vomiting
Cardiovascular:
- hypotension
- bradycardia
Respiratory distress
```
114
What electrolyte regulates water balance
Sodium
115
What electrolyte deals with acid/base regulation
Potassium (K)
116
what four electrolytes are essential for neuromuscular activity
sodium, potassium, calcium, chloride
117
4 functions of electrolytes
regulate water balance (mostly sodium)
acid/base regulation (potassium)
contribute to enzyme reactions
essential for neuromuscular activity (sodium, potassium, calcium, chloride)
118
Define electrolyte
: a substance that dissociates in solution to form charged particles, or ions
119
Define anion and cation
cations: positively charged particles
| anions: negatively charged particles
120
Electrolytes are found mostly in
cells
121
Serum levels may not accurately reflect
intracellular levels. (ex: 28 times more K in cells)
122
Normal sodium
135-147 meq/l
123
Minimum RDA of sodium vs how much Americans average
500mg/day
Americans average 6-15 g/day
124
Regulation of sodium
Kidneys
125
Where is sodium lost from
GI tract, skin
126
Hormonal regulation of kidneys
aldosterone increase retains sodium and therefore water as well. Angiotensin II, ACTH, and cortisol increase the production of aldosterone
127
Main function of sodium
Fluid retention
128
Target organ of sodium
Brain
129
Hyponatremia (sodium deficit) causes
```
Excessive Sodium Losses
- sweating
- gastrointestinal losses
- diuresis
Sodium Dilution
- excess sodium-free IV's
- psychogenic polydipsia
- repeated tap water enemas
Renal disease that impairs water elimination
Increased ADH Levels
- trauma, stress, pain
- SIADH
- Use of medications that increase ADH
```
130
S/S hyponatremia
```
Laboratory Values
- serum sodium below 137 meq/l
- decreased serum osmolality
- dilution of other blood components, esp. chloride, hematocrit, and BUN
Increased Water Content of Brain and Nerves
- headache
- mental depression
- personality changes
- confusion
- apprehension and feeling of impending doom
- lethargy and weakness
- stupor, convulsions, coma
Gastrointestinal Disturbances
- anorexia, nausea and vomiting
- abdominal cramps
- diarrhea
Increased Intracellular Fluid
- Fingerprinting over sternum
```
131
Hypernatremia causes
- excessive oral intake (sodium bicarbonate)
- rapid or excessive IV solutions with sodium chloride or sodium bicarbonate
Decreased extracellular water (concentration)
Increased water losses
- adrenal cortical hormone excess
- diabetes insipidus
- tracheobronchitis
- watery diarrhea
- hypertonic tube feedings
Decreased water intake
- unconsciousness or inability to swallow
- impaired thirst mechanism
- NPO for therapeutic reasons
132
S/S hypernatremia
```
Laboratory Findings
- serum sodium above 147 meq/l
- increased serum osmolality
Thirst
Urine Output
- oliguria or anuria
- high specific gravity
Intracellular Dehydration
- mucous membranes dry and sticky, skin dry and flushed
- subcutaneous tissue firm and rubbery
- central nervous system: agitation, restlessness, decreased reflexes, maniacal behavior, convulsions and coma
- Increased body temperature
- Decreased vascular volume with tachycardia, decreased blood pressure, weak and thready pulse
```
133
because Na and Cl are most often bound together, signs and symptoms are...
generally similar
134
Normal phosphate range
2.5-4.5 mg/dl, infants up to 7.0
135
Sources of phosphates
dairy products, green leafy vegetables (same as calcium)
136
Regulation of phosphates
kidneys
137
Hormonal regulation of phosphates
opposite of calcium. Parathyroid hormone lowers levels, calcitonin would raise them.
138
Main functions of phosphates
acid/base balance, ATP for energy, manufacture of blood components (WBC's, RBC, platelets).
139
Target organs of phosphates
neuromuscular function, blood
140
Calcium and phosphate are
reciprocal
141
when calcium is up, it drives phosphate
into the bone
| Ca x PO4 = 36
142
S/S hypocalcemia are similar to
HYPERphosphatemia, and vice versa
143
Hypophosphatemia causes
```
Increased loss from the GI tract
- antacids (aluminum and calcium bind with phosphates)
- severe diarrhea
- lack of vitamin D
Increased renal excretion
- alkalosis
- hyperparathyroidism
- diabetic ketoacidosis
- renal tubular defects
Decreased intake - malnutrition
Alcoholism
Increased movement into the cell
- intravenous hyperalimentation
- recovery from malnutrition
- administration of insulin for ketoacidosis
```
144
S/S hypophosphatemia
```
Laboratory values: below 3.0 in adults or 4.0 in children.
Altered neural function
- intention tremor
- ataxia
- parasthesias
- hyporeflecia
- confusion
- stupor
- coma
- seizures
Altered musculoskeletal function
- muscle weakness
- joint stiffness
- bone pain
- osteomalacia
Gastrointestinal symptoms
- anorexia
- dysphagia
Hematologic disorders
- hemolytic anemia
- platelet dysfunction with bleeding disorders
- impaired function of white blood cells
```
145
Causes of hyperphosphatemia
Excess intake
- long-term use of laxatives or enemas containing phosphate.
- excess administration in parenteral fluid.
- treatment of cancers with chemotherapy that releases large amounts of phosphate into the bloodstream
Inadequate loss: acute or chronic renal failure
146
S/S hyperphosphatemia
Similar to low calcium levels, especially muscle cramps, twitches, and tetany.
Calcification of soft tissues in lungs, kidneys, joints.
147
Define acid
an electrolyte that ionizes in water to form hydrogen ions (H+) and anions. The anion is called the conjugate base of the acid.
148
Define base
a substance that can bind hydrogen ions. An alkali is a substance that contains a base.
149
Define pH
the percentage of hydrogen ions in a solution.
150
Normal blood pH/ where does death occur
7.4 with a range of 7.35 - 7.45. Death usually occurs below 6.8 or above 7.8
151
Volatile acids
can be excreted from the body as a gas. Example: CO2 + H20 = H2CO3 (carbonic acid) = H+ & HCO3- (bicarbonate)
152
nonvotaile acids
or fixed acids, cannot be made into a gas and must be excreted as a liquid by the kidneys. Example: lactic acid, ketones, phosphoric acid, sulfuric acid. The typical American diet causes an overload of fixed acids.
153
Excreting acids
The LUNGS excrete volatile acids. The KIDNEYS excrete nonvolatile acids and retain bicarbonate as a buffer for acids.
154
Causes of respiratory acidosis
HYPOVENTILATION
• COPD (chronic obstructive pulmonary disease)
• pneumonia, atelectasis
• barbituate or sedative overdose
• Guillain-Barre Syndrome, ALS, or other neuromuscular weakening diseases
• skeletal deformities and injuries to ribcage
155
Lab values of respiratory acidosis
* pH below 7.35
* CO2 above 45 mmHg.
* HCO3 normal at 24 test question
* urine pH less than 6
156
Manifestations of respiratory acidosis
* Neurological: drowsy, disoriented, coma
* Cardiovascular: hypotension, tachycardia
* Respiratory: shallow, tachypnea or bradypnea depending on cause.
* Muscular: weakness
157
Nursing application of treating a person in respiratory acidosis
GRAB AMBU BAG AND START GIVING OXYGEN, PT MIGHT NEED TO BE INTUBAED
158
Causes of respiratory alkalosis
```
HYPERVENTILATION
• anxiety
• encephalitis
• fever
• mechanical over-ventilation
```
159
Lab values of respiratory alkalosis
* pH above 7.45
* CO2 below 35 mmHG
* HCOs normal 24 mEq/L
* urine pH greater than 7
160
Manifestations of respiratory alkalosis
* Neurological: lethargic, confused, may have numbness or tingling of extremities
* Muscular: tetany, hyperreflexia
* Respiratory: hyperventilation
161
What to do if a patient is having an anxiety attack
alk them through box breathing (spase breathing) breathing in 4 breaths and out 4 breaths
162
Causes of metabolic acidosis
```
Excess production of acids
• diabetic ketoacidosis
• lactic acidosis
• starvation with lactic acidosis
Inadequate loss of acids
• uremia
• renal tubular acidosis
Excess loss of base: severe diarrhea (pts with c. diff are also at risk)
```
163
lab findings in metabolic acidosis
* pH less than 7.35
* CO2 less than 35 mm HG Kussmal’s a mechanism for metabolic acidosis, sweet smelling breath
* HCO3 - less than 24 mEq/L
* urine pH less than 6
164
Manifestations of metabolic acidosis
* Neurological: disoriented, weak, coma
* Gastrointestinal: nausea, vomiting, diarrhea, abdominal pain, dehydration
* Respiratory: hyperventilation
165
Metabolic alkalosis causes
```
*RARE*Loss of acids
• severe vomiting
• excess gastric suctioning
• diuretic therapy
Base or buffer imbalance
• potassium deficit (causes relative Na excess)
• excess NaHCO3 intake
```
166
Lab findings of metabolic alkalosis
* pH above 7.45
* CO2 above 45 mmHg.
* HCO3 above 24 mEq./l
* urine pH above 7
167
Manifestations of metabolic alkalosis
* Neurological: confusion, stupor, coma
* GI: anorexia, nausea, tremors, cramps
* MS: tetany
* Respiratory: hypoventilation
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Normal values in arterial blood gases
```
Normal Values
pa O2: above 90%
pa CO2: 40 range 38-43
pH: 7.4 range 7.35-7.45
HCO3: 24 range 22-26
O2 Sat: 93-100%
Hgb: 13-15
CO: 0
```
169
Steps in blood gas analysis
1. Is the pH acidic or basic?
2. Is the CO2 elevated (acidic) or decreased (basic)?
3. Does the CO2 match the pH? If yes, problem is probably respiratory. Confirm by step 4.
4. Is the O2 normal or decreased? If O2 confirms CO2, problem is probably respiratory.
5. Is the HCO3 elevated (alkalotic) or decreased (acidotic)? If the HCO3 matches the pH, the problem is probably metabolic.
6. If the ph is within normal but the CO2 and HCO3 are abnormal, the problem is a chronic one that has been compensated.
170
Normal potassium range
3.5 - 5.0 meq/l
171
Minimum RDA of potassium
50-100 meq/day
172
Sources of potassium
Fruits and vegetables
173
Regulation of potassium is in the
kidneys
174
hormonal regulation os potassium
aldosterone reduces potassium in the bloodstream. Na and K are exchange ions - when one goes up, the other goes down.
175
main function of potassium
smooth electrical conduction to the muscles
176
target organ of potassium
heart
177
what percentage of potassium is inside the cells?
98%
178
4 special considerations of potassium
Potassium follows water. Diuresis will wash out potassium from the bloodstream.
K will shift out of cells with acidosis.
Insulin will also drive K into cells.
A deficiency of Mg will cause intracellular K depletion regardless of serum K levels.
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causes of hypokalemia (potassium deficit)
```
Inadequate Intake
- Inability to eat
- Diet deficient in potassium
- Administration of K free IV solutions
Excessive Gastrointestinal Losses
- Vomiting
- Diarrhea
- Nasogastric Suctioning
- Fistula Drainage
Excessive Renal Losses
- Diuretic phase of renal failure
- Diuretic therapy (except K-sparing ones)
- Increased mineralcorticoid levels
Cushing's Syndrome
Primary aldosteronism
Glucocorticoid Therapy
Intracellular Shift
- Treatment for diabetic acidosis
- Alkalosis, metabolic or respiratory
```
180
S/S hypokalemia
```
Laboratory Values: Serum K below 3.5
Skeletal Muscles:
- tenderness, paresthesias, cramps
- weakness
- flabbiness
- paralysis
Cardiovascular System:
- Postural hypotension
- Increased sensitivity to digitalis
- Arrhythmias and tachycardia
Gastrointestinal Tract:
- Anorexia
- Vomiting
- Abdominal Distention
- Paralytic Ileus
Respiratory Muscles:
- Shortness of breath
- Shallow breathing
Kidneys:
- Polyuria
- Nocturia
- Low osmolality and low specific gravity
Thirst
Central Nervous System Function
- Confusion
- Depression
Acid-Base Balance: metabolic alkalosis
```
181
Causes of hyperkalemia
```
Excessive Intake or Gain
- Excessive Oral Intake
- Excessive or rapid parenteral infusion
- Tissue trauma, burns, and massive crushing injuries
Inadequate Renal Losses
- Renal failure
- Adrenal Insufficiency; Addison's Disease
- Potassium sparing diuretics
```
182
S/S hyperkalemia
```
Laboratory values: Serum K above 5.5 meq/l
Neural and skeletal muscle activity
- Paresthesias
- Weakness and dizziness
- Muscle cramps
Smooth muscle activity of the GI tract
- Nausea, diarrhea
- Intestinal colic and GI distress
```
Cardiac Electrophysiology
- Peaked T waves, depressed S-T segment
- Depressed P wave and widening of QRS segment
- Cardiac Arrest
