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respiratory
| Question | Answer |
|---|---|
| FRC decreases greatest ________ days and lasts _________ after surgery and most severe in _________ | 3-5 days and lasts 10 days to 2 weeks. most severe procedure seen following upper abdominal procedures. |
| what are the effects of surgery on lung FRC? | DECREASES FRC, widenening of the A-a gradient, promoting atelectasis, shunting, and hypoxia. |
| describe apneic oxygenation. | ungs denitrogenated with o2, airway connected to o2 source, mass movement of oxygen occurs. when apnea occurs o2 not delivered, co2 not eliminated creating a vacuum effect of o2 sucked into the lungs. done for an hour before without ill effects. |
| the fall in po2 will equal the rise in pco about _______ | 3-6 torr/minute |
| normally how much o2 are removed from the alveoli and how much co2 are produced for elimination by the lungs per minute? | 250cc/minute of oxygen. 200cc/minute of CO2. |
| what happens to ventilation and pulmonary blood flow in the supine position and why? | posterior lungs more dependent and better ventilated vs. anterior portions because compressed alveoli occupy the steeper portion of pressure volume curve. the frc decreases by 0.5 L and abd. contents push diaphragm upwards so harder to ventilate at bases |
| what is the best treatment is someone with ARDS following burn injury? | best treatment iS PEEP, not tidal volume or fio2. because of intrapulmonary shunting that is formed from lung injury and edema. |
| the treatment of pulmonary edema under anesthesia ? | 1. admininster 100%o2. 2. give NTG to decrease preload. 3. give inotrope-dopamine to increase contractility. 4. fluid restrict and give lasix. 5. start peep at 5cm and inc. to 10-15cm. 6. place a PA catheter. |
| what are the causes of pulmonary edema? | 1. increased capillary leak. 2. increased cappilary pressure. 3. decreased oncotic pressure from low albumin. 4. lymphatic obstruction by tumor ect. |
| what may cause increased capillary leak causing pulmonary edema? | 1. ARDS, 2. BURNS, 3. ASPIRATION. 4. NEUROGENIC |
| WHAT MAY CAUSE INCREASED CAPILLARY PRESSURE CAUSING PULMONARY EDEMA? | 1. MITRAL STENOSIS. 2. heart failure. 3. retention of fluid by diseased kidney. 4. negative pulmonary edema. |
| if pulmonary edema occurs what is important to diagnose? | if the cause is cardiogenic or noncardiogenic. |
| how can you tell if pulmonary edema is cardiogenic? | pcwp high (18mmhg), also associated with bibasilar rales, patchy infiltrates, pink, forthy sputum. |
| what is the treatment of cardiogenic pulmonary edema? | fluid restriction, diuretics, inotropes. |
| how do you treat noncardiogenic pulmonary edema? | cautious fluid administrtion. |
| how can you tell if pulmonary edema is noncardiogenic? | pcwp not elevated. bibasilar rales often present. usually associated with burns, smoke inhalation, sepsis, dic , massive blood tr |
| what are the causes of pulmonary hypertension? | 1. increased pulmonary blood flow. 2. increased pulmonary resistance. 3. increased backward pressure from mitral stenosis or mitral regurgitation. |
| the equation of PVR? | (PA mean - PCWP)x80/CO = PVR NORMAL IS 15-250 DYNES-SEC/CM^5 |
| pulmonary hypertension is diagnosed when this parameter exceeds a certain value? | PA systolic pressure greater then or equal to 30mmHg. |
| how is PE Diagnosed? | by VQ scan or pulmonary angiography. PA diastolic pressure is typically 5 mmHg. greater then or equal to PCWP. |
| how do you treat pulmonary or fat embolus? | support oxygenation, circulation, ventilation. heparinization may be indicated. |
| what is diffusion hypoxia? | nitrous oxide is 35 times more soluble then nitrogen, so N2O Is easily eliminated from the lungs at the end of surgery but at the same time may dilute alveolar Oxygen during elimination. |
| how can diffusion hypoxia be eliminated? | breathing high concentration of oxygen for several minutes. |
| what are the effects of smoking? | increase mucus, impairs clearance, small airway narrowing, airway irritability, increase carbon monoxide level (10-15%, nonsmokers <2.5%). tissue distruction and COPD. HYPOXIA. NICOTINE INCREASES SYMPATHETIC TONE. |
| how does smoking cause hypoxia? | increases closing capacity relative to FRC. and increase COHGB. |
| HOW CAN YOU DIFFERENTIATE BETWEEN OXYGENATED HEMOGLOBIN FROM COHgb? | by using a co-oximeter because COhgb produce falsely high reading on pulse ox. |
| what are the effects of COhgb in smokers? | produce a falsely high reading on pulse oximeter. left shift of the ox-hgb curve. |
| what are the postoperative effects of smoking? | atelectasis, pneumonia, hypoxia. |
| timing of cessation of smoking prior to surgery and their effects? | 12 hrs to 24-48 hours - COHgb, arterial o2 content and normalize p50 from a left shift all normalizes. 1 week - normalizes secretions and improve oxigenation. 8 weeks - maximal benefit. decrease secretions, normal lung tone and clearance. |
| when does smoking cessation cause an increase in bronchial reactivity and bronchospasm? what is usually recommended in this setting? | in asthmatics. pulmonary complications is decreased when cessation occur 6-8 weeks prior to surgery. |
| does peep decreases extra vascular lung water? | NO NO NO |
| WHAT IS THE MECHANISM OF NITRIC OXIDE? | ENDOTHELIAL DERIVED RELAXING FACTOR. IT DIFFUSES INTO VASCULAR SMOOTH MUSCLE CAUSING VASODILATION. SELECTIVELY VASODILATES PULMONARY CIRCULATION |
| TREATMENT OF NITRIC OXIDE IS USE FOR? DOSING? EFFECT? | PERSISTEN PULMONARYY HYPERTENSION IN NEONATEDS AND CHILDREN. 20-40PPM OF INHALED NO IMPROVES OXYGENATION BY CAUSING VASCULAR RELAXATION, DECREASES PULMONARY HTN AND V/Q MISMATCHING. |
| HOW IS NO INACTIVATED? | SYSTEMATICALLY BY BINDING TO HEMOGLOBIN. |
| WHAT DOES PEEP CAUSE? | COMBATS ALVEOLAR COLLAPSE AT END EXPIRATION AND PROMOTES GAS EXCHANGE. |
| WHAT ARE THE organ EFFECTS OF PEEP? | 1. PULMONARY 2. CARDIAC OUTPUT 3. OXYGEN DELIVERY. |
| WHAT ARE THE PULMONARY EFFECTS OF PEEP? | 1. INCREASE FRC. 2. INCREASE LUNG COMPLIANCE. 3. DECREASE SHUNT. 4. INCREASE DEAD SPACE BUT THE BENEFITS OF DECREASE SHUNT EXCEEDS INCREASE IN DEAD SPACE. 5. INCREAE PaO2-less toxic effect of fio2 needed to increase pao2. |
| what are cardiac complications of peep? | if increased airway pressure in setting of decreased lung compliance cardiac output decreases with decreased coronary blood flow and release of inotropic substances from lungs. |
| oxygen delivery is determined by ? | product of cardiac output, hemoglobin content, saturation. |
| how does peep effect oxygen delivery? | depends on changes in both saturation and cardiac output. if saturation increases but CO decreases then oxygen delivery may remain the same or even decrease depends upon how much CO DECREASES. |
| IN REGARDS TO THE USE OF PEEP, WHEN CAN OXYGEN DELIVERY ACTUALLY IMPROVES? | WHEN SATURATION INCREASES BUT CARDIAC OUTPUT IS NOT DECREASED. |
| what should never be used alone to measure the effects of peep? | arterial oxygen levels. it should be monitored in conjunction with effects of peep to cardiac output. the best peep is when o2 saturation increases without decrease in cardiac output. |
| draw the lung volumes and capacities | draw |
| equation of FRC | FRC = ERV + RV. |
| FRC decreases with? | PANGOS: 1. PREGNANCY. 2. ASCITES. 3.NEONATES. 4. GENERAL ANESTHESIA 5. OBESITY 6. SUPINE |
| WHEN CAN SHUNTING OCCUR DURING TIDAL BREATHING? | if closing capacity is greater then FRC. |
| FRC INCREASES WITH? | PEEP AND EMPHYESEMA |
| DEFINE CLOSING CAPACITY AND ITS EQUATION? | IT IS THE VOLUME AT WHICH SMALL AIRWAYS BEGIN TO CLOSE. CC = RV+CV. |
| CLOSING CAPACITY INCREASES WITH? | ACLS-S: 1. AGE. 2. CHRONIC BRONCHITIS. 3. LV FAILURE. 4. SURGERY 5. SMOKING |
| WHEN IS CLOSING CAPACITY AT THE LOWEST? | TEENS AND INCREASES AFTER THAT |
| WHAT IS THE MOST CRITICAL FACTOR IN EVALUATING THE ADEQUACY OF OXYGEN DELIVERY TO TISSUES? what the second way? | ARTERIAL OXYGEN CONTENT most critical factor. then comes evaluation of mixed venous oxygen level. |
| HOW IS OXYGEN PRESENT IN BLOOD? | IN 2 FORMS. 1. DISSOLVED IN PLASMA 2. BOUND TO HEMOGLOBIN. |
| WHAT IS THE MOST OBVIOUS INFORMATION GIVEN FROM THE ARTERIAL OXYGEN CONTENT EQUATION? | the greatest amount of oxygen is bound to hemoglobin. |
| write the equation for arterial oxygen content. | CaO2 = (1.34 x Hgb x sat) + (0.003 x pao2) |
| how much of oxygen is dissolved in plasma? | 1.5% |
| according to the arterial oxygen content equation the most efficient way to increase oxygen content is to? | increase amount of hemoglobin. |
| the oxy-hemoglobin dissociation curve reflect what? | how easily hemoglobin releases oxgyen to tissues. |
| what is P50? what is the normal value for adult and infants? | FROM THE OXY-HGB DISSOCIATION CURVE, IT MEANS THE PARTIAL PRESSURE OF OXYGEN WHEN 50% OF HEMOGLOBIN IS SATURATED. normal value in adult is 27. in infants is 19mmHg because of increase levels of fetal hemoglobin. |
| WITH THE DISSOCIATION CURVE. WHEN HEMOBLOBIN IS 90% SATURATED THIS CORRESPONDS TO ? | Pao2 of 60 |
| what does a right shift of oxy-hgb curve mean? what causes it? | right shifting means increase unloading of oxygen to tissues. increase with increase H+, inc. temp. inc. 23dpg, inc. CARBON DIOXIDE. |
| what increases 23dpg? | anemia, altitude, cirrhosis. |
| what causes a left shift of oxy-hgb curve? | alkalosis, decrease temp. hemoglobin variants such as methemoglobinemia. |
| what does the bohr effect mean? | oxy-hgb curve shifts with changes in carbon dioxide. |
| what does the haldane effect mean? | the more deoxygenated the blood the more CO2 it will carry. the ability of reduced hemoglobin to carry more CO2 In the form of carbaminohemoglobin without increasing the level of PaCO2. |
| how do you assess adequacy of oxygen delivery to tissues? | 1. the firs way is to assess the arterial oxygen content and 2. the second way is to assess the mixed venous oxygen levels. |
| mixed venous oxygen saturation provideds one of the most important _________ | assessment of tissue oxygen metabolism. |
| what are the factors that determine Pvo2 (mixed venous oxygen level)? | COAL 1. CARDIAC OUTPUT. 2. OXYGEN CONSUMPTION. 3. AMOUNT OF HEMOGLOBIN. 4. LOADING OF HGB (right shift of o2-hgb dissociation curve increase unloading and lowering pvo2). |
| what happens to pvo2 when there is a right shift of o2-hgb curve? | pv02 (mixed venous oxygen level) decreases. |
| what is the normal value for pvo2 and the saturation? | normal pvo2 is 35-45mmHg. and normal saturation is 65-75% |
| what modulates the ventilatory response to hypoxemia? what modulates ventilatory response to pH and PaCO2? | 1. peripheral chemoreceptors in aortic and carotic bodies modulate ventilatory response to hypoxema. (paO2 LESS THEN OR EQUAL TO 60MMHG. 2. central chemoreceptors in brainstem modulate ventilator response to pH and PaCO2. |
| activation of aortic bodies results priimarily in? | aortic bodies results primarily in circulatory changes. it also modulates ventilatory response to arterial hypoxemia. |
| CAROTID AND AORTIC BODIES RESPOND TO PaO2 LEVEL OF ________. THEY DO NOT RESPOND TO _______ | LESS THEN OR EQUAL TO 60. THEY DO NOT RESPOND TO LOW OXYGEN CONTENT OR LOW OXGYEN SATURATION. |
| THE AORTIC AND CAROTID BODIES AFFERENT AND EFFERENT LIMBS ARE? | AFFERENT IS GLOSOPHARYNGEAL AND EFFERENT LIMB IS THE VAGUS NERVE. |
| THE VENTILATORY RESPONSE TO INCREASE IN CO2 is? | increase minute ventilation (both increase in RR AND TV). |
| WHEN DOES THE CENTRAL VENTILATORY RESPONSE TO INCREASE IN CO2 OCCUR? | VERY RAPIDLY WITHIN 1 MINUTE OF A CHANGE IN PaCO2. |
| FOR CENTRAL VENTILATORY RESPONSE TO BE ACTIVATED. WHAT PASSES THROUGH THE BBB AND BLOOD-CSF BARRIER AND WHAT DOES NOT? | CO2 passes but not H+. because CO2 IS VERY SOLUBLE AND NONIONIZED. |
| WHERE IS THE CHEMOSENSITIVE AREAS OF THE CENTRAL VENTILATORY RESPONSE? WHAT IS IT IN CLOSE PROXIMITY TO? | THE BRAINSTEM MEDULLA IN CLOSE PROXIMITY TO GLOSOPHARYNGEAL AND VAGUS NERVE. |
| IN REGARDS TO CENTRAL VENTILAOTRY RESPONSE, HOW ARE THEY STIMULATED BY CO2? | CO2 crosses the bbb. once in csf, H+ is formed, since the buffering capacity in csf is small, csf acidosis occurs. |
| in regards to the carbon dioxide response curve, what is the relationship between co2 and the ventilatory response? | ventilatory response to carbon dioxide is linear between 20-80mmHg. |
| in regards to the co2 response curve when does ventilatory depression occur? | when the PaCO2 greater then or equal to 100 mmHg. |
| what does it mean when carbon dioxide response curve is shifted to the left? to the right? | to the left = increase sensitivity to changes in CO2. A SHIFT TO THE RIGHT = DECREASE SENSITIVITY TO CO2. |
| WHAT causes a left shift of the co2 response curve? | 1. arterial hypoxemia. 2. metabolic acidosis. 3. central causes (cirrhosis, anxiety, fear, increased ICP) |
| WHAT causes a right shift of the CO2 RESPONSE CURVE? | DECREASED SENSITIVITY TO CO2. 1. AMINOPHYLINE. 2. salicylates. 3. catecholamines. 4. narcotics. 5. physiologic changes (normal sleep, drugs, metabolic alkalosis, denervation of peripheral chemoreceptors). |
| draw the CO2 RESPONSE CURVE | DRAW |
| WHAT CAUSES THE CO2 RESPONSE CURVE TO SHIFT DOWN AND TO THE RIGHT? | 1. HIGH DOSE NARCOTICS. 2. VOLATILE - WITH INCREASING DOSE THE CURVE BECOMES HORIZONTAL WITH LITTLE RESPONSE TO CO2. |
| THE relationship between pao2 and fio2 | with every 10% increase in fio2, the pao2 increase about 50torr. |
| the normal pao2 at room air is ? | 100 torr. |
| at 50% fio2, pao2 increase to? at 100% fio2, pao2 increases to? | 250 torr. and at 100% fio2, pao2 increases to 500 torr. |
| draw the zones of the lung and their PAlv, Ppa, ppv. | draw. |
| at zone 1, zone2, zone3, zone4 of the lung? | ZONE 1 = Palv > Ppa> Ppv zone 2. = Ppa > Palv. > Ppv zone 3. = Ppa > Ppv > palv. zone 4. = Ppa > Pisf > ppv > palv. |
| name the zones of the lung in relation to arterial vessels. | zone 1 = collapse, zone 2 = waterfall zone 3 = distention zone 4 = interstitial pressure |
| what does HPV PROVIDE/ | minimizes shunting of blood and improves PaO2 by decreasing blood flow to hypoxic region of lung by 50%. |
| what stimulates HPV? WHICH IS MAIN STIMULUS AND WHICH ONE INDIRECTLY STIMULATES? | 1. PAO2 (DECREASED alveolar oxygen tension) is the main stimulus. 2. mixed venous oxygen tension (less then equal to 30mmHg) indirectly induces HPV. |
| WHAT DECREASES HPV? | 1. increased pvr. 2. increased cardiac output. 3. hypocapnia (hypercapnea) does not increase hpv. 4. acidosis and alkalosis. 5. hypothermia. 6. CCB. 7. HFV. 8. n20. 9. volatiles. 10. NTP, NTG, isoproterenol |
| what does not affect HPV? | 1. INJECTABLE IV ANESTHETICS. 2. HYPERCAPNEA. 3. DOBUTAMINE AND DOPAMINE. |
| what increases and decreases as one goes up to zone 1 of the lung? WHAT DECREASES MORE THEN THE OTHER? | V/Q MISMATCH INCREASES. BOTH VENTILATION AND PERFUSION DECREASES. AND PERFUSION DECREASES MORE CAUSING V/Q MISMATCH. |
| VIRTUALLY WHAT IS CAUSED BY V/Q MISMATCH OF SOME KIND? | VIRTUALLY ALL PO2 ABNORMALITIES ARE CASUED BY V/Q MISMATCH. |
| Equation for shunt fraction? | = (CcO2-CaO2) / (CcO2 - Cvo2) |
| the normal v/q ratio is ? the ratio for dead space is? the ratio for absolute shunt is? | 1. normal 0.8 2. dead space is infinity 3. absolute shunt is zero. |
| what does the shunt fraction and the A-a gradient represent? | a guide as to the efficiency of the lung for the movement of alveolar oxygen to the capillaries. |
| what does the alveolar PO2 depends on? | inspired oxygen (fio2) and altitude and age. |
| what is the equation for alveolar po2? | = (Pbar-Ph2o) x fio2 - (paco2/0.8) |
| an approximation of the normal A-a gradient is with this equation. normal gradient in room air? normal gradient in 100%o2? | = 1/4 (age) room air = 5-10mmhg 100% fio2 = 20-30 mmHg |
| name the causes of hypoxemia and their Associated A-a gradient. | 1. hypoventilation - normal a-A 2. DECREASED FIO2 - normal a-A 3. v/q mismatch - elevated 4. diffusion impairement - elevated 5. right to left intracardiac shunt - elevated. |
| what value for a-A gradient indicates intubation and mechanical ventilation? | if gradient is greater then or equal to 350mmHg on 100% fio2. |
| what is the most common cause of a widened a-A gradient? | shunting. |
| when is oxygen administration ineffective in the setting of shunt? | when shunt fraction is greater then 30%. if shunt is 10-20% o2 is of some benefit. |
| what is the normal QS/QT? | shunt fraction normally 4-5% |
| what is the prototypes of shunt? dead space? | shunt = pneumothorax dead space = PE |
| in regards to increased shunting what happens to the relationship between pao2 and shunt? paco2 and shunt? | increase shunt - linear decline pao2 increase shunt fraction only when > 50% - paco2 begin to increase |
| how is paco2 affected when shunt fraction is increased, this is secondary to what? | paco2 start to increase when shunt fraction exceeds 50% due to greater solubility of co2. |
| what disease process causes shunt? | pneumothorax, bronchospasm, thebesian veins, bronchial veins, right to left cardiac shunt, pneumonia. |
| WHAT is the equation for dead space and what is the normal value? | vd/vt = 0.3 = Paco2-Peco2 / paco2. |
| what does physiologic dead space represent? | fraction of tidal volume not involve in gas exchange. the sum of anatomic and alveolar dead space. lung ventilated but not perfused. |
| anatomic dead space is _______ and alveolar dead space is __________ | anatomic dead space is the conducting airways. that does not involve in gas exchange. |
| what happens to pco2 and po2 with increase dead space? | increase in pco2 and decrease in po2. |
| what factors increases physiologic dead space? | 1. age, anticholinergics 2. upright position 3. bronchodilators 4. hypotension, hypothermia, hypovolemia 5. smoking 6. pulmonary diseases - emphysema, PE, pulmonary hypoperfusion |
| how does volatile anesthetic effect the lung? | causes 1. atelectasis. 2. shunting. 3. hypoxemia. 4. increase a-A gradient due to changes in ventilation-perfusion. |
| how makes the a-A gradient increase and ventilation perfusion changes under general anesthesia in lateral position? | ventilation greatest at nondependent lung and perfusion greatest at dependent lung increasing v/q mismatch. |
| what happens to ventilation and perfusion in a spontaneously breathing awake patient in lateral position? | both ventilation and perfusion best at dependent lung. |
| what causes a-A gradient to increase under general anesthesia? | decrease in cardaic output, frc, chest wall and lung compliance. increase in airway resistance, increase in v/q mismatch. |
| ventilation and perfusion changes in an awake supine patient? | diaphragm moves cephalad, ventilation and perfusion both increase in posterior lung. |
| ventilation and perfusion changes in a paralysed controlled ventilation supine position? | ventilation is greatest anteriorly and perfusion is greatest posteriorly. |
| under general anesthesia, decreased cardiac output leads to? | increased dead space in west zone 1 and more v/q mismatch overall |
| what leads to decreased pulmonary compliance under general anesthesia/ | decreased in FRC. |
| what contributes to v/q mismatch under general anesthesia? | decreased lung and chest wall compliance and increased airway resistance. |
| what are the complications of peep? | 1. decreased cardiac output. 2. increased icp, 3. fluid retention, 4. barotrauma. |
| how is peep helpful in pulmonary edema? | decreases shunting, increases frc. but does not reduce lung water just redistributes it. |
| belief of peep use in localized lung disease? | not recommended because it increases v/q mismatch by overdistending normal lung and redirecting blood to diseased areas. |
| the belief of routine peep and for mediastinal bleeding? | not beneficial |
| the belief of propylactic peep? | does not decrease incidence of ards |
| what are the pulmonary effects of peep? | 1. increases frc - increasing compliance, increase oxygenation, decreased shunt fraction, redistribution of extravascular lung water to more compliant larger lympathics by the peribronchial and hilar regions. |
| what is the primary pulmmonary effect of peep? | 1. increases frc, decreasing shunting. however at amodest increase in dead space ventilation - west zone 1 opens up but distended alveoli decreases blood flow thereby increasing deadspace. |
| the effect of peep less then 10, more then 10mmHg to lungs. | less then 10 maintains already distended open alveoli. more then 10 recruits collapse alveoli indicated with improvement in oxygenation and compliance. |
| cardiac effects of peep mostly due to ? | left ventricular preload decreases. decreased LVEDV due to RV DYSFUNCTION OR INCREASED PVR (INCREASED INTRATHORACIC PRESSURE). |
| MOST CO2 RESPONSE VENTILATION IS MODULAED BY THE THE _________ BY _______ PERCENT | MEDULLA BY 85 PERCENT. OTHERS ARE CAROTID BODIES. |
| VENTILATORY RESPONSE TO CO2 IS DECREASED BY? | 1. SLEEP, 2. GENETIC, RACIAL. 3. PERSONALITY. 4. IN TRAINED ATHELETS AND DIVERS. 5. CASES WITH ICNREASED WORK OF BREATHING (OBESITY). |
| BEnzodiazepine affect to co2 response curve? | down but not to the right |
| droperidol effect to co2 response curve? | no effect. |
| the respiratory depressant effect is increased or prolonged with? | other anesthetics |
| how much does combined halothane and n2o effect co2 response curve versus halothane alone? | combined halothane and n2o < halonthane alone. |
| what attenuates the co2 response curve to hypoxia? | volatile anesthetics even at subanesthetic level. |
| 50% N20 effect of co2 response curve? | no effect. |
| hypoxia effect to co2 response curve? | up and to the left. |
| which produces a more profound co2 ventilatory depression halothane or isoflurane? how does it effect the co2 response curve? | iso more profound then halo. curve is right shifted. |
| when does hypoxic ventilatory drive becomes strong? | when the po2 is below 50 torr. |
| what are the factors which increases the Paco2 to PAco2 gradient (lowering the peco2)? | gradientnormal 3 mm. 1.v/q mismatch 2.high peep dec. perfusion. 3. dead space.4.rapid RR-no time for expiration.5.low pulm. blood flow-PE, cardiac arrest.6. high sampling rate of monitor+high fresh gas rate.7.kinktube,part disconnect,broken co2 analyzer. |
| what is the definitive test for PE? | pulmonary angiography |
| do you heparinize patients with PE who also have hemoptysis? | yes, hemoptysis is not a contraindication. |
| treatment for PE? | SUPPORTIVE CARE, HEPARINIZATION. |
| SIGN OF PE DURING ANESTHESIA? | 1.TRANSIENT UNEXPLAINED HYPOXEMIA. 2.HYPOTENSION. 3. TACHYCARDIA.4.BRONCHOSPASM. 5. EKG/CV/PA WITH RVF AND PULM HTN. 6.SUDDEN FALL ETCO2 WITH INCREASE DEAD SPACE. |
| EKG SIGNS OF PE INCLUDE? | right axis deviation, complete or incomplete RBBB, TALL PEAKED T WAVES. |
| WHAT ARE THE EFFECTS OF PE? | 1.DEAD SPACE 2. V/Q MISMATCH 3. PULM.INFARCTION 4. ATELECTASIS 5. INCREASE PVR 6. PULM HTN 7. BRONCHOCONSTRICTION 8. FALL ETCO2. 9. HYPOXEMIA. 10. EKG CHANGES. |
| HOW DOES PVR INCREASE IN ACUTE PE? | local release of vasoactive serotonin |
| why does bronchoconstriction happen during acute PE? | attempts to decrease v/q mismatch. |
| how does atelectasis develop during PE? | ALVEOLI POORLY PERFUSED BECOME DEFICIENT IN SURFACTANT BY 12-24 HOURS. |
| HOW DOES HYPOXEMIA DEVELOP DURING PE? | PULM AND CHEST WALL COMPLIANCE DECREASES WHILE PULM. RESISTANCE INCREASES. |
| what is equation FEV1%? WHAT IS THE NORMAL VALUE? what happens in obstructive disease? | FEV1% = FEV1/FVC. % OF VC EXHALED IN 1 SECOND USUALLY 75-80% and decreased in obstructive |
| why is FEV% highly specific but yet not sensitive? what is the alternative? | 1. it is patient's effort dependent during spirometry lowering the fvc so the fev1/fvc ratio is normalize despite obstructive disease. 2. in isolated small airway disease its value is normal 3. alternative is measuring MEFR (25-75%) |
| why does obstructive disease have lowered expiratory flow rates? | INCREASED AIRWAY RESISTANCE. |
| fev1 is only sensitive for _________, and does not measure ______________ | sensitive to large airway diesease and does not measure changes in more peripheral airways. |
| what type of pft is NOT INFLUENCED BY PATIENT EFFORT THEREBY IS A BETTER MEASUREMENT FOR? | MEFR. SMALL AIRWAY DISEASE MORE PERIPHERAL. W |
| what percentage fev is seen as a better improvement with bronchodilators? | fev increased by 15% |
| the pft results in copd? | low fev1/fvc, increased TLC due to increased RV. INCREASED RATIO OF RV/TLC SUGGEST OBSTRUCTIVE DISEASE. NORMAL VITAL CAPACITIES |
| PATIENTS WITH COPD GENERALLY HAVE? | NORMAL VITAL CAPACITIES REASON WHY FEV/FVC IS REDUCED. |
| IN PATIENTS WITH ASTHMA ATTACK, WHAT IS AN INDICATOR OF IMPENDING RESPIRATORY FAILURE THAT MAY REQUIRE INTUBATION? | PaCO2 greather then 50 |
| in asthma attacks, signs of respiratory failure are? | prolonged expiration, depressed mental status, anxiety, increased pulsus paradoxus, poor aeration, tachycardia, tachypnea, nasal flaring. |
| what regional technique is not recommended in copd patients? why? | any regional involving sensory above T6, MAY cause decrease expiratory reserve volumes. resulting in ineffective cough and clearing of secretions. |
| what are the factors affecting apneic oxygenation? | depends on patency of the airway and cfomposition of ambient gas. |
| how is apneic oxygenation affected when there is occlusion of the airway? | hypoxia in 90 seconds as po2 falls to the pvo2 level. rapid equilibrium between alveolar, arterial and mixed venous pco2 as co2 rises at rate of 3-6mmhg/min |
| how is apneic oxygenation affected when there is patent airway and ambient air as gas? | pco rapidly equilibrates, alveolar, arterial and mixed venous pco2 rises gradually at a rate of 3-6 mmhg/min but hypoxia in 2 minutes - ambient air is drawn in by mass movement down trachea. o2 is removed and N2 accumulates. |
| with apneic oxygenation with patent airway and oxygen as its ambient gas, what is this technique limited to? | build up of co2 (3mmhg/min) with respiratory acidosis and cardiac arrythmias especially in patients who have frc/body weight ratio of less then 50cc/kg. |
| how is apneic oxygenation affected when there is patent airway and oxygen as gas? | N2 is not added as in air as gas, oxygen via catheter in 10-15 liters/min with prior breathing of o2. pt's po2 will start at 660 |
| name the composition of alveolar gas? inhaled and exhaled? | N20 568 torr 74.4% inh(5.97mmHg) exh(566mmHg) O2 105 torr 13.8% inh(1.59) exh(120) CO2 40 torr 5.2 % inh(0.3) exh(27) H20 47 torr 6.1% inh(3.7) exh(47) |
| what does vapor pressure depends on? | liquid and its temperature. increases with inc. temperature. |
| in the presence of water vapor, what happens to other gases? | lowers the partial pressure of atmospheric air, o2, n2. |
| how much percent of water does air have that is fully saturated with water vapor at room temperature? and in trachea at body temperature? | since water vapor increases with increase temperature. fully saturated air at room temperature contains 2 volume percent of water while at body temperature in the trachea contains 6 volume percent of water. |
| eight or more weeks of smoking cessation is associated with what? | 66% reduction of postop pulmonary complications. and no more pulmonary complications when compared to paitents who never smoked before. |
| what can nicotine cause? and why? | adrenergic stimulus, increasing hr, bp, svr. |
| patients who stop smoking less then 8 weeks have what according to one study? | increased risk of pulmonary complications |
| in smokers what causes a reduced oxygen supply available to tissues? | 15 percent of binding sites of hemoglobin is occupied by carbon monoxide. |
| patients who stop smoking in 12 hours have? | decreased carboxyhemoglobin, increased blood oxygen content, and improved release of oxygen by hemoglobin. but no improvement in morbidity |
| the overall rate of postoperative pulm complications in smokers vs. non smokers? | 39% versus 11.4% |
| the depression of ventilation by opioids is due to? | decreasing the response of ventilation at the brainstem to co2. |
| how is ventilation affected with opioids at low dose versus at high dose? | at low dose, decreases RR while maintaining tidal volume, at high dose both are reduced. towards apnea. |
Created by:
michelledaryanani