pH< 7.35 acidosis
pH > 7.45 alkalosis
The body response to acid-base imbalance is called compensation
May be complete if brought back within normal limits
Partial compensation if range is still outside norms.
If underlying problem is metabolic, hyperventilation or hypoventilation can help : respiratory compensation.
If problem is respiratory, renal mechanisms can bring about metabolic compensation.
Principal effect of acidosis is depression of the CNS through ↓ in synaptic transmission.
Deranged CNS function the greatest threat
Severe acidosis causes -Disorientation,coma ,death
Alkalosis causes over excitability of the central and peripheral nervous systems.
It can cause :Nervousness,muscle spasms or tetany ,Convulsions ,Loss of consciousness,Death
Carbonic acid excess caused by blood levels of CO2 above 45 mm Hg.
Hypercapnia – high levels of CO2 in blood
Depression of respiratory center in brain that controls breathing rate – drugs or head trauma
Paralysis of respiratory or chest muscles
Adult Respiratory Distress Syndrome
Signs and Symptoms of Respiratory Acidosis
Lethargy and disorientation
Tremors, convulsions, coma
Respiratory rate rapid, then gradually depressed
Skin warm and flushed due to vasodilation caused by excess CO2
viability; the underlying mechanism is:
- increased volume within space
- decreased space for contents
- combination of both
Trauma with bleeding/swelling
Pneumatic antishock garment
Increased compartment pressure leads to increased venous pressure which decreases A-V gradient resulting in muscle and nerve ischemia.
Variables to Consider
Duration of elevated pressure
Metabolic demand of tissue
Lowered ischemic threshold of damaged muscle
Released in high levels at reperfusion
Toxic to glomeruli
Metabolic acidosis & hperkalemia
Together lead to:Renal failure,Cardiac arrhythmia & failure,Hypothermia and Shock
Clinical exam: the Ps(Pressure,Pain,Paresthesia,Paralysis,Pallor,Pulselessness)
Laboratory tests-CPK and Urine myoglobin
Causes / Risk Factors for Obstructive Sleep Apnea
Obesity, Obesity, Obesity
Tonsillar hypertrophy, nasal pathology
Alcohol, smoking and family history
Up to 90% of adult patients with OSA are obese
Obstructive Sleep Apnea is defined as a cessation of airflow for more than 10 seconds despite continuing ventilatory effort, 5 or more times per hour of sleep and a decrease of more than 4% in SaO2.
What Happens with Normal Sleep?
4 to 6 cycles of N-REM sleep followed by REM sleep
4 stages of N-REM with progressive slowing of EEG
Stage 3 and 4 N-REM and REM are very deep levels of sleep
Progressive generalized loss of muscle tone
Restorative periods of sleep
Progressive decrease in muscle activity and resultant increase in upper airway resistance.
Occurs with loss of muscle activity
Increased subatmospheric pharyngeal pressure
MRI reveal anterior and lateral wall collapse
Obesity Effects Airway Anatomy Adversely
Inverse relationship between obesity and pharyngeal area
Fat deposits in the uvula, tongue, tonsillor pillars, aryepiglottic folds and lateral pharyngeal walls.
SUDDEN ONSET OF MARKED BRADYCARDIA, RESITANT TO TREATMENT,PROGRESSING TO COMPLETE HEART BLOCK
CLINICALLY ENLARGED LIVER
METABOLIC ACIDOSIS WITH A BASE DEFICIT OF > 10 MMOL/L ON AT LEAST ONE OCCASION
RHABDOMYOLYSIS OR MYOGLOBINURIA
Propofol marketed in the USA since 11/1989.
PRIS has been described in both children and adult patients sedated with propofol.
FIRST CASE REPORTS- 1992
FDA Investigation of Deaths associated with Propofol
Reviewed reports of death with propofol as the suspect drug: pediatric pt(≤ 16y) and adults(>16y) for non-procedural sedation.
Time period= Nov 1989-Apr 2005.
Metabolic acidosis and/or rhabdomyolysis with progressive cardiac failure US deaths for Nonprocedural sedation reported to the FDA
2yo boy PICU s/p shot in the head with an air gun pellet.
Intubated and ventilated for right sided cerebral edema and rim of subdural blood.
Sedated with propofol rate of 4-5.4 mg/kg/h. over 72 h.
oliguria, increase in K+,BUN, Cr and then sudden, persistent bradycardia(HR= 28).
Propofol stopped, trans-venous pacer placed, restored HR but had persistent acidosis.
Diagnosis: PRIS- started dialysis. Complete recovery.
- Otorrhea is yellow and foul-smelling
- Otorrhea has not resolved with otic drops
- Occasional dizziness
- No fever
- Otalgia has subsided
- Intermittent unilateral tinnitus
- Hearing loss
Weber localizes to left
AC > BC AD
BC > AC AS
Facial nerve intact
Otherwise - within normal limits
- Jugular bulb anomalies (high riding bulb, dehiscent jugular bulb, and jugular bulb diverticulum), aberrant internal carotid artery (ICA), hemangioma, persistent stapedial artery
- Otitis Media, otitis externa, malignant otitis externa, tuberculous otitis
- Granulomatous Diseases (a.k.a., Wegener’s granulomatosis)s
- Retained PE tube, Foreign Body
- Cholesteatoma, paraganglioma / glomus tympanicum tumor, schwannoma, adenoma, endolymphatic sac tumor, cholesterol granuloma, polyps, adenocarcinoma, squamous cell carcinoma, adenoid cystic carcinoma
- Cholesteatoma, encephalocele
Congenital Cholesteatoma _Criteria
White mass medial to normal tympanic membrane
Normal pars flaccida and pars tensa
No prior history of otorrhea or perforations
No prior otologic procedures
means increased activity of the suprarenal cortex at puberty with increased production of adrenal androgens which lead to appearance of pubic and axillary hair.
Cause of puberty:
During childhood , the hypothalamus is extremely sensitive to the negative feedback exerted by the small quantities of estradiol & testosterone produced by the child's ovaries .
As puberty approaches , the sensitivity of the hypothalamus is decreased and subsequently , it increase the pulsatile GnRH secretion .
The anterior pituitary responds by progressive secretion of FSH and LH associated with increased secretion of growth hormone .
The ovaries respond to the increase Gonadotrophin secretion by follicular development & estrogen secretion .
Estrogen causes development of the genital organs and the appearance of the secondary sexual characters .
With increased estrogen secretion , menarche and cyclic estrogen secretion occurs .
Factors affecting the initiation of pubertal development :
1 - Height and weight ratio (nutritional factors).
2 - Maturation of the hypothalamus .
3 - Increased neurotransmitter output in CNS .
4 - Onset of adrenal androgen activity
FEMALE PRECOCIOUS PUBERTY
It means menarche or appearance of any of the secondary sexual characters before the age of 8 years.
1 - True precocious puberty
It is due to increased production of pituitary gonadotrophins.
2 - False(pseudo-precocious puberty)
It is of peripheral origin.
It is due to secretion of sex hormones; (estrogen or androgen) which is not dependent on pituitary gonadotrophins as in case of estrogenic or androgenic ovarian tumors.
3 - Incomplete precocious puberty .
In this case only one pubertal change as breast development is present before the age of 8 years without the presence of any other pubertal changes and in absence of increased estrogen production.
The other pubertal changes occur at the normal age.