Exam 1 Flashcards
Potassium Ranges (hypo/hyperkalemia)
3.5 - 5.3 mEq/L
Normal Sodium Ranges
135 - 145 mEq/L
Normal Calcium Range
9 - 11 mg/dL
Serum Osmolality normal range
275-295 mOsm/Kg
Hematocrit - males normal range
41% - 50%
Hematocrit - females normal range
36% - 48%
Chloride Ranges
95-105 mEq/L
Phosphorus Range
2.5 - 4.5 mg/dL
Magnesium Range
1.5 - 2.5 mEq/L
pH range
7.35 - 7.45 (acidosis to alkalosis)
PaCO2 range
35 - 45 (alkalosis to acidosis)
PaO2 range
75-100
HCO3
24 - 28 (acidosis to alkalosis)
Base Excess (BE)
-3 to +3
ROME
Respiratory
Opposite Direction (pH and CO2)
Metabolic
Equal (same direction) (pH and HCO3)
How is Sodium (Na+) regulated?
Renal reabsorption or excretion.
ADH (AntiDiuretic Hormone) keeps urine, which dilutes Na+.
Aldosterone increases Na+ reabsorption in the collecting duct of nephrons, which increases Na+
What is the function of Sodium (Na+)
Hypo/Hyper effect the neurological system!!
Major regulator of water balance
Regulates ECF volume and distribution
Maintains blood volume
Transmits nerve impulses
Contracts muscles
Hyponatremia Clinical Manifestations
<135
>Usually due to drains (NG tube or suctioning) diuretic use, fluid loss, diarrhea, sweating (diaphoresis)
>Results in muscle cramps, tremors, confusion, seizures
Hyponatremia types
2 mains of hyponatremia:
1. Hypovolemic –> loss of fluid and sodium TOGETHER
2. Hypervolemic –> excess amount of water
Hyponatremia RN Assessment
Mild –> fatigue, nausea vomiting, headache
Medium –> General malaise, altered LOC, lethargy
High –> Seizures, coma, respiratory arrest
Hyponatremia Signs & Symptoms
Heart –>
Hypovolemic: increased HR, Decreased BP, Increased RR
Hypervolemic: increased HR, Increased BP, Decreased RR
ST Elevations on ECG b/c the ventricles are cramping up
SOB and dyspnea
Nausea vomiting and abdominal cramping
Restlessness and confusion, which leads to seizures and coma
Addison’s Disease
Hyponatremia RN Interventions
Add salt!
>Administer IV saline sol’n (depending on what type of hyponatremia). Isotonic for hypovolemia.
>Diuretics or dialysis if there is hypervolemia.
> daily weights
> safety –> orthostatic hypertension risk
> Airway precuation –> patient is probably NPO due to confusion
> Limit water intake for patients with hypervolemic hyponatremia
>Teach about high salt diet -> avoid salad dressing, sauces, canned veggie juices, chinese food/ cup of noodle soup
Hypernatremia
Na+ > 145 mEq/L
Sodium maintains blood pressure and blood volume
Caused by:
Loss of fluid (infection, diarrhea, persistent sweating)
Diabetes –> dehydrates because it causes ADH insufficiency
Sodium Excretion Impaired –> Renal problems (caused by corticosteroids sometimes)
Too much processed foods
Deprivation of fluids (hemoconcentration)
IV Hypertonic sol’n excess (too much 3-5% saline)
Vitamins / sodium supplements like alka seltzer, aspirin, cough syrups
Aldosterone excess –>
(hypercortisolism) holds Na+ in the body, resulting in weight gain and moon face (Cushings’ disease)
Hypernatremia Signs & Symptoms
High Sodium –> Big and Bloated
no “FRIED” foods for you!
F: fever,flushed skin
R: Restlesness/confused
I: increased fluid retention
E: extremely confused
D: decreased urinary output, dry skin
Hypernatremia Nursing Interventions
> Restrict Na+ Intake from diet
Patient safety – they’re confused and agitated
MD may order an isotonic or hypotonic IV sol’n like 0.45% NS given slowly to rehydrate the cell. the patient is at risk for cerebral edema if given too quickly (confusion is an initial sign).
Educate about diet and signs/symptoms of increased salt level
Function of Potassium
Hypo/Hyper affects the cardiac system!
Vital for skeletal, cardiac, and smooth muscle regulation.
It’s concentrated mostly inside the cell (ICF).
Maintains acid/base balance.
Helps transmit nerve and other electrical impulses.
How is Potassium (K+) regulated?
Renal excretion and conservation.
Aldosterone increases K+ excretion.
Insulin helps move K+ into the cells.
Tissue damage and acidosis shift K+ out of the cells and into the ECF.
Hypokalemia (Causes)
< 3.5 mEq/L; <=2.5 is DANGEROUS!!
Caused by: “DITCH”
D: drugs, such as laxatives, diuretics, or corticosteroids
I: inadequate intake, due to NPO, anorexia, or really sick and not eating.
T: too much water intake dilutes K+
C: Cushing Syndrome = too much aldosterone
H: heavy fluid loss due to NG suction, vomiting, diarrhea, wounds
also hyper-insulinism
Hypokalemia S&S
Everything is slow & low
K+ plays an important role in muscle and nerve conduction. So, low K+ becomes slow and low (exhausted body):
weak, thready pulse
orthostatic HTN
Decreased bowl sounds
decreased deep tendon reflexes
flaccid paralysis (late with very low paralysis)
confusion
Shallow respirations/ diminished breath sounds (no K+ means low ability of accessory muscles)
7Ls:
Lethargic
Low/shallow breathing
Lethal cardiac changes
Loss of urine (diuretics)
Leg cramps
limp muscles
low BP & HR
EKG –> depressed ST segment, flat or inverted T wave, prominent U wave
Hypokalemia RN Interventions
Monitor:
> Heart rhythms
> respiratory status
> GI & Renal status
> I/O
> Magnesium (Mg+ and K+ are linked)
> Glucose, Ca2+, Na+ because of the roles in cell transport
> K+ supplement for 2.5 - 3.5; give with food to avoid GI upset
> K+ infusion for <2.5; this is NEVER given as an IV Push, or IM or SubQ. Give slowly via IV. no more than 20 mEq/L per hour. Watch for phlebitis and infiltration
> Hold diuretics that waste K+ and cause urination. Notify the MD. May switch to K+ sparing such as spironolactone/aldactone, dyazide, maxide, triamterene.
> Check apical pulse and AM labs before giving digoxin.
Potassium rich foods
“Potassium”
P = Potatoes, pork
O = oranges
T = tomatoes
A = avocados
S = strawberries
S = Spinach
I = fish
U = mushrooms
M = melons / cantaloupe
Also carrots, raisins, bananas
Hyperkalemia
<5.0; if >=7.0 DANGEROUS
Causes: body “CARED” too much for K+”
C = cellular mov’t of K+ from ICF to ECF due to trauma like burns/tissue damage/ acidosis
A = Adrenal insufficiency (Addison’s disease)
R = renal failure
E = excessive K+ intake
D = drugs (K+ sparing diuretics, NSAIDs, Ace Inhibitors)
Hyperkalemia S &S
“MURDER”
M = muscle weakness
U = low Urine production
R = respiratory failure due to muscle weakness or seizures
D = decreased cardiac contractility (weak pulse, low BP)
E = early signs of muscle twitching / cramping. Late sign is profound muscle weakness
R = rhythm changes: tall, peaked T wave; flat P wave; wide QRS; prolonged PR interval
Hyperkalemia RN interventions
Monitor cardiac, respiratory, neuromuscular, and GI status
Stop IV K+ infusions and hold supplements
Initiate K+ restricted diet
Prepare patient for dialysis
Kayexalate sometimes order PO or enema; it causes GI N+ absorption which promotes K+ excretion
MD may switch to K+ wasting diuretics (thiazides or lasiz/furosemide)
MD may order hypertonic sol’n or glucose and insulin to pull K+ back into the cell.
Calcium Regulation
PTH (ParaThyroid Hormone) and Calcitriol increase serum Ca2+ levels
Calcitonin decreases Ca2+ levels
Calcium Function
Vital in regulating muscle contraction, neuromuscular function, and cardiac function.
Sedative effect on neuromuscular transmission!
Forms bones and teeth
Transmits nerve impulses
Maintains cardiac pacemaker (automaticity)
Blood clotting
Actives enzymes such as pancreatic lipase and phospholipase
Ca2+ and Mg+ are aligned
Ca2+ and Phosphate are opposite
Hypocalcemia
<9.0
Manifestations:
Trousseau’s
Chvostek’s
3 Bs: Bones, Blood, heart Beats
Causes: “LOW CALI”
L: low PTH due to a thyroidectomy, pancreatitis
O: oral meds, such as corticosteroids, anti-seizure meds such as dilantin and phenobarbital; Phosphate enemas, Citrate (anticoagulant used in blood products)
W: wound drain (GI wounds)
C: chronic diseases like celiac and crohn’s/ chronic kidney issues, diuretics
A: antibiotics
L: low Vit D or Mg2+ levels
I: Increased Phosphate in the blood
hypocalcemia S&S
Weak bones / fractures
Weak clotting
Weak heart beats / dysrhythmias
Heart: excitability = ventricular tachycardia
EKG: prolonged QT and ST
Slow clotting factors
Lungs = narrowing of the windpipe, stridor
Dyspnea and crackles
GI = massive diarrhea, intestinal cramping
Neurological == seizures, confusion, personality changes, dementia, psychosis
Musculoskeletal:
Trousseau’s and Chvostek’s
Hypocalcemia Nursing Interventions
“FAST”
F = foods high in calcium: Leafy greens, sardines/tofu, dairy
A = Administer meds like calcium acetate, IV Calcium, Oral Calcium with vit D, aluminum hydroxide
S = safety, risk for falls/fracture/ bleeding. Fracture precautions / fall precautions
low clotting factors / risk for bleeding. Don’t bear down when pooping!
cardiac dysrhythmias
T = Teach
take Ca2+ boosters and avoid Ca2+ depletors like laxatives and loop diuretics.
Magnesium Regulation
Kidneys conserve and excrete Mg2+
Intestinal absorption is increased by Vit D and PTH (which means the serum levels are reduced by Vit D and PTH)
Magnesium Function
Relaxes muscle contractions!
Important for DNA synthesis, regulates cardiac & neuromuscular function
Intracellular Metabolism (transfer & store energy)
Operates the Na+ / K+ pump
Transmits nerve impulses
Regulates cardiac function
Regulates PTH, which regulates Ca2+
Metabolizes carbs, lipids, proteins
Regulates BP
Absorbed in the small intestine and excreted via the kidneys
Hypomagnasemia
<1.6 mg/dL
Causes: “LOW MAG”
L = Limited intake of Mg+ due to starvation
O = other electrolyte issues, such as hypOcalcemia and hypOkalemia
W= wasting Mg+ in the kidneys –> loop/furosemide or thiazide diuretics, cyclosporines
M = malabsorption issues due to Crohn’s, Celiac, vomiting.
Also proton-pump inhibitors like protonix, prilosec, any that end in ‘zole’ like Prazole
A = Alcoholism due to poor dietary habits, and alcohol stimulates the kidney to waste Mg+, and causes acute pancreatitis
G = Glycemic Issues, for example patients in DKA or who need insulin
hypomagnasemia S&S
“TWITCHING”
Neuromuscular excitability
T = Trousseau’s
W = weak respirations
I = irritability
T = torsades de pointes: goes along with alcoholism. It’s a lethal, abnormal heart rhythm. Tetany = abnormal twitching
C = Cardiac changes: moderately low = tall T waves and depressed ST segments
Severely low = prolonged PR and QT intervals with wide QRS complexes.
Wide QT –> Torsades indicator
also Chvostek’s
H = HTN and Hyper-reflexia
I = involuntary movement
N = nousea
G = GI issues - decreased bowel sounds and mobility
Hypomagnasemia RN Interventions
Monitor cardiac, GI, respiratory, neuro status
Put them on a cardiac monitor for EKG changes
MD might order K+ supplements, Ca2+ supplements w/ Vit D
*Administer Mg Sulfate IV infusion. Have to monitor the Mg levels very closely to avoid hypermagnasemia. Check deep tendon reflexes. Hypomagnasemia = lots of reflexes; if you get to hypermagnasemia they’re absent.
Seizure precautions
Oral Mg may cause diarrhea
Foods high in Mg+
Avocado
Green leafy veggies
Peanut butter and pork
Fish (canned tuna, mackeral)
Dark chocolate
Cauliflower
Legumes
nuts
Oranges
Milk
Hypermagnesemia
> 2.6 mg/dL
Causes: “MAG”
This is less common than hypomagnasemia. Can happen if you’re trying to correct hypomag.
M = Mg+ containing antacids and laxatives like magnesium sulfate - mylanta or malox
A = Addison’s disease (adrenal insufficiency)
G = Glomerular filtration insufficiency or renal failure. Filtration <30mL/min. Kidneys are conserving too much Mg+.
Hypermagnasemia S&S
Mild cases are without symptoms. Symptoms only present with very high Mg+ levels.
“LETHARGIC”
L = profound lethargy
E = EKG changes: PR and QT interval prolonged and wide QRS complex
T = tendon reflexes are absent / dimished
H = hypOtension
A = Arrhythmias, such as bradycardia or heart blocks
R = respiratory arrest
G = GI issues like nausea and vomiting
I = impaired breathing due to the weakness of the skeletal muscles
C = Cardiac Arrest
Hypermagnasemia RN Interventions
Monitor cardiac, respiratory, neuro, GI, renal system. Place the patient on a cardiac monitor for EKG changes.
Ensure patient safety due to lethargy / drowsiness
Prevention: avoid giving the patient renal failure due to excessive Mg+ containing antacids / laxatives, checking for high Mg+ during infusions, not giving foods high in Mg+
MD order of K+ wasting diuretics like furosemide/lasix (loop diuretics)
If in renal failure, prep for dialysis
IV Ca2+ can be ordered to reverse side effects of Mg+, although have to watch for infiltration. A central line is preferred for this.
Chloride (Cl-) Regulation
Excreted and reabsorbed along with Na+ in the kidneys
Aldosterone increases chloride reabsorption with Sodium
Chloride (Cl-) Function
Linked with Na+ –> same impacts
HCl production - aids in digestion
Helps Na+ maintain ECF balance and vascular volume
Regulates acid/base balance
Buggers O2 / CO2 exchange in RBCs
Hypochloremia
<97
Causes: “CHAMP”
C: Chloride loss from fluid loss, like vomiting, diarrhea, NGT suctioning, sweating, fever, or burns
H: HypOnatremia
A: Addison’s disease and renal crisis
M: Medications such as diuretics
P: pH imbalances from metabolic alkalosis (fluid loss from GI from vomiting)
Hypochloremia S&S
Same as hypOnatremia!
Generally depressed and deflated.
Hypotension (low BP)
EKG: dysrhythmias
Respiratory: depressed and deflated – dyspnea from a deflated diaphragm muscle
SOB
Neugological depressed – agitation, irritability, seizures, coma, confusion
GI: diarrhea, nausea, vomiting
Musculoskeletal: tremors and muscle cramps
Hypochloremia RN interventions
Give salt, because Cl- will follow salt!
IV NS or 0.45% NS
Avoid free water
Hyperchloremia
> 107
Same as hypERnatremia
Causes:
Trauma (head injury)
Dehydration
Hyperparathyroidism
Respiratory alkalosis (hyperventilating)
Hyperchloremia S&S
Same as hypERnatremia (big and bloated!)
Hypertension
EKG: dysrthythmias
Lung: tachypnea, respiratory alkalosis
Neurological: ICP, cognitive changes, altered level of consciousness
GI: diarrhea, diuresis, dehydration
MSK: muscle weakness
Hyperchloremia RN interventions
Treat the causes!
Restore fluid imbalance via IV LR (lactated ringers) or Sodium Bicarbonate
Phosphate Regulation
2.5 - 4.5 mg/dL
Excretion and reabsorption by the kidneys
PTH decreases phosphate levels by increasing renal excretion
Opposite relationship with Ca2+ –> increasing Ca2+ will decrease phosphate levels and vice versa
Vit D plays a role in phosphate absorption
Phosphate functions
forming bones and teeth (stored mainly in the bone)
Metabolizes carbs, proteins, and fats
Cellular metabolism: producing ATP and DNA
Muscle, nerve, and RBC function
Regulate acid/base
Regulate Ca2+ levels
Hypophosphatemia Causes
<2.7 mg/dL
low “PHOSPHATE”
P = Pharmacy: aluminum hydroxide and aluminum based antacids cause malabsorption which reduces phosphate absorption. Also, lack of Vit D.
H = Hyperparathyroidism: PTH is too high in the serum, which inhibits the reabsorption of phosphate in the kidneys and it is excreted.
O = oncogenic osteomalacia –> kidneys waste phosphate due to bones softening.
S = syndrome of refeeding. Watch for this on patients TPN; occurs in malnutrition or starvation pathologies. The body was in starvation mode and when it gets nutrients, it releases way too much insulin. It then releases phosphate and magnesium to help digest (but they were already too low to begin with)
P: pulmonary issues due to respiratory alkalosis b/c phosphate moves out of the blood and into the cell.
H: Hyperglycemia leads to glycosuria, polyuria, and ketoacidosis. Causes the kidney to waste phosphate.
A: Alcoholism impacts the body’s ability to absorb phosphate. plus, alcoholism is associated with malnutrition.
T: thermal burns – extreme burns causes a shift of phosphate out of the blood and into the cells.
E: electrolyte imbalances cause low phosphate levels like hypERcalcemia, hypOmagnasemia, and hypOkalemia.
Hypophosphatemia S&S
“BROKEN” (the patient is at risk for bone fractures and every system of the body is breaking down!)
B = breathing problems due to muscle weakness
R = Rhabdomyolysis, an electrolyte disturbance due to low levels of Phosphate, K+. Affects the muscles and causes rapid necrosis of the muscles. This releases myoglobulin into the blood, which is toxic to the kidneys causing tea-colored urine, muscle-weakness, and pain.
also deep tendon reflexes will decrease
O = osteomalacia: bone fractures, deformities
Also, Cardiac outpute is decreased
K= kills immune system through decreased platelet aggregation (increased bleeding)
E = extreme weakness and ecchymoses ( due to decreased platelets)
N = neuro changes such as irritability, confusion, seizures
Hypophosphatemia RN Interventions
MD orders oral phosphorous w/ vit D to help with absorbption
Monitor patients on TPN for muscle pain and weakness (rhabdomyolosis), also re-feeding syndrome
Ensure patient safety (bed down, call light in reach) due to risk for fractures and confusion
Encourage foods rich in phosphate
If <1.7 the MD may order IV phosphate. Be careful with patients who are in renal failure, because they can’t clear the phosphate.
Monitor Ca2+ level, as this can decrease if the phosphate gets higher.
Monitor phosphate levels to avoid hyperphosphatemia
Monitor EKG changes
Foods rich in Phosphate
Fish
Organ meats
Nuts
Pork
Beef
Whole grains
(essentially meat)
Hyperphosphatemia Causes
> 4.5 mg/dL
“PHOSHI” –> note that Phoslo is a phosphate binding drug that patients in renal failure take to keep phosphate low (because the kidneys can’t get rid of phosphate anymore)
P: Phospho-soda overuse. Laxatives and enema overuse
H: HypOparathyroidism causes high phos levels due to PTH being too low. PTH causes the kidneys to keep too much phosphate.
O: overuse of Vit D, which supports absorption of phosphate
S: syndrome of tumor lysis, which occurs with chemo. Chemo kills off good and bad cells. This lets out the phosphate which is normally inside the cell into the ECF.
H: rHabdomyolysis –> rapid necrosis of muscles. Dead muscles release myoglobulin into the blood, which is toxic to the kidneys, which sends the patient into renal failure and phosphate excretion is decreased.
I: insuffiency of the kidneys (ESRF) which means phosphate won’t be excreted.
Hyperphosphatemia S&S
Same as the symptoms of hypOcalcemia
Confusion
Hyperactive reflexes
Anorexia
Muscle spasms in calves/feet, seizures, tetany
Positive Trousseau’s sign and Chvostek’s sign
Hyperphosphatemia RN Interventions
Administer phosphate-binding drugs (Phoslo) which works on the GI system. Give with food or right after a meal.
Don’t give phosphate laxatives or enemas.
Restrict foods that are high in phosphorous.
Prepare patient for dialysis due to renal failure.
Bicarbonate (HCO3-) regulation
Excretion and reabsorption by the kidneys
Regeneration by the kidneys
Bicarbonate Function
Major body buffer involved in acid/base regulation
Isotonic
Isotonic IV Solutions: 0.9 NS, LR, D5W
Hypertonic
Hypertonic IV Solutions: D5 LR, D10W, D20W, D50W, D5 0.45%, D5 NS, 3% NaCl, 5 % NaCl
Hypotonic
Hypotonic solutions have less salt (lower osmolality) than the cells, so water goes into the cell.
1/2 NS or 0.45%
1/3 NS or 0.33%
1/4 or 0.25% NS
NEVER use with ICP patients
NEVER use with diabetics who are at risk for HYPERglycemia
Used to help with cellular dehydration, which is when the cells are thirsty – hypERnatremia and HHNS (type 2 diabetic disorder with uncontrolled high blood sugar, which causes cellular dehydration).
Also used with DKA (type 1 diabetics; involves burning ketones instead of sugar for energy –> causes dehydrated cells)
D5W
isotonic in the bag
Hypotonic in the body
due to sugar!
NEVER use with diabetics who are at risk for HYPERglycemia
Hypotonic RN Interventions
NEVER given for ICP patients
Give SLOWLY to prevent cellular edema
Watch out for hypovolemia signs and symptoms such as tachycardia, decreased BP, cellular edema, and cell damage.
Be cautious with liver disease, trauma, burn patients.
HypERtonic fluid
The fluid is escaping from inside the cell to outside the cell.
Hypertonic solutions have higher concentrations than the ICF. Thick, concentrated solution - higher osmolality.
Will pull fluids out of the cells and making the cell more skinny.
3% NS
5% NS
D10W
D5.5 NS
D5LR
D50W
Used for hypOvolemia, heat related (heat exhaustion)
HypERtonic RN Interventions
Infuse slowly, no boluses! too quick could cause a massive fluid shift that can domino into cellular dehydration and fluid volume overload.
S&S –> bounding pulses, high BP, jugular vein distention, crackles, edema.
Isotonic fluids
“iso-perfect” Causes no fluid shifts, so fluid remains in the vesicle. Used primarily to treat fluid volume deficit.
Same osmolality as body fluids
0.9% NS
LR (which contain potassium, so no liver impaired patients! like cirrhosis)
D5W is isotonic in the bag and hypotonic in the body due to sugar
Monitor for S&S of hypovolemia: tachycardia, weak pulse, hypotension.
Monitor for S&S of hypervolemia: HTN, bounding pulse, crackles, dyspnea, jugular vein distention, extra heart sounds such as S3.
Fluid Volume Deficit
Causes
Fluid output> Fluid intake, which causes hypOvolemia / dehydration
Causes:
Loss of fluids from thoracentesis, paracentesis, hemorrhage, NG tube, trauma, GI losses - vomiting and diarrhea, polyuria (caused by diabetes or diuretics)
Third spacing, such as caused by burns and ascites (volume from the vessels goes to the cells due to truama)
Fluid Volume Deficit S &S
Decreased weight overall
Increased HR (weak and thready)
Decreased BP
Decreased CVP (Central Venous Pressure)
Increased RR
Decreased Urinary Output due to not enough fluid to urinate or because they’re holding on to it.
Decreased skin turgor (tenting), dry mucous membranes, thirst
Flat neck veins
Labs - INCREASED serum osmolality, urine specific gravity, hematocrit, Na+, BUN
Fluid Volume Deficit Treatment
Replace the fluid loss! either PO or IV
Monitor for fluid volume overload when using IV
Safety precautions – orthostatic HTN is a risk (rise slowly)
Daily I/O
Daily Weight –> same time, same scale, same clothes
Fluid Volume Excess Causes
=Hypervolemia
Caused by:
Heart Failure
Kidney dysfunction (can’t excrete excess volume)
Cirrhosis
Increased Na+ intake
FVE S&S
Increased weight due to water weight
increased HR because the heart wants to push volume forward. Bounding HR!
Increased BP due to increased volume
Increased CVP
Wet lung sounds (crackles) due to the backflow of fluids from the heart.
Polyuria, large amounts of dilute urine from the kidney
Edema in the skin
Distended neck veins (JVD = jugular vein distention)
Labs: diluted, DECREASED:
serum osmolality, urine specific gravity, hematocrit, Na+, BUN
FVE Treatment
Low Na+ diet
Daily I/O and weight
Diuretics
high /semi fowler’s position
Respiratory Acidosis Pathophysiology
Hypoventilation –> causes CO2 to increase in the blood (hypercapnia), causing a drop in blood pH. Hypercapnia then causes papilledema (swelling of the optic nerve) and peripheral vasodilation.
Narcotic overdose
Chest Trauma
Airway Obstruction
HypERkalemia
Hypoventilation, air trapping, bronchoconstriction
Secondary to neuro-muscular disorder, COPD, asthma, sleep apnea, pneumonia, sedation.
Respiratory Acidosis
pH<7.35
CO2> 45
Kidneys may compensate by retaining HCO3 (HCO3 will be >28)
Respiratory center is stimulated as well to increase the RR so that you exhale CO2 and raise the pH
Respiratory Acidosis S&S
HypERkalemia
Tachycardia
Headache, feeling of fullness
Mental cloudiness, decreased LOC
dizziness, muscle twitching, seizures
dysrhythmias due to hypERkalemia
Hypotension, which can lead to CNS depression
Respiratory Acidosis Nursing Interventions
> After the primary assessment is the focused respiratory assessment - look at mental status and lung sounds.
Monitor ABG
Monitor K+
Vital Signs –> tachycardia, LOC, safety protocols
Correct the underlying cause
Restore effective gas exchange in the lungs: symptoms are activity intolerance and SOB.
Chest Physiotherapy
O2
Fluids
Fowlers position
Meds: bronchodilators to open up airways and decrease bronchospasms; antibiotics to treat infections
Deep breathing and coughing
Oral suction
Respiratory Acidosis Patient Education
Prevention
Pursed Lip Breathing
Suctioning airways (even in infants)
Respiratory Acidosis Diagnostic Tests
ABG
PFT
ECG
X-ray
Sputum studies
Respiratory Alkalosis
Due to an increase of HCO3
ABGs:
pH >7.45; CO2 <35
Compensation: kidneys conserve H and get rid of HCO3
HypOkalemia
HypOcalcemia
Respiratory center compensates by becoming depressed, decreasing the rate and depth to retain CO2
Respiratory Alkalosis Clinical Manifestations
HyPERventilation causes a CO2 deficit, which leads to respiratory alkalosis due to a decreased concentration of carbonic acid (H2CO3) in the blood.
HypERventilation is rapid breathing, causing the person to feel dizzy, cramping of the hands and feet, and the feeling that you’ll black out.
HypOkalemia, HypOcalcemia - tetany
Cardiac arrythmias
Blurred vision
Headache
Warm/flushed skin
high pulse rate
muscle weakness
Dyspnea, chest tightness, dizziness, anxiety, panic, blurred vision
Hyperthermia can cause the hyperventilation
Hypokalemia –> K+ moves out from the cells in exchange for H+ ions
HypOcalcemia –> alkalosis causes binding of Ca2+ to albumin, causing symptoms of hypocalcemia: numbness and tingling of the mouth and fingers.
Trousseaou, Chvostek
Decreased/normal BP
Tachycardia
Deep, rapid breathing
Respiratory Alkalosis Nursing Interventions
Provide calm and reduce the respiratory rate.
If on a ventilator, decrease the tidal volume to increase the CO2 level.
Monitor labs, ECG,neurologic changes
Assess lungs and respiratory style
Assess cardiac rhythms
Give O2 as needed
A paper bag on someone’s head can increase the CO2 level, but be careful not to induce hypoxia.
Consider referral to counseling for anxiety
Give anti-anxiety meds (diazepam/valium)
Respiratory Alkalosis Patient Education
Relaxation techniques
Stress management
Keep aspirin out of the reach of children
Maintain safety protocols
Seek help for anxiety
Respiratory Alkalosis Diagnostic Tests
ABG
ECG
WBC, Sputum testing to rule out infection
Respiratory Alkalosis Failure to Rescue
HypOkalemia related to dysrhythmias can lead to ventricular fibrillation
Increased RR, decreased BP –> patient tires out and can no longer continue breathing
Assess the potential of respiratory arrest and if the patient is deteriorating.
Metabolic Acidosis
Metabolic acidosis is due to DKA, Shock, Sepsis
pH<7.35; HCO3<24
Also likely a low O2 level<75
Metabolic Acidosis Causes / Risk Factors
Eating Disorders
Laxative Abuse
Renal failure
Aspirin turns into acid when it breaks down, which causes metabolic acidosis.
GI: starvation, malnutrition
Diarrhea (mostly in children)
Metabolic Acidosis Clinical Manifestations
Decreased pH; HCO3<24
HypOmagnasemia
Compensation from the kidneys - conservation of HCO3
HypOtensive
Decreased BP
HypERkalemia
Abdominal pain, nausea, vomiting
Kaussmal respirations (rapid, deep breathing)
Mental status changes
Alcoholic keto-acidosis due to abrupt alcohol cessation; treated with 5% dextrose in NS, Mg+/K+ replacements, and optional thiamine and folate treatment
Metabolic Acidosis Diagnostics
ABG
ECG
Electrolyte Panel
Metabolic Acidosis Nursing interventions
I/O, Daily Weight
K+ and ECG
Vital Signs
LOC
GI Function
Protect from injury
Hydration - (0.9% NS)
Replace electrolytes
Insulin
HCO3
Sodium Lactate
Meds to prevent diarrhea
Meds for DKA/ dialysis
Metabolic Acidosis Complications
Hypotension, dysrthythmias, decreased LOC, hyperkalemia can lead to lethal cardiac rhythms such as ventrical fibrillation
Metabolic Acidosis Patient Education
Adequate nutrition
Take meds as prescribed
Educate about signs and symptoms of metabolic acidosis if the patient is on meds such as diuretics, ACE inhibitors, and anticonvulsants
Metabolic Alkalosis
High pH
High HCO3 >28
High respirations as compensation
Metabolic Alkalosis Pathophysiology
Loss of H due to vomiting, NG tube suctioning, increase of bicarbonate (Alka seltzer)
Purging / on purpose vomiting, diarrhea, abuse of laxatives or diuretics. Anything that makes the stomach contents leave the body.
Hypochloremia –> Cl- is replaced by HCO3- leading to increased alkalinity
Post-cardiac surgery in young children.
Metabolic Alkalosis common causes/risk factors
severe vomiting
NG suctioning
Diuretic therapy
Lots of black licorice
Excessive use of sodium bicarbonate (alka seltzer)
Metabolic Alkalosis Labs/Diagnostics
ABG
ECG
Electrolyte panel
HypOkalemia
HypOcalcemia
HypOnatremia
Metabolic Alkalosis Clinical Manifestations
confusion
Nausea, vomiting, diarrhea
Tremors, muscle cramps, tingling of fingers and toes
HypOkalemia
HypOcalcemia
HypOnatremia
Excitatory effect on the CNS
Restlessness followed by lethargy
Dysrhythmias
Bradypnea
HypOtension
Metabolic Alkalosis Nursing Intervention
Restore hydration and electrolytes
Monitor I/O, ABG
ECG, vital signs
Protect patient from injury
Meds such as 0.90% NS, histamine 2 receptor antagonist to help reduce the loss of H from GI damage
Identify altered temperature regulation, irregular breathing pattern, fall risks
Hypokalemia, Hypocalcemia, Hyponatremia
Metabolic Alkalosis Complications
Hypotension, dysrhythmias, drops in the respiratory rate to maintain O2 (compensation)
Metabolic Alkalosis Education
Teach about proper positioning in infants to avoid aspiration
Take antacids appropriately
Signs / Symptoms of hypOkalemia
Physiology of Oxygenation
Cilia protect the airway from unwanted, small particles.
Epiglotis helps protect foods from passing into the airway system
Trachea bifurcates, gives access to right and left lungs
Right lung has 3 lobes and is small/shorter than the left lung, which has 2 lobes
Pleural lining helps protect, aids in respiration, has two layers: visceral pleura (lung side) and parietal (rib side)
Early S&S of Hypoxia
Restlessness
Confusion
Anxiety
Increased BP
Increased HR
Increased RR
Dyspnea
Late S&S of Hypoxia
Decreased LOC
Decreased activity level
Hypotension
Bradycardia
Metabolic Acidosis
Cyanosis
Chronic S&S of Hypoxia
Clubbing of the fingers and toes
Peripheral edema
Right-sided heart failure
Respiratory Acidosis
O2 saturation <87%
RR Normal Ranges
Adults: 12-20
Newborn: 30-80
Tachypnea
breathing too fast (RR>20 for adults and >80 for infants)
Bradypnea
Breathing too slow (RR<10 for adults and <30 for infants)
Leads to inadequate O2 and possibly too high CO2
Apnea
No breathing, can lead to cardiac arrest.
Obesity can cause apnea.
Dyspnea
labored breathing - subjective assessment by the patient that they’re having trouble breathing
Orthopnea
Can’t breathe in certain physical positions, like on their back.
Asthma and pneumonia can cause orthopnea.
Hypoxemia
mild impairment in oxygenation, can lead to hypoxia
Pneumothorax
lung collapse; asymmetrical respiration.
While pneumothorax may occur spontaneously, most occur as the result of trauma.
Oxygenation RN Assessment
Physical:
Patency
Bilateral symmetry
View anterior & posterior chest
Auscultate lungs
Gag reflex & need for suctioning to prevent aspiration
Ability to cough up sputum and need for percusion/vibration/positioning
History:
Smoking history
Corticosteroid use: if stopped abruptly can cause hypOtension, tachycardia, cardiovascular collapse
Oxygenation Diagnostic Tests
Sputum (use coughing technique or suction sample)
ABG
Pulse Ox (expect 95+)
PFTs- changes in lung function
Peak Expiratory Flow Rate (PEFR): for asthma, gives an indication of improvement
Chest X-ray for pneumothorax, hemothorax, pneumonia
Pulmonary Angiogram
Pulmonary V/Q scans for oxygenation and perfusion
Bronchoscopy - to view the pulmonary structures
Thoracentesis - to get fluid from between the pleural lining for testing
Oxygenation Treatment
O2 as indicated (be careful with COPD)
Incentive Spirometry – air flow of lung volumes (how much/how quickly exhale)
Lung reduction surgery - diffuse emphysema
Frequent turning b/c tissue hypoxia increases skin breakdown
Deep breathing exercises
Positioning - fowlers and possibly (prone)
Encourage smoking cessation
Pulmonary hygeine, suctioning
Chest physiotherapy
Bronchoscopy to remove mucus
Thoracentesis to remove fluid from interpleural space
Kussmaul Respirations
Deep, rapid exhalations.
Increases CO2 exhalation
Indicates respiratory alkalosis
Cheyne Stokes Respirations
rapid breathing, then shallow and apnea
Indicative of HF, increased ICP, drug overdose
Biot Respirations
shallow type breathing with apnea
Indicative of neurological issues
Tracheal sounds
Normal tracheal sounds are harsh and high pitched. These should diminish over the bronchi and become almost nonexistent over the alveoli.
The strongest vibration should be felt over the trachea.
Bronchiovascular sounds
Medium in loudness and pitch. They are heard between the scapulae, posteriorly and next to the sternum.
Vesicular sounds
soft and low pitched.
They are longer on inhalation and exhalation
Bronchial sounds
loud, high pitched sounds next to the trachea
Stridor
wheezing when breathing in, usually in the trachea area.
High pitched sound; most often can be heard when people are taken off the ventilator.
Caused by narrow airway passages.
Wheezing
narrowing of the bronchi, heard on expiration
Crackles / rales
popping / bubbly type sound like pouring milk over rice krispies.
Caused by fluid in the lung and atelectasis.
Coughing can clear it up.
Rhonchi
low pitched sound that is continuous throughout inspiration.
It’s a blockage of the airway, a loud and rumbling sound, usually caused by sputum that could be cleared by coughing.
Pleural rub
low pitched, dry grating, rubbing sound caused by inflamed pleura.
Present during inspiration and expiration.
Absent lung sounds
collapsed lungs or surgically removed lobes.
Nasal Canula
Used for patients who are noncritical, with minor breathing problems. Or for those who can’t/won’t wear a mask.
O2 concentrations of 24-44%
Flow rates 1-6L
Always use humidification for >4L/min
Provide nose care every 4 hours
Face Mask
Used for clients who require a moderate flow rate for a short period of time.
40-50% O2
Flow rates 5-8L/min
Because CO2 can build up, don’t use a flow rate lower than 6L/min; use a humidifier above 4L/min
Replace sterile water at least every 24 hrs or per facility policy
Nonrebreather mask
used when CO2 is too high and the patient needs more O2.
Always used with higher than 6L/min
The reservoir fills with pure O2, allowing the patient to breath pure O2. (keep this at least 2/3 inflated as this is the O2 source!!)
95-100% O2
Flow rates 10-15 L/min
Face Tent
used for patients who are getting claustrophobic with the face mask, but it’s hard to keep in place.
24-100% O2
Flow rates of at least 10L/min
Venturi Mask
used for clients with COPD when an accurate FiO2 is essential and CO2 buildup has to be kept to a minimum.
24-50%; 4-12L
No humidifiers.
Color-coded adaptors based on flow rate.
Interferes with eating and talking, so might be paired with nasal canula during meals.
Tracheotomy mask
Small mask that fits over the tracheostomy site.
Flow rate is usually 10L/min
CPAP (Continuous Positive Airway Pressure)
Commonly used for sleep apnea because the continuous pressure keeps the airway open.
Pressure is usually between 5-20 cm of water.
BiPAP (Bilevel Positive Airway Pressure)
Provides assistance during inspiration and keeps the airway open during exhalation.
It increases the amount of air in the lungs at the end of expiration, reduces airway closure, and improves O2.
Asthma Etiology
In Asthma, the airway becomes constricted and histamine is released. Most common in kids.
Usually caused by exposure to an allergy or trigger, such as dander, foods, nuts, drugs, exercise induced, weather induced (usually cold), irritants, genetics, exposure to smoke, allergies, or a respiratory infection.
The loss of heat or moisture from the bronchial surface is a characteristic of exercise-induced asthma, which is triggered by exercising in cold, dry air.
Asthma Clinical Manifestations
coughing, wheezing, tachycardia, tachypnea
Most common symptom in older adults is cough, which might also indicate COPD, CHF, or pulmonary fibrosis.
Dyspnea, tachypnea, and rhinitis typically occur in children and younger adults.
Asthma Risk Factors
Race (African Americans), exposure to irritants, genetics, allergies, and respiratory infection.
Asthma Nursing Assessment
Apparent level of distress and LOC
Respiratory rate and excursion
Breath sounds
Skin color / Vital signs
Inspect/palpate chest for symmetry
Assess for use of accessory muscles –> this indicates respiratory distress and rapid intervention is needed!
Assess for presence and nature of pulmonary secretions.
Asthma diagnostic tests
Allergy/skin testing –> scratch or patch testing and IgE testing can be used to determine the severity of the patient’s allergies.
SpO2
chest x-ray
ABGs
PFT
WBC count
Serum IgE and eosinophils
Asthma Nursing Interventions
Acute episodes are managed by ‘rescue medications’ such as bronchodilators (Albuterol), Anticholinergics (Atrovent) - to prevent further bronchoconstriction, and steroids such as methylprednisone to reduce inflammation.
LT mgmt use of Long-Acting Beta Agonists
Assess respiratory and O2 status
Identify triggers/precipitating factors
Create an Asthma Action Plan
Asthma Patient Education
Teach to avoid asthma triggers!
Rescue vs. maintenance
Proper use of meds
Anticholinergics (tiotropium / Spiriva) Mechanism of Action in Asthma
Blocks the cholinergic receptors of the Parasympathetic Nervous System, which allows the Sympathetic Nervous System to dominate.
Releases Epinephrine, relaxes smooth muscles around the airways, and promotes bronchodilation.
Tiotropium is administered through inhalation.
Anticholinergics (tiotropium / Spiriva)
Nursing Considerations
Assess for allergies to soybean/peanuts
Use cautiously during lactation, pts with glaucoma, prostatic hypertrophy
Assess for improved gas exchanged, decreased chest tightness, and decreased dyspnea
After use, offer mouth rinses to relieve dry mouth and bitter taste.
SABA - Short Acting Beta-2 Adrenergics
(Albuterol and Levalbuterol)
Mechanism of Action
Activates the Sympathetic Nervous System beta-2 receptors to relax bronchial smooth muscles causing bronchodilation.
Relieves bronchospasms for improved gas exchange in patients experiencing an acute asthma attack.
“Rescue inhaler” – works within minutes
SABA & LABA
Nursing Considerations
Use cautiously in pts with high BP, CAD, cardiac arrhythmias, and diabetes.
Inhalation is the desired route to minimize adverse systemic effects.
Should be administered with a MDI, DPI, or nebulizer.
Desired effects are a reduction in tachypnea, work of breathing, wheezing, and anxiety
Observe for signs of tremors, as beta2 agonists may activate the beta2 receptors in skeletal muscles.
SABA & LABA
Delivery Education
MDI is the most common method of delivery
Instruct the patient to depress the canister while taking slow, deep breaths for the most precise dose.
When 2 puffs are needed, wait for 1 minute between puffs.
Take Rescue inhaler 5 minutes before any other inhaled drugs, since the bronchodilator effects will impact those.
Monitor HR for tachycardia (SABAs have systemic effects)
Long Acting Beta Agonist
(arformeterol/Brovana; Formoterol / Perforomist; indacaterol / Arcapta)
Mechanism of Action
Not recommended for acute attacks due to a 30 minute onset.
Some LABAs (salmeterol) have an increased risk of asthma-related deaths b/c patients try to use them as a Rescue Inhaler.
Combination products include a LABA with a corticosteroid.
Corticosteroids for Asthma
(beclomethasone/Qvar; fluticasone/Flovent; prednisolone/Orapred)
Mechanism of Action
Not beneficial for acute attack!
Suppress inflammation in the airways and decrease mucus production.
Reduces the impact of exacerbations, improves speed of recovery, and decreases rate of relapse.
Combination salmeterol/fluticasone lasts as long as 12 hours, but takes 30 minutes to work so can’t be used for acute attacks.
Corticosteroid Nursing Considerations
Administer each dose of the corticosteroid about 5-10 minutes after the inhaled dose of bronchodilators to enhance the distribution of medication into the lungs.
Assess for throat irritation, nasal dryness, and oral/laryngeal candidias.
Administer antifungals or gargles as directed by HCP.
Corticosteroid Patient Education
Rinse mouth after each use to decrease throat irritation and reduce the risk of fungal infections.
NOT for acute attacks!
Could take a couple of weeks to experience the beneficial effects.
Take the medication continuously and refrain from stopping during symptom-free periods to ensure that therapeutic levels are maintained.
Leukotriene Modifiers
(Monelukat/singulair; zafirlukast/accolate; zileuton/Zyflo)
Mechanism of Action
NOT FOR ACUTE ATTACKS. These are a 2nd line therapy if an ICS cannot be used or adjunctive if ICS is insufficient.
Suppress inflammation and the release of leukotrienes/other inflammatory mediators. This results in less edema, mucus production, and airway obstruction.
May have adverse effects of depression and suicidal thinking.
Leukotriene Modifiers
Nursing Considerations
With Exercise-Induced Bronchoconstriction (EIB), take meds at least 2hours before exercising.
NOT for an acute attack!
Monitor liver function tests
May increase levels of warfarin, resulting in bleeding.
Mast Cell Stabilizers
(cromolyn)
Stabilize mast cell membranes and prevent the release of inflammatory mediators, such as leukotrienes, histamines.
This reduces edema, mucus production, and airway obstruction.
Also used to prevent asthma attacks triggered by inflammation/allergens.
Administered by MDI or nebulizer and are relatively safe with few side effects.
Mast Cell Stabilizers (Cromolyn)
Nursing Considerations & Education
Assess for decreased frequency of asthma attacks, wheezing, and bronchoconstriction.
Use daily, even when asymptomatic.
Use the MDI correctly!! (use teach-back when training)
NOT FOR ACUTE ATTACKS.
Methylxanthines
(aminophylline and theophylline)
Mechanism of action
Dual actions: CNS stimulant and bronchodilator.
As a CNS stimulant, methylxanthines decrease drowsiness and fatigue, but higherdoses may produce nervousness, insomnia, and tremors.
As a bronchodilator, they relax the bronchial smooth muscles.
Methylxanthines are infrequently used, as there is a narrow margin of safety and many side effects.
Methylxanthine Nursing Considerations
Avoid caffeine, as this increases the level of toxicity.
Adverse effects include insomnia, gastric distress, nausea, vomiting, and CNS stimulation. Cardiac dysrhythmias may be observed at higher dosages.
Monitor serum levels of the drugs to assure they’re at a therapeutic level.
Methylxanthine Patient Education
NOT a rescue inhaler
Contact HCP about OTC drugs due to possible interactions.
Monitor serum theophylline levels to avoid toxicity.
Educate on adverse effects and tell patient to report adverse effects.
Monoclonal Antibodies
(benralizumab/Fasenra; dupilumab/Dupixent; Mepolizumab/nucala)
Inhibits several types of interleukins to decrease an inflammatory response.
Administer by subcutaneous injection, except for reslizumab - which is given IV.
Instruct the patient or family member how to do a subQ injection.
COPD def’n
Incurable, irreversible chronic lung disorder with two main components:
1. chronic bronchitis – inflammation and excessive mucus. productive cough that has lasted 3+ months in 2 consecutive years.
2. Emphysema– alveolar membranes break down (usually due to a long history of cigarette smoking)
Low pO2 becomes the stimulus for breathing, so it’s important to only give the lowest amount of O2 possible to remain stable.
COPD Etiology
Age related - 50+
Current/past smoker
Respiratory infection - frequent trigger for exacerbation of symptoms
Occupation - chemicals, dust, air pollution, infections
Antitrypsin deficiency - “AAT” inherited, it normally protects the lungs from injury.
COPD Clinical Manifestations
Easily fatigued
Frequent URIs
Use of accessory muscles to breathe
Orthopneic
Wheezing
pursed lip breathing
Chronic cough
Barrel chest
Dyspnea
Prolonged expiratory time
Bronchitis - increased sputum
Digital clubbing
Worsening ABGs
COPD Collaborative Treatments
Stop smoking!!
low flow O2 (goal is 88-92%)
CPAP or BiPAP
breathing treatments
sitting position or tripod position
Breathing techniques:
> abdominal breathing relieves the work of the accessory muscles
> pursed lip breathing slows the respiratory rate and helps maintain open airways.
Huff Coughing: inhale deeply while leaning forward, exhale sharply with a ‘huff’ sound
Controlled Coughing: inhale deeply, hold breath briefly, cough twice; inhale by sniffing
Small meals that are high in protein; hydration
Chest physiotherapy
What is Pneumonia
Pneumonia is acute inflammation of the lung.
The inflammatory response causes fluid to accumulate in the alveoli and edema to form as alveolar capillaries dilate and allow fluid to leak into interstitial tissues. This results in impaired gas exchange, causing the patient to become dyspneic.
Bacterial Pneumonia
70% of cases
Upper respiratory tract infection
Risk factors: air pollution, cigarette smoking, medication, alcohol, COPD, heart failure, kidney failure
Aspiration pneumonia
patient aspirates gastric contents into the lungs, and this causes pneumonia.
Risk is highest during emergency surgery, because the patient hasn’t stopped eating.
other risks include decreased LOC, dysphagia, nasogastric intubation, 65+ yo, abdominal/chest surgery, tube feeding, vomiting
Viral pneumonia
10% of the adult population.
Flu and adenovirus are most common causes, but herpes and measles can also lead to pneumonia.
Mostly found in immunosuppressed patients.
Pneumonia Clinical Manifestations
Cough
Chills
Fever
Tachypnea
Dyspnea
Chest pain
Sputum
Fatigue
Decreased LOC
Diagnostics / Labs for Pneumonia
Chest X-Ray
Pulse Ox
Sputum –> the sputum gram stain can rapidly identify the infecting organisms, which allows the provider to select the correct antibiotic.
Blood cultures
ABGs
WBCs
Pneumonia Treatment
Prevention
incentive Spirometry (prevents alveoli collapse)
Chest PT
Suction
Fowlers position
O2 to prevent hypoxemia
Small meals, high in calorie/protein, los in carbs
Encourage movement!
Fluids
Sleep Apnea
Sleeping disorder when a person stops breathing. The average adult needs 7-9 hours of sleep.
Considered sleep apnea when there are 5+ apneic periods in an hour.
30+ episodes in an hour is considered severe.
Sleep Apnea Risk Factors
Women who are 60+
Anyone with a mental disorder
Large neck / abdominal circumference
Smoking
Alcohol
Could be genetically linked
Sleep Apnea Clinical Manifestations
Snoring
Sleeplessness, excessive sleepiness (always tired/irritable)
Fatigue
Irritability
Distractibility
Hard time focusing
Confusion
Morning headaches
Sleep Apnea diagnostics
Polysomnography Test (PSG) –> records O2 levels, eye movements.
ECG ==> used to measure brain waves
Sleep Apnea Treatment
Sleep maintaining behaviors
Stimulants for daytime
CPAP
Weight reduction
Possibly surgery to remove the obstruction
Avoid alcohol
Sleep Apnea Nursing Assessment
Assess apnea episodes
Assess wakefullness
Assess O2 status, SpO2, PaO2, CO2
Headaches
Sleep Apnea Patient Education
Deep breathing exercises
Positioning upright
promote secretion clearance
limit liquid at night
encourage smoking & alcohol cessation
avoid naps during the day
improve diet
O2 therapy
Exercise regimen
