abg&acid base balance

الرحمن الله الرحمن بسم الله بسم الرحيمالرحيم

ABG analysis &Acid-base ABG analysis &Acid-base ImbalanceImbalance

By/Dr.Babiker Mohd. AhmedBy/Dr.Babiker Mohd. Ahmed

DR/ALA ELDIN HASSNDR/ALA ELDIN HASSN..

SHAAB T.HSHAAB T.H..

What is an ABGWhat is an ABGArterial Blood Gas

Drawn from artery- radial, brachial, femoral

It is an invasive procedure.

Caution must be taken with patient on anticoagulants.

Arterial blood gas analysis is an essential part of diagnosing and managing the patient’s oxygenation status, ventilation failure and acid base balance.

PrecautionsPrecautions Excessive Heparin Decreases bicarbonate

and PaCO2

Large Air bubbles not expelled from sample PaO2 rises, PaCO2 may fall slightly.

Fever or Hypothermia, Hyperventilation or breath holding (Due to anxiety) may lead to erroneous lab results

Care must be taken to prevent bleeding

ABG analysisABG analysis

•Why do we care? –Critical care requires a good understanding –Helps in the differential and final diagnosis–Helps in determining treatment plan–Treating acid/base disorders helps medications work better

(i.e. antibiotics, vasopressors, etc.)–Helps in ventilator management–Severe acid/base disorders may need dialysis–Changes in electrolyte levels in acidosis (increased K+ and

Na+, and decreases in HCO3)

Normal Arterial Blood Gas Normal Arterial Blood Gas ValuesValues**

PH 7.35-7.45PH 7.35-7.45 35-4535-45 mm Hg mm Hg PaCO PaCO22

70-10070-100 m Hgm Hg PaO PaO22

SaOSaO2 2 95-100%95-100% 22-2622-26 mEq/L mEq/L -- HCO3 HCO3--

% %MetHb <2.0%MetHb <2.0%< < 3.0%3.0% %%COHbCOHb

16-2216-22 ml Oml O22/dl/dl CaO CaO22

* * At sea level, breathing ambient air ** Age-At sea level, breathing ambient air ** Age-dependentdependent

COMPONENTS OF THE COMPONENTS OF THE ABGABG

pH: Measurement of acidity or alkalinity, based on the hydrogen (H+)

7.35 – 7.45Pao2 The partial pressure oxygen that is dissolved in arterial blood.

80-100 mm Hg. PCO2: The amount of carbon dioxide dissolved in arterial blood.

35– 45 mmHgHCO3

: The calculated value of the amount of bicarbonate in the blood 22 – 26 mmol/L

B.E: The base excess indicates the amount of excess or insufficient level of bicarbonate. -2 to +2mEq/L(A negative base excess indicates a base deficit in blood)

SaO2:The arterial oxygen saturation. >95%

Stepwise approach to ABGStepwise approach to ABG

•Step 1: Acidemic or Alkalemic? •Step 2: Is the primary disturbance

respiratory or metabolic? •Step 3. Asses to Pa O2. A value below 80mm

Hg indicates Hypoxemia. For a respiratory disturbance, determine whether it is acute

or chronic. •Step 4. For a metabolic acidosis, determine

whether an anion gap is present. •Step 5. Assess the normal compensation by

the respiratory system for a metabolic disturbance

Interpretation: pHInterpretation: pH–Normal arterial pH = 7.36 to 7.44

•Determine Acidosis versus Alkalosis

–1 .pH <7.35: Acidosis

–2 .pH >7.45: Alkalosis

•Metabolic Conditions are suggested if

–pH changes in the same direction as pCO2/HCO3-

–pH is abnormal but pCO2 remains unchanged Respiratory Conditions are suggested if:

–pH changes in the opp direction as pCO2/HCO3-

–pH is abnormal but HCO3- remains unchanged

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EFFECTS OF pHEFFECTS OF pH•The most general effect of pH changes

are on enzyme function–Also affect excitability of nerve and muscle

cells

pHpH

ExcitabilityExcitability

PH {Potential PH {Potential Hydrogen}Hydrogen}

The pH is a measurement of the acidity or alkalinity of the blood. It is inversely proportional to the no. of (H+) in the blood. The normal pH range is 7.35-7.45.Changes in body system functions that occur in an acidic state decreases the force of cardiac contractions, decreases the vascular response to catecholamines, and a diminished response to the effects and actions of certain medications.An alkalotic state interferes with tissue oxygenation and normal neurological and muscular functioning.Significant changes in the blood pH above 7.8 or below 6.8 will interfere with cellular functioning, and if uncorrected, will lead to death.

pH is inversely related to [HpH is inversely related to [H++]; a pH change ]; a pH change of 1.00 represents a 10-fold change in [Hof 1.00 represents a 10-fold change in [H++]]

pH [H+] in nanomoles/L

7.00 1007.10807.30 50 7.40 40 7.52 30 7.70208.00 10

Assess the PaCOAssess the PaCO22

•In an uncompensated state – when the pH and paCO2 moves in the same direction: the

primary problem is metabolic.

•The decreasing paco2 indicates that the lungs acting as a buffer response (blowing of the

excess CO2)

•If evidence of compensation is present but the pH has not been corrected to within the

normal range, this would be described as metabolic disorder with the partial respiratory

compensation.

Assess the HCOAssess the HCO33

•The pH and the HCO3 moving in the opposite directions, we

would conclude that the primary disorder is respiratory and the

kidneys acting as a buffer response: are compensating by retaining HCO3 to return the pH

to normal range.

HCO3- (bicarbonate):

SB (standard bicarbonate)

AB (actual bicarbonate)

SB: the contents of HCO3- of serum of arterial

blood in 38 , PaCO2 40mmHg, SaO℃ 2 100%.

Normal: 22-27mmol/L

mean: 24mmol/L

AB: The contents of HCO3- in actual

condition. In normal person: AB=SB

AB and SB are parameters to reflect metabolism, regulated by kidney.

Difference of AB-SB can reflect the

respiratory affection on serum HCO3

-.

Respiratory acidosis: AB>SB

Respiratory alkalosis: AB<SB

Metabolic acidosis: AB ＝ SB<Normal

Metabolic alkalosis: AB=SB>Normal

Assessing OxygenationAssessing Oxygenation

•Normal value for arterial blood gas 80-100mmHg decreased progressively with

age•Normal value for venous blood gas

40mmHg•Normal SaO2

–Arterial: 97%–Venous: 75%–Hypoxemia is PaO2 < 80 mm Hg at RA

Acceptable PaO2 Values on Acceptable PaO2 Values on Room AirRoom Air

Age GroupAccepable PaO2 (mm Hg)

Adults upto 60 yrs & Children

<80

Newborn40-70

70 yrs <70

80 yrs <60

90 yrs <50

60 yrs 80 mm Hg 1mm Hg/yr

INDICATORS OF OXYGENATIONINDICATORS OF OXYGENATION

•Assessing the efficiency of oxygenation requires knowledge of

•Ventilation is the mechanical movement of air. Oxygenation is the process of transporting oxygen

from the alveolus across capillary membranes into pulmonary circulation.

A-a gradient (Alveolar to arterial gradient):

• Provides an assessment of alveolar-capillary gas exchange. To calculate you need the alveolar PO2

(PAO2) and arterial pO2 (paO2). The larger the gradient, the more serious the respiratory compromise

P(A-a)OP(A-a)O22

P(A-a)O2 is the alveolar-arterial difference in partial pressure of oxygen. It is commonly called the “A-a gradient,” though it does not actually result from an

O2 pressure gradient in the lungs. Instead, it results from gravity-related blood flow changes within the lungs (normal ventilation-perfusion imbalance) .

PAO2 is always calculated based on FIO2, PaCO2, and barometric pressure .

PaO2 is always measured on an arterial blood sample in a “blood gas machine ”.

Normal P(A-a)O2 ranges from 5 to 25 mm Hg breathing room air (it

increases with age). A higher than normal P(A-a)O2 means the lungs are not transferring oxygen properly from alveoli into the pulmonary capillaries.

Except for right to left cardiac shunts, an elevated P(A-a)O2 signifies some sort of problem within the lungs.

Compare Compare PPAAOO22 to P to PaaOO22

•Healthy people: PAO2 = PaO2

•Two Approaches to Comparison–)PAO2 - PaO2 (difference

–PaO2 / PAO2 ratio

.

A-a difference increases with pulmonary disease

a/A ratioa/A ratio

•Normally averages just over 0.8 (Am. Rev. Resp.

Dis. 109: 142-145, 1974).•a/A ratio falls with pulmonary disease.•Lower limit normal:

–young (room air) : 0.74 –older (room air) : 0.78 –Both groups (100% O2): 0.82

•A-a gradient = PAO2 - PaO2PaO2 (partial pressure of O2 in the artery)

--obtained from the arterial blood gases.PAO2 (partial pressure of O2 in the

alveoli)-- obtained from the Alveolar Gas equation.

Alveolar Gas EquationAlveolar Gas Equation

PAO2 = PIO2 - 1.2 (PaCO2)where PIO2 = FIO2 (PB – 47 mm Hg)

Except in a temporary unsteady state, alveolar PO2 (PAO2) is always higher than arterial PO2 (PaO2). As a result,

whenever PAO2 decreases, PaO2 also decreases. Thus, from the AG equation:

If FIO2 and PB are constant, then as PaCO2 increases both PAO2 and PaO2 will decrease (hypercapnia causes hypoxemia).

If FIO2 decreases and PB and PaCO2 are constant, both PAO2 and PaO2 will decrease (suffocation causes hypoxemia).

If PB decreases (e.g., with altitude), and PaCO2 and FIO2 are constant, both PAO2 and PaO2 will decrease (mountain climbing leads to hypoxemia).

Oxygen SaturationOxygen Saturation

•Oxygen Saturation ( SaO2 )

–This refers to the amount of oxygen being carried by the haemoglobin (Hb) molecules

•The Hb molecule is divided into two portionsGlobin - made of protein

•Haem - made of iron

•There are 4 groups of haem on each molecule of Hb

•Each haem group can bind 1 O2 molecule

Important points for assessing Important points for assessing tissue oxygenationtissue oxygenation

•This is the O2 that’s really available at the tissue level.

•Is the THb normal?–Low THb means the ability of the blood to

carry the O2 to the tissues is decreased

•Is perfusion normal?–Low perfusion means the blood isn’t even

getting to the tissues

PvO2: Oxygenic partial pressure of mixed venous blood.

Normal: 35-45mmHg

mean: 40mmHg

Significance: Pa-vO2 is to reflect the tissue absorbing oxygen.

CaO2: The content of the oxygen of the arterial blood .

Normal: 19-21mmol/L

Significance: a comprehensive parameter to evaluate arterial oxygen.

SaOSaO22 and Oxygen Content and Oxygen Content

Tissues need a requisite amount of oxygen molecules for metabolism. Neither the PaO2 nor the SaO2 tells how much

oxygen is in the blood. How much is provided by the oxygen content, CaO2 (units = ml O2/dl). CaO2 is calculated as:

CaO2 = quantity O2 bound + quantity O2 dissolved to hemoglobin in plasma

CaO2 = (Hb x 1.34 x SaO2) + (.003 x PaO2)

Hb = hemoglobin in gm%; 1.34 = ml O2 that can be bound to each gm of Hb; SaO2 is percent saturation of hemoglobin with

oxygen; .003 is solubility coefficient of oxygen in plasma: .003 ml dissolved O2/mm Hg PO2.

SaOSaO22 – is it calculated or measured – is it calculated or measured??

SaO2 is measured in a ‘co-oximeter’. The traditional ‘blood gas machine’ measures only pH, PaCO2 and PaO2,, whereas the co-oximeter measures SaO2, carboxyhemoglobin, methemoglobin

and hemoglobin content. Newer ‘blood gas’ consoles incorporate a co-oximeter, and so offer the latter group of

measurements as well as pH, PaCO2 and PaO2.

Always make sure the SaO2 is measured, not calculated. If it is calculated from the PaO2 and the O2-dissociation curve, it provides no new information, and could be inaccurate --

especially in states of CO intoxication or excess methemoglobin. CO and metHb do not affect PaO2, but do lower

the SaO2.

Carbon monoxide – an important Carbon monoxide – an important cause of hypoxemiacause of hypoxemia

•Normal %COHb in the blood is 1-2%, from metabolism and small amount of ambient CO (higher in traffic-congested areas)

• All smokers have excess CO in their blood.•CO binds @ 200x more avidly to hemoglobin than O2, displacing

O2 from the heme binding sites .•CO : 1) decreases SaO2 by the amount of %COHb present, and 2)

shifts the O2-dissociation curve to the left, retarding unloading of oxygen to the tissues.

•CO does not affect PaO2, only SaO2. To detect CO poisoning, SaO2 and/or COHb must be measured (requires co-oximeter). In the presence of excess CO, SaO2 (when measured) will be lower

than expected from the PaO2.

Physiologic causes of low PaOPhysiologic causes of low PaO22

Non-Respiratory P[A-a]O2Cardiac Right to Left Shunt IncreasedDecreased Pio2 NormalRespiratoryPulmonary Right to Left Shunt IncreasedV/Q Imbalance IncreasedDiffussion barrier IncreasedHypoventilatio [increased CO2] Normal

Anion GAPAnion GAP

•Calculation of AG is useful approach to analyse metabolic acidosis

AG = (Na+ + K+) – (cl- + Hco3-)• *A change in the pH of 0.08 for each 10

mm Hg indicates an ACUTE condition.* A change in the pH of 0.03 for each 10 mm Hg indicates a CHRONIC condition.

Anion gap (AG): the difference of undetermined anion

and undetermined cation in serum.AG={Na + K}-(Cl-+ HCO3

- )Normal: 8-16mmol/L Significance :

AG = acidosis: ketoacidosis, kidney failure AG normal acidosis: Cl , diarrhea, fixed

acid decrease to evaluate mix acid-basic disorder

ANION GAPANION GAP

•The AG is estimated by substracting the sum of Cl and Hco3 concentration from the plasma Na: Na+unmeasured cations=Cl +Hco3 +unmeasured anions:

•AG={Na} – {Cl} +{Hco3}•The major unmeasured cations are

calcium,magnesium and potassium.•The major unmeasured anions are

albumin,sulphate, phosphate,lactate.

ELEVATED AG ACIDOSISELEVATED AG ACIDOSIS

•Causes are best remembered by mnemonic KULT:

•K: Ketoacidosis (DKA,alcoholic ketoacidosis,starvation)

•U: Uraemia•L: Lactic acidosis

•T; Toxins (Ethylene glycol,methanol,salicylates,paraldehyde,INH{

• K etoacidosis

•Uremia

• S epsis•Salicylate & other drugs

• M ethanol• A lcohol (Ethanol)

•Lactic acidosis• Ethylene glycol

REMEMBER

BASE EXCESSBASE EXCESS

•Base Excess (BE)

•Rising levels of bicarbonate make the blood more alkaline and a depletion of

bicarbonate makes it more acidic

•Base excess refers to the amount of base (alkali) which needs to be added or taken

away from the blood to return the pH to 7.4


•Base Excess can be used in the following

•To interpretate change in Hco3 levels:

•1-If the base excess is between -2 and +2 then there is no metabolic acidosis or alkalosis based on observed Hco3 change.

BASES EXCESSBASES EXCESS

•2- If the base excess is less than -2 {Base deficit} then there is metabolic acidosis which may be primary or compensatory process.


•3-If the base excess is greater than +2 then there is metabolic alkalosis which may be primary or compensatory process.

•=BASE EXCESS alone cannot differentiate between primary or compensatory process.

FormulaFormula•With the base excess is -10 in a 50kg

person with metabolic acidosis mM of Hco3 needed for correction is:

= 0.3 X body weight X BE = 0.3 X 50 X10 = 150 mM

Compensated or Uncompensated—Compensated or Uncompensated—what does this meanwhat does this mean??

.1Evaluate pH—is it normal? Yes

.2Next evaluate pCO2 & HCO3

•pH normal + increased pCO2 + increased HCO3 = compensated respiratory acidosis

•pH normal + decreased HCO3 + decreased pCO2 = compensated metabolic acidosis

COMPENSATIONCOMPENSATION

•A patient can be uncompensated or partially compensated or fully compensated

•pH remains outside the normal range•pH has returned within normal range- fully

compensated though other values may be still abnormal

•Be aware that neither the system has the ability to overcompensate

Partially compensatedPartially compensated

pHpaco2Hco3

Res.Acidosis

Res.Alkalosis

Met. Acidosis

Met.Alkalosis

FULLY COMPENSATEDFULLY COMPENSATEDpHpaco2Hco3

Resp.AcidosisNormal

but<7.40

Resp.AlkalosisNormal

but>7.40

Met. AcidosisNormal

but<7.40

Met. AlkalosisNormal

but>7.40

Clinical SignificanceClinical Significance

To evaluate respiratory failure

type 1 or type 2

To evaluate acid-basic disorder

HypoxiaHypoxia

Mild: 80-60mmHgMediate: 60-40mmHgSevere: <40mmHg

Respiratory FailureRespiratory Failure

PaO2<60mmHg respiratory failure

Notice: sea level, quiet, inspire air rule off other causes ( heart

disease)

Classification of Respiratory FailureClassification of Respiratory Failure

Type 1 Type2 PaO2 (mmHg) <60 <60 PaCO2 (mmHg) ≤50 >50

Other ParametersOther Parameters

SaO2: Saturation of arterial blood oxygen

Normal: 0.95-0.98

Significance: a parameter to evaluate hypoxia, but not sensitive

ODC ( Dissociation curve of oxygenated hemoglobin): “S” shape

PH 2,3DPG temperature CO2

ODC to right deviation

Oxygenated hemoglobin release oxygen to tissue, prevent hypoxia of the tissue. But absorbed oxygen of hemoglobin is decreased from the alveoli.

Bohr effect: movement of ODC place is

induced by PH.

SaO2%

PO2

Oxygen dissociation curve

Oxygen dissociation curve: SaOOxygen dissociation curve: SaO22 vs. PaO vs. PaO22

Also shown are CaOAlso shown are CaO2 2 vs. PaOvs. PaO22 for two different hemoglobin contents: 15 gm% for two different hemoglobin contents: 15 gm%

and 10 gm%. CaOand 10 gm%. CaO22 units are ml O units are ml O22/dl. P/dl. P5050 is the PaO is the PaO22 at which SaO at which SaO22 is 50% is 50% . .

ODCODC

•Oxygen Dissociation Curve •The curve highlights the affinity of oxygen

to haemoglobin•When PO2 is high, oxygen is strongly

affiliated to haemoglobin, so oxygen saturation will be high

•When PO2 is low there is less affinity of oxygen to haemoglobin, so oxygen

saturation drops

ODCODC

•Oxygen Dissociation Curve •It can be seen from the shape of the oxygen

dissociation curve that initially there is a slight drop in SaO2 when there is a reduced PO2

•However, at a certain point there is a sudden drop in saturation as indicated by the steep

decline in the curve–Therefore, SaO2 normally only drops sharply if the

PO2 is at a very low level8 kPa is the point at which the patient is hypoxaemic and is in respiratory failure

Classification of Acid-basic DisorderClassification of Acid-basic Disorder

PH PaCO2 HCO3-

Rest. acidosis

Rest. alkalosis

Meta. Acidosis

Meta. Alkalosis

Respiratory Acid Base DisordersRespiratory Acid Base Disorders

•Respiratory alkalosis most common of all the 4 acid base disorders (23-46%) -followed by met alkalosis - review of 8289 ABG analysis in ICU

pts Kaehny WD, MCNA 67(4), 1983 p 915-928

•Resp acidosis seen in 14-22% of pts•Attention to possibility of hypoxemia and its

correction always assumes priority in analysis of pts with a possible respiratory acid-base

disorder

59

RESPIRATORY RESPIRATORY ACIDOSISACIDOSIS

•is defined as a pH less than 7.35 with a paco2 greater than 45 mmHg.

•Acidosis –accumulation of co2, combines with water in the body to

produce carbonic acid, thus lowering the pH of the blood.

•Any condition that results in hypoventilation can cause

respiratory acidosis.

Res. Acidosis

61

RESPIRATORY ACIDOSISRESPIRATORY ACIDOSIS•Caused by hyperkapnia due to

hypoventilation–Characterized by a pH decrease

and an increase in CO2

62

RESPIRATORY ACIDOSISRESPIRATORY ACIDOSIS•The speed and depth of breathing control

the amount of CO2 in the blood

•Normally when CO2 builds up, the pH of the blood falls and the blood becomes acidic

•High levels of CO2 in the blood stimulate the parts of the brain that regulate breathing, which in turn stimulate faster and deeper

breathing

63

RESPIRATORY ACIDOSISRESPIRATORY ACIDOSIS•Respiratory acidosis can also develop when

diseases of the nerves or muscles of the chest impair the mechanics of breathing

•In addition, a person can develop respiratory acidosis if overly sedated from narcotics and

strong sleeping medications that slow respiration

64

RESPIRATORY ACIDOSISRESPIRATORY ACIDOSIS•The treatment of respiratory acidosis aims

to improve the function of the lungs•Drugs to improve breathing may help

people who have lung diseases such as asthma and emphysema

65

RESPIRATORY ACIDOSISRESPIRATORY ACIDOSIS•Decreased CO2 removal

can be the result of:(1Obstruction of air

passages(2Decreased respiration

(depression of respiratory centers)

(3Decreased gas exchange between pulmonary

capillaries and air sacs of lungs

(4Collapse of lung

Manifestations of Resp Manifestations of Resp AcidosisAcidosis

•NEUROMUSCULAR: Related to cerebral A vasodilatation & Cerebral BF

.1Anxiety

.2Asterixis

.3Lethargy, Stupor, Coma

.4Delirium

.5Seizures

.6Headache

.7Papilledema

.8Focal Paresis

.9Tremors, myoclonus

•CARDIOVASCULAR: Related to coronary vasodilation

.1Tachycardia with N BP

.2Ventricular arrythmias (related to hypoxemia and not hypercapnia per se)

.3Senstivity to digitalis

•BIOCHEMICAL ABNORMALITIES: tCO2

Cl-

PO43-

Homeostatic Response Homeostatic Response toto Respiratory AcidosisRespiratory Acidosis

•Imm response to rise in CO2 (& H2CO3) blood and tissue buffers take up H+ ions, H2CO3 dissociates and

HCO3- increases with rise in pH .•Steady state reached in 10 min & lasts for 8 hours.•PCO2 of CSF changes rapidly to match PaCO2.•Hypercapnia that persists > few hours induces an

increase in CSF HCO3- that reaches max by 24 hr and partly restores the CSF pH.

•After 8 hrs, kidneys generate HCO3 -•Steady state reached in 3-5 d

•predicts rise in PaCO2 obligatory hypoxemia in pts breathing R.A .

•Resultant fall in PaO2 limits hypercapnia to 80 to 90 mm Hg

•Higher PaCO2 leads to PaO2 incompatible with life .

•Hypoxemia, not hypercapnia or acidemia, that poses the principal threat to life .

•Consequently, oxygen administration represents a critical element in the management

Causes of Chronic Respiratory Causes of Chronic Respiratory AcidosisAcidosis

•EXCRETORY COMPONENT PROBLEMS:

.1Ventilation:COPD

Advanced ILD•Restriction of thorax/chest wall:

Kyphoscoliosis, Arthritis

Fibrothorax

Hydrothorax

Muscular dystrophy

Polymyositis

Treatment of Respiratory Treatment of Respiratory AcidosisAcidosis

•Ensure adequate oxygenation - care to avoid inadequate oxygenation while

preventing worsening of hypercapnia due to supression of hypoxemic resp drive

•Correct underlying disorder if possible•Avoid rapid decrease in ch elevated

PCO2 to avoid post hypercapnic met alkalosis (arrythmias, seizures

adequate intake of Cl-)

•Alkali (HCO3) therapy rarely in ac and never in ch resp acidosis only if acidemia directly inhibiting

cardiac functions•Problems with alkali therapy:

.1Decreased alv ventilation by decrease in pH mediated ventilatory drive

.2Enhanced carbon dioxide production from bicarbonate decomposition

.3Volume expansion .•COPD pts on diuretics who develop met alkalosis

often benfefited by acetazolamide

73

RESPIRATORY RESPIRATORY ALKALOSISALKALOSIS

Manifestations of Resp Manifestations of Resp AlkalosisAlkalosis

•NEUROMUSCULAR: Related to cerebral A vasoconstriction & Cerebral BF

.1Lightheadedness

.2Confusion

.3Decreased intellectual function

.4Syncope

.5Seizures

.6Paraesthesias (circumoral, extremities)

.7Muscle twitching, cramps, tetany

.8Hyperreflexia

.9Strokes in pts with sickle cell disease

•CARDIOVASCULAR: Related to coronary vasoconstriction

.1Tachycardia with N BP

.2Angina

.3ECG changes (ST depression)

.4Ventricular arrythmias

•GASTROINTESTINAL: Nausea & Vomitting (cerebral hypoxia)

•BIOCHEMICAL ABNORMALITIES:

tCO2PO43-

Cl- Ca2+

76

RESPIRATORY ALKALOSISRESPIRATORY ALKALOSIS•Can be the result of:

–1 (Anxiety, emotional disturbances

–2 (Respiratory center lesions

–3 (Fever–4 (Salicylate poisoning

(overdose)–5 (Assisted respiration

•6 (High altitude (low PO2)

77

RESPIRATORY ALKALOSISRESPIRATORY ALKALOSIS•Anxiety is an emotional

disturbance

•The most common cause of hyperventilation, and

thus respiratory alkalosis, is anxiety

78

RESPIRATORY ALKALOSISRESPIRATORY ALKALOSIS•Usually the only treatment needed is to

slow down the rate of breathing

•Breathing into a paper bag or holding the breath as long as possible may help raise

the blood CO2 content as the person breathes carbon dioxide

back in after breathing it out

79

RESPIRATORY ALKALOSISRESPIRATORY ALKALOSIS•Respiratory center

lesions–Damage to brain

centers responsible for monitoring

breathing rates•Tumors•Strokes

80

RESPIRATORY ALKALOSISRESPIRATORY ALKALOSIS•Fever

–Rapid shallow breathing blows off

too much CO2

81

RESPIRATORY ALKALOSISRESPIRATORY ALKALOSIS•Salicylate poisoning

(Aspirin overdose)–Ventilation is stimulated

without regard to the status of O2, CO2 or H+ in

the body fluids

82

RESPIRATORY ALKALOSISRESPIRATORY ALKALOSIS•Assisted Respiration

–Administration of CO2 in the exhaled air of the care - giver

Your insurance won’t cover a ventilator any longer, so Bob here will be giving you mouth to mouth for the next several days

83

RESPIRATORY ALKALOSISRESPIRATORY ALKALOSIS•High Altitude

–Low concentrations of O2 in the arterial blood reflexly stimulates ventilation in an attempt to

obtain more O2

–Too much CO2 is “blown off” in the process

84

RESPIRATORY ALKALOSISRESPIRATORY ALKALOSIS•Kidneys compensate by:

–Retaining hydrogen ions

–Increasing bicarbonate excretion

H+

HCO3-

HCO3-

HCO3-

HCO3-

HCO3-

HCO3-

HCO3-

HCO3-

HCO3-

HCO3-

H+

H+

H+

H+

H+

H+

H+

H+

H+

H+

85

RESPIRATORY ALKALOSISRESPIRATORY ALKALOSIS•Decreased CO2 in the lungs will

eventually slow the rate of breathing–Will permit a normal amount of CO2 to

be retained in the lung

Homeostatic Response to Resp Homeostatic Response to Resp AlkalosisAlkalosis

•In ac resp alkalosis, imm response to fall in CO2 (& H2CO3) release of H+ by blood and tissue buffers react with HCO3- fall in HCO3- (usually not less than

18) and fall in pH•Cellular uptake of HCO3- in exchange for Cl-•Steady state in 15 min - persists for 6 hrs•After 6 hrs kidneys increase excretion of HCO3- (usually

not less than 12-14) •Steady state reached in 11/2 to 3 days .•Timing of onset of hypocapnia usually not known except

for pts on MV. Hence progression to subac and ch resp alkalosis indistinct in clinical practice

METABOLIC ACIDOSISMETABOLIC ACIDOSIS

Metabolic AcidosisMetabolic Acidosis

•Bicarbonate less than 22mEq/L with a pH of less than 7.35.

•Renal failure•Diabetic ketoacidosis•Anaerobic metabolism•Starvation•Salicylate intoxication

89

METABOLIC ACIDOSISMETABOLIC ACIDOSIS•The causes of metabolic acidosis can

be grouped into five major categories–1 (Ingesting an acid or a substance that is

metabolized to acid

–2 (Abnormal Metabolism

–3 (Kidney Insufficiencies

–4 (Strenuous Exercise

–5 (Severe Diarrhea

90

METABOLIC ACIDOSISMETABOLIC ACIDOSIS•Unregulated

diabetes mellitus causes

ketoacidosis–Body metabolizes fat

rather than glucose–Accumulations of

metabolic acids (Keto Acids) cause

an increase in plasma H+

91

METABOLIC ACIDOSISMETABOLIC ACIDOSIS•This leads to excessive production of

ketones:–Acetone–Acetoacetic acid–B-hydroxybutyric acid

•Contribute excessive numbers of hydrogen ions to body fluids

Acetone

Acetoacetic acid

Hydroxybutyric acid

H+

H+

H+

H+

H+H+H+

92

METABOLIC ACIDOSISMETABOLIC ACIDOSIS•2 (Abnormal Metabolism

–The body also produces excess acid in the advanced stages of shock, when lactic

acid is formed through the metabolism of sugar

93


•3 (Kidney Insufficiencies

–Even the production of normal amounts of acid

may lead to acidosis when the kidneys aren't

functioning normally

94

METABOLIC ACIDOSISMETABOLIC ACIDOSIS•3 (Kidney Insufficiencies

–Kidneys may be unable to rid the plasma of even the

normal amounts of H+ generated from metabolic

acids

–Kidneys may be also unable to conserve an

adequate amount of HCO3-

to buffer the normal acid load

95

METABOLIC ACIDOSISMETABOLIC ACIDOSIS•3 (Kidney Insufficiencies

–This type of kidney malfunction is called renal tubular acidosis or uremic

acidosis and may occur in people with kidney failure or with abnormalities that

affect the kidneys' ability to excrete acid

96

METABOLIC ACIDOSISMETABOLIC ACIDOSIS•Treating the underlying cause of metabolic

acidosis is the usual course of action–For example, they may control diabetes with

insulin or treat poisoning by removing the toxic substancefrom the blood

–Occasionallydialysis is needed

to treat severeoverdoses and

poisonings

97


•Metabolic acidosis may also be treated directly

–If the acidosis is mild, intravenous fluids and

treatment for the underlying disorder may be all that's

needed

METABOLIC ALKALOSISMETABOLIC ALKALOSIS

Metabolic alkalosisMetabolic alkalosis

•Bicarbonate more than 26m Eq /L with a pH more than 7.45

•Excess of base /loss of acid can cause•Ingestion of excess antacids, excess use of

bicarbonate, or use of lactate in dialysis.•Protracted vomiting, gastric

suction,hypchoremia,excess use of diuretics, or high levels of aldesterone.

100

METABOLIC ALKALOSISMETABOLIC ALKALOSIS•A reduction in H+ in the case of metabolic

alkalosis can be caused by a deficiency of non-carbonic acids

•This is associated with an increase in HCO3-

101


•Treatment of metabolic alkalosis is most often accomplished by replacing water and

electrolytes (sodium and potassium) while treating the underlying cause

•Occasionally when metabolic alkalosis is very severe, dilute acid in the form of

ammonium chloride is given by IV

102

METABOLIC ALKALOSISMETABOLIC ALKALOSIS•Can be the result of:

–1 (Ingestion of Alkaline Substances

–2 (Vomiting ( loss of HCl )

103


•Baking soda (NaHCO3) often used as a remedy for gastric hyperacidity

–NaHCO3 dissociates to Na+ and HCO3-

104

METABOLIC ALKALOSISMETABOLIC ALKALOSIS•Bicarbonate neutralizes high

acidity in stomach (heart burn)•The extra bicarbonate is

absorbed into the plasma increasing pH of plasma as

bicarbonate binds with free H+

105


•Commercially prepared alkaline products for gastric hyperacidity are not

absorbed from the digestive tract and do not alter the pH status of the plasma

106

METABOLIC ALKALOSISMETABOLIC ALKALOSIS•2 (Vomiting (abnormal loss of HCl)

–Excessive loss of H+

Gastric juices contain large amounts of HClHCl

During HClHCl secretion, bicarbonate is added to the plasma

The bicarbonate is neutralized as HClHCl is reabsorbed by the plasma from the digestive tract

During vomiting H+H+ is lost as HClHCl and the bicarbonate is not

neutralized in the plasmaLoss of HClHCl increases the

plasma bicarbonate and thus results in an increase in pHpH

of the blood

107


•Reaction of the body to alkalosis is to lower pH by:

–Retain CO2 by decreasing breathing rate–Kidneys increase the retention of H+

CO2 CO2

H+

H+

H+

H+

MIXED DISORDERSMIXED DISORDERS

.

Mixed Acid-Base DisordersMixed Acid-Base Disorders

•Patients may have two or more acid-base disorders at one time

•Delta GapDelta HCO3 = HCO3 + Change in anion gap

< 24 = metabolic alkalosis

Mixed Acid-base Disorders are Mixed Acid-base Disorders are CommonCommon

In chronically ill respiratory patients, mixed disorders are probably more common than single disorders, e.g., RAc

+ MAlk, RAc + Mac, Ralk + MAlk.

In renal failure (and other conditions) combined MAlk + MAc is also encountered.

Always be on the lookout for mixed acid-base disorders. They can be missed!

Tips to Diagnosing Mixed Tips to Diagnosing Mixed Acid-base DisordersAcid-base Disorders

TIP 1. Do not interpret any blood gas data for acid-base diagnosis without closely examining

the serum electrolytes: Na+, K+, Cl-, and CO2 .•A serum CO2 out of the normal range always represents some

type of acid-base disorder (barring lab or transcription error).•High-serum CO2 indicates metabolic alkalosis &/or

bicarbonate retention as compensation for respiratory acidosis.

•Low-serum CO2 indicates metabolic acidosis &/or bicarbonate excretion as compensation for respiratory alkalosis.

•Note that serum CO2 may be normal in the presence of two or more acid-base disorders.

Tips to Diagnosing Mixed Acid-base Tips to Diagnosing Mixed Acid-base Disorders Disorders (cont.)(cont.)

TIP 2. Single acid-base disorders do not lead to normal blood pH. Although pH can end up in the normal range

(7.35 - 7.45) with a single mild acid-base disorder, a truly normal pH with distinctly abnormal HCO3

- and PaCO2 invariably suggests two or more primary disorders .

Example: pH 7.40, PaCO2 20 mm Hg, HCO3- 12 mEq/L in a

patient with sepsis. Normal pH results from two co-existing and unstable acid-base disorders - acute respiratory alkalosis and

metabolic acidosis.

Tips to Diagnosing Mixed Acid-base Tips to Diagnosing Mixed Acid-base Disorders Disorders (cont)(cont)

TIP 3. Simplified rules predict the pH and HCO3- for a given

change in PaCO2. If the pH or HCO3- is higher or lower

than expected for the change in PaCO2, the patient probably has a metabolic acid-base disorder as well .

The next slide shows expected changes in pH and HCO3- (in

mEq/L) for a 10-mm Hg change in PaCO2 resulting from either primary hypoventilation (respiratory acidosis) or

primary hyperventilation (respiratory alkalosis).

Expected changes in pH and HCOExpected changes in pH and HCO33-- for for a 10-mm Hg a 10-mm Hg

changechange in PaCOin PaCO22 resulting from either primary resulting from either primary hypoventilation (respiratory acidosis) or primary hypoventilation (respiratory acidosis) or primary

hyperventilation (respiratory alkalosis)hyperventilation (respiratory alkalosis):: ACUTE CHRONIC

Resp Acidosis

pH ↓ by 0.07pH ↓ by 0.03HCO3

- ↑ by 1*HCO3- ↑ by 3 - 4

Resp AlkalosispH ↑ by 0.08pH ↑ by 0.03HCO3

- ↓ by 2HCO3- ↓ by 5

Units for HCO3- are mEq/L

Predicted changes in HCOPredicted changes in HCO33-- for a directional for a directional

change in PaCOchange in PaCO22 can help uncover mixed can help uncover mixed

acid-base disordersacid-base disorders . .(aA normal or slightly low HCO3

- in the presence of hypercapnia suggests a concomitant metabolic acidosis, e.g., pH 7.27,

PaCO2 50 mm Hg, HCO3- 22 mEq/L. Based on the rule for

increase in HCO3- with hypercapnia, it should be at least 25

mEq/L in this example; that it is only 22 mEq/L suggests a concomitant metabolic acidosis.

b)A normal or slightly elevated HCO3- in the presence of hypocapnia

suggests a concomitant metabolic alkalosis, e.g., pH 7.56, PaCO2 30 mm Hg, HCO3

- 26 mEq/L. Based on the rule for decrease in HCO3

- with hypocapnia, it should be at least 23 mEq/L in this example; that it is 26 mEq/L suggests a

concomitant metabolic alkalosis.

TIP 4. In maximally-compensated metabolic acidosis, the numerical value of PaCO2 should be the same

(or close to) as the last two digits of arterial pH. This observation reflects the formula for expected

respiratory compensation in metabolic acidosis:Expected PaCO2 = [1.5 x serum CO2] + (8 ± 2)

In contrast, compensation for metabolic alkalosis (by increase in PaCO2) is highly variable, and in some cases there may be no or

minimal compensation.

Tips to Diagnosing Mixed Acid-base Tips to Diagnosing Mixed Acid-base Disorders Disorders (cont.)(cont.)

117

RESPONSES TO:RESPONSES TO:ACIDOSIS AND ALKALOSISACIDOSIS AND ALKALOSIS

•Mechanisms protect the body against life-threatening changes in hydrogen

ion concentration–11 ( (Buffering Systems in Body FluidsBuffering Systems in Body Fluids

–22 ( (Respiratory ResponsesRespiratory Responses

–33 ( (Renal ResponsesRenal Responses

•44 ( (Intracellular Shifts of IonsIntracellular Shifts of Ions

118

(1(1Buffer SystemsBuffer Systems 2) Respiratory Responses2) Respiratory Responses3) Renal Responses3) Renal Responses4) Intracellular Shifts of Ions4) Intracellular Shifts of Ions

119

BUFFERSBUFFERS•A buffer is a combination of chemicals

in solution that resists any significant change in pHpH

•Able to bind or release free HH++ ions

120

BUFFERSBUFFERS•Buffering systems provide an

immediate response to fluctuations in pH: pH: 1) Phosphate1) Phosphate

–22 ( (ProteinProtein

–33 ( (Bicarbonate Buffer SystemBicarbonate Buffer System

121

BUFFERSBUFFERS•Chemical buffers are able to react immediately

(within milliseconds)

•Chemical buffers are the first line of defense for the body for fluctuations in pHpH

122

•Regulates pHpH within the cells and the urine

–Phosphate concentrations are higher intracellularly and within the kidney tubules

–Too low of aconcentration in

extracellular fluidto have much

importance as anECFECF buffer system

PHOSPHATE BUFFER PHOSPHATE BUFFER SYSTEMSYSTEM

123

•11 ( (Phosphate buffer systemPhosphate buffer system

Na2HPO4 + H+ NaH2PO4 +

Na+ –Most important in the intracellular system

PHOSPHATE BUFFER PHOSPHATE BUFFER SYSTEMSYSTEM

124

PROTEIN BUFFER SYSTEMPROTEIN BUFFER SYSTEM

•22 ( (Protein Buffer SystemProtein Buffer System–Behaves as a buffer in both plasma and

cells

–Hemoglobin is by far the most important protein buffer

125

PROTEIN BUFFER SYSTEMPROTEIN BUFFER SYSTEM

•Proteins are excellent buffers because they contain both acid and base groups

that can give up or take up HH++

•Proteins are extremely abundant in the cell

•The more limited number of proteins in the plasma reinforce the bicarbonate

system in the ECFECF

126

PROTEIN BUFFER SYSTEMPROTEIN BUFFER SYSTEM•Hemoglobin buffers HH++ from metabolically

produced COCO22 in the plasma only

•As hemoglobin releases OO22 it gains a great affinity for HH++

HHbb

O2

O2 O2

O2

127

BICARBONATE BUFFER BICARBONATE BUFFER SYSTEMSYSTEM

•33 ( (Bicarbonate Buffer SystemBicarbonate Buffer System–Predominates in extracellular fluid (ECFECF)

HCOHCO33- - + added H+ added H++ H H22COCO33

128


•This system is most important because the concentration of both components can

be regulated:–Carbonic acidCarbonic acid by the respiratory system

•BicarbonateBicarbonate by the renal system

BICARBONATE BUFFER SYSTEMBICARBONATE BUFFER SYSTEM

•HH22COCO33 <=> HH++ + HCO + HCO33--

–Hydrogen ions generated by metabolism or by ingestion react with bicarbonate base

to form more carbonic acid

BICARBONATE BUFFER SYSTEMBICARBONATE BUFFER SYSTEM

•Equilibrium shifts toward the formation of acid

–Hydrogen ions that are lost (vomiting) causes carbonic acid to dissociate yielding

replacement HH++ and bicarbonate

131

Loss of HCl

Addition of lactic acid


HH++ HCOHCO33--

HH22COCO33HH22

OOCOCO22+ ++

Exercise

Vomiting

132

RESPIRATORY RESPONSERESPIRATORY RESPONSE•Neurons in the medulla oblongata and

pons constitute the Respiratory CenterRespiratory Center•Stimulation and limitation of respiratory

rates are controlled by the respiratory center

•accomplished byresponding to CO2

and H+

concentrations inthe blood

133

CHEMOSENSITIVE AREASCHEMOSENSITIVE AREAS•Chemosensitive areas of the respiratory

center are able to detect blood concentration levels of CO2 and H+

•Increases in CO2 and H+ stimulate the respiratory center

–The effect is to raiserespiration rates

•But the effectdiminishes in1 - 2 minutes

134

CHEMOSENSITIVE AREASCHEMOSENSITIVE AREAS•The effect of

stimulating the respiratory centers by increased CO2 and H+

is weakened in environmentally

increased CO2 levels

•Symptoms may persist for several days

135

CHEMORECEPTORSCHEMORECEPTORS•Chemoreceptors are also present in the

carotidcarotid and aorticaortic arteries which respond to changes in partial pressures of O2 and CO2

or pH•Increased levels of

CO2 (low pHpH) ordecreased levels of

O2 stimulaterespiration rates

to increase

136

CHEMORECEPTORSCHEMORECEPTORS•Overall compensatory response is:

–HyperventilationHyperventilation in response to increased CO2 or H+ (low pHpH)

–HypoventilationHypoventilation in response to decreased CO2 or H+ (high pHpH)

137

RENAL RESPONSERENAL RESPONSE•The kidney compensates for Acid - Acid -

BaseBase imbalance within 24 hours and is responsible for long term control

•The kidney in response:–To AcidosisTo Acidosis

•Retains bicarbonate ions and eliminates hydrogen ions

–To AlkalosisTo Alkalosis•Eliminates bicarbonate ions and retains

hydrogen ions

Intracellular Shifts of IonsIntracellular Shifts of Ions

139

HYPERKALEMIAHYPERKALEMIA•HyperkalemiaHyperkalemia is generally associated

with acidosis–Accompanied by a shift of H+ ions into

cells and K+ ions out of the cell to maintain electrical neutrality

140

HYPOKALEMIAHYPOKALEMIA•HypokalemiaHypokalemia is generally associated with

reciprocal exchanges of H+ and K+ in the opposite direction

–Associated with alkalosis

•Hypokalemia is a depressed serum K+

141

ELECTROLYTE SHIFTSELECTROLYTE SHIFTS

cell

HH++

KK++

AcidosisAcidosisCompensatory Response Result

- HH++ buffered intracellularly

- Hyperkalemia

HH++

KK++

cell

AlkalosisAlkalosisCompensatory Response Result

- Tendency to correct alkalosis

- Hypokalemia

Arterial Blood Gases: Arterial Blood Gases: Test Your Overall UnderstandingTest Your Overall Understanding

Case 1. A 55-year-old man is evaluated in the pulmonary lab for shortness of breath. His regular medications include a diuretic for hypertension and one aspirin a day. He smokes a pack of cigarettes a day.

FIO2 .21 HCO3- 30 mEq/L

pH 7.53 %COHb 7.8%

PaCO2 37 mm Hg Hb 14 gm%

PaO2 62 mm Hg CaO2 16.5 ml O2/dl SaO2 87%

How would you characterize his state of oxygenation, ventilation, and acid-base balance?


Case 1 - Discussion

OXYGENATION: The PaO2 and SaO2 are both reduced on room air. Since P(A-a)O2 is elevated (approximately 43 mm Hg), the low PaO2 can be attributed to V-Q imbalance, i.e., a pulmonary problem. SaO2 is reduced, in part from the low PaO2 but mainly from elevated carboxyhemoglobin, which in turn can be attributed to cigarettes. The arterial oxygen content is adequate.

VENTILATION: Adequate for the patient's level of CO2 production; the patient is neither hyper- nor hypo-ventilating.

ACID-BASE: Elevated pH and HCO3- suggest a state of metabolic alkalosis,

most likely related to the patient's diuretic; his serum K+ should be checked

for hypokalemia.


Case 2. A 46-year-old man has been in the hospital two days with pneumonia. He was recovering but has just become diaphoretic, dyspneic, and hypotensive. He is breathing oxygen through a nasal cannula at 3 l/min.

pH 7.40

PaCO2 20 mm Hg

%COHb 1.0%

PaO2 80 mm Hg

SaO2 95%

Hb 13.3 gm%

HCO3- 12 mEq/L

CaO2 17.2 ml O2/dl

How would you characterize his state of oxygenation, ventilation, and acid-base balance?


Case 2 - Discussion

OXYGENATION: The PaO2 is lower than expected for someone hyperventilating to this degree and receiving supplemental oxygen, and points to significant V-Q imbalance. The oxygen content is adequate.

VENTILATION: PaCO2 is half normal and indicates marked hyperventilation.

ACID-BASE: Normal pH with very low bicarbonate and PaCO2 indicates combined respiratory alkalosis and metabolic acidosis. If these changes are of sudden onset, the diagnosis of sepsis should be strongly considered, especially in someone with a documented infection.


Case 3. A 58-year-old woman is being evaluated in the emergency department for acute dyspnea.

FIO2 .21

pH 7.19

PaCO2 65 mm Hg

%COHb 1.1%

PaO2 45 mm Hg

SaO2 90%

Hb 15.1 gm%

HCO3- 24 mEq/L

CaO2 18.3 ml O2/dl

How would you characterize her state of oxygenation, ventilation, and acid-base balance?


Case 3 - Discussion

OXYGENATION: The patient's PaO2 is reduced for two reasons - hypercapnia and V-Q imbalance - the latter apparent from an elevated P(A-

a)O2 (approximately 27 mm Hg).

VENTILATION: The patient is hypoventilating.

ACID-BASE: pH and PaCO2 are suggestive of acute respiratory acidosis plus metabolic acidosis; the calculated HCO3

- is lower than expected from acute respiratory acidosis alone.

148

ENDEND ACID - BASE ACID - BASE

BALANCEBALANCE

[

ENDEND

abg&acid base balance

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