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THORACIC SURGERY > 1/3 > Flashcards

1/3 Flashcards

0
Q

WHAT HAPPENS TO AIR (AND O2) AS IT ENTERS THE NOSE?

A

TURBULANT FLOW AROUND CONCHAE FORCES AIR INTO CONTACT WITH THE MUCOSA….THE AIR BECOMES HUMIDIFIED (70-80% HUMIDITY AT THE NASOPHARYNX…100% AT THE CARINA) AND O2 CONCENTRATION IS DILUTED WITH H2O. 160%O2 TO 150% O2.

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1
Q

WHAT CONSTITUTES THE UPPER AIRWAY?

A

UPPER AIRWAY IS ABOVE THE CORDS AND MAKES UP 30-50% OF ANATOMIC DEADSPACE.

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2
Q

WHAT ARE YOUR CENTRAL AND PERIPHERAL AIRWAYS?

A

CENTRAL (LARGE) AIRWAY=BRONCHI
PERIPHERAL (SMALL) AIRWAY= BRONCHIOLES

THE BRONCHILES ARE WHAT SNAPS SHUT DURING ASTHMA ATTACK.

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3
Q

WHAT IS THE FUNCTION OF THE LOWER AIRWAY?

A

EXTERNAL RESPIRATION AKA THE TRANSFER OF GASES FROM AND TO THE ATMOSPHERE. IE LUNGS.

…AS OPPOSED TO INTERNAL RESPIRATION WHICH IS THE O2 UTILIZATION BY THE CELLS. IE MITOCHONDRIA

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4
Q

WHAT ARE THE STATS ON THE GENERATIONS OF THE LOWER AIRWAY? #1-26.

A

TRACHEA-#0: 10-13CM LONG. 1.5-2.5 CM DIAMETER. FORMED OF 16-20 C SHAPED CARTILAGINOUS RINGS. CORDS AT C4-5. CARINA IS AT T4-6.

MAINSTEM BRONCHI (1): RIGHT 25 DEGREES; LEFT 40-60 DEGREES.

LOBAR BRONCHI(#2): 3 RIGHT, 2 LEFT.

SUBSEGMENTAL BNRONCHI (4-9): CARTILAGE AND SIZE DECREASE SO 80% OF AIRWAY RESISTANCE BELOW THE GLOTTIS OCCURS HERE.

BRONCHIOLES (10-15): < 1MM DIAMETER. NO CARTILAGE IN WALLS SO PATENCY DEPENDS ON THE ELASTICITY OF SURROUNDING LUNG TISSUE. AND THERE ARE SO MANY OF THESE BRONCHILES THAT THE TOTAL AREA INCREASES DRAMATICALLY HERE. <20% OF AIRWAY RESISTANCE IS FOUND HERE DUE TO THIS FACT EVEN THOUGH THEY HAVE SMALL DIAMETER.

TERMINAL BRONCHIOLES (16): THE LAST PART OF THE CONDUCTING AIRWAY. IE NO GAS EXCHANGGE YET

RESPIRATORY BRONCHIOLES (17-19): BEGINNING OF LUNG PARENCHYMA AND THUS GAS EXCHANGE.

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5
Q

WHAT ARE THE 3 LAYERS IN THE LUNG?

A

-ALVEOLAR EPITHELIUM: 3 TYPES OF CELLS. 1, 2, AND 3.
1-FORM THE ALVEOLAR WALL AND SPECIALIZE IN GAS EXCHANGE. MOST ARE OF THIS TYPE.
2- COVER 10% OF ALVEOLAR SURFACE. PRODUCE SURFACTANT AND REGENERATE TYPE 1 CELLS.
3- PHAGOCYTIC MACROPHAGES THAT CLEAN DEBRIS.
-INTERSTITIAL SPACE
-CAPILLARY EPITHELIUM

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6
Q

HOW IS RESPIRATION CARRIED OUT WITH MUSCLES?

A

INSPIRATION IS ACTIVE AND INVOLVES 3 MUSCLES:
DIAPHRAM
EXTERNAL INTERCOSTALS
ACCESSORY MUSCLES IE: STERNOCLEIDOMASTOID, SCALENES, PEC MAJOR/MINOR, AND TRAPEZIUS.
EXPIRATION IS PASSIVE AND INVOLVES ABDOMINAL MUSCLES, LAT DORSI AND INTERNAL INTERCOSTALS.

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7
Q

HOW IS RESPIRATION CARRIED OUT WITH CHEMORECEPTORS?

A

CENTRAL AND PERIPHERAL CHEMORECEPTORS.
CENTRAL-IN MEDULLA SENSE CHANGE IN CSF PH. INCR CO2 CAUSES A INCR IN RESPIRATION. THIS SYSTEM IS WHAT WE DO NORMALLY AT REST.
PERIPHERAL- IN CAROTID BODY RESPOND TO DECREASE O2 SUPPLY. THIS IS WHEN YOURE DYING….PO2<50!

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8
Q

WHAT DOES STIMULATION OF CENTRAL CHEMORECEPTORS CAUSE?

A

INCREASE TIDAL VOLUME FOLLOWED BY RESPIRATORY RATE.

ALSO INCREASE CO AND SVR.

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9
Q

WHAT IS VAPOR PRESSURE OF H2O AT BODY TEMP? (37 C)

A

47 TORR.

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10
Q

DO CHANGES IN ALVEOLAR PRESSURE OF CO2 AFFECT ALVEOLAR PRESSURE OF O2?

A

YES! pA O2 WILL FALL ABOUT 1.2 MM HG FOR EVERY 1 MM HG RISE IN pA CO2.

HYPOVENTILATION (INCR CO2) POSTOP CAUSES HYPOXEMIA WHICH IS EASILY REVERSIBLE WITH O2 SUPPLEMENTATION.

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11
Q

WHY IS ARTERIAL O2 ALWAYS LESS THAN ALVEOLAR O2?

A

BECAUSE THERE IS ALWAYS A SMALL AMOUNT OF SHUNTED BLOOD THAT GOES FROM THE RIGHT HEART WITHOUT GOING TO THE ALVOLI.

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12
Q

WHAT DOES pA O2 - pa O2 MEASURE?

A

THE ADEQUACY OF O2 TRANSFER FROM LUNGS TO ART BLOOD. IF THIS GRADIENT INCREASES IT MEANS THAT DIFFUSION IS IMPAIRED OR THERE IS AN INCREASE IN PULMONARY ADMIXTURE. (BLOOD SHUNTED FROM RIGHT TO LEFT)
THIS GAP WILL ALSO INCREASE AS WE AGE BECAUSE paO2 IS AGE DEPENDENT (DECREASES AS WE GET OLDER) WHEREAS pAO2 IS INDEPENDENT OF AGE.
AN ELEVATED ALVEOLAR-ARTERIAL GRADIENT REFLECTS LUNG DISEASE.

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13
Q

WHAT IS THE EQUATION FOR pAO2?

A

pAO2= (FiO2 X [BAROMETRIC PRES -47]) - ( 1.2 X paCO2)

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14
Q

WHAT IS THE LITER FLOW AND EXPIRED FiO2 OF SUPPLEMENTAL OXYGEN?

A

NASAL CANNULA: EVERY 1L FLOW INCREASE; FiO2 INCREASES 4%….SO 1-6 L/MIN AND 24-44% O2.
FACE MASK: 8-10L ; 40-60%
NON REBREATHER: 6-10L ; 60-100% O2. (10% INCR/1L)
MOUTH TO MOUTH: 17% O2
AMBU BAG: 15L =100%

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15
Q

WHAT ARE THE HAZARDS OF O2 THERAPY?

A

IF YOU HAVE 100% O2 FOR THE MAJORITY OF A DAY YOU CAN GET O2 TOXICITY WHICH CAUSES SUBSTERNAL DISTRESS AND LUNG DAMAGE. DENITROGENATION ABSORPTION ATELECTASIS.
IT CAN ALSO REDUCE HYPOXIC VENT DRIVE IF YOURE DOING SEDATION. PLUS YOU SHOULD ALWAYS GIVE NEONATES LESS O2 SO SHUNTS DONT REOPEN.

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16
Q

WHY DOES paO2 FALL WITH AGE?

A

DUE TO INCREASING VA/Q INEQUALITY.

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17
Q

WHAT ARE THE 3 ANCHORS OF THE Hb-O2 DISSOCIATION CURVE?

A

MIXED VENOUS BLOOD-PO2 40, SAT 75%
ARTERIAL BLOOD- PO2 100; SAT 97%
THE “KNEE” - PO2 60; SAT 90%

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18
Q

WHAT ARE 5 CAUSES OF HYPOXEMIA?

A

HYPOVENTILATION, DIFFUSTION IMPAIRMENT (LUNGS FLOODED), SHUNT, VA/Q MISMATCH, REDUCTION OF FiO2 (as in HIGH ALTITUDE OF ANESTHETIC MISHAP)

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19
Q

WHAT IS HYPOVENTILATION USUALLY CAUSED BY?

A

A DISEASE OUTSIDE THE LUNGS LIKE OVERDOSE, SLEEP APNEA, OR ANXIETY. OR PICKWICKIAN SYNDROME.

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20
Q

WHAT ARE THE 2 CARDINAL FEATURES OF HYPOVENTILATION?

A
  1. INCREASED PaCO2 (VA CUT IN HALF; PaCO2 WILL DOUBLE. )
  2. HYPOXEMIA IS EASILY ABOLISHED BY INCREASING FiO2. (THIS CAN BE DANGEROUS FOR SEDATED PTS BECAUSE WE CAN MAKE PULSE OX LOOK GOOD BUT THEYRE PH IS STILL LOW AND CO2 HIGH…..THINK RESPIRATION IS ADEQUATE WHEN ITS NOT!
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21
Q

WHAT IS THE ONLY CAUSE OF HYPOXEMIA WHICH FAILS TO RESPOND TO O2 THERAPY?

A

A SHUNT.

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22
Q

WHAT ARE THE 2 TYPES OF DEAD SPACE?

A

MECHANICAL (ETT) AND PHYSIOLOGIC (BOTH ANATOMIC AND ALVEOLAR)

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23
Q

WHAT ARE THE 3 TYPES OF SHUNTS?

A
  • ANATOMIC (BRONCHIAL, PLEURAL, THEBESIAN VEINS ) 3-5% OF CO GOES STRAIGHT FROM RIGHT FROM LEFT.
  • CAPILLARY: BLOOD FLOW WITHOUT VENTILATION AS IN PNEUMONIA OR PULMONARY EDEMA
  • SHUNT EFFECT AKA V/Q MISMATCH. BLOOD FLOW WITH LOW VENTILATION. (BLOOD/AIR OUT OF SYNCH…BAD COMMUNICATION)
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24
Q

WHY DOES ZONE 1 ENLARGE WHEN YOURE IN SHOCK?

A

BECAUSE PA SYSTOLIC IS LOWER SO PERFUSION DOESNT TRAVEL AS HIGH UP IN THE LUNG.

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25
Q

WHAT IS ANOTHER NAME FOR SHUNT EFFECT AND WHAT DISEASE IS IT RELATED TO?

A

V/Q MISMATCH. AND ITS RESPONSIBLE FOR MOST HYPOXEMIA OF COPD.

AKA…THE AIR AND BLOOD ARE GOING TO DIFFERENT PLACES.

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26
Q

WHAT IS NORMAL ARTERIAL PCO2? AND WHAT IS ARTERIAL PCO2 A DIRECT REFLECTION OF?

A

37-43 MMHG. AGE HAS NO EFFECT. FALLS A BIT WITH HEAVY EXERCISE AND RISES A BIT DURING SLEEP.
ITS A DIRECT REFLECTION OF THE ADEQUACY OF ALVEOLAR VENTILATION…..AS ALVEOLAR VENTILATION GOES UP PCO2 GOES DOWN.

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27
Q

WHAT ARE 2 MAJOR CAUSES OF CO2 RETENTION?

A

HYPOVENTILATION AND V/Q MISMATCH.

28
Q

HOW CAN PATIENTS WITH V/Q MISMATCH BE HYPOXEMIC BUT HAVE A NORMAL paCO2?

A

INITIALLY THEY ARE HYPOXEMIC AND HYPERCARBIC…WHICH IS WHAT YOU WOULD EXPECT. THEN, THE CHEMORECEPTORS CAUSE INCREASED VENTILATION (INCR. RR) ….THIS CORRECTS THE HYPERCARBIA BUT DOES NOTHING FOR THE HYPOXEMIA.

FREQUENTLY PTS WITH V/Q MISMATCH DO HAVE LOW O2 BUT NORMAL CO2.

29
Q

WHY DO SOME PATIENTS DEVELOP CO2 RETENTION?

A

BECAUSE THEY HAVE INCREASED WORK OF BREATHING….OFTEN DUE TO AIRWAY RESISTANCE (BRONCHITIS). THEY ELECT TO RAISE THEYRE CO2 RATHER THAN EXERT ENERGY TO INCREASE VENTILATION. BRONCHITIS USUALLY RETAINS CO2….ASTHMA OR EMPHYSEMA MAY NOT.

30
Q

WHAT IS THE CHANGE IN ARTERIAL PH IF CO2 IS RETAINED?

A

INCREASE IN CO2 OF 10 TORR YIELDS A 0.1 PH DECREASE.

IE: 40 TO 80 CO2 MEANS PH GOES FROM 7.4 TO 7.0

31
Q

IS THERE A CHANGE IN BICARB IF CO2 BUILDS UP?

A

NOT IF ITS AN ACUTE RETENTION OF CO2….THE PH WILL FALL RAPIDLY, BICARB WILL NOT BUFFER.
HOWEVER IF PT HAS CHRONIC CO2 RETENTION THE PT WILL HAVE A SMALLER CHANGE IN PH BECAUSE THE KIDNEYS WILL COMPENSATE BY RETAINING BICARB. THIS IS CALLED COMPENSATED RESPIRATORY ACIDOSIS.

32
Q

WHAT ARE SOME CAUSES OF ALKALOSIS?

A

RESPIRATORY ALKALOSIS DUE TO PAIN OR FEAR….OR IT CAN BE CHRONIC IF THEY LIVE AT A HIGH ALTITUDE. ALSO, IF A PT LIVES WITH COMPENSATED RESPIRATORY ACIDOSIS BECAUSE THEY HAVE LUNG DISEASE AND CRNA VENTILATES THEM TOO ENTHUSIASTICALLY TO A paCO2 OF 40 OR LESS. (KINDNEYS CANT ADJUST THAT QUICKLY…THEYRE STILL MAKING BICARB)

33
Q

WHAT ARE THE 2 TYPES OF METABOLIC ACIDOSIS AND HOW DO THEY DIFFER?

A

CAUSED OUTSIDE VS INSIDE THE BODY.
OUTSIDE: WILL SEE INCREASED ANION GAP. (NORM=8-12) CAUSES ARE POISONS
INSIDE: NO INCREASE IN ANION GAP. CAUSES ARE RENAL/GI BICARB LOSS.

34
Q

WHAT IS COMPENSATION ASSOCIATED WITH PRIMARY DISTURBANCE IN CO2?

A

ITS THE BODY’S ATTEMPT TO CORRECT PH DUE TO A CO2 IMBALANCE. IT IS NOT A CORRECTION OF THE PRIMARY ABNORMAL PROCESS!

35
Q

WHAT IS AVERAGE INTRAPLEURAL PRESSURE?

A
  • 4-5 CM H2O AT END EXPIRATION RELATIVE TO ATMOSPHERIC PRESSURE.
36
Q

WHAT PRESSURE GRADIENTS ARE INDICATIVE OF TRANSAIRWAY PRESSURE AND TRANSPULMONARY PRESSURE?

A

TRANSAIRWAY: PMOUTH-PALVEOLI
TRANSPULMONARY: PMOUTH-PINTRAPLEURAL

37
Q

WHAT IS THE LAW OF LAPLACE?

A

P = 2T/R
THE PRESSURE NEEDED TO MAINTAIN ALVEOLI OPEN IS EQUAL TO THE SURFACE TENSION/RADIUS OF THE ALVEOLI.
SINCE NOT ALL ALVEOLI ARE THE SAME SIZE YET THE PRESSURE IS EQUAL THROUGHOUT THE LUNG….THE SURFACE TENSION MUST VARY.

38
Q

HOW DOES SURFACE TENSION VARY WITHIN THE LUNG?

A

SURFACE TENSION DECREASES AS THE ALVEOLAR SURFACE AREA IS REDUCED

39
Q

WHAT IS ALVEOLAR CRITICAL VOLUME?

A

THE VOLUME BELOW WHICH ELASTIC FORCES OF ALVEOLI WOULD CAUSE THEM TO COLLAPSE. WITHOUT SURFACTANT THE SMALLEST ALVEOLI WOULD TEND TO COLLAPSE.

40
Q

WHAT IS COMPLIANCE?

A

COMPLIANCE = CHANGE IN VOL/CHANGE IN PRESSURE.
SO THE LESS THE VOLUME CHANGE PRODUCED BY A GIVEN CHANGE IN PRESSURE, THE LESS THE COMPLIANT THE LUNG. THIS IS GRAPHICALLY REPRESENTED BY A PRESSURE VOLUME LOOP. IF THE INHALATION LINE (TO THE RIGHT) IS MORE HORIZONTAL….THAT MEANS DECREASED COMPLIANCE BECAUSE MORE PRESSURE IS NEEDED TO DELIVER A GIVEN TIDAL VOLUME.

41
Q

WHAT TYPE OF LOOP DEPICTS AIRWAY RESISTANCE?

A

A FLOW VOLUME LOOP.

RESISTANCE =CHANGE IN PRESSURE/ FLOW.

42
Q

HOW WILL FLOW VARY BASED ON IF THERE IS LAMINAR, TURBULENT, OR TRACHOEOBRONCHIAL FLOW?

A

LAMINAR: GREATEST FRICTION AT SIDES OF TUBE WITH CONSTANT DRIVING PRESSURE. FLOW VARYS DIRECTLY WITH THE 4TH POWER OF THE RADIUS OF TUBE. IE SMALL CHANGES IN AIRWAY TUBE WILL GREATLY CHANGE DELIVERY OF AIR TO ALVEOLI.
TURBULENT: FLOW IS RANDOM WITH RESISTANCE EVENLY DISTRIBUTED ACROSS LUMEN…IT IS ASSOCIATED WITH HIGHER FLOW RATES AND INCREASED RESISTANCE.
TRACHEOBRONCHIAL: MIXTURE OF LAMINAR AND TURBULANT FLOWS. A VENT CONNECTED TO AIRWAY TREMENDOUSLY INCREASES AIRWAY RESISTANCE.

43
Q

WHAT ARE 2 COMMON CAUSES OF AIRWAY RESISTANCE BELOW THE GLOTTIS?

A

INFLALMMATION AND BRONCHOSPASM.

44
Q

WHAT IS THE BREAKDOWN OF AIRWAY RESISTANCE?

A

UPPER AIRWAY = 45% (INCREASES WITH UPPER AIRWAY OBSTRUCTION.

LOWER AIRWAY = 55%
80% FOUND IN CENTRAL AIRWAYS (SUBSEGMENTAL BRONCHI)

45
Q

HOW IS RR SELECTED FOR A GIVEN VENT PATTERN?

A

RR IS SELECTED TO EXERT MINIMAL AMOUNT OF EFFORT AS OPPOSED TO EFFICIENT VENTILATION. THERFORE A HIGH RR IS NOT NECESSARILY INDICATIVE OF HYPER (ALVEOLAR) VENTILATION.

46
Q

AT A CONSTANT VOLUME DEEP SLOW BREATHING IS OPPOSED BY WHAT FORCES?

A

ELASTIC.

RAPID SHALLOW BREATHING IS OPPOSED BY AIRWAY RESISTANCE.

47
Q

HOW MUCH O2 IS CONSUMED BY A NORMAL ADULT?

A

250 ML/MIN. BUT IN SEVERE DISEASE STATES….THE VENT SYSTEM CAN BE SO INEFFICIENT THAT O2 GAINED THROUGH INCREASED VENTILATION IS CONSUMED ENTIRELY BY THE INCREASED VENTILATORY WORK OF THE MUSCLES.

48
Q

WHAT DOES A PIC OF AN EMPHYSEMATOUS LUNG LOOK LIKE?

A

ALVEOLI ARE LARGE AND THE SURROUNDING ELASTIC TISSUE THAT KEEPS THEM PATENT HAS DEGENERATED.

49
Q

WHAT ARE 2 DETERMINATES OF PULMONARY PERFUSION?

A

GRAVITY AND CARDIAC OUTPUT.
PULM ART PRESSURE IS GREATER AT BASES THAN AT APEX OF LUNG DUE TO GRAVITY…BUT THE ALVEOLAR PRESSURES ARE EQUAL THROUGHOUT THE LUNG….THIS IS WHAT GIVES YOU THE 3 LUNG ZONES. -DIFFERING IN LEVELS OF PERFUSION AND VENTILATION.

BLOOD GOES TO DEPENDENT REGIONS SO IF CO INCREASES…BLOOD IS SENT HIGHER IN LUNG SO ZONE 3 INCREASES.

50
Q

HOW DO THE 3 LUNG ZONES DIFFER FROM EACH OTHER?

A

ZONE 1: NO BLOOD FLOW
ZONE 2: INTERMITTENT FLOW..AT SYSTOLE NOT DIASTOLE.
ZONE 3: CONSTANT BLOOD FLOW..AT SYSTOLE AND DIASTOLE.

51
Q

WHERE IN THE LUNG IS INTRAPLEURAL PRESSURE THE LEAST (MOST NEGATIVE)?

A

AT THE APEX. THIS NEGATIVE PRESSURE STRETCHES LUNG TISSUE AND MAKES THESE ALVEOLI LARGER THAN THE ALVEOLI AT THE BASES WHERE THE WEIGHT OF THE LUNG PRESSES DOWN, AND REDUCES ALVEOLI SIZE.

52
Q

WHERE IN THE LUNG DOES INSPIRED GAS VENTILATE MOST IN AN UPRIGHT PERSON?

A

THE BASES MORE THAN THE APICES BECAUSE LARGE ALVEOLI ARE LESS COMPLIANT AND INTRAPLEURAL PRESSURE FLUCTUATES MORE WITH DIAPHRAMATIC MOVEMENT AT THE BASES.

53
Q

WHERE IS VENTILATION PERFUSION RATIO THE GREATEST IN AN UPRIGHT INDIVIDUAL?

A

THE APEX….DONT CONFUSE THIS WITH STRAIGHT UP VENTILATION.

THE RATIO IS 1 THROUGH MUCH OF THE LUNG.

54
Q

WHAT IS MINUTE VENTILATION?

A

THE AMOUNT OF AIR MOVING IN OR OUT OF LUNGS PER MINUTE.
VE=RR X VT

TO GET ALVEOLAR VENTILATION YOU MUST SUBTRACT DEADSPACE FROM TIDAL VOLUME.

55
Q

DOES HYPERVENTILATION MEAN BREATHING FAST?

A

NO. IT MEANS HAVING A LOW CO2.

56
Q

WHAT IS THE HALLMARK OF VENTILATORY FAILURE?

A

INCREASED paCO2.

57
Q

WHAT ARE 3 REASONS FOR VENTILATORY FAILURE? (HIGH CO2 LOW O2) (DECREASED VENT. ALVEOLAR)

A
  1. DECREASED VE (AKA. MINUTE VENTILATION)…RESP DEPRESSION OR CHEST BELLOWS DYSFUNCTION LIKE FLAIL CHEST.
  2. INCREASED VD (AKA DEADSPACE)…..(SEEN IN ALL RESTRICTIVE/OBSTRUCTIVE PATHOLOGY THAT LEADS TO CO2 RETENTION).
  3. DIMINISHED VE AND INCREASED VD AT SAME TIME. ANESTHETIZED PATIENTS ARE A GOOD EXAMPLE OF THIS. NORM VD/VT=.33, INTUBATED= .46, MASK= .65 (DEAD SPACE INCREASING AND VT DECREASING IS BAD)
58
Q

WHAT IS BY FAR THE MOST COMMON ETIOLOGY OF ARTERIAL HYPOXEMIA AS IN ASTHMA, ATELECTASIS, BRONCHITIS, EPHYSEMA, PNEUMONIA, AND PE?

A

V/Q MISMATCH

59
Q

HOW DOES V/Q RATIO VARY FROM TOP TO BOTTOM OF LUNG IN AN UPRIGHT PERSON?

A

AT TOP CAN BE 3
AT BOTTOM OF LUNG CAN BE LESS THAN 1

BOTH VENTILATION AND PERFUSION INCREASE TOWARD TEH BOTTOM OF THE LUNG, BUT THE EFFECT IS GREATER ON BLOOD BECAUSE IT HAS WEIGHT.

60
Q

WHAT ARE THE 2 COMPONENTS OF PHYSIOLOGICAL DEAD SPACE?

A

1: ANATOMIC…GAS THAT OCCUPIES THE CONDUCTING AIRWAYS IE TRACHEA.
2: ALVEOLAR…GAS IN ALVEOLI THAT ARE UNPERFUSED IE ZONE 1

PHYSIOLOGIC DEADSPACE CAN BE MADE WORSE BY MECHANICAL DEADSPACE IN PTS WHO ARE VENTILATED.

61
Q

WHAT DOES A PHYSIOLOGIC (TOTAL) SHUNT CONSIST OF? (3 TYPES OF SHUNTS)

A

1: ANATOMIC SHUNT: Q WITHOUT ANY V. 2-5 % OF CO.
2: CAPILLARY SHUNT: Q WITHOUT NORMAL V. WHEN BLOOD FLOWS PAST TOTALLY UNVENTILATED ALVEOLI SEGMENTS DUE TO PNEUMONIA.
3: SHUNT EFFECT(AKA V/Q MISMATCH): Q WITH MINIMAL V.
PERFUSION IN EXCESS OF VENTILATION. HYPOXEMIA DUE TO THIS TYPE OF SHUNT IS RESPONSIVE TO O2 THERAPY AS OPPOSED TO THE OTHER 2 TYPES.

THE FINAL EFFECT OF ALL SHUNTS IS BLUE BLOOD BEING PASSED FROM RIGHT TO LEFT.

62
Q

WHAT WILL THE CO2 LOOK LIKE FOR PTS HYPOXIC FROM V/Q MISMATCH? AND WHY?

A

CO2 IS USUALLY LOW OR NORMAL BECAUSE THE REGIONS THAT YOU CAN VENTILATE CAN MAKE UP FOR REGIONS THAT YOU DONT (AS IN ONE LUNG VENTILATION) BUT YOU CANNOT DO THIS FOR O2.

63
Q

WHAT CHANGES IN VOLUMES WILL YOU SEE IN A PERSON WITH OBSTRUCTIVE DEFECTS? RESTRICTIVE?

A

OBSTRUCTIVE: ELEVATED TLC, FRC, AND RV….MAYBE EVEN AT THE EXPENSE OF THE VC.

RESTRICTIVE: DECREASED TLC, VC, AND NORMAL OR DECREASED FRC.

64
Q

WHEN EVALUATING PFT WHEN WILL FLOW RATES BE THE GREATEST?

A

AT HIGH LUNG VOLUMES. BECAUSE EXPIRATORY FLOW IS MAINLY DETERMINED BY THE RECOIL FORCE OF THE LUNG. LARGE LUNG VOLUMES GENERATE MORE RECOIL THUS HIGHER FLOWS.

REDUCTION OF RECOIL REDUCES FLOW.

65
Q

WHAT IS A NORMAL FEV1? (FORCED EXPIRED FROM TLC IN 1ST SECOND ….DURING PFT) EXPRESSED AS PERCENT OF FVC.

A

70% OF FVC. MEANING AT LEAST 70% OF VITAL CAPACITY IS EXHALED WITHIN THE 1ST SECOND.

THIS NUMBER IS A SENSITIVE INDICATOR OF AIRWAY OBSTRUCTION AND RESPONSE TO BRONCHODILATORS.

66
Q

WHAT IS MEASURED BY PLOTTING FLOW AGAINST VOLUME?

A

AIRWAY RESISTANCE.

67
Q

WHAT IS MEASURED BY PLOTTING PRESSURE AGAINST VOLUME?

A

COMPLIANCE

68
Q

WHEN IS A FLOW TIME DIAGRAM USEFUL?

A

USEFUL IN IDENTIFYING IF THE LUNGS ARE EMPTYING COMPLETELY BEFORE ANOTHER BREATH IS INITIATED. IF NOT ADJUST THE I/E RATIO. AND IN DIAGNOSING LEAKS.

THORACIC SURGERY (3 decks)

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