Acid base and Fluids Flashcards

1
Q

describe Acid-Base Homeostasis

normal arterial pH?

  • Respiratory mechanism
  • Renal mechanism
A

•Arterial pH is maintained between 7.35 – 7.45 by extracellular and intracellular chemical buffering systems along with respiratory and renal mechanism

•Respiratory mechanism:control arterial CO2 tension (PaCO2 )

•Renal mechanism: control plasma bicarbonate (HCO3 - )

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2
Q

components of Abg

uses?

A

pH

Oxygen tension (Pa02 )

Carbon dioxide tension (PaCO2 )

Oxyhemoglobin saturation (Sa02 )

Bicarbonate concentrations (HCO3 -)

USES

Identify acid-base disturbances

Measures partial pressures of O2 and CO2

Assessment of the response to therapeutic interventions

Procurement of blood samples in emergencies when venous blood is not feasible

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3
Q

blood pH values identify:

  • Acidemia –
  • Alkalemia –
  • Acidosis –
  • Alkalosis –
A
  • Acidemia – arterial pH < 7.35
  • Alkalemia – arterial pH > 7.45
  • Acidosis – ↓extracellular fluid pH
  • Alkalosis – ↑extracellular fluid pH
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4
Q

describe changes seen in (pH, HCO3, CO2)

  • Metabolic acidosis –
  • Metabolic alkalosis –
  • Respiratory acidosis –
  • Respiratory alkalosis -
A
  • Metabolic acidosis – ↓serum HCO3- & pH
  • Metabolic alkalosis – ↑serum HCO3- & pH
  • Respiratory acidosis – ↑arterial pCO2 & ↓ pH
  • Respiratory alkalosis - ↓ arterial pCO2 & ↑pH
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5
Q

define

  • Primary respiratory disturbance →
  • Primary metabolic disturbances →
A

•Primary respiratory disturbance →

  • primary change in PaCO2 →
  • invokes compensatory metabolic response →
  • secondary change in HCO3 –

•Primary metabolic disturbances →

  • primary change in HCO3 - →
  • invokes compensatory respiratory response →
  • secondary change in PaCO2
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6
Q

arrows in

  • Metabolic acidosis –
  • Metabolic alkalosis –
  • Respiratory acidosis –

Respiratory alkalosis

A

pH & CO2

Opposite = respiratory process

Same direction = metabolic process

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7
Q

CO2 in

Respiratory Acidosis

Respiratory Alkalosis:

A

Respiratory Acidosis: TOO MUCH CO2 = TOXIC

Respiratory Alkalosis: LOSING TOO MUCH CO2

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8
Q

Hyperventilation Syndrome: panic attack causes what ?

A

Respiratory Alkalosis

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9
Q

arrow in

Respiratory Acisodis

Respiratory Alkalosis

A

pH & CO2 going in OPPOSITE directions!!!

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10
Q

arrows in

Metabolic acid

Metabolic Alk

A

OPPOSITE DIRESTION

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11
Q

resp acidosis is caused by?

tx?

A
  • Severe pulmonary failure
  • Respiratory muscle fatigue
  • Abnormalities in ventilatory control

Reverse underlying cause

Tracheal intubation and assisted mechanical ventilation

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12
Q

si/sx of Respiratory Alkalosis:

A

Dizziness

Mental confusion

Seizures

Hypotension

Decreased cardiac output

Cardiac arrhythmias

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13
Q

metabolic acidosis causes

A
  • ↑ endogenous acid production (lactate or ketoacid)
  • Loss of bicarbonate (diarrhea)
  • ↑endogenous acid bc of ↓ excretion of acid by the kidneys (CKD)
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14
Q

si/sx of metabolic acidos

A

LOOK SICK

  • Increase in ventilation and TV (Kussmaul respirations)
  • ↓cardiac contractility
  • Peripheral arterial vasodilation
  • Central venous constriction
  • Decrease in central and pulmonary vascular compliance → pulmonary edema
  • Depressed CNS function → headache, lethargy, stupor, coma
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15
Q

normal anion gap acidosis is defines as

A

The presence of a metabolic acidosis with a normal anion gap and hyperchloremia

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16
Q

causes of high anion gap met acidosis

A

MUD PILES

  • Methanol
  • Uremia
  • Diabetes
  • Paraldehyde
  • Iron (and Isoniazid)
  • Lactate
  • Ethylene glycol
  • Salicylate
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17
Q

non-anion gap avidosis is describes ad

A

Bicarbonate loss from the GI tract or kidneys – kidneys over excrete bicarb

  • Vomiting
  • Diarrhea
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18
Q

si/sx of Metabolic Alkalosis

what electro;yte abnorm are seen?

A
  • ↑ in HCO3 –
  • ↓ nonvolatile acid (usually HCl) from the extracellular fluid (vomiting or NG tube suction)
  • Failure of the kidneys to eliminate HCO3 –

Often accompanied by hypochloremia and hypokalemia

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19
Q

si/sx Metabolic Alkalosis

A

Similar to those of hypocalcemia

  • Mental confusion
  • Obtundation
  • Predisposition to seizures
  • Paresthesia
  • Muscle cramping
  • Tetany
  • Aggravation or arrhythmias
  • hypoxemia
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20
Q

_Frequently occurs as a mixed disorder in association wit_h

  • respiratory acidosis
  • respiratory alkalosis,
  • metabolic acidosis
A

Metabolic Alkalosis

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21
Q

tx of Metabolic Alkalosis

A

Treat hypokalemia with potassium replacement

  • Stop loop / thiazide diuretics
  • Acetazolamide – Diamox = weak diuretic makes you hold onto your bicarb!
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22
Q

arrows in

metabolic acid

metabolic alk

A

pH CO2 in SAME direction

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23
Q

causes of high anion gap acidosis

Lactic Acidosis= ↑lactateKetoacidosis

Drug/Toxin Induced

Chronic Kidney Disease

A

Lactic Acidosis= ↑lactate

  • Poor tissue perfusion (type A)
  • Aerobic disorders (type B)
  • D-Lactic acid acidosis

Ketoacidosis

  • Diabetic Ketoacidosis (DKA)
  • Alcoholic Ketoacidosis (AKA)

Drug/Toxin Induced

  • Salicylates
  • Ethylene Glycol
  • Methanol
  • Propylene Glycol
  • Isopropyl Alcohol
  • Pyroglutamic Acid

Chronic Kidney Disease

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24
Q

caused by injestion of asprin & accompanied by a respiratory alkalosis

A

high anion gap met acidosis - Salicylates

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25
Often accompanied by **a high osmolar gap** ## Footnote **urine oxalate crystals**
Ethylene Glycol
26
Methanol / ___ alcohol: lead to severe damage of???
Wood Alcohol : Leads to severe damage of: Optic nerve & CNS
27
toxicity Seen in ICU settings with patients on continuous infusions of medications what meds?
Propylene Glycol Diazepam • Lorazepam • Phenobarbital • Nitroglycerine
28
Increase is osmolar gap is present, but Labs might not show high anion FALSe NORMAL ANION GAP)
Isopropyl Alcohol Labs might not show high anion gap because _isopropyl alcohol is metabolized to acetone, which is excreted_ rapidly (FALSO NORMAL ANION GAP)
29
Accumulation of 5-oxoproline is seen w/ what toxicity
Pyroglutamic Acid: Acetaminophen overdose
30
CKD w/ high anion gap causes
Caused by poor filtration and reabsorption of organic anions _→ uremic acidosis_
31
Steps to Interpreting ABGs
**•Step 1** – Determine the primary disorder **•Step 2** – Determine appropriate compensation verse the presence of mixed acid-based disorder by calculating the range of compensation **•Step 3** – Calculate the ion gap **•Step 3a** – Calculate the corrected HCO3- concentration if the anion gap is increased **•Step 4 –** Examine the patient to determine whether the clinical signs are compatible with the acid base analysis
32
•If the compensation is not appropriate, this is evidence of ??
a second acid base disorder
33
**•Primary metabolic acidosis: INC/DEC in ____ indicates?** * mixed metabolic acidosis and r_espiratory acidosis_ * metabolic acidosis and _respiratory alkalosis_ **•Primary respiratory acidosis: INC/DEC in ____ indicates? pH** respiratory acidosis and _metabolic acidosis_ respiratory acidosis and _metabolic alkalosis_
**•Primary metabolic acidosis** metabolic acidosis and _respiratory acidosis:_ ↑ pCO2, metabolic acidosis and _respiratory alkalosis:_ _↓ pCO2,_ **•Primary respiratory acidosis** respiratory acidosis and _metabolic acidosi_s: _↓HCO3 ↓pH_ respiratory acidosis and _metabolic alkalosis_: _•↑HCO3, pH normal_ _• pH might be “normal” appearing_
34
•Should suspect a mixed disorder based on:
* The patient’s history * pCO2 or HCO3 - is abnormal and pH is normal or did not change as expected * pCO2 and HCO3 - move in the opposite direction
35
to check compensation you start with? pCO2 or HCO3 ? Resp? Metabolic
Resp - pCO2 (-40) Metabolic- HCO3 (-35)
36
pCO2 & HCO3 going in SAME direction in respiratory pathology - think??
– MIXED ## Footnote NORMALLY •pCO2 and HCO3 going in OPPOSITE direction
37
pCO2 and HCO3 going in OPPOSITE directions in metabolic pathology???
– MIXED ## Footnote NORMALLY •pCO2 and HCO3 going in SAME direction
38
what must be calcukated w/ ALL patients with metabolic acidosis\*\*\* what is inportant to remeber about this calculation?
Anion Gap •Normal anion gap 6 – 12 mEq/L **use CO2 value from the patient’s BMP or CMP = HCO3** * •WE DO NOT USE Abg Value !!! * •If you get sodium and chloride in question always calculate anion gap\*
39
In patients with a high anion gap metabolic acidosis what must be calculated? how is this interpreted?
dekta ration ## Footnote If one metabolic acidosis is going on OR 2
40
* Anion gap, \> 20 mEq/L = ??? * Anion gap \> 30 mEq/L =
**•Anion gap, \> 20 mEq/L** : primary metabolic acid-base, usually acidosis •regardless of the serum pH or serum bicarb level **•Anion gap \> 30 mEq/L** = metabolic acidosis
41
Calculate the corrected HCO3- concentration if..? ## Footnote * If corrected bicarb is \< 22 = ?? * If corrected bicarb is \> 26 = ??
the anion gap is increased ## Footnote * If corrected bicarb is \< 22 = additional metabolic acidosis present * If corrected bicarb is \> 26 = additional metabolic alkalosis present
42
steps to calculations in metabolic acidosis
Metabolic acidosis: ## Footnote 1. Confirm compensation: HCO3 2. Calculate serum _anion gap_ (HCO3 use CO2) 3. If HIGH anion gap c_alculate delta ration_ (use CO2) 4. _Confirm delta ration w/ corrected HCO3_ using measured HCO3
43
when calculating anion gap & delta ration what vaules do we use?
anion : CO2 value from the patient’s BMP or CMP = HCO3 delta ration - patients Abg HCO3
44
INC anion gap is =
\>12
45
Osmolality measured in mOsmol/L is defined as * Increased serum osmolality = * Decreased serum osmolality=
•Number of dissolved particles in a fluid. Range 285-295 * •Concentration of solutes/electrolytes per liter of solution/water sodium, potassium, glucose and urea * •Check when sodium levels are UP!! **•Increased serum osmolality** =volume depletion and concentration of electrolytes **•Decreased serum osmolality**=volume overload and dilution of electrolyte
46
Dysnatremias occur as a malfunction of this feedback mechanism within the kidneys
ADH is secreted by the posterior pituitary gland and functions to help body hold onto water
47
define osmoreceptiors and their role in water balance??
_Osmoreceptors_ are sensory receptors in hypothalamus which monitor serum osmolality. 1. The hypothalamus then triggered the p_ituitary glad = release ADH_ 2. _ADH tells the kidney to hold onto H2O_ via the renin-angiotensin system. 3. _↑ADH = ↑H2O_ 4. _↑production of angiotensin II_ =stimulate aldosterone release from adrenals. 5. _Aldosterone_ =stimulates reabsorption of Na+ in distal tubules in kidney, water thus flows with sodium.
48
3 classifications of fluids
* Colloids- solutions that do not cross the cell membrane * Crystalloids are commonly prescribed for volume depletion and maintenance fluids * Blood Products should be used when there is acute blood loss
49
•3 types of cystalloid solutions based on tonicity:
\***Isotonic**- same concentration of solutes in blood- cells content stays the same no movement between extracellular and intracellular \***Hypotonic**- lower concentration of solutes than in the cell solutions move into cells causing them to enlarge- swell **Hypertonic**- higher concentration of solutes in solution -solutions pull fluid from the cells- shrink
50
name 3 isotonic fluids
Normal Saline – 0.9% LR D5W
51
Only fluid which is compatible with blood transfusions
Normal Saline – 0.9%
52
Most closely mimics the blood and plasma concentration indications?
LR acute blood loss hypovolemia from third spacing fluid shifts electrolyte imbalances metabolic acidosis
53
•Provides some minimal calories while patient is NPO – diabetics Will hemolyze blood products CI????
D5W ## Footnote Should not be used for dehydration alone as it dilutes the plasma electrolytes _CI -_ arly post op recovery resuscitation increased ICP
54
CI in patients with liver failure who are unable to metabolize lactate and patients with a pH \>7.5
LR ## Footnote Careful in renal patients as Potassium chloride in solution
55
Hypotonic- fluid uses?
.45% NS “half normal” treat hypernatremia DKA hyperosmolar hyperglycemia Prevent dehydration w/ high sugars
56
Draws water out of cells and into intravascular space Volume expanders
Hypertonic- * 3% NaCl * 5% Na Cl * concentrations of solutes
57
•Cure for severe Hyperkalemia
Concentrated dextrose \>10% Higher – followed by insulin bolus
58
Indicated in the following situations: •Shock, Severe burns, pancreatitis, peritonitis, hepatorenal syndrome Risk of anaphylaxis\*\*
Colloids * Albumin * Hespan •“Volume” expanders – they draw fluid into the blood vessels via oncotic pressure
59
Hyponatremia Si/Sx * Mild ( * Mod * Severe
* Mild (130-134) * Mod (120-129) * Severe (\<120) **\<125 = 1st sx is weakness** 140 - 130 * •Thirst * •Impaired taste * •Anorexia * •DOE * •Fatigue/weakness * •¯ sensation **130 ® 120**: Severe GI Sx (ex. vomiting, abdominal cramps) **110-115** * •Confusion * •Lethargy * •Muscle twitching * •Seizures * •Stupor/coma
60
Goal rate of correction in severe hyponatremia is to raise serum sodium concentration by \_\_\_\_mEq/L in a 24 hour period •Maximum rate correction no more than ___ mEq/L in 24 hours
Goal rate of correction in severe hyponatremia is to raise serum sodium concentration by **4-6 mEq/L** in a 24 hour period •Maximum rate correction no more than **8 mEq/**L in 24 hours
61
tx of hyponatremia
**Na \<130: asymptomatic** * 50 mL bolus 3% * Remeasure hourly **Na \<130: symptomatic** * 100 mL of 3% * If sx follow à 2 more 100mL bolus in 30 mins
62
si/sx of Overcorrected Tx hyponatermia
Central pontine myelinolysis destruction of myelin covering nerve cells in the brainstem •Confusion, encephalopathy, lethargy Weakness, paralysis Cerebral edema Brain stem herniation Osmotic demyelination syndrome
63
SIADH is characterized by
**Excess ADH secretion** - DEC diuresis DEC urine and water excretion = INC ­total body water **Dilutional hyponatremia** * the urine is very concentrated. * Not enough water is excreted = too much water in the blood. * This dilutes many substances in the blood such as sodium.
64
* HA/confusion * Lethargy * Anorexia _Euvolemic – but Na is LOW_ _Dx?? & LABS_
SIADH * •↓Serum osmolality - \<280 * •↑ urine osmolality * INC urine Na – conc. Na * DEC blood Na Urine is concentrated but sodium is LOW
65
Tx SIADH
Treat underlying causes •Fluid restriction _•Demeclocycline_ - inhibiting release of ADH * Vasopressors * Salt tablets
66
Hypernatremia \>145 is caused by
_­ INC NA intake (ex. IVF)_ _DEC NA loss_ (ex. Cushing syndrome, hyperaldosteronism) _DEC free body water:_ (ex. GI loss, sweating, burns, diabetes insipidus, osmotic diuresis) Psychogenic polydipsia
67
si/sx ofHypernatremia \>145
* AMS * Ataxia * Seizures * Hyperreflexia * Spasticity/twitching * Irritability * Lethargy • Altered thirst mechanism psychiatric patients elderly institutionalized patients
68
common cause of hypovolemic hypernatremia
**Diabetes Insipidus** Passage of large volumes of dilute urine Cause hypovolemic hypernatremia through 2 mechanisms: 1. Decreased secretion of ADH from posterior pituitary 2. Increased renal resistance to ADH cannot concentrate urine Most common cause is damage after trauma or surgery to the region of the pituitary and hypothalamus
69
The goal in tx of hypernatremia is to lower serum sodium by ____ per hour in less than 24 hours what other 2 tx??
The goal in tx of hypernatremia is to lower serum sodium by **1-2 mEq/l per ho**ur in less than 24 hours ## Footnote **•DSW IV 3-6 mL/kg/hr - monitor every 2 hr** **•Desmopressin (DI)**
70
complication of hypernatremia
**Primary hyperaldosteronism-** problem with the adrenals * usually a benign tumor * excess production of aldosterone- hormone responsible for NA+ and K+ balance * increased sodium and water and decreased potassium
71
ECG changes in ## Footnote Hypokalemia Hyperkalemia Hypocalcemia
**Hypokalemia** - * flat T-waves * ST depression * U waves **Hyperkalemia** * •Tall/peaked T-waves * •Widened QRS * •Flat P-waves **Hypocalcemia**: prolonged QT interval)
72
Meds that cause ## Footnote Hypokalemia Hyperkalemia
**Hypokalemia** •Cellular redistribution (insulin) diuretics, steroids, β-adrenergic agonists) **Hyperkalemia** * ACEI – lisinopril * ARBs – Losartan * aldosterone antagonists – spironolactone
73
* Hyperreflexia * Tetany * Muscle spasms Dx?
Hypocalcemia
74
* Chvostek sign - ?? * Trousseaus sign - ?? Dx??
Hypocalcemia Chvostek sign - facial spasm following the percussion of the facial nerve •Trousseaus sign - spasm of the hand elicited by inflation of a BP cuff
75
Mag deficnecy needs to be tx FIRST in what dzs??
**Hypokalemia** ## Footnote •Supp. Mg - \*\* It is a difficult task to replete potassium in the setting of low magnesium. Therefore be sure to replete magnesium if needed prior to the potassium **Hypocalcemia** •Supp. Mg - Because of the effect of magnesium on calcium balance You must correct a magnesium deficit first
76
Tx of Hyperkalemia
**IV Ca (ex. gluconate, chloride) – FIRST** * •Cardioprotective does not decrease K+ IV **hypertonic glucose w/ regular insulin** – * •moves excess K+ into the cells **IV diuretics (loop or thiazide)** **Kayexalate** - Given resins that bind K+ and excreted in stool Hemodialysist
77
“Bones, Stones, Groans, & Psychiatric Moans” dx?
Hypercalcemia ## Footnote * Bone pain * Muscle weakness * Nephrolithiasis * Fatigue/lethargy * Confusion * Constipation * Depression * Nausea
78
causes of Hypercalcemia
CHIMPANZEE C-CALCIUM SUPPLEMENTS H- HYPERPARATHYROIDISM I- IATROGENIC, IMMOBILIZATION M-MULTIPLE MYELOMA P-PARATHYROID HYPERPLASIA A-ALCOHOL N-NEOPLASM
79
tx of Hypercalcemia
**ITotal Calcium \<12 no immediate treatment.** * Remove contributing factors such as thiazide diuretics, lithium, calcium carbonate. * Encourage hydration **12-14 mg/dL** •IVF _NS_ and _Bisphosphonates_ **\>14 - need aggressive therapy** _Isotonic Salin_e at 200-300 ml/hr and make sure urine output is 100- 150mL/hr _Calcitonin_ – 4 IU/kg and then repeat Calcium level in 4 hrs _Zolendronic acid or Pamindronate_ * •If severe renal impairment - _Denosumab_
80
causes of Hypomagnesemia
•Chronic ETOH use DEC intestinal absorption INC renal excretion INC GI loss (ex. vomiting, diarrhea) * Refeeding syndromes * Starvation
81
si/sx of Hypomagnesemia
* Lethargy * Confusion * Tremors * Convulsions **•Hyperreflexia** •Paresthesia’s
82
si/sx Hypermagnesemia
**DEC DTR’s** * Bradycardia * Hypotension * Flaccid paralysis * Cardiac arrest * Nausea * HA * Hypocalcemia
83
si/sx & ECG differentiating ## Footnote Hypomagnesemia Hypermagnesemia
**Hypomagnesemia**: Hyperreflexia * _ECG_ (widened QRS, ST depressions) **Hypermagnesemia**: DEC DTRs * _ECG_ * peaked T-waves * widened QRS * escape beats
84
tx Hypomagnesemia
**mild asymptomatic cases** - _PO magnesium salts_- precaution may develop osmotic diarrhea * •Mag-Ox- magnesium oxide * •Slow-Mag- magnesium chloride * •Mag-Tab- magnesium lactate • **severe or symptomatic deficienc** - IV replacement * • 1-2 g IV Magnesium sulfate over 2-15 min * •Careful monitoring for rebound hypermagnesemia and arrhythmias * •Caution when giving Mg+ to renal patients
85
\_\_\_\_Cr = ↓kidney function
INCREASE IN **Cr** = ↓kidney function ## Footnote •Better indicator of renal function - Excreted only by the kidney
86
Etiology : pH and ____ changes ## Footnote Respiratory Acidosis Respiratory Alkalosis
pH & pCO2 in OPPOSITE DIRECTION _Respiratory Acidosis_: Due to inadequate ventilation * ↓pH \< 7.35 * ↑PaCO2 \> 45 mmH _Respiratory Alkalosis_ : Due to hyperinflation * ↑pH \> 7.45 * ↓PaCO2 \< 35mm Hg
87
Etiollogy and pH & ____ changes ## Footnote Metabolic Acidosis Metabolic Alkalosis
pH & HCO3 in SAME direction **Metabolic Acidosis**: Due to gain of acid or loss of base Excessive GI loss * ↓pH \< 7.35 * ↓HCO3 22 mEq/L **Metabolic Alkalosis:** Due to loss of acid or gain of base Vomiting / Gastric suction * ↑pH \> 7.45 * ↑HCO3 \>26 mEq/L
88
Hyperkalemia: is assoc w/ metabolic ??? Hypokalemia: is assoc w/ metabolic ???
**Hyperkalemia**: is assoc w/ _metabolic acidosis_ **Hypokalemia**: is assoc w/ _metabolic alkalosis_
89
ECG (flat T-waves, ST depression, U waves) dx?
Hypokalemia
90
ECG (TWiFP) * Tall/peaked T-waves * Widened QRS * Flat P-waves
Hyperkalemia
91
•ECG (prolonged QT interval)
Hypocalcemia