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1 Arterial Blood Gas Analysis in patients with respiratory failure 울산의대서울아산병원호흡기내과 홍상범

2 Case 1 30 갑 / 년의흡연력을가진 58 세남자가평소건강히지내던중내원 5 일전부터열, 식욕부진, 전신쇠약감이있었고, 내원당일고열과노란색객담, 복통및호흡곤란보이며의식소실이있어응급실로왔다. 혈압 190/120 mmhg, 맥박수 120 회 / 분, 호흡수 24 회 / 분, 체온 38.3 이었다. 급성병색을보였으며의식은혼돈상태였다. 양쪽흉부하부에서흡기시수포음이청진되었다. 심음은정상이었다.

3 Case 1 혈액검사소견상백혈구 15,100 /ul ( 호중구 90%) 이었고, Na+, K+, Cl 는각각 143, 4.4, 106 mmol/l 이었다. 단순흉부엑스선사진상양쪽폐하엽에경화 (consolidation) 소견이관찰되었다. 산소마스크로 10 L/min 공급상태에서동맥혈가스분석검사는 ph 7.438, PaO mmhg, PaCO mmhg, HCO mmol/l, base excess -3.7 mmol/l, SaO2 94% 이었다. 동맥혈가스분석검사의해석은?

5 Case 1 1) 진단은폐렴에의한패혈증환자이다. 2) 산소화상태는산소마스크로 10 L/min 공급상태에서 PaO2 가 67.2 mmhg 로저산소혈증을보이고있다. High-flow oxygen system 이아니므로일정한양의산소가공급되지않아 A-aDO2 는정확한계산이어렵다. 그러나 O2 의공급에도 PaO2 가상당히낮은것을보면 shunt 가저산소증의주된역할을할가능성이있다.

6 3) 산 - 염기상태 : ph 는정상범위를보이고있다. HCO3 와 base excess 가낮아서대사산증이있는것으로추정된다. anion gap 은 143 ( ) = 17.6 으로증가되어있어서 high anion gap 대사산증이다. AG/ HCO3- = ( )/( ) <1 ~ 2> Case 1 PaCO2 의예상감소는공식을이용하면 1.2 ( ) = 5.52 이므로 34.5 mmhg (40-5.5) 가예상치이다. 그러나실제측정치는 29.4 mmhg 이므로호흡알카리증이동반. 4) 결론적으로대사산증그리고호흡알카리증이동반된예로해석된다.

7 동맥혈가스분석검사의결과는 ph- PCO2 (mm Hg)-PO2 (mm Hg)- HCO3-(mEq/L) 순으로표기한다.

8 동맥혈채취법은피검자의환기상태와가스교환, 산소화상태및산 - 염기의상태를분석하기위해시행하는검사이다. 특히호흡곤란이나청색증등을호소하는천식, 만성폐쇄성폐질환및급성호흡곤란증후군등의호흡기질환뿐만아니라약물중독, 당뇨또는알코올성케톤산혈증, 패혈증쇼크, 심부전, 급성심근경색증, 심폐소생술전후등의 위중하고급박한환자의상태를빠르게분석

9 Buffer ph = O 2 CO 2 H + Arterial blood Clark Electrode Sanz Electrode Serveringhaus Electrode With the use of blood gas electrodes, the amount of oxygen (O 2 ), carbon dioxide (CO 2 ), and hydrogen ions (H + ) dissolved in the blood can be measured.

10 Normal blood gas ph PCO 2 PO 2 HCO - 3 SO 2 ABGA mmhg mmhg meq/l 98 % VBGA mmhg mmhg meq/l 75 %

11 Information from ABGA 1. Oxygenation 2. Ventilation 3. Gas exchange 4. Acid-Base balance

12 Air PO 2 = 159 mmhg Alveoli PO 2 = 100 mmhg Arterial blood PO 2 = 95 mmhg Venous blood Oxygen cascade PO 2 = 40 mmhg We can now trace the transfer of O2 from air to tissues via a pathway known as the oxygen cascade.

13 Listlessness Agitation Confusion Disorientation Hypoxia The signs and symptoms of hypoxia are nonspecific and may include listlessness, agitation, confusion, and disorientation.

14 Gas Exchange Since the PaO 2 is higher than the PvO 2, O2 will diffuse from the lungs into the blood.

15 O 2 A-aDO 2 CO 2 P A O 2 = [F I O 2 (P B -PH 2 O)]-P a CO 2 R Normal A-aDO 2 = mm Hg in room air = mm Hg in 1.0 of FiO 2

16 Diagnostic approach to the patients with hypoxemia

17 The saturation of Hb with O 2 will vary according to the level of PaO 2 and is expressed by a curve called the oxyhemoglobin dissociation curve.

18 Right shift : increased PCO2, H+, Temperature, or 2,3- DPG Example : M/23, AGC with lung metastasis, pneumonia (-10.2) (FIO2 60%) Recommand : SaO2 88 ~ 95 %

19 PaCO 2 = Alveolar Ventilation

20 Ventilation Minute ventilation = alveolar ventilation + dead space ventilation Physiologic dead space = anatomical dead space + alveolar dead space

21 인공환기기의분당환기량을설정시 현재분당환기량 PaCO2 = 새로운분당환기량 목표 PaCO2 의공식을이용하여구하면된다. 단조직에서의 CO2 의생산과사강환기가일정하다는가정

22 Approximate Paco 2 -ph Relationship Paco 2 [HCO 3- ]P* (mm Hg) ph (mmol3/l) [HCO 3- ]p = plasma bicarbonate concentration

23 Sudden accumulation of CO 2 1. Acute respiratory acidosis : affect heart and brain function 2. Effect of rapid rise in PaCO 2 : vasodilation, cerebral edema 3. Associated fall in PaO 2

24 Traditional Conception of ph PaCO 2 H 2 CO 3 = PaCO 2 (0.03) = Respiratory component [HCO 3- ] Metabolic component 7.4 ph Acid-base balance ph ([H + ]) is not an independent variable. [H + ] is passive, being determined to some extent by each of the independent variables.

25 ph determinants Strong ion difference : Na+, K+, CL-, lactate,, The total weak acid buffers (Atot) : albumin, phosphate PCO2

26 Sequential response to a H + load H + load Extracellular buffering by HCO 3 - Respiratory buffering by decreasing PCO 2 Intracellular and bone buffering Renal H + excretion Immediately Minutes to hours Two to four hours Hours to days

27 Response to an increase in the PCO 2 PCO 2 Intracellular buffering 10 to 30 min Renal H + excretion Hours to days

28 Approximate compensatory response to primary acid-base disorder Metabolic acidosis Δ PaCO 2 = Δ 1.2HCO 3- Metabolic alkalosis Δ PaCO 2 = Δ 0.7HCO 3- Respiratory acidosis Acute Δ HCO 3- = Δ 0.1PaCO 2 Chronic (after 3-5d) Δ HCO 3- = Δ 0.35PaCO 2 Respiratory alkalosis Acute Δ HCO 3- = Δ 0.2PaCO 2 Chronic (after 3d) Δ HCO 3- = Δ 0.4PaCO 2

29 Respiratory? Acidosis Metabolic? Respiratory? Alkalosis Metabolic? These are the four primary conditions that can disturb overall acida cid- base balance.

30 ph = Alkalemia PaCO 2 = Normal or high = Simple metabolic alkalosis HCO 3- = High When alkalemia is caused exclusively by a high HCO 3-, we are dealing with a simple metabolic alkalosis.

31 Causes of Metabolic alkalosis Loss of hydrogen -GI loss -Renal loss - H+ movement into cells Retension of bicarbonate - Massive blood transfusion - Administration of NaHCO3 - Milk-alkali syndrome Contraction alkalosis (fluid loss contain Cl - ) - Loop or thiazide-type diuretics - Gastric loss in pts. with achlorhydria - Sweat loss in CF

32 ph = Acidemia PaCO 2 = Normal or low = Simple metabolic acidosis HCO 3- = low When acidemia is caused exclusively by a low [HCO 3- ], we are dealing with a simple metabolic acidosis.

33 Respiratory compensation - begin 1-2 h ~ max h - as much as 30 L/min (VT > RR) - To PCO 2 of 10 to 15 mmhg - Last for only a few days - Increasing MV WOB respiratory m. fatigue RF diversion of blood flow from vital organ to respiratory m. organ injury - Acidemia arrhythmia & myocardial O2 demand

34 Anion Gap Major cation (Na + ) Major anion (Cl - + HCO 3- ) Unmeasured anion unmeasured cation K+, Ca2+, Mg2+ Protein, p, sulfate, organic anion Normal value : 5 11 meq/l Adjusted in case of hypoalbuminemia - AG 2.5 meq/l for plasma albumin 1 g/dl

35 Increased AG in ICU Ketosis DKA, AKA Lactic acidosis Poisoning Renal failure sepsis

36 Δ AG/Δ HCO 3 - H + + BHB - HBHB More than 50% of H + is buffered by the cells, not by HCO 3 - Δ AG/Δ HCO ~2, uncomplicated high AG MAc - below 1, combined high and normal AG MAc - above 2, MAc with MAlk

37 대사산증의임상증상 호흡기증상으로는호흡곤란과 Kussmaul 호흡이관찰되고동맥혈 ph 가 이하로되면심실성부정맥, 심근수축력저하, 카테콜라민에대한반응저하를유발한다. 신경증상으로는기면 (lethargy) 및혼수가초래될수있고수소이온의골완충 (bone buffer) 과정에서칼슘, 인삼염등이유리되어골질환이초래될수있다.

38 치료 (1) 신장에서산배설장애또는중탄산염재형성 (regeneration) 장애 만성신부전의경우는투석을하고원위세뇨관성산증에는중탄산염을하루 30~60 meq 투여한다. (2) 체외로중탄산염소실위장관을통한중탄산염소실이되면중탄산염을투여한다. (3) 유기산 (organic acid) 의축적젖산산증은조직관류 (perfusion) 를개선시키고당뇨병성케톤산증은인슐린을투여하고산증이매우심한경우에서만 (ph < 7.1 또는 [HCO3-]<6~8 meq/l) 중탄산염을투여한다. 살리실산염 (salicylate), 메타놀및에틸렌글리콜 (ethylene glycol) 중독의경우는혈액투석으로제거한다.

39 치료의일반원칙 (1) 경구투여 나트륨중탄산염 (sodium bicarbonate) 의보충은 1 g 하루 3회로시작하여조절한다. Shohl's solution(sodium citrate와 citric acid의혼합물, 1 ml = 1 meq HCO3-) 을사용한다. (2) 정맥투여 나트륨중탄산염을 50~150 meq/l의농도로투여량은목표 ph 7.2 으로한다. 이때 [H+] = 63 nanomole/l이므로 [H+] = 24 PCO2/[HCO3-], 63 = 24 PCO2/[HCO3-] target [HCO3-] = 24/63 PCO2 0.4 PCO2 [HCO3-] deficit = 0.4~0.6 체중 (kg) (desired[hco3-]-measured[hco3-])

40 M/35 alcoholic ketoacidosis After hydration on the same day

41 Case 5 Alcholic ketoacidosis Renal failure & Hydration Pulmonary edema & respiratory failure (-30)-3-100%, BP 70/50 MV, Norepinephrine 200 ug/min Uncontrolled acidosis Bicarbonate infusion with dialysis (-18.4) %, BP 110/80

42 F/70 AMI, pneumonia

산 - 염기불균형과간호 (OCW 2) 1

산 - 염기불균형과간호 (OCW 2) 1 학습목표 본과제를학습한후학생들은아래의내용을설명할수있다. 1. 산, 염기의특성을설명할수있다. 2. 혈액내산 - 염기균형을위한신체기전을요약할수있다 3. 혈액내산 - 염기불균형의유형, 원인, 증상및효과적인중재법을제시할수있다. 2 산과염기특성 산 (Acid) 염기 (Base) 신맛맛쓴맛 리트머스 : 청 a 적 무색 리트머스