How CO 2 is transported in the blood?
Examiner will give you a pen and paper and tell you to write the equationof bicarbonate
Q3: where dose this equation happens?
Chloride shift?
Examiner will give you an ABG, interpret?
Reduce
Low pH, high PCOz, normal bicarb
Q6: Cause?
Why still no metabolic compensation?
Where is the respiratory center?
CO2 + H20 = H2CO3 = H + HCO3
НCО3* → diffuses out to the plasma
H+ → binds to Hb
Cl → diffuses into the RBC
in RBCs
Chloride diffuses into the red cell to maintain cellular balance, as HCO3 moves out
uncompensated respiratory acidosis
Morphine overdose (depresses CNS)
Kidney takes time to react 3 days in average
Centeral: Pons and Medulla oblongata / peripheral: carotid & aortic bodies
Why is bicarb normal?
The receptor in the body which responsible for respiration?
where is the centeral chemoreceptors located? and their role?
Q: where to find peripheral chemoreceptors?
In acute respiratory acidosis, compensation occurs in 2 steps
• The initial response is cellular buffering that occurs over minutes to hours. Cellular buffering elevates plasma bicarbonate (HCO3−) only slightly, approximately 1 mEq/L for each 10-mm Hg increase in PaCO2 .
• The second step is renal compensation that occurs over 3–5 days. With renal compensation, renal excretion of carbonic acid is increased and bicarbonate reabsorption is increased.
In pons and medulla. They detect PH level in blood and sent signals to respiratory centers in the brain to adjust respiration accordingly.
What type of respiratory failure is that?
Types of respiratory failure and what are their causes?
Response mechanisms to hypercarbia?
Why PaO 2 is in normal range?
Where to manage this patient?
Management? (ITU)
How morphine act?
Dose of Naloxone? Side effects:
Indications of ITU admission
Type 2 (hypercapnia)
Type 1 Ventilation/perfusion (V/Q) mismatch; the volume of air flowing in and out of the lungs is not matched with the flow of blood to the lungs
• Pneumonia • Bronchitis • PE • Pneumothorax
Type 2 Caused by inadequate alveolar ventilation; both O2 /CO 2 are affected.
Defined as the buildup of carbon dioxide levels (PaCO2 ) that has been generated by the body but cannot be eliminated. The underlying causes include:
• Increased airways resistance (COPD, asthma, suffocation)
• Reduced breathing effort (drug effects, brain stem lesion, extreme obesity)
• A decrease in the area of the lung available for gas exchange (such as in chronic bronchitis)
• Neuromuscular problems
• Deformed (kyphoscoliosis)
Elevation in CO 2 leads to central acidosis, which stimulates central chemoreceptors and leads to increased respiratory rate in order to blow off extra CO2 .
Because FiO 2 is 0.6 = 60%
ITU
• ABC, managed according to CCrISP protocol
• Ensure adequate oxygenation by humidified O2
• Ensure adequate ventilation either noninvasive or invasive (intubation and invasive respiratory support or CPAP)
• Management of the underlying cause
• Morphine antagonist: (Naloxone)
By binding to mu receptors on the respiratory center causing respiratory depression
0.4 -2 mg IV initially and repeat every 2-3 min if no response, to a maximum of 10 mg
Nausea, vomiting, sweating, tachycardia, abdominal cramps, pulmonary edema, cardiac arrest
ITU admission is indicated for multi-organ mechanical support:
• Respiratory: mechanical ventilation, non-invasive ventilation
• Renal: continuous hemofiltration, intermittent hemodialysis.
• Cardiac: advanced cardiac output monitoring, inotropic support.
• Neurological: intracranial pressure monitoring.
Q12: why to manage in ITU?
Q: Where to give naloxone? why?
Q: How morphine causes respiratory failure?
Q: causes of Respiratory acidosis?
Q: Side effects of morphine?
Patient needs monitoring as naloxone can cause cardiac arrest and it has short half life, and requires ventilation
Naloxone is given in ICU because the patient requires close monitoring — it can precipitate cause arrhythmia or cardiac arrest, especially in chronic opioid users. It also has a short half-life (30–60 minutes), so repeated doses or infusion may be needed. Ventilatory support should be available as respiratory depression can recur once naloxone wears off.
Morphine depresses the brainstem respiratory center so that the normal rise in CO₂ and fall in O₂ no longer stimulate respiration, leading to hypoventilation and respiratory failure
-pneumonia, Asthma, COPD, morphine overdose
M
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P
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MORPHINE SIDE EFFECTS
“MORPHINE”
M -MYOSIS
O -OUT OF IT (SEDATION)
R-RESPIRATORY DEPRESSION
P-PNEUMONIA (ASPIRATION)
H-HYPOTENSION
I-INFREQUENCY (CONSTIPATION, URINARY RETENTION)
N-NAUSEA
E-EMESIS