6 resp part 2

Question 1

V/Q mismatch

Answer 1

Ventilation compared to perfusion of alveoli, normal is 0.8-0.9 and is some mismatch in normal individuals
V/Q of lower lobes better than apexes
Greater compliance and pul perfusion AFFECTED by gravity
Body position can alter it (gravity dependent area have greater V/Q)

Question 2

Hypoxemia Hypercapnia numbers

Answer 2

PaO2<80mmHg
PaCO2>45mmHg
Low V/Q is inadequate ventilation
High V/Q is inadequate perfusion (more oxygen doesn’t help)

Question 3

Ventilation problems are

Answer 3

LOW V/Q
From lack of resp rate (drugs, neuro damage etc)
Or airway/alveoli disorders
Asthma, chronic bronchitis, pulmonary edema, pneumonia

Question 4

High V/Q

Answer 4

High ventilation low perfusion

Question 5

Pulmonary circulation problems

Answer 5

High V/Q
Hypoxic vasoconstriction from low alveolar PO2 causes vasoconstriction to shunt blood to oxygenated areas
Acidemia causes pulm artery constriction
Biochemical factors of inflammation can cause it

Question 6

Cardiovascular effects that will cause pulm circ issues creating High V/Q

Answer 6

CHF, hypovolemia, pul embolus

Question 7

Right to Left shunting

Answer 7

V/Q LOW
Blood passes through large portions of lung without ventilation, no oxygenation occurs then mixes with oxygenated blood (hypoxemia)
O2 won’t help because cap beds are not exposed to O2

Question 8

Right to L shunting (low V/Q) occurs in

Answer 8

ARDS, newborn resp distress, atelectasis

Question 9

Pulmonary Hypertension

Answer 9

High pressure in pulm arteries
Higher than 22mmHg at rest or 30mmHg during physical activity (AHA)
Normal pressure in pulm arteries at rest is 8-20mmHg

Question 10

Primary pulmonary hypertension

Answer 10

Persistent elevation over 25mmHg without secondary causation like increased L sided heart pressure (idiopathic changes in pulm arteries)

Question 11

3 possible causes of primary pulmonary hypertension

Answer 11

Abnormal proliferation and contraction of arterial smooth muscle
Coagulation abnormalities in pulm arteries
Fibrosis of intimal lining of pulm arteries

Question 12

Fibrosis of intimal lining in primary pulm htn pathogensis

Answer 12

Autosomal dominant trait which leads to decrease in receptor subtypes on endothelial and smooth muscle cells
Receptors control certain growth factors that suppress prolif of endothelial and smooth muscle

Question 13

Causes of secondary pulm HTN

Answer 13

COPD
L sided failure (aortic valve disorders, mitral valve disorders)
Pulmonary emboli

Question 14

COPD secondary pulm htn pathology

Answer 14

Chronic hypoxia causes chronic pulm vasoconstriction

Question 15

L sided failure causing secondary pulm htn

Answer 15

Will lead to retrograde transmission of pressure into pulm veins and vasculature

Question 16

Pulm emboli causing second pulm htn

Answer 16

If untreated will lead to a back up of pressure into arterioles and pulm arteries that feed the terminal occlusion

Question 17

Clinical manifestations of pulmonary hypertension

Answer 17

Tachypnea tachycardia
fatigue
Syncope
Ischemic chest pain
Cor pulmonale (enlarged R head)
Peripheral edema
Decreased cardiac output

Question 18

ARDS definition

Answer 18

Form of resp failure characterize by acute lung inflammation and diffuse alveocap injury

Question 19

ARDS etiology

Answer 19

Most common causes are sepsis and multi trauma
Other causes
Pneomonia, burns, toxins, CABG, pancreatitis, OD, blood transfusion, radiation therapy, DIC, aspiration

Question 20

Patho of ARDS

Answer 20

24-48 hours after inflammatory phase, hyaline membranes form and fibrosis progressively obliterates alveoli (7 days)
Same mediators often cause MODS

Question 21

Clinical manifestations of ARDS

Answer 21

Rapid shallow breathing with resp alkalosis
Dyspnea, decreased compliance
Hypoxemia unresponsive to O2
Diffuse alveolar infiltrates, crackes, metabolic acidosis
Hypotension, decreased CO and death

Question 22

Pleural effusion

Answer 22

Fluid in pleural space from vessels or lymph or an abscess or lesion
Pleura is relatively permeable and fluids that accumulate in lung can cross, can be transudate or exudate
It can cause compression atelectasis but not lung collapse
Can cause dyspnea

Question 23

Transudate

Answer 23

Extravascular fluid with low protein content

Question 24

Empyema

Answer 24

Infected pleural effusion or pus in pleural space
Complication of resp infection, breath sounds decreased over empyema
Manifests as toxicity, cyanosis, fever, tachycardia, cough and pleural pain

Question 25

Pleurisy

Answer 25

Inflammation of pleura
Pleura become reddened and covered with exudate and lymph, fibrin, cellular elements
S&S chills, fever, pain on inspiration, pleural friction rub

Question 26

Pulmonary contusion

Answer 26

From trauma, presents with hypoxemia

Question 27

Flail and rib fractures

Answer 27

Three or more adjacent ribs in two or more places

Paradoxical movements

Question 28

Hemothorax

Answer 28

Blood collects in pleural space, same effect as tension pneumo shifting mediastinum
Compounded by shock
Hypotension and dullness on percusion (otherwise same as tension)

Question 29

Pneumothorax

Answer 29

Rupture in visceral pleura or parietal pleura
Air separates visceral and parietal pleura which destroys negative pressure of pleural space, disrupting equilibrium between elastic recoil of lung and chest wall

Question 30

Types of pneumo

Answer 30

All cause pulmonary atelectasis
Closed/simple
Open
Tension

Question 31

Clinical manifestations of pneumo

Answer 31

Simple is pleural pain, tachypnea, mild dyspnea

Tension - severe hypoxemia, dyspnea, hypotension, decreased venous return, JVD, tracheal shift