Altitude Flashcards
Define moderate and high altitude
Moderate between 5000-8000 feet
High between 8000-14000
Discuss acclimatization
Begines as the o2 saturation of art blood falls below sea level values.
The altitude at which this occurs depends on the rate of ascent, the duration of exposure and individuals physioloyg.
Increased MV - occurs wihtin minutes (hypoxic ventilatiory response)
Kidneys incerase bicarbonate excretion – acetazolamide enhances this reaching a max at 6-8 days
Increase catecholamines increase CO and elevatees HR , SV, BP and venous ntone.
EPO and increased HB –> long term leads to increased plasma volume and total blood volume.
Increased in 2,3 dpg leading to rightward shift and offloading of o2
Discuss the pathophysiology of Acute mountain sickness and high altitude cerebral oedema
All start with exposure to hypoxia due to barametric reduction in o2. Physiological response starts in minutes with AMS, HACE and HAPE take 2-4 days to develop
Within minutes of exposure to hypoxia, cerebral vasodilation occurs with increased arterial blood velocity and volume
Hypocapnia creates a countervailing cerebral vasoconstriction. The end product is increased cerebral blood flow.
CNS hypoxia leads to impaired vascular autoregulation causing increased pressures within the brains capillary beds.
In addition systemic hypertension from strenous activity at high altitude + symptathetic discharge can overwhelm the brain vasculature resutlign in transcapillary leak and vasogenic oedema.
Inflammatory mediates (endothelial growth factor, nitric oxide, reactive cytokines and free radicals all likley play a role)
Hypobaria itself likley plays a role –> less incidence of AMS in hypoxia induced at normal pressure.
Tight fit hypothesis suggest that it is not the amount of swelling that maters as much as the person ability to tolerate the swelling. Individuals with less intracranial and intraspinal CSF buffering capacity are at increased risk
Discuss the pathophys of high altitude pulmonary oedema
Results from hypoxia induced acute pulmonary hypertension leading to stress failure of pulmonary capillaries with consequent alveolar and interstitial oedema.
Hypoxic pulmonary vasocstriction response can vary greatly between people and even in different regions of the lung. This uneveness is thought to contribute to pathogenesis
Uneven vasoconstrictrion forces the pulmonary hjyppertension to be transmitted to delicate capillary vessels in an uneven fashion leading to the failure of apillary endothelium.
This uneven nature explains the patchy infiltrate seen on CXR
Inflammatory markers than appear to worsen the situation
Discuss factors that predispose patient to HAPE
male gender, cold ambient temperatures, preexisting respiratory infection, and vigorous exertion
Pre-exisiting factors that lead to icnrfeased pulmonary blood flow and hypertension or increased pulmonary vascular reactivity predispose patient to HAPE
- primary pulmonary hypertension,
- congenital absence of one pulmonary artery,
- left-to-right intracardiac shunts, such as atrial septal defects and ventricular septal defects
Discuss clinical features of AMS`
Lake loiuse criterai for the diagnosis of AMS requries a patient to have recently ascended at least 8000ft with a report of a headache and at least on of the following
- GIT upset (anorexia, nasuea or vomting)
- general weakness or fatigue
- dizziness or light headiness
- difficulty sleeping, nocturnal periodic breathing
The headache varies from mild to severe is generally bitemporal and throbbing in nature
Can use ultrasound to measure ONSD can be used as diagnostic tool and monitoring of improvement
Discuss DDX of AMS
Tension headache viral sydnrome ETOH intoxication CO poisoning Dehydration Caffeine withdrawal Migraine headache infectious intracranail haemorrhage or mass CNS aneurysms Venous sinus thrombosis Abdominla process Acute angule closure gluacoma
Discuss treatment of AMS
Do not ascend to a higher sleeping altitdue until symptoms resolve and acclimatization occurs
If develop any signs of HACE or HAPE immediate decent is indicated
O2- all forms of altitude illnes including AMS are effectively treated with supplemental o2.
Analgesics and antiemetics
- NSAIDs paracetamol and antiemetics can be used to treat patient symptomatically
- do not use opiates due to respiratory depressant effect
Acetazolamide
-Periodic breathing causes insomnia which is best reated with the respiraotry stimulant acetazolamide
-accelerates acclimitization and if given early in AMS may rapidly resolve sympomts
-dose 250mg BD and 2.5mg/kg in kids all BD
Benefits -
-improves renal correction of resp alkalosis
- encourages ventilation to reduce nocturnal apnoea
-diuretic and so attentuates fluid retention
-lowers CSF voume and pressure
-beneficial chemorecepotor effects on ventilatory dirve
Adverse effects
-nausea, diarrhoea, drowsiness, tinnitus, and transietn myopia
-sulfa drug risk of allergy
Dexamethasone
- initial dose of 8 mg followed by 4mg QID
-
Discuss HACE
Least common but most severe form of High altitude illness
Death from HACE is reported at 8200ft most occur over 1200 feet
Mild AMS can progress to severe HACE with coma in as few as 12 hours althoguh severe symptoms usually develop within 1-3 days they may not occur until 5-9 days
Discuss clinical features of HACE
Characterised by evidence of global cerebral dysfunction
Symptoms include
-Severe AMS (headache fatigue and vomiting)
-HAPE
-HACE specific signs
—Ataxia - one of the first signs due to particular sensitivty of the cerebellum to hypoxia
—-slurred speech
—– altered Mental state (range from mild emotional lability to hallucinations and worsening obtundation that may progress to comma or death()
Discuss management of HACE
- Securing of airway
- all efforts to increase o2
- -High flow O2 if available
- decent
- Decrease ICP
- –Hyperventialtion
- –diuretics (frusemide)
- – Hypertonic saline
- Steroid therapy as per AMS
Hyperbacis
Discuss HAPE
Most common fatal manifestation of severe high altitude illness
Uncommon below 10000 feet although can occur and be fatal
Some individuals are susceptible and experience HAPE with each ascent to altitude. Rarely the congenital absence of a pulmonary artery exaggerates te pulmonary vascular repsonse to hypoxia
Discuss clinical features of HAPE
Usually begins insidiusly 2-4 days after arrival at high altitude
Marked dyspnoea on exertion, fatigue with minimal to moderate effort and prologned recovery time, and dry cough are early manifestations
As the HAPE patient worsens usually throughout the night the dyspnoea worsens and is not releived by rest. Dyspnoea at rest is a red flag
Copious amount of watery sputum and haemyotosis in severe cases
Widespread rhales as the disease progresses
Disucss IX HAPE
US
- B lines and effusions
CXR
- patchy alverolar infiltrates
- nil cardiomegaly, batwing distribution or kerley blines
ECHO and ECG
- RAD
- tall rwaves and s-wave laterally
Discuss management of HAPE
Warm and minimize exertion
O2 therapy
-high flow rate of 6-8L by mask should be delivered
-these flows can be reduced with decent
-Hyperbaric chambers can be used (portable lightweight fabric chambers haqve been used)
Nifedipein SR 20mg TDS
- lower pulmonary artery pressure, pulmonary blood flow and vascular resistance
- HAPE does not result from excessive intravascular volume or failed cardiac pump as such diuretics have no role
Phosphodiesterase type 5 inhibitors (sildenafil)
- agument pulmonary vasodilatory effects of nitric oxide
Steroids
Beta agonist
- upregulate fluid clearance
