CAIRAN TUBUH, ELEKTROLIT, KESEIMBANGAN ASAM BASA

Ginus Partadiredja

Massa Tubuh Total

Perempuan

Laki-laki

45%

Solids

40%

Solids

55%

Fluids

60%

Fluids

2/3 ICF

1/3 ECF

ICF = Intra cellular fluid = CIS = cairan intra selular

ECF = extra cellular fluid = CES = cairan ekstra selular

80%

20%

Cairan interstisial

Plasma

CES: - Plasma

- Cairan interstisial:

- Cairan limfe - Aqueous humor & vitreous body

- Cairan serebrospinal - Endolimfe, Perilimfe

- Cairan synovial - Cairan pleura, pericardium,

peritoneum

Pertukaran cairan dan elektrolit:

Filtrasi - Difusi Reabsorbsi - Osmosis

Sumber-sumber cairan (input & output)

2500

2000

1500

1000

500

0

Minum

1600 ml

Ginjal

1500 ml

Metabolik 200 ml

Makanan

700 ml

Kulit 600 ml

Paru 300 ml

GIT 100 ml

Metabolik respirasi seluler aerobik (produksi ATP)

sintesis dehidrasi

(glukosa + fruktosa sukrosa + H2O)

Input

Output

Dehidrasi

Saliva

Volume darah

Osmolaritas darah

Mulut & pharynx

kering

Stimulasi osmoreseptor

hypothalamus

Tekanan darah

Produksi renin oleh

Sel2 juxtaglomeral

ginjal

Angiotensin II

Stimulasi pusat

Haus hypothalamus

Rasa haus

Minum

Cairan tubuh

Regulasi Pemasukan Cairan

Asupan NaCl

Konsentrasi plasma Na+

& Cl-

Osmosis air dari CIS

Interstisial plasma

Volume darah

Regangan atrium jantung

Produksi renin

Atrial Natriuretic Peptide (ANP)

Angiotensin II

GFR

Aldosterone

Reabsorbsi NaCl oleh ginjal

Na+ & Cl- via urine (Natriuresis)

Kehilangan air di urine via osmosis

Volume darah

Regulasi Hormonal Na+ & Cl- Renal

Osmolaritas cairan tubuh ADH protein aquoporin 2 membran apical sel permeabilitas terhadap air osmosis ke darah Volume darah Dehidrasi Hiperventilasi Vomitus ADH Diare Demam Keringat banyak Combustio (luka bakar)

Pertukaran air Konsumsi banyak air keracunan air Kehilangan cairan ganti air tawar osmolaritas CES osmosis CES CIS Enema

Konsentrasi Elektrolit & Anion Protein di Plasma, Cairan Interstisial, dan Cairan Intrasel

mEq/L

175

150

125

100

75

50

25

0

Na+ K+ Ca+2 Mg+2 Cl- HCO3- HPO42- SO42- Anion

Protein

Plasma

Cairan interstisial

Cairan intra sel

142 145

10

4 4

140

5 3 0.2

2 2 35

100 117 3

24 27 15

2 2 100

1 1 20

20 2 50

Fungsi ion dari elektrolit:Kontrol osmosis airKeseimbangan asam basaAliran listrik potensial aksi (pada neuron)Kofaktor enzimCairan interstisial >< plasma protein tekanan koloid osmotik plasmaCairan ekstra sel: Na+ & Cl-Cairan intra sel: K+, protein, HPO42-

Natrium Pengaruhi osmolaritas CES (142 mOsm/L dari 300 mOsm/L) Aldosteron reabsorbsi Na+ meningkat Hyponatremia ADH ekskresi air meningkat Hormon ANP ekskresi Na+ meningkat Gagal ginjal retensi Na+ volume darah , Hiperaldosteronisme edema Insufisiensi adrenal aldosteron Diuretik ekskresi Na+ hipovolemia

Chlorida Mudah keluar masuk antara CES & CIS Untuk keseimbangan anion

O2 + HbH HbO2 + H+

H+ + HbO2 HbH + O2

Kalium Resting membrane potential & repolarisasi Aldosterone sekresi K+ Bicarbonate (HCO3-) Ginjal: pengatur utama HCO3- Kalsium 98% skeleton & gigi Pembekuan darah, neurotransmiter, tonus otot, eksitabilitas saraf & otot Hormon parathyroid & calcitriol Ca2+

Ca2+ plasma PTH stimulasi osteoclasts

lepas Ca2+ darah (resorbsi )

reabsorbsi Ca2+ (ginjal)

Calcitriol absorbsi Ca2+ (GIT)

Fosfat (H2PO4-, HPO42-, PO43-) 85% kalsium fosfat (tulang) HPO42- buffer H+, molekul organik, asam nukleat, ATP PTH resorbsi HPO42- darah

inhibisi reabsorbsi HPO42-

Calcitriol absorbsi fosfat & Ca+2 Magnesium Kofaktor enzim Pompa Na+ K+ Aktivitas neuromuskular Transmisi sinaps Fungsi myokardium

Orang-orang beresiko: Bayi, orang tua, infus, drainase, kateter, diuretik, atlit, militer, dll. Penyakit kronik (gagal jantung kongestif, diabetes, chronic obstructive pulmonary diseases (COPD), kanker)

Mekanisme eliminasi H+Sistem bufferEkshalasi CO2Ekskresi H+ via ginjalSistem bufferKebanyakan: asam lemah & garamnyaKonversi asam/ basa kuat lemah

Sistem Buffer Protein Protein Hb & Albumin

R R

NH2 C COOH NH2 C COO- + H+

H H

(sebagai asam, ketika pH meningkat)

R R

NH2 C COOH + H+ +NH3 C COOH

H H

(sebagai basa, ketika pH turun)

Darah di kapiler sistemik:

CO2 + H2O H2CO3

H2CO3 H+ + HCO3-

Hb-O2 + H+ Hb-H + O2

O2 + HbH HbO2 + H+

Sistem Buffer Asam Karbonat Bikarbonat Ginjal mensintesis & reabsorbsi HCO3-

pH turun H+ + HCO3- H2O + CO2 paru

(basa lemah)

pH naik H2CO3 H+ + HCO3-

(asam lemah)

- Tak dapat mengkoreksi pH gangguan respirasi (CO2)

Sistem Buffer Fosfat

- H2PO4- = dihydrogen fosfat (asam lemah)

- HPO42- = monohydrogen fosfat (basa lemah)

OH- + H2PO4- H2O + HPO42- H+ + HPO42- H2PO4- Ekshalasi CO2 CO2 H+ pH

CO2 + H2O H2CO3 H+ + HCO3-

- Ventilasi CO2 H+ pH

Stimulus

pH ( [H+] )

Reseptor kemoreseptor sentral & perifer

(medulla oblongata, aorta, & a. karotis)

Area inspirasi medulla oblongata

Diafragma kontraksi

Ekshalasi CO2

H2CO3 , pH

Umpan Balik Negatif pH Darah oleh Sistem Respirasi

Ketidak Seimbangan Asam Basa pH darah normal 7,35 7,45 Asidosis & alkalosis Asidosis: Depresi sistem saraf pusat, koma, mati Alkalosis: Eksitabilitas saraf meningkat, spasme otot, kejang, mati Kompensasi: sempurna/ parsial pH berubah (metabolik) kompensasi respiratorik (jam) pH berubah (respiratorik) kompensasi renal (berhari-hari) Asidosis/ alkalosis respiratorik pCO2 Asidosis/ alkalosis metabolik HCO3-

Asidosis respiratorik CO2 exhalation pH Emphysema, edema paru, obstruksi jalan nafas, gangguan otot respirasi, kerusakan pusat respirasi di medulla oblongata. Kompensasi oleh ginjal: - Ekskresi oleh H+

- Reabsorbsi HCO3-

- Terapi ventilasi, HCO3- intra vena

Alkalosis respiratorik pCO2 < 35 mmHg Hiperventilasi, defisiensi O2 (ketinggian), rangsangan pada area inspirasi batang otak, penyakit paru, stroke, cemas Kompensasi renal: - Ekskresi H+

- Reabsorbsi HCO3-

Asidosis metabolik

- HCO3- < 22 mEq/ L

Diare, disfungsi renal, ketosis, kegagalan ginjal mengeluarkan H (protein) Terapi: hiperventilasi (kompensasi respiratorik), NaHCO3 intra vena Alkalosis metabolik HCO3- > 26 mEq/ L Vomitus, gastric suctioning, diuretik, penyakit-penyakit endokrin, obat alkalin (antasida), dehidrasi Terapi: hipoventilasi, cairan koreksi defisiensi Cl-, K+

Diagnosis Gangguan Asam Basa

pH HCO3- - pCO2

pH Alkalosis/ asidosis?pCO2/ HCO3-?pCO2 respiratorik; HCO3- metabolik

Usia & Keseimbangan Cairan/ Asam - Basa

BayiDewasaProporsi air75% - 90%CES > CIS (2x)55% - 60%CIS > CES (2x)Rate input output7x >Metabolic rate2x >Perkembangan ginjalBayi x efisiensi dewasaRasio luas permukaan : volume3x >Frequensi nafas30 80x/ menitKonsentrasi ionK+, Cl- >

Orang tua: Volume CIS menurun, K+ menurun, lemak meningkat Orang tua rawan dehidrasi, hipernatremia, hiponatremia, hipokalemia, asidosis. Referensi

1. GJ Tortora & B Derickson. Principles of Anatomy & Physiology, Chapter 27: Fluid, Electrolyte, and Acid-Base Homeostasis

Haemoglobin binds both CO2 and H+ and so is a powerful buffer. Deoxygenated haemoglobin has the strongest affinity for both CO2 and H+; thus, its buffering effect is strongest in the tissues. Little CO2 is produced in red cells and so the CO2 produced by the tissues passes easily into the cell down a concentration gradient. Carbon dioxide then either combines directly with haemoglobin or combines with water to form carbonic acid. The CO2 that binds directly with haemoglobin combines reversibly with terminal amine groups on the haemoglobin molecule to form carbaminohaemoglobin. In the lungs the CO2 is released and passes down its concentration gradient into the alveoli.

The buffering of hydrogen ions formed from carbonic acid is more complicated. The chain of events that occurs within the red cell is most easily understood by referring to figure 6.In the tissues, dissolved CO2 passes into the red blood cell down its concentration gradient where it combines with water to form carbonic acid. This reaction is catalysed by the enzyme carbonic anhydrase. Carbonic acid then dissociates into bicarbonate and hydrogen ions. The hydrogen ions bind to reduced haemoglobin to form HHb. Bicarbonate ions (HCO3-) generated by this process pass back into the plasma in exchange for chloride ions (Cl-). This ensures that there is no net loss or gain of negative ions by the red cell. In the lungs this process is reversed and hydrogen ions bound to haemoglobin recombine with bicarbonate to form CO2 which passes into the alveoli. In addition, reduced Hb is reformed to return to the tissues.

Filtered bicarbonate combines with secreted hydrogen ions forming carbonic acid. Carbonic acid then dissociates to form CO2 and water. This reaction is catalysed by carbonic anhydrase, which is present in the brush border of the renal tubular cells. This CO2 readily crosses into the tubular cell down a concentration gradient.

Inside the cell the CO2 recombines with water, again under the influence of carbonic anhydrase, to form carbonic acid. The carbonic acid further dissociates to bicarbonate and hydrogen ions. The bicarbonate passes back into the blood stream whilst the H+ passes back into the tubular fluid in exchange for sodium. In this way, virtually all the filtered bicarbonate is reabsorbed in the healthy individual.

The predominant buffers in the urine are phosphate (HPO42-) and ammonia (NH3). Phosphate is freely filtered by the glomerulus and passes down the tubule where it combines with H+ to form H2PO4-. Hydrogen ions are secreted in exchange for sodium ions; the energy for this exchange comes from the sodium-potassium ATPase that maintains the concentration gradient for sodium.

Ammonia is produced in renal tubular cells by the action of the enzyme glutaminase on the amino acid glutamine. This enzyme functions optimally at a lower (more acidic) than normal pH. Therefore, more ammonia is produced during acidosis improving the buffering capacity of the urine. Ammonia is unionised and so rapidly crosses into the renal tubule down its concentration gradient. The ammonia combines with H+ to form the ammonium ion, which being ionised does not pass back into the tubular cell. The ammonium ion is therefore lost in the urine, along with the hydrogen ion it contains

*

This results when the PaCO2 is above the upper limit of normal, >6kPa (45mmHg). The relationship between hydrogen ion concentration and CO2 was discussed earlier (Production of Hydrogen Ions). Respiratory acidosis is most commonly due to decreased alveolar ventilation causing decreased excretion of CO2. Less commonly it is due to excessive production of CO2 by aerobic metabolism.

a) Inadequate CO2 Excretion: the causes of decreased alveolar ventilation are numerous, they are summarised in Fig 10. Many of the causes of decreased alveolar ventilation are of interest to theanaesthetist and many are under our control.

b) Excess CO2 Production: respiratory acidosis is rarely caused by excess production of CO2. This may occur in syndromes such as malignant hyperpyrexia, though a metabolic acidosis usually predominates. More commonly, modest overproduction of CO2 in the face of moderately depressed ventilation may result in acidosis. For example, in patients with severe lung disease a pyrexia or high carbohydrate diet may result in respiratory acidosis

Whats normal?

http://faculty.ucc.edu/biology-atsma/misc/resp102.htm

http://humanisamiracle.imanisiteler.com/6_clip_image018.jpg

*

Bronchodilators such as beta agonists (eg, albuterol and salmeterol), anticholinergic agents (eg, ipratropium bromide and tiotropium), and methylxanthines (eg, theophylline) are helpful in treating patients with obstructive airway disease and severe bronchospasm. Theophylline may improve diaphragm muscle contractility and may stimulate the respiratory center.

Oxygen TherapyBecause many patients with hypercapnia are also hypoxemic, oxygen therapy may be indicated. Oxygen therapy is employed to prevent the sequelae of long-standing hypoxemia. Patients with COPD who meet the criteria for oxygen therapy have been shown to have decreased mortality when treated with continuous oxygen therapy. Oxygen therapy has also been shown to reduce pulmonary hypertension in some patients. Oxygen therapy should be used with caution because it may worsen hypercapnia in some situations. For example, patients with COPD may experience exacerbation of hypercapnia during oxygen therapy. This observation is thought by many to be primarily a consequence of ventilation-perfusion mismatching, in opposition to the commonly accepted concept of a reduction in hypoxic ventilatory drive. The exact pathophysiology, however, remains controversial. Hypercapnia is best avoided by titrating oxygen delivery to maintain oxygen saturation in the low 90% range and partial arterial pressure of oxygen (PaO2) in the range of 60-65 mm Hg.