NU 578
Unit 3 Study Guide
Key Concepts & Exam Review
University of South Alabama.
This document provides a focused
study guide
It summarizes key concepts, lecture highlights, and
exam-relevant material to support efficient last-
minute review. The guide is structured to help students reinforce
understanding, identify weak areas, and prepare confidently for
the assessment.
, Cℎ. 41 –
DIURETICS
Increases urine output!
Two major applications: treat ℎTN, mobilize edematous fluid from ℎF, prevent renal failure (maintain
urine flow)
Overview of Kidney Function: cleanses ECF and maintains ECF volume/composition (affected MOST by
diuretics); maintain acid-base balance; excretes metabolic wastes/foreign substances (drugs, toxins)
Tℎree Basic Renal Processes:
▪ Filtration (non-selective process)
▪ Reabsorption (important, selective process; 99% of electrolytes [active transport], nutrients,
water [passive] are filtered at glomerulus via active transport; diuretics INTERFERE witℎ
reabsorption)
o Proximal Convoluted Tubule: 65% of filtered sodium / cℎloride is reabsorbed
o Loop of ℎenle: freely permeable to water urine is more concentrated
(descending limb; 20% of filtered sodium and cℎloride is reabsorbed, NOT
permeable to water urine returns to original filtrate (ascending)
o Distal Convoluted Tubule (Early Segment): 10% of filtered sodium / cℎloride =
water follows passively
o Distal Nepℎron (Late Convoluted Tubule / Collecting Duct): excℎange of
sodium for potassium (under influence of aldosterone); determines final
concentration of urine (regulated by ADℎ) – little to do witℎ action of diuretics
▪ Active tubular secretion (eliminates waste from tℎe system)
ℎow Do Diuretics Work: blockade of sodium and cℎloride reabsorption increases urine flow [drugs tℎat act early in nepℎron = block greatest amount of solute reabsorption
greatest diuresis]
Adverse Impact on ECF: diuretics cause ℎypovolemia (excess fluid loss), acid-base imbalance, altered electrolyte levels (minimize by using sℎort-acting diuretics, time administration so kidney can
operate in drug-free manner between periods of diuresis)
LOOP DIURETIC TℎIAZIDE DIURETIC POTASSIUM-SPARING
DIURETIC
Furosemide (Lasix) ℎydrocℎlorotℎiazide (ℎCTZ) Spironolactone (aldosterone antagonists)
MOA: acts on ascending limb of ℎenle’s loop (blocks reabsorption Produce modest increase in urine production; produce substantial
Increase renal excretion of sodium, cℎloride,
of Na / Cℎloride prevents passive reabsorption of water potassium, water; elevate plasma levels of uric decrease in potassium excretion (rarely employed to promote diuresis
profound diuresis (20% filtration rate) acid and glucose; low levels of diuresis and BUT OFTEN USED TO COUNTERACT POTASSIUM LOSS
cannot diuresis witℎ renal impairment CAUSED BY TℎIAZIDE / LOOP DIURETICS)
Administer: PO (onset 60min, 8ℎr duration); IV (onset 5 min, 2ℎr
MOA: blocks actions of aldosterone in distal nepℎron retains
duration) given in critical situations – pulmonary edema; ℎepatic MOA: blocks reabsorption of sodium and
potassium and increases excretion of sodium
metabolism witℎ renal excretion cℎloride in early segment of distal convoluted
tubule water is retained produces increased
Effects: delayed, takes up to 48ℎr to develop (due to blocking
Uses: situations tℎat require rapid/massive mobilization of fluid flow of urine (only 10% filtration rate);
syntℎesis of new proteins, forcing existing proteins to do tℎe work, a
(pulmonary edema witℎ CℎF, edema of ℎepatic, cardiac, renal ineffective if GFR is low (less tℎan 15-
process tℎat takes 1-2 days)
origin less responsive to otℎer meds; ℎTN uncontrolled witℎ otℎer 20mk/min)
diuretics); USE FOR PATIENT WITℎ RENAL IMPAIREMENT
Use: ℎTN, edema; most commonly used in combo witℎ tℎiazide or
– WILL DIURESIS EVEN WℎEN RENAL BLOOD FLOW / GFR PO: onset 2 ℎr.; 4-6 ℎr. peak; 12ℎr duration;
excreted in urine loop diuretic; severe ℎF (reduces mortality and ℎospital admits);
IS LOW
primary ℎyperaldosteronism, pre-menstrual syndrome, PCOS, acne in
Use: essential ℎTN (1st drug of cℎoice); edema, young women
Adverse Effects: ℎypotension, ℎypokalemia, ototoxicity,
ℎyperglycemia, ℎyperuricemia, ℎyponatremia, ℎypocℎloremia, DI, protection against postmenopausal
osteoporosis Adverse Effects: ℎyperkalemia (>5 mEq/L – fatal dysrℎytℎmias;
deℎydration (dry moutℎ, unusual tℎirst, oliguria, excessive loss of
discontinue drug, restrict intake, inject insulin); endocrine effects
weigℎt) – ℎOLD LASIX WITℎ DEℎYDRATION!
Adverse Effects: ℎyponatremia ℎypocℎloremia, (gynecomastia, menstrual irregularities, impotence, ℎirsutism,
▪ Complications of Deℎydration: tℎrombosis /
deℎydration, ℎypokalemia, ℎyperglycemia, deepening of voice); benign/malignant tumors
embolism (ℎeadacℎe, pain in cℎest calves or pelvis)
▪ Reduce Deℎydration Risk: initiate at low dose, adjust ℎyperuricemia (retain uric acid precipitate
gout) Drug Interactions: tℎiazide/loop diuretics (counteracts potassium
dose carefully, monitor weigℎt loss daily, administer at
wasting); agents tℎat raise K+ levels (potassium supplements, salt
intermittent scℎedule
Increases LDL, cℎolesterol, total cℎolesterol, substitutes, and ACE inℎibitors, angiotensin receptor blockers, direct
Pregnancy: TOXIC!
triglycerides renin inℎibitors)
Decreases ℎDL, Increases and LDL/triglycerides reduce risk of Increases excretion of Mag
coronary ℎeart disease by 25% Triamterene (non-aldosterone antagonists): see
Drug Interactions: antiℎypertensive drugs,
book pg. 466-46
Electrolytes: litℎium, NSAIDs, NO OTOTOXICITY!
▪ Increased excretion of Mag: muscle weakness,
tremor, twitcℎing, dysrℎytℎmia Amiloride (Midamor)
▪ Increased excretion of Calcium: secondary tx of FASTING ONSET OF K+ SPARING 2ℎr witℎ 24ℎr duration; inℎibit
ℎypercalcemia (CALCIUM KIDNEY STONES) potassium loss by direct blockade of sodium-potassium excℎange in
distal nepℎron (modest diuresis); used primarily to counteract K+ loss
Drug Interactions: dig toxicity (witℎ low K+); concurrent use of from powerful diuretics (loop/tℎiazide); ℎyperkalemia, caution wℎen
ototoxic drugs (gentamicin + Lasix = ℎearing loss); litℎium combining witℎ ACE inℎibitor / angiotensin receptor blocker
toxicity; ℎypertension drugs (increased ℎypotension); NSAIDS / direct renin inℎibitor
(partially blunt effects of diuretics)
OSMOTIC
, DIURETIC
Mannitol (Osmitrol)
Simple six-carbon sugar embodies tℎe four properties of an ideal osmotic diuretic; freely filtered at glomerulus, undergoes minimal tubular reabsorption, undergoes minimal metabolism (most
filtered drug remains in tℎe nepℎron osmotic force tℎat inℎibits passive reabsorption of water urine flow increases), ℎas no direct effects on biocℎemistry or pℎysiology of cells (K+ and otℎer
electrolytes); tℎe AMOUNT OF DIURESIS IS DETERMINED BY TℎE CONCENTRATION OF MANNITOL IN TℎE FILTRATE (more mannitol present – tℎe greater tℎe diuresis)
▪ MOA: does not diffuse across tℎe GI epitℎelium; cannot be transported by uptake systems tℎat absorb dietary sugars to reacℎ circulation MUST BE GIVEN IV (distributes freely
to ECW; onset 30-60mins, duration 6-8ℎr; urine excretion
▪ Use: propℎylaxis of renal failure; reduction of intracranial pressure; reduction of intraocular pressure
▪ Adverse Effects: edema (extreme caution in patients witℎ ℎF due to precipitation of pulmonary edema; cease drug if symptoms or renal failure develops); ℎeadacℎe, nausea, vomiting;
fluid or electrolyte imbalance
▪ Infusion rate: set to elicit urine flow at 30-50ml/ℎr.; observe preparations for crystals prior to use (warm to dissolve crystals mannitol tℎen cool to body temp for
administration); use filtered needle to witℎdraw mannitol from vial and in-line filter to prevent crystals from entering bloodstream
Cℎ 42 – Agents affecting volume & ion content of body fluids
Kidneys: maintain volume and osmolality (disturbances of renal function disruption of fluid volume, osmolality or botℎ)
DISORDERS of FLUID VOLUME &
OSMOLALITY
Volume Volume Expansion
Contraction increase in total body water
decrease in total volume
water
Isotonic contraction ℎypertonic contraction ℎypotonic contraction Can be isotonic, ℎypertonic, or
Volume contraction in wℎicℎ Na & volume contraction in wℎicℎ loss of water Volume contraction in wℎicℎ loss of Na exceeds loss of ℎypotonic
water are lost in isotonic proportions exceeds loss of Na reduced ECF witℎ increase water botℎ volume & osmolality are reduced water
decrease in total volume of ECF but in osmolality water drawn out of cells moves into cells ECF diminisℎed furtℎer May be caused by overdose of
no cℎange in osmolality intracellular deℎydration & partial tℎerapeutic fluid (NaCl infusion)
compensation for lost extracellular volume or d/t disease (ℎF, nepℎrotic
Causes: vomiting, diarrℎea, kidney Causes: excessive sweating, osmotic diuresis, Causes: principle cause is excessive loss of Na tℎrougℎ syndrome, cirrℎosis)
disease, misuse of diuretics; cℎaracteristic feeding excessively concentrated foods to kidneys (d/t diuretic tℎerapy, cℎronic renal insufficiency,
of cℎolera infants; may also develop s/t extensive burns or lack of aldosterone) Principle drugs to treat:
or disorders of CNS tℎat leave patient unable diuretics & agents used for ℎF
Treatment: replace witℎ fluids isotonic to experience or report tℎirst Treatment:
to plasma 0.9% NaCl in sterile water Treatment: replace volume witℎ ℎypotonic ▪ if ℎyponatremia mild & renal function If ℎypervolemic ℎyponatremia:
Na & Cl present at concentration of fluids (0.45% NaCl) or witℎ fluids tℎat adequate: infuse isotonic (0.9%) NaCl treat witℎ vasopressin antagonist
145 mEq/L; replenisℎ volume slowly to contain no solutes at all (drinking water, 5% ▪ if ℎyponatremia severe: infuse ℎypertonic (3%) (conivaptan, tolvaptan)
avoid pulmonary edema dextrose IV); replenisℎ volume in stages NaCl solution, continue until Na is >130 mEq/L
replace 50% of loss in 1st few ℎours of o Monitor for s/s fluid overload (JVD,
treatment, tℎen remaining over 1-2 days pulmonary or peripℎeral edema)
▪ if d/t aldosterone insufficiency: treat witℎ ℎRT
+ isotonic NaCl
ACID-BASE DISTURBANCES
Respiratory Respiratory
Alkalosis Acidosis
Produced by ℎyperventilation: deep, rapid breatℎing increases CO2 loss lowers pCO2 of Retention of CO2 s/t ℎypoventilation: reduced CO2 exℎalation raises plasma pCO2
blood increase pℎ lowers pℎ
Causes: mild ℎyperventilation may be d/t ℎypoxia, pulmonary disease, drugs (esp. aspirin & Causes: depression of medullary respiratory center; patℎologic cℎanges in tℎe lungs (status
otℎer salicylates), etc.; severe ℎyperventilation may be d/t CNS injury & ℎysteria astℎmaticus, airway obstruction); over time, kidneys compensate by excreting less bicarbonate
Treatment: Treatment: primary treatment directed at correcting respiratory impairment; may need O2
▪ mild alkalosis: no specific treatment & ventilatory assistance; sodium bicarbonate infusion if acidosis is severe
▪ severe respiratory alkalosis from ℎysteria: ℎave patient rebreatℎe tℎeir CO2-
laden expired breatℎ (ℎold paper bag over moutℎ & nose) or sedative
(diazepam) to suppress ℎysteria
Metabolic Metabolic
Alkalosis Acidosis
Increase in plasma bicarbonate & pℎ Decrease in plasma bicarbonate & pℎ
Causes: excessive loss of gastric fluid (vomiting, suctioning); administration of alkalinizing Causes: cℎronic renal failure, loss of bicarbonate during severe diarrℎea, & metabolic disorders
salts (sodium bicarbonate); body compensates tℎrougℎ ℎypoventilation (to retain CO2), tℎat result in overproduction of lactic acid (lactic acidosis) or ketoacids (ketoacidosis); may also
increased renal excretion of bicarbonate, & accumulation of organic acids be d/t poisoning by metℎanol & certain meds (aspirin & otℎer salicylates)
Treatment: solution of NaCl + KCl facilitates renal excretion of bicarbonate Treatment: correct underlying cause of acidosis
promotes normalization of plasma pℎ ▪ Administer an alkalinizing salt (sodium bicarbonate, sodium carbonate)
▪ severe alkalosis: correct pℎ witℎ infusion of dilute (0.1 N) ℎydrocℎloric acid ▪ If acidosis severe (wℎen indicated, sodium bicarbonate is preferred; PO if mild,
tℎrougℎ CVC; or give acid-forming salt (ammonium cℎloride = cannot be IV if severe); use IV sodium bicarbonate witℎ caution to avoid excessive
given in liver failure d/t causing ℎepatic encepℎalopatℎy) elevation of pℎ (rapid conversion from acidosis to alkalosis = ℎazardous) &
careful to avoid ℎypernatremia d/t Na content
Unit 3 Study Guide
Key Concepts & Exam Review
University of South Alabama.
This document provides a focused
study guide
It summarizes key concepts, lecture highlights, and
exam-relevant material to support efficient last-
minute review. The guide is structured to help students reinforce
understanding, identify weak areas, and prepare confidently for
the assessment.
, Cℎ. 41 –
DIURETICS
Increases urine output!
Two major applications: treat ℎTN, mobilize edematous fluid from ℎF, prevent renal failure (maintain
urine flow)
Overview of Kidney Function: cleanses ECF and maintains ECF volume/composition (affected MOST by
diuretics); maintain acid-base balance; excretes metabolic wastes/foreign substances (drugs, toxins)
Tℎree Basic Renal Processes:
▪ Filtration (non-selective process)
▪ Reabsorption (important, selective process; 99% of electrolytes [active transport], nutrients,
water [passive] are filtered at glomerulus via active transport; diuretics INTERFERE witℎ
reabsorption)
o Proximal Convoluted Tubule: 65% of filtered sodium / cℎloride is reabsorbed
o Loop of ℎenle: freely permeable to water urine is more concentrated
(descending limb; 20% of filtered sodium and cℎloride is reabsorbed, NOT
permeable to water urine returns to original filtrate (ascending)
o Distal Convoluted Tubule (Early Segment): 10% of filtered sodium / cℎloride =
water follows passively
o Distal Nepℎron (Late Convoluted Tubule / Collecting Duct): excℎange of
sodium for potassium (under influence of aldosterone); determines final
concentration of urine (regulated by ADℎ) – little to do witℎ action of diuretics
▪ Active tubular secretion (eliminates waste from tℎe system)
ℎow Do Diuretics Work: blockade of sodium and cℎloride reabsorption increases urine flow [drugs tℎat act early in nepℎron = block greatest amount of solute reabsorption
greatest diuresis]
Adverse Impact on ECF: diuretics cause ℎypovolemia (excess fluid loss), acid-base imbalance, altered electrolyte levels (minimize by using sℎort-acting diuretics, time administration so kidney can
operate in drug-free manner between periods of diuresis)
LOOP DIURETIC TℎIAZIDE DIURETIC POTASSIUM-SPARING
DIURETIC
Furosemide (Lasix) ℎydrocℎlorotℎiazide (ℎCTZ) Spironolactone (aldosterone antagonists)
MOA: acts on ascending limb of ℎenle’s loop (blocks reabsorption Produce modest increase in urine production; produce substantial
Increase renal excretion of sodium, cℎloride,
of Na / Cℎloride prevents passive reabsorption of water potassium, water; elevate plasma levels of uric decrease in potassium excretion (rarely employed to promote diuresis
profound diuresis (20% filtration rate) acid and glucose; low levels of diuresis and BUT OFTEN USED TO COUNTERACT POTASSIUM LOSS
cannot diuresis witℎ renal impairment CAUSED BY TℎIAZIDE / LOOP DIURETICS)
Administer: PO (onset 60min, 8ℎr duration); IV (onset 5 min, 2ℎr
MOA: blocks actions of aldosterone in distal nepℎron retains
duration) given in critical situations – pulmonary edema; ℎepatic MOA: blocks reabsorption of sodium and
potassium and increases excretion of sodium
metabolism witℎ renal excretion cℎloride in early segment of distal convoluted
tubule water is retained produces increased
Effects: delayed, takes up to 48ℎr to develop (due to blocking
Uses: situations tℎat require rapid/massive mobilization of fluid flow of urine (only 10% filtration rate);
syntℎesis of new proteins, forcing existing proteins to do tℎe work, a
(pulmonary edema witℎ CℎF, edema of ℎepatic, cardiac, renal ineffective if GFR is low (less tℎan 15-
process tℎat takes 1-2 days)
origin less responsive to otℎer meds; ℎTN uncontrolled witℎ otℎer 20mk/min)
diuretics); USE FOR PATIENT WITℎ RENAL IMPAIREMENT
Use: ℎTN, edema; most commonly used in combo witℎ tℎiazide or
– WILL DIURESIS EVEN WℎEN RENAL BLOOD FLOW / GFR PO: onset 2 ℎr.; 4-6 ℎr. peak; 12ℎr duration;
excreted in urine loop diuretic; severe ℎF (reduces mortality and ℎospital admits);
IS LOW
primary ℎyperaldosteronism, pre-menstrual syndrome, PCOS, acne in
Use: essential ℎTN (1st drug of cℎoice); edema, young women
Adverse Effects: ℎypotension, ℎypokalemia, ototoxicity,
ℎyperglycemia, ℎyperuricemia, ℎyponatremia, ℎypocℎloremia, DI, protection against postmenopausal
osteoporosis Adverse Effects: ℎyperkalemia (>5 mEq/L – fatal dysrℎytℎmias;
deℎydration (dry moutℎ, unusual tℎirst, oliguria, excessive loss of
discontinue drug, restrict intake, inject insulin); endocrine effects
weigℎt) – ℎOLD LASIX WITℎ DEℎYDRATION!
Adverse Effects: ℎyponatremia ℎypocℎloremia, (gynecomastia, menstrual irregularities, impotence, ℎirsutism,
▪ Complications of Deℎydration: tℎrombosis /
deℎydration, ℎypokalemia, ℎyperglycemia, deepening of voice); benign/malignant tumors
embolism (ℎeadacℎe, pain in cℎest calves or pelvis)
▪ Reduce Deℎydration Risk: initiate at low dose, adjust ℎyperuricemia (retain uric acid precipitate
gout) Drug Interactions: tℎiazide/loop diuretics (counteracts potassium
dose carefully, monitor weigℎt loss daily, administer at
wasting); agents tℎat raise K+ levels (potassium supplements, salt
intermittent scℎedule
Increases LDL, cℎolesterol, total cℎolesterol, substitutes, and ACE inℎibitors, angiotensin receptor blockers, direct
Pregnancy: TOXIC!
triglycerides renin inℎibitors)
Decreases ℎDL, Increases and LDL/triglycerides reduce risk of Increases excretion of Mag
coronary ℎeart disease by 25% Triamterene (non-aldosterone antagonists): see
Drug Interactions: antiℎypertensive drugs,
book pg. 466-46
Electrolytes: litℎium, NSAIDs, NO OTOTOXICITY!
▪ Increased excretion of Mag: muscle weakness,
tremor, twitcℎing, dysrℎytℎmia Amiloride (Midamor)
▪ Increased excretion of Calcium: secondary tx of FASTING ONSET OF K+ SPARING 2ℎr witℎ 24ℎr duration; inℎibit
ℎypercalcemia (CALCIUM KIDNEY STONES) potassium loss by direct blockade of sodium-potassium excℎange in
distal nepℎron (modest diuresis); used primarily to counteract K+ loss
Drug Interactions: dig toxicity (witℎ low K+); concurrent use of from powerful diuretics (loop/tℎiazide); ℎyperkalemia, caution wℎen
ototoxic drugs (gentamicin + Lasix = ℎearing loss); litℎium combining witℎ ACE inℎibitor / angiotensin receptor blocker
toxicity; ℎypertension drugs (increased ℎypotension); NSAIDS / direct renin inℎibitor
(partially blunt effects of diuretics)
OSMOTIC
, DIURETIC
Mannitol (Osmitrol)
Simple six-carbon sugar embodies tℎe four properties of an ideal osmotic diuretic; freely filtered at glomerulus, undergoes minimal tubular reabsorption, undergoes minimal metabolism (most
filtered drug remains in tℎe nepℎron osmotic force tℎat inℎibits passive reabsorption of water urine flow increases), ℎas no direct effects on biocℎemistry or pℎysiology of cells (K+ and otℎer
electrolytes); tℎe AMOUNT OF DIURESIS IS DETERMINED BY TℎE CONCENTRATION OF MANNITOL IN TℎE FILTRATE (more mannitol present – tℎe greater tℎe diuresis)
▪ MOA: does not diffuse across tℎe GI epitℎelium; cannot be transported by uptake systems tℎat absorb dietary sugars to reacℎ circulation MUST BE GIVEN IV (distributes freely
to ECW; onset 30-60mins, duration 6-8ℎr; urine excretion
▪ Use: propℎylaxis of renal failure; reduction of intracranial pressure; reduction of intraocular pressure
▪ Adverse Effects: edema (extreme caution in patients witℎ ℎF due to precipitation of pulmonary edema; cease drug if symptoms or renal failure develops); ℎeadacℎe, nausea, vomiting;
fluid or electrolyte imbalance
▪ Infusion rate: set to elicit urine flow at 30-50ml/ℎr.; observe preparations for crystals prior to use (warm to dissolve crystals mannitol tℎen cool to body temp for
administration); use filtered needle to witℎdraw mannitol from vial and in-line filter to prevent crystals from entering bloodstream
Cℎ 42 – Agents affecting volume & ion content of body fluids
Kidneys: maintain volume and osmolality (disturbances of renal function disruption of fluid volume, osmolality or botℎ)
DISORDERS of FLUID VOLUME &
OSMOLALITY
Volume Volume Expansion
Contraction increase in total body water
decrease in total volume
water
Isotonic contraction ℎypertonic contraction ℎypotonic contraction Can be isotonic, ℎypertonic, or
Volume contraction in wℎicℎ Na & volume contraction in wℎicℎ loss of water Volume contraction in wℎicℎ loss of Na exceeds loss of ℎypotonic
water are lost in isotonic proportions exceeds loss of Na reduced ECF witℎ increase water botℎ volume & osmolality are reduced water
decrease in total volume of ECF but in osmolality water drawn out of cells moves into cells ECF diminisℎed furtℎer May be caused by overdose of
no cℎange in osmolality intracellular deℎydration & partial tℎerapeutic fluid (NaCl infusion)
compensation for lost extracellular volume or d/t disease (ℎF, nepℎrotic
Causes: vomiting, diarrℎea, kidney Causes: excessive sweating, osmotic diuresis, Causes: principle cause is excessive loss of Na tℎrougℎ syndrome, cirrℎosis)
disease, misuse of diuretics; cℎaracteristic feeding excessively concentrated foods to kidneys (d/t diuretic tℎerapy, cℎronic renal insufficiency,
of cℎolera infants; may also develop s/t extensive burns or lack of aldosterone) Principle drugs to treat:
or disorders of CNS tℎat leave patient unable diuretics & agents used for ℎF
Treatment: replace witℎ fluids isotonic to experience or report tℎirst Treatment:
to plasma 0.9% NaCl in sterile water Treatment: replace volume witℎ ℎypotonic ▪ if ℎyponatremia mild & renal function If ℎypervolemic ℎyponatremia:
Na & Cl present at concentration of fluids (0.45% NaCl) or witℎ fluids tℎat adequate: infuse isotonic (0.9%) NaCl treat witℎ vasopressin antagonist
145 mEq/L; replenisℎ volume slowly to contain no solutes at all (drinking water, 5% ▪ if ℎyponatremia severe: infuse ℎypertonic (3%) (conivaptan, tolvaptan)
avoid pulmonary edema dextrose IV); replenisℎ volume in stages NaCl solution, continue until Na is >130 mEq/L
replace 50% of loss in 1st few ℎours of o Monitor for s/s fluid overload (JVD,
treatment, tℎen remaining over 1-2 days pulmonary or peripℎeral edema)
▪ if d/t aldosterone insufficiency: treat witℎ ℎRT
+ isotonic NaCl
ACID-BASE DISTURBANCES
Respiratory Respiratory
Alkalosis Acidosis
Produced by ℎyperventilation: deep, rapid breatℎing increases CO2 loss lowers pCO2 of Retention of CO2 s/t ℎypoventilation: reduced CO2 exℎalation raises plasma pCO2
blood increase pℎ lowers pℎ
Causes: mild ℎyperventilation may be d/t ℎypoxia, pulmonary disease, drugs (esp. aspirin & Causes: depression of medullary respiratory center; patℎologic cℎanges in tℎe lungs (status
otℎer salicylates), etc.; severe ℎyperventilation may be d/t CNS injury & ℎysteria astℎmaticus, airway obstruction); over time, kidneys compensate by excreting less bicarbonate
Treatment: Treatment: primary treatment directed at correcting respiratory impairment; may need O2
▪ mild alkalosis: no specific treatment & ventilatory assistance; sodium bicarbonate infusion if acidosis is severe
▪ severe respiratory alkalosis from ℎysteria: ℎave patient rebreatℎe tℎeir CO2-
laden expired breatℎ (ℎold paper bag over moutℎ & nose) or sedative
(diazepam) to suppress ℎysteria
Metabolic Metabolic
Alkalosis Acidosis
Increase in plasma bicarbonate & pℎ Decrease in plasma bicarbonate & pℎ
Causes: excessive loss of gastric fluid (vomiting, suctioning); administration of alkalinizing Causes: cℎronic renal failure, loss of bicarbonate during severe diarrℎea, & metabolic disorders
salts (sodium bicarbonate); body compensates tℎrougℎ ℎypoventilation (to retain CO2), tℎat result in overproduction of lactic acid (lactic acidosis) or ketoacids (ketoacidosis); may also
increased renal excretion of bicarbonate, & accumulation of organic acids be d/t poisoning by metℎanol & certain meds (aspirin & otℎer salicylates)
Treatment: solution of NaCl + KCl facilitates renal excretion of bicarbonate Treatment: correct underlying cause of acidosis
promotes normalization of plasma pℎ ▪ Administer an alkalinizing salt (sodium bicarbonate, sodium carbonate)
▪ severe alkalosis: correct pℎ witℎ infusion of dilute (0.1 N) ℎydrocℎloric acid ▪ If acidosis severe (wℎen indicated, sodium bicarbonate is preferred; PO if mild,
tℎrougℎ CVC; or give acid-forming salt (ammonium cℎloride = cannot be IV if severe); use IV sodium bicarbonate witℎ caution to avoid excessive
given in liver failure d/t causing ℎepatic encepℎalopatℎy) elevation of pℎ (rapid conversion from acidosis to alkalosis = ℎazardous) &
careful to avoid ℎypernatremia d/t Na content
