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107 Cards in this Set

  • Front
  • Back

Thirst center loc


-stimulated by (2)

Hypothalamus control center


Stimulated by drop in blood volume


Increase in serum osmolality (We are talking about Salt)

Thirst mechanism decreases with


-who is at risk of not responding appropriately to thirst

Thirst mechanism decreases with age


Confused or altered mental status patients are at risk of not responding appropriately to thirst.

Kidneys main fx


-% fluid reabsorbed


-kidney fx is tied to

Filtration


99% of fluid is reabsorbed


Kidney function is tied to perfusion of the kidneys by the cardiac system

Normal urine output : mL/day, mL/hour


Minimum mL/h

Normal urine output is about 1500mL/day or 60mL/hr


Minimum 30mL/hr

Kidneys response to low perfusion is

Kidneys response to low perfusion is the release of renin--multiple steps-Angiotensin II.
Angiotensin II effects on body

Vasoconstrictor


Stimulates thirst


Kidneys to retain sodium and water


Stimulates the adrenal cortex to release Aldosterone

Aldosterone fx
Aldosterone promotes sodium and water retention by the distal portion of the nephrons

ADH


-osmoreceptors where? & respond to..


-what releases ADH

Antidiuretic Hormone (ADH)


Osmoreceptors in the hypothalmus respond to increase serum osmolality


Posterior pituitary gland releases ADH

ADH acts on


-causing urine output to


-thus blood volume... leads to

Distal tubules and makes them reabsorb more water


Urine output falls


Blood volume increases – leads to -serum osmolality decreases.

ADH release is increased by:
Stress, nausea, pain, surgery, anesthesia, narcotic, nicotine
ADH release is decreased by:

Alcohol


Phenytoin


Increased blood volume


Decrease serum osmolality

Atrial Natriuretic Peptide (hormone)


-comes from


-opposes


-effects (2)

-Comes from stretched atrial muscle cells (Fluid Overload)


-Opposition of the renin-angiotensin aldosterone system.


-Sodium wasting and increased urine output.

R-A-A system


-decreased (2) set off... leading to


-increased levels of aldosterone regulate (4) through ...

-Decreased blood volume and renal perfusion set off a chain of reactions leading to release of aldosterone from the adrenal cortex.


-Increased levels of aldosterone regulate serum K+ and Na+, blood pressure, and water balance through effects on the kidney tubules.

What stimulates release of ADH


-ADH increases

Increased serum osmolality or a fall in blood volume stimulates the release of ADH from the posterior pituitary.


-ADH increases the permeability of distal tubules, promoting water reabsorption.

Fluid Volume Deficit def

Decrease in intravascular, interstitial, and/or intracellular fluid in the body
Causes of fluid loss

Vomiting and diarrhea


Gastrointestinal suctioning, intestinal fistulas, and intestinal drainage


Diuretics, renal disorders, and endocrine disorders


Hot environment and hemorrhage

Manifestations of fluid loss

-Rapid weight loss and pale skin


-Decreased skin turgor and urine output


-Tachycardia


-Decreased systolic blood pressure and venous pressure

Fluid Volume Deficit Nursing care

Rehydration through oral, intravenous, or enteral routes


-By mouth, by IV, by NG or G-tube

fluid volume deficit further complications (2)

Hypovolemic shock


Electrolyte disturbances

Teach prevention of FVD : STOP

Stop fever, pain, nausea, vomiting & diarrhea
Fluid Volume Excess results when
Results when both water and sodium are retained in the body or by impairment of the mechanisms that maintain homeostasis
Causes of fluid excess (5)

-Heart or renal failure


-Cirrhosis of the liver


-Adrenal gland disorders


-Corticosteroid administration


-Stress conditions causing release of ADH and aldosterone (ie surgery)

Manifestations of fluid excess

-Peripheral or pulmonary edema


-Full bounding pulse and tachycardia


-Hypertension and ascites


-Reduced oxygen saturation


-Changes in urine output (think about cause and effect).

Fluid Volume Excess Nursing Care


-teach


-CHF pt about


-intervention

Teach prevention in patients at risk


-CHF patient about not taking in too much NaCL and H20


-Weigh same time every day

Ascites def


-diseases that produce this complications

Excessive accumulation of fluid in the abdominal cavity


-Chronic cirrhosis


-Malignancies of GI tract


-Heart failure


-Pancreatitis

Ascites presentation

Abdominal distention


Weight gain – water retention


DiscomfortNausea


Dyspnea – sudden/severe shortness of breath

Dyspnea
sudden/severe SOB

Acid-Base balance must be maintained to..


ex (4)

Be maintained to sustain proper body function and life


Basic cellular function


Enzyme activity


Electrolyte balance


Muscle contraction

ph is the


-range


-neutral

pH is the negative logarithm of hydrogen ion concentration


1-14


(7 is neutral – pure water)

Respiratory control is the primary control of
carbonic acid (H2CO3)
carbonic acid is exhaled as
is exhaled as CO2 and H2O
CO2 is the stimulator of the
respiratory center
increase in CO2 =
increase rate and depth of respirations
decrease in CO2=
decrease rate and depth of respirations
increase and decrease in CO2 occurs within ___ of change in ___

minutes


pH

Hbg will hold onto/release o2 depending on
the chemical environment
02 rich environment will cause Hgb to
hold onto o2
Acid environment will cause Hgb to
Acid environment will release O2 to the tissue and carry CO2 back to the lungs
carbonic acid:

A weak acid Carbon Dioxide dissolved in water is in equilibrium with carbonic acid:H2CO3


CO2 + H2O ⇌ H2CO3 it leaves to body in the lungs as C02 and H20

Normal PaCo2 range


+def

35-45 mm/hg


symbol for partial pressure of carbon dioxide in the arterial blood

some CO2 is dissolved in the
plasma (PaCO2)
The remaining CO2 (not PaCo2) is where
carried on the Hgh molecule inside the red blood cells

PaCo2 can rapidly change by


-so PaCo2 indicates

PaCo2 can be rapidly changes by alveolar ventilation


…So this is the value indicates effective alveolar ventilation.

Acidosis def
Hydrogen ion concentration above normal (pH below 7.35)

Alkolosis def

Hydrogen ion concentration below normal (pH above 7.45)
Normal ratio of bicarbonate to carbonic acid is

20:1


-pH remains w/in normal range of: 7.35-7.45

Respiratory acidosis ratio
20:2

Respiratory Acidosis aka


-characterized by pH ___ and PaCO2 ___


-results from ____ caused by _____


-can be (2)

Characterized by pH < 7.35 and a PaCO2 > 45 mmHg


Results from carbon dioxide retention caused by alveolar hypoventilation


Can be acute or chronic

Manifestations of Resp Acidosis



Headache, irritability, and decreased level of consciousness


Warm skin and blurred vision


Cardiac arrest

Manifestations of chronic Resp. Acidosis

Weakness, dull headache, impaired memory, and personality changes


Sleep disturbances and daytime sleepiness

Respiratory Alkalosis
O.6 part carbonic acid: 20 parts bicarbonate HCO3-
Respiratory Alkalosis pH
Characterized by pH > 7.45 and a PaCO2 < 35 mmHg
Respiratory Alkalosis causes

Anxiety with hyperventilation


High fever or hypoxia


Gram-negative bacteria


Thyrotoxicosis

Resp Alkalosis manifestations

Lightheadedness, tremors, and tinnitus


Panic feeling, difficulty concentrating, and sensation of chest tightness


Seizures and circumoral and distal extremity paresthesias

Metabolic acidosis ratio
1 carbonic acid + 18 bicarbonate (HCO3-)
Metabolic Acidosis characterized by __ pH and __ + 24
Characterized by low pH <7.35) and low bicarbonate < 24 mgEq/L
Metabolic Acidosis caused by

Caused by excess acid or loss of bicarbonate


Tissue hypoxiaDiabetic ketoacidosisAcute or chronic renal failure

Metabolic Acidosis Manifestations

Headache, weakness, and fatigueAnorexia, nausea, and vomiting


Flushed skin, stupor, and possible coma


Dysrhythmias and cardiac arrest


Deep and rapid respirations

Metabolic Alkalosis ratio
1 carbonic acid: 26 bicarbonate

Metabolic Alkalosis aka


-characterized by ____ pH _____ bicarbonate ____

Bicarbonate Excess



Metabolic Alkalosis caused by

Caused by loss of acid or excess bicarbonate



Metabolic Alkalosis


-secondary to


-associated w/


-tmt w/

Secondary to hospitalization


Hypokalemia


Treatment with alkalinizing solutions

Metabolic Alkalosis manifestations like


-ex.

manifestations like hypocalcemia


-Muscle spasms, numbness, and tingling


-Tetany, confusion, and dizziness


-Depressed respirations and possible respiratory failure

5 easy steps to ABG analysis

1.Is the pH normal?


2. Is the CO2 normal?


3. Is the HCO3 normal?


4. Match the CO2 or the HCO3 with the pH


5.Does the CO2 or the HCO3 go the opposite direction of the pH?


6. Are the pO2 and the O2 saturation normal?

Step 1


-below


-above


-if normal, which side does it fall on?

Analyze the pH


Below 7.35 it is acidic


Above 7.45 it is alkalotic


If normal, which side does it fall on


-Lower than 7.4 is normal/acidic


-Higher than 7.4 is normal/alkalotic


-Label it!

Step 2


-normal


-below is


-above is


and..

Analyze the CO2


Normal 35-45


Below is alkalotic


Above is acidic


Label it!

Step 3


-normal


-below


-above

Analyze the HCO3


Normal 22-26


Below 22 is acidotic


Above 26 is alkalotic


Label it!

Step 4


-if pH is acidotic and CO2 is acidotic, then it is


-if pH is alkalotic and HCO3 is alkalotic, then it is

Match the CO2 or HCO3 w/ th pH


-If pH is acidotic and CO2 is acidotic, then it is respiratory acidosis


-If the pH is alkalotic and HCO3 is alkalotic, then it is metabolic alkalosis

Step 5

Analyze the pO2 and O2 saturation


-If they are below normal there is evidence of hypoxemia

Objectives of IV Therapy (3)

-Maintain daily body fluid requirements


-Restore previous body fluid losses


-Replace current body fluid losses

Isotonic solutions


-osmolarity?


-fluid shifts?


-used to (2)


-potential dangers of use

Isotonic Solutions


-Have similar osmolality to plasma


-No fluid shifts in or out of the cells


-Used to: replace or maintain blood volumetreatment of hypotension (r/t hypovolemia)


-Potential Dangers of Use:circulatory overloadD5W: hyponatremic encephalopathy

Hypotonic Solutions


-osmolarity?


-fluid shifts?


-used to (2)


-potential dangers of use (2)

-Have osmolality lower than plasma


-Fluid shifts into and swells the cells


-Used to: replace cellular fluid (DKA-diuretic therapy)provide free water (to maintain renal function)


-Potential Dangers of Use:water intoxicationRisk for Increased Intracranial Pressure (ICP) and 3rd spacing

Hypertonic solutions


-osmolarity?


-fluid shifts?


-used to (3)


-Potential dangers of use?

-Higher osmolality than plasma


-Fluid shifts out of cells and cells shrink


-Used to: decrease post-op edema, stabilize blood pressure, maintain urinary output


-Potential Dangers of Use:cellular dehydration (especially with heart failure, hypernatremia)

Commonly used Isotonic IV solutions

-0.9% Sodium Chloride (NS*


-Lactated Ringers (LR)*


-5% Dextrose (D5W)

Commonly used Hypotonic IV solutions

-0.45% Sodium Chloride (½ NS)


-2.5% ----Dextrose



Commonly used Hypertonic IV solutions

-D5 0.9% Sodium Chloride


-D5 Lactated Ringers


-50% Dextrose


-3% Sodium Chloride

General Rule for combination fluids


-ex

Combination fluids are usually Hypertonic.




Examples: D5NS is (ISO)+(ISO) = hypertonicD5 1/2NS (D5W and 0.45%NS) is (ISO)+(hypo)=hypertonic


D5LR is (ISO)+(ISO) = hypertonic

Normal adult fluid intake

~2000 ml/24 hrs

Considering IV rates

Rate based on purpose of therapy

TKO/KVO rate

rate depends on facility


(~8-15ml)

Maintenance IV rate

75-100 ml/h

Replacement IV rate

100-150 ml/h

Severe loss replacement IV rate

>150 ml/h

Bolus

250ml + in less than an hour




(usually 500ml)

Dangers of using D5W in Post-op patients (nice to know)


-why

Hyponatremic Encephalopathy


-D5W is electrolyte free – dilutes sodium concentration


-First 2-4 post-op days: increased ADH (as much as 50%)


-Water from diluted plasma moves into cellsBrain cells unable to tolerate > 5% tissue expansion


-Leads to cerebral herniation --- sudden death

phlebitis def

Inflammation of one or more layers of the vein

Mechanical causes of phlebitis

-Cannula too large for vein


-Cannula inserted near a joint, creating piston motion against vein wall when patient moves


-Inadequate dressing and securement

phlebitis mechanical management

-Remove IV cannula and reinsert appropriate vascular access device in new location.


-Apply warm moist compress (ie. body temperature) to site for 20 mins, 6 hourly for 24 hours (non cytotoxic drugs only)


-Use smallest gauge cannula in largest vein possible

Phlebitis chemical causes


-chemical def

(irritation by IV medication)


-Infusion Alkaline solutions: - e.g. acyclovir, ganciclovir, phenytoin or Acid solutions - vancomycin, thiamine, glucagon, haloperidol


-Infusion of hyper/hypotonic solutions


- Speed and method of infusion delivery

Phlebitis chemical management

-Remove IV cannula and reinsert appropriate vascular access device in new location.


-Apply warm moist compress (i.e. body temperature) to site for 20 mins, 6 hourly for 24 hours for non cytotoxic drugs only


-Use smallest gauge, cannula in largest vein possible


-Dilute irritating solutions to acceptable dilutions in consultation with pharmacy


-Decrease infusion rate

Phlebitis bacterial causes +def

(irritation by bacteria or bacterial toxins)


-Break in aseptic technique during insertion or routine care.


-Inadequate skin preparation and/or hand hygiene


-Use of contaminated/expired IV solution or medication.


-Cannula remaining in situ past date of expiry

Phlebitis bacterial management

Remove IV cannula and reinsert appropriate vascular access device in new location.


-Send IV cannula to lab for culture, if inflammation or sepsis is suspected.


-Obtain swab for culture if there is ooze from the site.


-Apply warm moist compress (ie. Body temperature) to site for 20 mins, 6 hourly for 24 hours (non cytotoxic drugs only)

Extravasation of vesicant drugs / fluids into the tissues is a complication that can occur due to:

-Vein injury during cannula insertion


-Too large a cannula for the vein


-Cannula dislodgement during infusion


-Inadequate securement of the cannula


-Constriction of the vein above infusion site. e.g. clothing, patient ID bracelet

s/sx of extravasation

-Swelling


-Burning and or pain at the insertion site. Pain may be severe if the IV solution is hypertonic (e.g. solutions greater than 5% Dextrose), acid or alkaline


-Slowing of the infusion rate


-Lack of blood return from cannula

Extravasation

-Do not flush the line


-Attempt to aspirate drug from the cannula


-Remove the cannula once aspiration is complete


-Notify medical staff


-Contact pharmacy regarding the ongoing management of the site in relation to the particular drug extravasation


-Re cannulate away from the affected area


-Document the above actions and assessments


-Ensure there is adequate follow up assessment of the site

Extravasation prevention

-Ensure the cannula is the appropriate size and well secured


-Blood return on aspiration is observed before flushing cannula


-The insertion site must be visible at all times during administration


-Check cannula site at least hourly or more often if there is any concern during an infusion




Note: the insertion site should never be over an area of flexion.Splints are never to be used

Cellulitis def

inflammation of the t.

cellulitis s/sx

-Erythema (superficial reddening of the skin)


-Pain


-Tenderness


-Swelling

cellulitis management

-The cannula does not necessary require removal


-Antibiotic treatment as ordered by medical team


-Mark the site and monitor any deterioration/improvement of site Q8


-Document the above actions and assessments

hyponatremia


-causes


-manifestations

-Causes: diuretics, kidney disorders, adrenal insufficiency, vomiting, diarrhea, and gastrointestinal suction


-Manifestations: muscle cramps, weakness, fatigue, depression, irritability, personality changes, and possible coma with very low levels

hypernatremia


-occurs when (2)


-manifestations

-Occurs when: sodium is gained in excess of water, or when water is lost in excess of sodium


-Manifestations: thirst, lethargy, weakness, irritability; can progress to seizures, coma, and death



hypocalcemia


-causes


-manifestations

-Causes: hypoparathyroidism resulting from surgery and acute pancreatitis


-Manifestations: hypotension; tetany, paresthesias, muscle spasms; ventricular dysrhythmias; bone pain and fractures

Hypercalcemia


-causes


-manifestations

-Causes: hyperparathyroidism and malignancies


-Manifestations: muscle weakness and fatigue; anorexia, nausea, vomiting, and constipation; lethargy, personality changes, and coma; increased blood pressure

Hypomagnesemia


-normal range


-causes


-manifestations

normal 1.8-3.0 mg/dL


-Causes: chronic alcoholism, protein–calorie malnutrition, diabetic ketoacidosis, kidney disease, and medications


-Manifestations: dysphasia; muscle weakness and tremors; tetany; paresthesias; seizures; confusion and mood changes; increased heart rate and ventricular dysrhythmias. Cardiac arrest and sudden death can occur.



Hypermagnesemia


-causes


-manifestations

-Causes: less common, but can occur with renal failure, especially if magnesium is administered


-Manifestations: nausea and vomiting; hypotension; as levels increase, can show signs of CNS depression; marked elevations cause respiratory depression, coma, and compromised cardiac function

Positive Chvostek's sign def


-most often seen in

A spasm of the facial muscles following a tap on the facial nerve.


- Most often seen in hypocalcemic tetany.

Positive Trousseau's sign def


-indicative of

A muscular spasm of the hand and wrist from pressure on the nerves and vessels of the upper arm.


- It is indicative of latent tetany, usually as a result of hypocalcemia. (Cuff above SBP for 2-5 minutes)