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Pathophysiology 2 > Hypobarism and Hyperbarism > Flashcards

Hypobarism and Hyperbarism Flashcards

1
Q

Hypobarism

A
  • A decrease in atmospheric pressure
  • Can result in pathology
    • Altitude sickness
    • HAPE
    • HACE
    • Decompression Sickness
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2
Q

Hyperbarism

A

A increase in atmospheric pressure

Can result in pathology

Can be used as a therapeutic intervention

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3
Q

Henry’s Law

A

States that the amount of gas dissolved in a liquid is directly proportional to the partial pressure of the gas above the solution and the solubility coefficient of the gas

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4
Q

Daltons’s Law of Partial Pressure

A

The total pressure of a mixture of gases is the sum of the pressure that each gas would exert if it were present alone

Pt= P1 + P2 + P3 + …+Pn

Consider air

  • 21% oxygen and 79% nitrogen
  • At sea level the total pressure is 760 mmHg
  • The partial pressure of oxygen then is 0.21 x 760 mmHg = 160 mmHg
  • The partial pressure of nitrogen is 0.79 x 760 mmHg = 600 mmHg
  • We calculated PiO2 at 3ATA to be 480 mmHg (with FiO2 0.21). When 1.0 then the PiO2 is 2280 mmHg!
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5
Q

Dalton’s Law and HBOT

A
  • If hyperbaric therapy is done with air (21% O2 and 79% N2) both the partial pressure of nitrogen and oxygen are increased in the tissues
  • Nitrogen has narcotic effect at increased pressures “Rapture of the Deep”
    • 2.5-3 ATA can result in mild euphoria
    • 4-6 ATA can result in significant intoxication which could lead to procedures being performed erroneously
      • Confirmation by someone outside the chamber may be required
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6
Q

Boyle’s Law

A

When temperature of a gas is constant, any increase in pressure causes a proportional decrease in the volume of the gas

Thus at a given temperature

P1V1=P2V2

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7
Q

Boyle’s Law and HBOT

A
  • Changes in pressure lead to predictable changes in volume
    • When the pressure is doubles then the volume is halved
    • Tripling the pressure reduced the volume to 1/3 of original size
  • Example- Pneumothorax and “Ascent”
    • Consider what will happen to ETT cuff volumes and pressures
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8
Q

Altitude Sickness

A
  • Altitude Sickness; Acute Mountain Sickness – AMS
  • Generally speaking, not seen below 10,000 feet
    • Generally seen in people who do not properly acclimatize when ascending to high altitudes
  • Incidence depends upon three things:
    • The altitude the individual is ascending to
    • Their rate of ascent – how fast are they climbing
    • The individual’s own susceptibility
  • ​The etiology of AMS = Hypoxemia
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9
Q

Altitude Sickness Signs and Symptons

A

Generally start within the first 6 to 12 hours after entering altitude, increase in severity over first 48 hours, and lessen after 72 hours at altitude

Can include:

  • Severe fatigue, progressive muscle strength loss, inability to walk
  • Headache, dizziness, confusion, insomnia
  • SOB, paroxysmal nocturnal dyspnea, periodic breathing
  • May progress to pulmonary edema (HAPE) and cerebral edema (HACE)
  • Symptoms are worse at night, when the respiratory drive is lessened
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10
Q

Altitude Sickness Treatment

A
  • Three options: descend, acclimatize, or descend “artificially”
    • With severe AMS the CNS is severely affected
  • They need to descend immediately or they will die
  • “Artificial” Descent
    • Portable & inflatable hyperbaric tent (Gamow Bag)
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11
Q

Altitude Sickness

Proper Acclimatization

A

Generally takes the better part of a week (5 to 6 days ), where the individual ascends at a slow pace to allow for RBC’s due to stimulation of the hormone erythropoietin (due to ¯PaO2 ) and results in increased oxygen carrying capacity

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12
Q

Altitude Sickness Prevention

A

Ascend to altitude slowly

Climb high and sleep low

Don’t go up until symptoms go down

If symptoms get worse – descend

Keep well hydrated

Don’t over exert yourself

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13
Q

Altitude Sickness Protective Agents

A
  • Diamox (acetazolomide)
    • Carbonic anyhydrase inhibitor; diuretic
    • Can decrease manifestations of mild edema (e.g. headaches)
    • Can induce a relative metabolic acidosis and lead to further respiratory stimulation
  • Dexamethasone
    • Used prophylactically to prevent HAPE and HACE
    • Must be started 5 days prior to ascent
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14
Q

Hyperbarism Indication for Acute Conditions

A

Decompression Sickness (the “bends”)

Air embolism

CO poisoning

Cyanide poisoning

Thermal injuries

Acute traumatic ischemia

Clostridial gangrene

Necrotizing soft-tissue infection

Ischemic skin graft/flap

Exceptional blood loss

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15
Q

Hyperbarism Indication for Chronic Conditions

A

Nonhealing wounds

Refractory osteomyelitis

Radiation necrosis

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16
Q

Hyperbarism Contraindications

A

High fevers

Hypercapnia (> 60 mmHg)

Obstructive airway disease

Optic neuritis

Seizure disorders

Pneumothorax (*Absolute)

Sinusitis

Upper respiratory tract infections

Viral infections

17
Q

Hyperbarism Primary Physiological Effects

A

Hyperoxygenation

Reduction in bubble size

18
Q

Hyperbarism Secondary Physiological Effects

A

Angiogenesis

Vasoconstriction

Increased leukocyte oxidative killing

Bactericidal/bacterial static for anaerobic/ facultative anaerobic bacteria

19
Q

Hyperbarism Effects on the Cardiovascular System

A

HR: decreased

Cardiac output: decreased (due to decreased HR)

BP: possible minimal increase

SVR: Increased (vasoconstriction 2° increased oxygenation)

This results in increased afterload which could be detrimental to patients with CHF

Treatment for DCS/AE can sometimes be at up to 6 ATA for more severe cases, but, as always, depends on the institution’s protocols.

20
Q

Hyperbarism Effects on Blood Gases

A

other than the obvious increase PaO2!

Transport of CO2 in the blood occurs as bicarbonate (~75%), carbaminohemoglobin (~20%) and dissolved in the plasma (~5%)

As described by the Haldane Effect, in the presence of oxygen, hemoglobin has less affinity for CO2, thus CO2 is not carried on hemoglobin in a hyperbaric environment

This results in increased levels of CO2 dissolved in the blood

21
Q

HBOT: Principles of Application

A
  • Uses standardized protocols
  • E.g. Gas Bubble Disease
    • Eg. Decompression sickness (the “bends”) or iatrogenic gas embolism
    • Patient is compressed to 2.8 ATA and then decompressed to 1.9 ATA
    • Periods of 100% O2 breathing are interspersed with short “air breaks”
    • Minimizes oxygen toxicity
    • This treatment schedule proposed for mild DCS
22
Q

Carbon Monoxide Poisoning

A

Hemglobin binds with CO 200-250 times more readily than with O2

So patient commonly pressurized to 203 ATA times vary depening on the protocol

23
Q

Gas Ambient Pressure and Mean Half Life

A

Air

  • Ambient Pressure
    • 1
  • Mean Half Life
    • > 5 hours

Oxygen

  • Ambient Pressure
    • 1
  • Mean Half Life
    • 80 min

Oxygen

  • Ambient Pressure
    • 3
  • Mean Half Life
    • 23 min
24
Q

Hyperbarism and Barotrauma

A
  • Can occur in any gas containing organ or cavity in the body
  • Middle ear (Most common)
  • Sinuses
  • GI tract
  • Teeth
    • If infected or restored
  • Lungs
    • Patients coached during decompression to avoid breath holding
25
Q

Hyperbarism and Oxygen Toxicity

A

Effects may occur at any point in the treatment

Correlated more to the duration of the treatment rather than the number of treatments

Can avoid by giving “ait breaks”

26
Q

Hyperbarism and CNS Signs and Symptons

A

Nausea/vomiting

Sweating

Visual changes

Hallucination

Decreased LOC

Seizures

27
Q

Hyperbarism and Respiratory Signs and Symptons

A

Dry cough

SOB

Chest pain

Sub sternal

Pulmonary edema

28
Q

The “Bends”

A

A mild form of decompression sickness

Caused by the formation of gas bubbles in the body during rapid ascent (normal ascent allows nitrogen to slowly move out of the body)

29
Q

The “Bends” Signs and Symptons

A
  • Consists of “pain only” manifestations
  • The pain occurs in the joints
    • Due to bubble accumulation
    • Patients avoid or are unable to bend affected joints
  • Can also include skin mottling and itching
30
Q

Decompression Sickness

A

Potentially lethal

Signs and symptoms will appear gradually

First symptom will tend to appear at 20 min and the second at 2 hours

31
Q

Decompression Sickness Signs and Symptons

A

Pain

Mild headache

Blurred vision

Paresthesia

Shortness of breath

Cough

Vertigo

Paralysis

Shock

32
Q

DCS and Arterial Gas Embolism

A

Thus, these bubbles generally become trapped in the pulmonary circulation

Arterial gas embolism occurs when there are air bubbles in the arterial system

These usually arise due to pulmonary expansion barotrauma! (eg. From a breath hold ascent)

Can be lethal depending on location of air embolus

33
Q

Decompression Sickness the Four Cs

A

Another way to look as the signs and symptoms: The four “C’s“:

Creeps: sensation of tiny insects moving underneath the skin – bubble formation

Cramps: the bends: pain localized in the large joints of the body – severe

Chokes: rare: substernal chest pain, SOB, a dry, non-productive cough – caused by pulmonary air emboli

Collapse: the end stage, death

34
Q

Nitrogen Narcosis: “Rapture of the Deep”

A

Pathologydue to the hyperbaric environment (i.e. not during removal from)

Only at risk if breathing air (not oxygen) in a hyperbaric environment (\deep sea diving as well!)

Due to the high partial pressure of N2 in the tissues (specifically in the brain)

35
Q

Nitrogen Narcosis Clinical Manifestations

A

Euphoria

Impaired judgment

Decreased coordination

Light-headedness

Inattention

Hallucinations

Coma

Death

36
Q

Nitrogen Narcosis Treatment

A

= Decompression

Fully, or at least to a depth where symptoms disappear.

Pathophysiology 2 (9 decks)

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