Keseimbangan cairan, asam dan basa dan elektrolit

Fungsi Air dalam Fisiologi Manusia

1. Media semua reaksi kimia tubuh 2. Berperan dalam pengaturan distribusi kimia &
3. 4. 5. 6. 7.

biolistrik dalam sel Alat transport hormon & nutrien Membawa O2 dari paru-paru ke sel tubuh Membawa CO2 dari sel ke paru-paru Mengencerkan zat toksik dan waste product serta membawanya ke ginjal dan hati Distribusi panas ke seluruh tubuh

Distribusi Cairan Tubuh

Volume cairan tubuh

- wanita (17-39 th) : 50% BB - pria (17-39 th): 60% BB

Distribusi cairan tubuh - cairan intrasel (CIS) = 2/3 cairan tubuh - cairan ekstrasel (CES) = 1/3 cairan tubuh

* intravaskular (plasma) = 25% CES * intersisial = 75% CES

Komposisi Ion pd Cairan Tubuh

1.
2.

Perpindahan Cairan & Elektrolit Difusi

perpindahan molekul dari tekanan/konsentrasi tinggi ke tekanan/konsentrasi rendah Osmosis perpindahan air dari konsentrasi zat terlarut rendah ke konsentrasi zat terlarut tinggi osmolaritas: ukuran konsentrasi suatu larutan - isotonus konsentrasi larutan = plasma darah Transport aktif perpindahan molekul dari tekanan/konsentrasi rendah ke konsntrasi tinggi dgn menggunakan energi

3.

Tekanan Cairan
1. Tekanan osmotik & onkotik
Tekanan osmotik: tekanan untuk mencegah aliran osmotik cairan Tekanan onkotik: gaya tarik s/ koloid agar air tetap berada dalam plasma darah di intravaskular

2. Tekanan hidrostatik ( filtration force)

tekanan yang digunakan oleh air dalam sistem tertutup

Perpindahan cairan di kapiler

Selektivitas Permeabilitas Membran

Membran sel

lipid bilayer

Permeabilitas membran sel bersifat selektif

terhadap: ion (kanal ion), air (aquaporin)

Pengaturan Keseimbangan Cairan & Elektrolit

1. Pengaturan volume cairan ekstrasel * Asupan cairan
* Peranan Ginjal * Pengontrolan tekanan darah - Hormon Atriopeptin (Atrial Natriuretic peptide) * Pengontrolan keseimbangan garam - Sistem Renin-Angiotensin-Aldosteron

2. Pengaturan osmolaritas cairan ekstrasel

* Perubahan osmolaritas di nefron * Peranan Vasopresin

PENGATURAN VOLUME CAIRAN EKSTRASEL

Peranan ginjal

Filtrasi, Reabsorpsi, Sekresi & Ekskresi di Nefron

Respons thd Peningkatan Tekanan Darah

Respons thd Penurunan Tekanan Darah

Peranan Atriopeptin

Peranan Renin-Angiotensin-Aldosteron

Respons thd Asupan Garam

PENGATURAN OSMOLARITAS CAIRAN EKSTRASEL

Perubahan osmolaritas di Nefron

Peranan Vasopresin

Mekanisme Kerja Vasopresin/ADH

Pengaturan Neuroendokrin dalam Keseimbangan Cairan

1.

Sistem saraf Reseptor

- Baroreseptor di arkus aorta & sinus karotis - Reseptor regang tekanan rendah di thorak

2.

Sistem saraf simpatis Sistem endokrin

- Angiotensin II reabsorpsi Na - Aldosteron reabsorpsi Na - Antidiuretic hormone (ADH) reabsorpsi air - Atrial natriuretic peptide (ANP/atriopeptin) ekskresi Na & air

Perubahan Volume & Osmolaritas Cairan

Faktor-faktor yang mempengaruhi Keseimbangan Cairan & Elektrolit

Umur

Suhu lingkungan
Diet Stres Penyakit

Keseimbangan Asam & Basa

Keseimbangan asam-basa pengaturan konsentrasi ion H+ dalam cairan tubuh
Ion H+ sbg hasil dari metabolisme:
C6H12O6 + O2 CO2 + H2O H2CO3 H+ + HCO3-

[H+] dlm plasma pH plasma darah = 7,4 Sistem dapar (buffer) menghambat

perubahan pH yang besar jika ada penambahan asam atau basa

Sistem Dapar
1.
2. 3. 4.

Asam karbonat:Bikarbonat sistem dapar di CES untuk asam non-karbonat Protein sistem dapar di CIS & CES Hemoglobin sistem dapar di eritrosit untuk asam karbonat Phosphat sistem dapar di ginjal dan CIS

Keseimbangan ion H+

Mekanisme Regulasi Keseimbangan Asam-Basa

Sistem dapar hanya mengatasi ketidakseimbangan

asam-basa sementara Ginjal: meregulasi keseimbangan ion H+ dengan menghilangkan ketidakseimbangan kadar H+ secara lambat; terdapat sistem dapar fosfat & amonia Paru-paru: berespons scr cepat thd perubahan kadar H+ dalam darah & mempertahankan kadarnya sampai ginjal menhilangkan ketidakseimbangan tersebut

Regulasi Pernapasan dlm Keseimbangan Asam-Basa

Kadar CO2 meningkat pH menurun Kadar CO2 menurun pH meningkat Kadar CO2 & pH merangsang kemoreseptor

yg kemudian akan mempengaruhi pusat pernapasan hipoventilasi meningkatkan kadar CO2 dlm darah hiperventilasi menurunkan kadar CO2 dlm darah

Regulasi Pernapasan dlm Keseimbangan Asam-Basa

Regulasi Ginjal dlm Keseimbangan Asam-Basa

Sekresi H+ ke dalam filtrat & reabsorpsi HCO3- ke CES menyebabkan pH ekstrasel meningkat HCO3- di dlm filtrat diabsorbsi
Laju sekresi H+ meningkat akibat penurunan

pH cairan tubuh atau peningkatan kadar aldosteron Sekresi H+ dihambat jika pH urin < 4,5

Gangguan Keseimbangan Asam-Basa

1. 2.

3.
4.

Asidosis respiratori hipoventilasi retensi CO2 H2CO3H+ Alkalosis respiratori hiperventilasi CO2 banyak yg hilang H2CO3 H+ Asidosis metabolik Diare, DM HCO3- PCO2 H+ Alkalosis metabolik muntah H+ HCO3- PCO2

Kompensasi Sistem Pernafasan terhadap Asidosis Metabolik

Kompensasi Ginjal terhadap Asidosis Respiratorik

Nomogram Davenport

INTERPRETASI AGD
Lihat pH darah

pH < 7,35

pH > 7,45

ASIDOSIS

ALKALOSIS

Lihat pCO2

Lihat HCO3-

< 40mmHg

> 40 mmHg

< 24 mM

> 24 mM

METABOLIK

RESPIRATORIK RESPIRATORIK

METABOLIK

TERKOMPENSASI atau TIDAK?

Lihat pH kembali - jika mendekati kadar normal (7,35-7,45) terkompensasi - jika belum mendekati normal tidak terkompensasi atau terkompensasi sebagian Jika asidosis respiratorik dgn HCO3- < 24 mM terkompensasi sebagian Jika asidosis metabolik dgn pCO2 < 40 mmHg terkompensasi sebagian Jika alkalosis respiratorik dgn HCO3- > 24 mM terkompensasi sebagian Jika alkalosis metabolik dgn pCO2 > 40 mmHg terkompensasi sebagian

LATIHAN

pH 7.32, PCO2 40, HCO3 19 pH 7.55, PCO2 20, HCO3 22 pH 7.55, PCO2 37, HCO3 30 pH 7.49, PCO2 35, HCO3 29 pH 7.30, PCO2 50, HCO3 29 pH 7.43, PCO2 53, HCO3 30 pH 7.44, PCO2 38, HCO3 26 pH 7.43, PCO2 32, HCO3 20

Asidosis metabolik tdk terkompensasi Alkalosis respiratorik tdk terkompensasi Alkalosis metabolik tdk terkompensasi

Alkalosis metabolik tdk terkompensasi

Asidosis respiratorik terkompensasi sebagian Alkalosis metabolik terkompensasi

normal
Alkalosis respiratorik terkompensasi

Dr. SUHAEMI, SpPD, Finasim

GANGGUAN ELEKTROLIT

Electrolyte and protein anion concentrations in plasma, interstitial fluid, & intercellular fluid

Electrolytes
sodium (Na+)

potassium (K+)
chloride (Cl-) calcium (Ca2+) magnesium (Mg2+) bicarbonate (HCO3-) phosphate (PO42-) sulfate (SO42-)

Korey Stringer

1974 - 2001
Korey Stringer was a professional football player for the Minnesota Vikings. He collapsed during practice from excessive heat and died the following day.

Electrolytes
Charged particles in solution Cations (+) Anions (-) Integral part of metabolic and cellular

processes

Positive or Negative?
Cations (+)
Sodium

Anions (-)
Chloride Bicarbonate

Potassium
Calcium Magnesium

Phosphate
Sulfate

Major Cations

EXTRACELLULAR
SODIUM (Na+)

INTRACELLULAR
POTASSIUM (K+)

Electrolyte Imbalances
Hyponatremia/

Hypocalcemia/

hypernatremia
Hypokalemia/

Hypercalcemia
Hypophosphatemia/

Hyperkalemia
Hypomagnesemia/

Hyperphosphatemia
Hypochloremia/

Hypermagnesemia

Hyperchloremia

Sodium
Major extracellular cation Attracts fluid and helps preserve fluid volume Combines with chloride and bicarbonate to help

regulate acid-base balance

Normal range of serum sodium 135 - 145 mEq/L

Sodium and Water

If sodium intake suddenly increases, extracellular fluid concentration also rises
Increased serum Na+ increases thirst and the

release of ADH, which triggers kidneys to retain water Aldosterone also has a function in water and sodium conservation when serum Na+ levels are low

Sodium-Potassium Pump
Sodium (abundant outside cells) tries to get into cells
Potassium (abundant inside cells) tries to get out of cells Sodium-potassium pump maintains normal concentrations Pump uses ATP, magnesium and an enzyme to maintain sodium-potassium

concentrations Pump prevents cell swelling and creates an electrical charge allowing neuromuscular impulse transmission

Hypokalemia
Usually secondary to:
GI loss (vomiting, diarrhea) Urinary losses (diuretics, RTA)

Also think about : co-existing electrolyte abnormality (hypomagnesemia), hyperaldosteronism, insulin therapy, albuterol, alkalosis)

Indications for replacement:

Evidence of potassium loss Significant deficit in body potassium Acute therapy in redistributive disorders (periodic

paralysis, thyrotoxicosis)

Hypokalemia
Symptoms: usually manifest when serum K <3.0
Muscle weakness (K <2.5), cramps, rhabdomyolysis

Respiratory muscle weakness

GI symptoms: anorexia, nausea, vomiting Cardiac arrhythmias: atrial tachycardia, junctional

tachycardia, AV block, ventricular tachycardia or fibrillation EKG abnormalities: PAC, PVC, sinus bradycardia, ST segment depression, decreased amplitude of T-wave, increased amplitude of U-wave (mostly in V4-V6) If prolonged hypokalemia: functional changes in the kidney and glucose intolerance

Therapy
Calculate potassium deficit (if normal distribution is present-

do NOT use in DKA or HONK)

Acute: .27meq/L decrease in serum K+ for every 100meq reduction in total

potassium stores Chronic: 1meq/L decrease in serum K+ for every 200-400meq reduction in total potassium stores

Simplified: Goal K Serum K x 100 = total meq K required serum Cr 10meq of KCL will raise the serum K by ~.1meq/L

Formulations
Potassium Chloride : PREFERRED AGENT
Most patients with hypokalemia and acidosis are also chloride

depleted Raises serum potassium at a faster rate Available as salt substitute, liquid, slow release tablet or capsule, and IV

Oral: 40meq tid-qid; IV: Peripheral line 10meq/hr

Central line 20meq/hr

Potassium Bicarbonate/Citrate/Acetate:
can be used in patients with hypokalemia and metabolic acidosis

Potassium Phosphate:
Rarely used (Fanconi syndrome with phosphate wasting)

Example

72 year old female admitted for weakness and dehydration

due to acute gastroenteritis. She is having up to 6 BM/day. Her serum K on admission is 2.5 meq and serum Cr is 2.0. EKG reveals u-waves. 1. How much potassium do you order?
4-2.5 x 100 = 75meq 2

2. 3.

What formulation do you choose?

KCL; if bicarb is low then consider potassium bicarb or acetate

What route should the potassium be administered? 40meq

(initial) oral and 40meq IV; (re-assess 2-4 hours later and give more orally if needed and tolerating po)

4.

Serum potassium remains low, what else could be contributing?

Low magnesium, ongoing diarrhea

Hypomagnesemia
Average daily intake: 360mg Presence of low magnesium (nearly 12% of hospitalized

patients) suspected in following cases:

Chronic diarrhea Hypocalcemia Refractory hypokalemia Ventricular arrhythmias

Symptoms/Signs :
Tetany (seizures in children/neonates) Hypokalemia Hypoparathyroidism hypocalcemia (<1.2mg/dL) Vitamin D deficiency (due to low calcitriol) EKG changes: widened QRS, peaked T-waves, dimunition, PR interval prolongation, Ventricular arrhythmias (especially during ischemia or bypass), think TORSADES

What Do You See?

CNS
Altered LOC

Confusion
Hallucinations

What Do You See?

Neuromuscular
Muscle weakness

Leg/foot cramps
Hyper DTRs

Tetany
Chvosteks & Trousseaus signs

What Do You See?

Cardiovascular
Tachycardia

Hypertension
EKG changes

What Do You See?

Gastrointestinal
Dysphagia

Anorexia
Nausea/vomiting

Therapy
IV if symptomatic (magnesium sulfate)

1.5-1.9mg/dL 2g magnesium sulfate IV 1.2-1.4mg/dL4g .8-1.1mg/dL 6g <.8mg/dL 8g Torsades: 2g IV push Low K/Ca w/ tetany/arrhythmia: 50meq (~6g) of IV Mg given slowly over 8-24 hrs

Oral if asymptomatic: each tablet contains 60-84mg, give 2-4

tabs/day in mild cases, 6-8 tabs for severe depletion -Slow Mag (magnesium chloride) -Mag-Tab SR (magnesium lactate) -Magnesium Oxide (formulary at the VA)

Avoid replacement in patients with reduced GFR Treat underlying disease (PPI, diuretics, alcohol, uncontrolled
diabetes)

Therapy
Goal of therapy:
maintain plasma magnesium concentration over 1.0mg/dL acutely in

symptomatic patients In cardiac patients, maintain Mg >1.7 (usually goal 2.0mg/dL) to avoid arrhythmias Serum levels are poor reflection of actual body stores (mostly intracellular) so aim for high-normal serum level

Adverse effects:
Abrupt elevation of plasma Mg can remove the stimulus for Mg

retention and lead to increased excretion Diarrhea Drug interactions Magnesium intoxication, Aluminum intoxication

Mag Sulfate Infusion

Use infusion pump - no faster than 150

mg/min Monitor vital signs for hypotension and respiratory distress Monitor serum Mg++ level q6h Cardiac monitoring Calcium gluconate as an antidote for overdosage

Hypocalcemia
Clinical Manifestations:
Acute: serum Ca <7.5mg/dL
Neurologic: tetany (from paresthesias to seizures and bronchospasm) Cardiac: prolonged QT, hypotension, heart failure, arrhythmia Papilledema Psychiatric manifestations

Chronic:
EPS, dementia, cataracts, dry skin

Etiology:

Vitamin D PTH Hypomagnesemia Drugs

Therapy
Correct for albumin
Ca lower by .8mg/dL for every 1g/dL reduction in serum albumin or check ionized calcium

Level can be altered by acid/base disturbance Symptomatic or acute serum Ca <7.5mg/dL:

IV Calcium gluconate 1-2g(amp) over 10-20min (temporary rise for

2-3 hrs, must be followed by slower infusion 50mL/hr if Ca remains low)

Asymptomatic and serum Ca >7.5mg/dL or chronic:

Oral therapy: calcium carbonate or citrate 1-2g/day (500mg bid-

qid)

Add Vitamin D in following cases:

Hypoparathyroidism: Vitamin D (Calcitriol .25-.5mcg bid) Vitamin D deficiency: 50,000IU/week for 6-8 weeks then 800-1000IU

daily
Erogcalciferol (D3) Cholecalciferol (D2)

Therapy
Goals of therapy:
Treat and prevent manifestations of hypocalcemia In hypoparathyroidism: to raise serum Ca to low-normal range (8.0-

8.5mg/dL)

Adverse Effects:
Rapid infusion- bradycardia, hypotension
Extravasation- tissue necrosis Hypercalcemia Hypercalciuria

Constipation
Hypophosphatemia Milk-alkali syndrome

Example
35 y/o male with hypoparathyroidism secondary to DiGeorges presents with serum Ca of 6.2, albumin of 3.8, ionized Ca .77. Has some mild muscle cramps, otherwise asymptomatic.
1.

How do you initially treat his hypocalcemia?

- IV Calcium Gluconate 1g IV over 10-20min

2. Repeat serum Ca is 6.6, how do you proceed with treatment?

-start Calcium gluconate 1mg/mL in D5W 50mL/hr infusion

2. After initial treatment, what maintenance regimen should you

initiate?
-Calcitriol (.5mcg bid, titrated up in this patient) -Calcium carbonate (1950mg po tid in this patient)

Preferred Route

Preferred Formulation Potassium Chloride

Dosage

Response

Potassium

Oral

10meq tabs

.1 increase serum K for 10meq given

Magnesium

Oral

Magnesium Oxide Magnesium Sulfate Calcium Gluconate

2-4 tabs/day
(420mg; 20meq/tab)

IV- arrhythmia Calcium IV- acute

2g IVP or slow infusion 1-2amp (rapid) 1mg/mL in D5W, 50mL/hr Infusion

.5 increase for 2g (50meq) IV

.5mg/dL increase serum Ca for 1g given

Oral- maintenance Calcium Carbonate Phosphate Oral Sodium Phosphate (neutra-phos)

1-2g/day
1-2 packet tidqid
1packet=250mg or 8mmol

1.2mg/dL increase serum PO4

(weight based)

Electrolyte Imbalances
Electrolyte
Sodium Na+ Potassium K+ Hydrogen carbonate HCO3Chloride Cl-

Normal range (mmol / L) 135 - 145 3.5 5.0 24 - 30 100 - 106

Excess
Hypernatremia (increased urine excretion; excess water loss) Hyperkalemia (renal failure, low blood pH)

Defiency
Hyponatremia (dehydration; diabetesrelated low blood pH; vomiting, diarrhea) Hypokalemia (gastointestinal conditions)

Hypercapina (high blood pH; hypoventilation) Hyperchloremia (anemia, heart conditions, dehydration)

Hypocapnia (low blood pH; hyperventilation; dehydration) Hypochloremia (acute infections; burns; hypoventilation)

Regulation of Sodium
Renal tubule reabsorption affected by hormones:

Aldosterone

Renin/angiotensin
Atrial Natriuretic Peptide (ANP)

75

Electrolyte imbalances: Sodium

Hypernatremia (high levels of sodium)
Plasma Na+ > 145 mEq / L Due to Na + or water Water moves from ICF ECF Cells dehydrate

76

77

 Hypernatremia Due to:

Hypertonic IV soln. Oversecretion of aldosterone

Loss of pure water

Long term sweating with chronic fever Respiratory infection water vapor loss Diabetes polyuria Insufficient intake of water (hypodipsia)

78

Clinical manifestations of Hypernatremia

Thirst
Lethargy Neurological dysfunction due to dehydration

of brain cells Decreased vascular volume

79

Treatment of Hypernatremia
Lower serum Na+

Isotonic salt-free IV fluid Oral solutions preferable

80

Hyponatremia
Overall decrease in Na+ in ECF Two types: depletional and dilutional

Depletional Hyponatremia
Na+ loss: diuretics, chronic vomiting Chronic diarrhea Decreased aldosterone Decreased Na+ intake

81

 Dilutional Hyponatremia:
Renal dysfunction with intake of hypotonic fluids Excessive sweating increased thirst intake of

excessive amounts of pure water Syndrome of Inappropriate ADH (SIADH) or oliguric renal failure, severe congestive heart failure, cirrhosis all lead to:

Impaired renal excretion of water

Hyperglycemia attracts water

82

 Neurological symptoms

Clinical manifestations of Hyponatremia

Lethargy, headache, confusion, apprehension, depressed

reflexes, seizures and coma

Muscle symptoms
Cramps, weakness, fatigue

Gastrointestinal symptoms
Nausea, vomiting, abdominal cramps, and diarrhea

Tx limit water intake or discontinue meds

83

What Do You See?

Think S-A-L-T
Skin flushed Agitation

Low grade fever

Thirst

Neurological symptoms

Signs of hypovolemia

What Do We Do?
Correct underlying disorder
Gradual fluid

Monitor for s/s of cerebral edema

Monitor serum Na+

replacement

level Seizure precautions

Hypokalemia
Serum K+ < 3.5 mEq /L
Beware if diabetic

Insulin gets K+ into cell Ketoacidosis H+ replaces K+, which is

lost in urine

adrenergic drugs or epinephrine

86

Causes of Hypokalemia
Decreased intake of K+
Increased K+ loss

Chronic diuretics Acid/base imbalance Trauma and stress

Increased aldosterone
Redistribution between ICF and ECF
87

Clinical manifestations of Hypokalemia

Neuromuscular disorders Weakness, flaccid paralysis, respiratory

arrest, constipation

Dysrhythmias, appearance of U wave Postural hypotension Cardiac arrest Others table 6-5 Treatment Increase K+ intake, but slowly, preferably by foods

88

What Do You See?

Think S-U-C-T-I-O-N
Skeletal muscle weakness U wave (EKG changes) Constipation, ileus Toxicity of digitalis glycosides Irregular, weak pulse Orthostatic hypotension Numbness (paresthesias)

What Do We Do?
Increase dietary K+
Oral KCl supplements IV K+ replacement Change to K+-sparing diuretic Monitor EKG changes

IV K+ Replacement
Mix well when

adding to an IV solution bag Concentrations should not exceed 40-60 mEq/L Rates usually 10-20 mEq/hr

NEVER GIVE IV PUSH POTASSIUM

Hypocalcemia
Hyperactive neuromuscular reflexes and tetany

differentiate it from hypercalcemia Convulsions in severe cases Caused by:

Renal failure Lack of vitamin D Suppression of parathyroid function Hypersecretion of calcitonin Malabsorption states Abnormal intestinal acidity and acid/ base bal. Widespread infection or peritoneal inflammation
92

Hypocalcemia
Diagnosis:
Chvosteks sign

Trousseaus sign

Treatment
IV calcium for acute Oral calcium and vitamin D for chronic

93

Hyperkalemia
Serum K+ > 5 mEq/L
Less common than Caused by altered

kidney function, increased intake (salt

hypokalemia

substitutes), blood
transfusions, meds (K+sparing diuretics), cell death (trauma)

What Do You See?

Irritability Paresthesia Muscle weakness (especially legs)

EKG changes (tented T wave)

Irregular pulse Hypotension Nausea, abdominal cramps, diarrhea

What Do We Do?
Mild
Loop diuretics (Lasix) Dietary restriction

Emergency
10% calcium gluconate

for cardiac effects

Sodium bicarbonate for

Moderate
Kayexalate

acidosis

Electrolytes

water, dextrose, potassium citrate, sodium chloride and sodium citrate. Nonmedicinal ingredients: FD&C Blue #1 and Red #40 (grape flavor) and FD&C Red #40 (bubblegum flavor). Per 8 fl oz Sodium 10.6 mg Potassium 4.7mg Chloride 8.3 mg Dextrose 5.9g Calories 24

water, sucrose syrup, glucosefructose syrup, citric acid, natural and artificial flavors, salt, sodium citrate, monopotassium phosphate, ester gum, sucrose acetate isobutyrate, red 40, blue 1 Per 8 fl oz Total fat 0g Sodium 110mg Potassium 30mg Total carbs 14g Sugars 14g Calories 50