HYPERCARBIA

&
HYPOCARBIA



NORMAL CO LEVELS

Normal arterial PCO = 35-45 mmHg

Normal venous PCO = 46 mmHg

Normal alveolar PCO = 40 mmHg


DEFINITION

HYPERCAPNIA- defined as an arterial PCO above 46 mmHg
that does not represent compensation for a metabolic alkalosis.
PaCO CO production
1/ alveolar ventilation
so, PaCO = K VCO/V
A


HYPOCAPNIA- arterial PCO
2
less than 35 mmHg that does not
represent compensation for metabolic acidosis.

PHYSIOLOGY
CO
2
is the end product of aerobic metabolism
Production - awake pt. = 200 ml/min
- paralysed pt. = 160 ml/min
Produced in mitochondria and is excreted out through
lungs
In lungs - PaCO of blood entering in pulmonary
capillaries (46 mmHg) > P
A
CO(40 mmHg)
So CO
2
diffuses out from blood Alveoli
Expired gases.




CO
2
levels
46
Arterial end Venous end
PaCO2=40mmHg PvCO2= 45mmHg
45


R = V
CO2
/V
O2

normal = 0.8
carbohydrates = 1
fats = 0.7
proteins = 0.7

CO TRANSPORT:-
100ml blood 48 ml CO

2.5ml (5%) dissolved form in plasma
2.5ml (5%) carbamino compounds
43ml (90%) - HCO
3
-
RESPIRATORY QUOTIENT (R)
BOHR EFFECT

Describes effect of PCO on ODC.
Hypercapnia and acidosis shift ODC to rt. ed O release ( in
tissues )
Hypocapnia and alkalosis shift ODC to lt. ed O uptake ( in
lungs )

HALDANE EFFECT

Describes effect of oxygenation of Hb on CO dissociation curve.
-ed oxy Hb shift to lt. ed uptake of CO (tissues)

-ed oxy Hb shift to rt. ed release of CO (lungs)

CLASSIFICATION
According to onset:-

1. Acute Hypercapnia - acute respiratory acidosis

2. Chronic Hypercapnia compensated respiratory acidosis

CAUSES OF HYPERCAPNIA IN AWAKE PATIENT

It is mainly because of hypoventilation which can be due to-

i. Brainstem resp. depression-
- Drugs (opioids)
- Obesity hypoventilation syndrome

ii. Peripheral neuropathy-
- Critical illness polyneuropathy
- Guillian-Barre Syndrome

iii. Muscle weakness-

- hypophosphatemia
- magnesium depletion
- myasthenia gravis











CAUSES OF HYPERCAPNIA UNDER ANAESTHESIA


A. INADEQUATE VENTILATION-

CO production is constant but alveolar ventilation is decreased


Decrease in V
A
increase in P
A
CO

UNDER ANAESTHESIA
when pt. is breathing spontaneously- hypoventilation may occur
due to:-

i) Difficulty in breathing -
- Increased airway resistance
- Abnormal surgical position
- Decreased lung compliance

ii) Less drive to breath -
- Because of anaesthetic agents



B. INCREASED DEAD SPACE VENTILATION

i) Age

ii) Rapid short respiration

iii) Increase anatomical dead space-

- 33% -46% during intubation (longer tube)
- 33% -64% during mask ventilation



i . i n c r e a s e a n a t o m i c a l d e a d s p a c e -
- % - 4 6 % d u r i n g i n t u b a t i o n ( l o n g e r
t u b e )
- 3 3 % - 6 4 % d u r i n g m a s k v e n t i l a t i o
iv) Decreased pulmonary art pressure (esp. deliberate hypotension)
increase in zone 1 inc. alveolar dead space


v) Increased airway pressure during PEEP inc. zone 1


vi) Pulmonary embolism, thrombosis & vascular obliteration
( kinking, clamping or blocking of pulm. art. during surgery)
V/Q mismatch




C. ANAESTHESIA APPARATUS RELATED CAUSES

i. Absorbant failure

ii. Unidirectional valve problem

iii. Inadequate fresh gas flow to Mapelson system




D. INCREASED CO PRODUCTION

- Pyrexia

- Malignant hyperthermia

- Shivering

- Tube Light anaesthesia

- Hyperthyroidism

- Overfeeding


E. EXOGENOUS HYPERCAPNIA-


During laparoscopy - CO insufflation


-At 15 mmHg abd press-
- PaCO by 10 mmHg
- P
A
CO by 4 mmHg


F. SHUNT

a. Atelectasis (collapse of lung ) or consolidation
(pneumonia, edema, obliterative
process)complete cessation of ventilation in a region


b. Right to left shunt


CLINICAL SIGNS OF HYPERCAPNIA
Hyperventilation cardinal sign
but is absent in - paralysed pt.
- in those in whom hypercapnia is
result of hypoventilation e.g. COPD
Dyspnoea may or may not be present
Other signs Flushing of skin
- Full and bounding pulse
-ed BP
- Muscle twitching & flaps of hands
- Convulsions
- Coma

EVALUATION OF HYPERCAPNIA
MEASURING CO PRODUCTION

V
CO2
can be measured at the bed side by specialized metabolic
carts that are normally used to perform nutritional assessment.

In steady state condition, the rate of CO excretion is equivalent
to V
CO2.

Normal V
CO2
is 90 130 lit/min/m
2
which is roughly 80% of V
O2

Under anaesthesia can be measured by capnography.


Normal waveform


Phase I (EA) - latter part of inspiration, during which the CO
2

level remains at zero.

Phase II (BC) - emptying of connecting airways and the
beginning of the emptying of alveoli.

Phase III (CD) - alveolar plateau. Because of uneven emptying
of alveoli, the slope continues to rise gently.

Phase IV (DE) - as the patient inhales, CO
2
-free gas enters the
patient's airway, and the CO
2
level abruptly falls to zero.

angle - angle between Phases II and III
- 100 and 110 degrees.
- decreased with obstructive lung disease
capnometer's response time, sweep speed, respiratory
cycle time.

angle - angle between the end of Phase III and the
descending limb of the capnogram.
- 90 degrees.
- increased with rebreathing.
- decreased if the slope of Phase III is increased.



Factors that change EtCO2 during anaesthesia

Elements that change co2 production

Increase in EtCO2
- Increases in metabolic
rate
- Hyperthermia
- Sepsis
- Malignant hyperthermia
- Shivering
- Hyperthyroidism

Decrease in EtCO2
- Decreases in metabolic
rate
- Hypothermia
- Hypothyroidism
Elements that change CO2 elimination
Increase in EtCO2

- Hypoventilation
- Hypoperfusion
Decrease in EtCO2

- Hyperventilation
- Rebreathing
- Pulmonary embolism
Low EtCO2
Elevated EtCO2

EFFECTS OF HYERCAPNIA

A) Central Nervous System

It has five major effects on the brain-
i) Effect on CBF
ii) Secondary effect on CSF pressure
iii) Influence on intracellular pH in neurons
iv) Effect on RAS & hypothalamus
v) Inert gas/ vapor narcotic effect

1) Effect on consciousness
CO
2
narcosis-
- Reversible narcosis
- Begins at PCO
2
>90-120 mmHg (12-16 kPa)
- Occurs due to formation of H
+
ion which leads to decreased
intracellular pH with consequent metabolic derangements.
Associated with-
i. Marked ventilatory & circulatory changes
ii. Increased muscle tone
iii. Cortical seizure activity




Depressant effects-

i)Direct depression of synaptic transmission in brain & spinal cord
ii) Depressant effect on intracellular functions mediated via reduction
of intracellular pH .

Stimulatory effects-

i)Excitation of RAS- arousal influence on cortex
ii)Enhanced activity of hypothalamus


2) Effects on cerebral blood flow
CBF - normal = 50 ml/100gm/min

Increased by 1-2ml/100gm/min for each 1mmHg increase in
PaCO & vice versa, till max vasodilatation at PaCO= 120mmHg

With chronic exposure acclimatization occurs- CBF returns
back to eucapnic levels.


EFFECT OF HYPERCAPNIA ON CBF
MECHANISM

in CBF is due to
- Cerebral vasodilatation
- in BP

in PaCO
2

extra-cellular pH in region of arterioles

Alters intracellular Ca
++
levels directly and indirectly via NO
production and formation of cyclic GMP.

Cerebral vasodilatation & in CBF
ANAESTHESIA


All inhalational agents increases normocapnic CBF.

Also accentuate the response to both hypocapnia & hypercapnia.

IV anaesthetics e.g. thiopentone & propofol reduce CBF at normal
PCO
2
in accordance with ed cerebral O
2
consumption.

3) Effect on intracranial pressure-

ICP tends to rise with ing PCO
2
as a result of cerebral
vasodilatation.


Previously hyperventilation was used as method of acutely
reducing ICP after head injury.



4) Effects on autonomic nervous system-

symp. Activity secretion of NA at n. endings.
Adrenal medulla adrenal secretion.
At PaCO
2
< 200 mmHg NA = Adr.
> 200 mmHg Adr. >> NA
Hypercapnia modifies reactivity of adrenergic neuro- effector cells.
Mod. Hypercapnia enhances effects of exogenous
catecholamines.
>15% CO
2
depression of chronotropic, ionotropic and pressor
response of exo. catecholamines.



B) Pulmonary gas exchange

Hypercapnia hyperdynamic circulation es CO ed O flux
to tissues ed arterio-venous O difference ed O
2
content of
venous blood ed Alv.-Art. O
2
gradient.

Slight increase in PaO- offset by impaired uptake of O by Hb due to
Bohr effect.

Reverse of this occurs in hypocapnia.
C) Circulatory Response To Hypercapnia

DIRECT EFFECTS - depressive effect on CVS

myocardial contractility. - vascular tone
LVEF
HR
Altered rhythm. (pH < 7.0 )


INDIRECT EFFECT - sympathetic stimulation

myocardial contractility
HR




NET EFFECT variable balance b/w the two

Increase-

HR

Myocardial
contractility

Cardiac index

Stroke volume




Decrease-


Ejection time
( because of hyperdynamic
circulation)
D) Change In Cardiac Rhythm
Hypercapnia change in cardiac conduction
change in rhythm
esp. PaCO > 90 mmHg & pH < 7.0

- ECG changes A-V junctional rhythm with or without variable
T-wave changes

Halothane , enflurane , isoflurane asso. with Torsades De Pointes,
VT-VF
E) Effect On Skeletal Muscle
PaCO
2
5468 mmHg decrease contractility (10-30%)
earlier fatigue of diaphragm

K levels leakage of K from cells to plasma takes time to
go intra-cellular after correction of hypercapnia

- Repeated bouts of hypercapnia step ladder increase in K
levels dangerous hyperkalemia

Limb blood flow-

Balance b/w vasodilatation (CO
2
) & vasoconstriction (symp.
System)

During anaesthesia
predominant vasodilatation in skin flushing
predominant vasoconstriction in muscles


F) Effect On Regional Blood Flow
Pulmonary circulation

Hypercapnia increased pulmonary blood flow
(d/t increased CO)

-Increased pulmonary vascular resistance blood
shunted away to better ventilated alveoli decreased V/Q
mismatch.

Coronary circulation
Hypercapnia coronary artery dilatation

- increased coronary blood flow
- increased coronary sinus PO
2
a-v O
2

difference across coronary circulation.

PERMISSIVE HYPERCAPNIA
In order to minimise pulmonary damage, minute volume of
ventilation is maintained deliberately low and the arterial
PCO
2
is allowed to increase.

Used in cases where, there are chances of lung damage, e.g.-
-COPD
-ARDS

HYPOCAPNIA
P
a
CO
2
<36 mmHg
It is due to hyperventilation-
1. active
2.passive

ACTIVE HYPERVENTILATION
- action of the pt.s respiratory muscles leading to ed resp. drive
resulting from
Hypoxemia - CHD (Rt. to Lt. shunt)
- High altitude
- Collapse/consolidation of lung
Metabolic acidosis
-DKA
-Severe hemorrhagic shock
Hysteria, anxiety, head injuries.
Pregnancy
Light plane of anesthesia with pt. breathing spontaneously.

PASSIVE HYPERVENTILATION
- Caused by external agency
Iatrogenic (IPPV)
Pt. on ventilator

EFFECTS OF HYPOCAPNIA

A) EFFECTS ON CNS

Signs of CNS depression (d/t cerebral hypoxia).

Confusion, euphoria like mild alc. intoxication & occasionally
loss of cons.

Considerable amount of analgesia is also seen with hypocapnia.

a) EFFECT ON CEREBRAL CIRCULATION-

- PCO cerebral vasc. resistance CBF


- If PCO from 40 mmHg to 20 mmHg CBF by 50%


- Marked hypocapnia marked cerebral vasocons.
cerebral hypoxia prevents further vasocons.





b) EFFECTS ON JUGULAR VENOUS PO
2
-

- Mod. Hypocapnia cerebral vasocons. CBF ( as
metabolic demand of brain is same ) O extraction
from CBF ed jugular venous PO
2


c) EFFECTS ON CEREBRAL METABOLISM-

- Extreme hypocapnia dec. cerebral O consumption.(upto
10%)
- Cerebral venous lactate (d/t anaerobic meta. d/t CBF)



d) EEG CHANGES-
App. Of delta waves (slow waves) d/t
- Cerebral hypocapnia per se
- Cerebral hypoxemia


B) EFFECTS ON CVS-

- Isolated heart prep.- force of contraction or no effect.
- In awake pt. CO ( venous return)
- In anaesthetised pt.- passive hyperventilation CO upto
30% (when PCO-20 mmHg)


a) CARDIAC RHYTHM & BP

Hypocapnia is produced by hyperventilation under light
anaesthesia

- Little tendency for arrhythmia
- No change in pulse rate
- MAP declines a little ( d/t CO) but less remarkable as
TPR increases

b) PERIPHERAL CIRCULATION-
CO2- direct action- V.D
-sympathetic stimulation- V.C
Balance decides the net effect
Light anesthesia increases TPR during hypocapnia
Hypocapnia cutaneous V.C & V.D in muscle increases
B.F through limbs

c) PULMONARY CIRCULATION
hypocapnea pulm V.D increased flow
Alveolar arterial O2 tension difference- increase in G.A
which is further compounded by hypocapnea

C) EFFECTS ON RESPIRATION

Hypocapnia


decreased excitatory stimulus from Peripheral &
central chemoreceptor


decrease activity of respiratory neurons


respiratory depression

HYPOCAPNIA IN ANAESTHESIA

1. Hypocapnia cerebral hypoxia
(CBF & shift of ODC to Lt.)
2. CO
3. Vasoconstriction of systemic circulation


POST HYPERVENTILATION APNOEA
-Hyperventilation decreased CO
2
in blood and tissues

decreased resp drive

apnoea
-As hyperventilation does little to O
2
reserve risk of
arterial hypoxemia if breathing air O
2
in post-op is
important



Initiation of spontaneous ventilation after
hypocapnia

-hypocapnia during anesthesia difficulty in
initiation of spon ventilation


-Inhalational agents, narcotics spon ventilation
starts PCO > normal

Hence, narcotics and inhalational agents should be timed
properly.



Thank you