Disorders Of Pulmonary Circulation

Front 1

Normal capillary wedge pressures:

Back 1

6-12 mmHg

Front 2

What type of catheter measures capillary wedge pressure?

Back 2

Pulmonary artery (Swan-Gantz) catheter

Front 3

Tall spiking wave forms on PA catheter indicate you are located in the ?

Back 3

RV

Front 4

If you're in the PA, pressures you measure just behind the balloon reflect pressures in ?

Back 4

LA

Front 5

10-15% of all hospital mortalities!

Back 5

pulmonary embolism

Front 6

3 Reasons for clot (Wirchow's triad):

Back 6

1) stasis
2) vessel wall abnormalities
3) alterations in coagulation system

Front 7

Four effects of PE on pulmonary fxn:

Back 7

1) circulation - vessels constrict and blood is shifted to other areas of lung
2) ventilation - bronchoconstriction in obstructed area, shifting ventilation to better perfused areas
3) ventilation/perfusion mismatch
4) loss of surfactant

Front 8

Risk factors for venous thromboembolism:

Back 8

IMMOBILITY, hypercoaguable states (pregnancy, malignancy), CHF, trauma, burns, shock, lupus, prior VTE, high estrogen, protein deficiencies (protein C, protein S, AT3)

Front 9

The ____the prevalence of underlying CV disease the ___ likely that you will survive an embolic event.

Back 9

greater, less

Front 10

Symptoms of PE:

Back 10

dyspnea, pleuritic pain, cough, hemoptysis, palpitations, wheezing, leg swelling

Front 11

Signs of PE:

Back 11

tachypnea, crackles/rales, tachycardia, S4, increased P2, fever, RV lift, pleural rub, cyanosis, DVT

Front 12

Alveolar arterial O2 gradient

Back 12

non-specific tool to determine normality of pulmonary fxn

Front 13

How do you calculate alveolar O2?

Back 13

PAO2 = FiO2(Pbar - PH2O) - (PCO2/R)

Front 14

How do you calculate arterial O2?

Back 14

ABG

Front 15

Normal A-a gradient:

Back 15

8-10 mmHg

Front 16

DDx for PE:

Back 16

AMI, PEdema, Asthma, COPD exacerbation, atelectasis, pericarditis, dissecting aneurysm, pneumonia, pleurisy, PA thrombosis, pneumothorax

Front 17

Gold standard for diagnosing PE

Back 17

pulmonary angiography

Front 18

Potential problems w/ pulmonary angiography:

Back 18

1) cath in pulmonary circulation
2) renal dysfxn b/c dye is nephrotoxic
3) done by interventional radiologist

Front 19

Why is CT better than pulmonary angiography?

Back 19

1)no special technique
2)rapid
3)contrast through regular IV

Front 20

Mainstay of treatment for PE

Back 20

anticoagulation w/ heparin or warfarin

Front 21

Used for patients w/ PE that can't tolerate anticoagulation.

Back 21

Vena Cava Interruption (Filter)

Front 22

Supportive measures for PE

Back 22

fluids for BP, supplemental O2

Front 23

What are some other things that can cause a PE besides a clot?

Back 23

fat, bone marrow, amniotic fluid, foreign bodies, air, tumors

Front 24

Pulmonary HTN is an increase in ?

Back 24

Pulmonary Arterial Pressure

Front 25

Pulmonary HTN defined as ?

Back 25

sytolic P > 30 mmHg
diastolic P > 15 mmHg
mean P > 18-20 mmHg
w/ exercise systolic P > 35 w/ mean P > 30

Front 26

Gradual PA pressure increases will cause RV to?

Back 26

hypertrophy and dilate, ultimately failing

Front 27

Sudden PA increases (above 40 mmHg) will cause RV to?

Back 27

fail

Front 28

Three principal mechanisms for pulmonary HTN:

Back 28

1) increase in LA pressure
2) increase in pulm blood flow/volume
3) increase in pulm vasculature resistance

Front 29

Increases in pulm vasculature resistance can be caused by?

Back 29

vasoconstriction (hypoxemia), obstruction (PE), or obliteraion processes (tumors, emphysema)

Front 30

Precapillary pulm HTN is due to?

Back 30

vascular mechanisms - left to right shunting, primary pulm HTN, PTE disease

Front 31

Pleuropulmonary HTN is due to?

Back 31

emphysema, pulmonary fibrosis, ARDS, severe air space disease, interstitial disease
alveolar hypoventilation by way of chronic hypoxemia

Front 32

Postcapillary pulmonary HTN is due to?

Back 32

LV failure, mitral valve disease

Front 33

Pulmonary venous HTN is due to?

Back 33

Pulmonary Occlusive Disease, mediastinal granulomas/neoplasms

Front 34

Pulmonary HTN is ____ in general population.

Back 34

very low

Front 35

How does pulmonary HTN progress?

Back 35

eventually CO will fall, pulmonary pressuress fall, leading to right heart failure

Front 36

Primary PHTN is more common in?

Back 36

pre-menopausal females

Front 37

What is the initial symptom of primary PHTN?

Back 37

dyspnea

Front 38

What does primary PHTN look like histologically?

Back 38

increase in smooth muscle of small pulmonary arterioles

Front 39

What appetite suppressant was associated w/ PHTN?

Back 39

Fen Phenylalanine

Front 40

Right sided heart disease due to any pulmonary lung disease.

Back 40

Cor Pulmonale

Front 41

Pulmonary emboli that don't resolve or go away leading to scarring of pulmonary vasculature.

Back 41

Chronic thromoboembolic PHTN

Front 42

Treatment of Chronic Thromboembolic PHTN.

Back 42

surgery

Front 43

Manifestations of PHTN.

Back 43

exertional dyspnea, chest pain, syncope, hemoptysis, hoarseness, precordial discomfort, cyanosis, increased P2, S4, RV heave

Front 44

Treatemnt of PHTN:

Back 44

modify factors leading to disease, Ca channel blockers, surgery

Front 45

Surgical opttions for PHTN:

Back 45

atrial septostomy
pulmonary thromboendoarterectomy
lung transplant

Front 46

Classes of PHTN by NYHA

Back 46

Class I - no symptoms, 58.6 months
Class II - 58.6 months
Class III - 31.5 months
Class IV - can't get out of bed, 6 months

Front 47

Abnormal accumulation of liquid and solute in extravascular spaces and tissues in the lung.

Back 47

pulmonary edema

Front 48

Two stages of pulmonary edema:

Back 48

interstitial edema - fluid invades interstitial space, widening of alveolar walls and lymphatic channels, impairment of gas exchange
alveolar edema - fluid and solute in alveolar spaces, gas exchange is further impaired

Front 49

Pathogenesis of PEd often seen w/ heart disease.

Back 49

increase capillary hydrostatic pressure

Front 50

What can cause PEd due to decrease in interstitial pressure?

Back 50

rapid evacuation of an effusion or pneumothorax

Front 51

Pathophysiology involved with PEd caused by nephrotic syndrome

Back 51

decrease in colloid osmotic pressure b/c of protein loss

Front 52

HAPE stands for?

Back 52

high altitude pulmonary edema

Front 53

Consequences of PEd?

Back 53

decreased lung compliance
increased airway resistance
shorter breaths
hypoxemia
hyperventilation
increased pulmonary vascular resistance

Front 54

Symptoms of PEd due to cardiogenic dysfxn?

Back 54

orthopnea, S3, paroxysmal nocturnal dyspnea, and increasd JVD, peripheral edema

Front 55

Management of PEd?

Back 55

treat underlying cause, diuretics, O2, morphine, bronchodilators, vasodilators, and inotropic support

Front 56

Abnormal connection btwn artery and vein in lung.

Back 56

Pulmonary arterio-venous malformation

Front 57

Pulmonary AV malformations are usually?

Back 57

congenital (half due to Hereditary Hemorrhagic Telangectasia, AKA Osler-Weber-Rendu Disease)

Front 58

Inheritance of HHT/OWR disease?

Back 58

AD

Front 59

Characteristics of HHT/OWR disease.

Back 59

recurrent nose bleeds, telagectasia

Patients develop cyanosis, clubbing, and polycythemia due to chronic hypoxemia.

Front 60

Complicationns of AV malformations?

Back 60

paradoxical embolus, brain abscess, and hypoxemia

Front 61

Why do AV malformations lead to infarcts, abscesses, etc?

Back 61

b/c the capillary bed is bypassed where bacteria and clots are usually trapped

Front 62

Causes of Pulmonary artery aneurysms?

Back 62

congenital, infection, vasculitis

Front 63

Treatment of pulmonary artery aneurysms?

Back 63

surgery