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RC Test 4 > B4.067 - Pulmonary Vascular Disease > Flashcards

B4.067 - Pulmonary Vascular Disease Flashcards

1
Q

3 major diseases of pulmonary vessels

A

Pulmonary embolism Pulmonary hypertension Pulmonary edema

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2
Q

what is the swan ganz catheter

A

invasive hemodynamic measurement of pulmonary artery pressures

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3
Q

which part of the heart has the lowest pressure

A

right atrium

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4
Q

SVR calculation (systemic vascular resistance)

A

SVR = 80 x (MAP - RAP)/ (CO)

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5
Q

calculation of pulmonary vascular resistance (PVR)

A

PVR = 80 x (MAP - LAP)/Pulmonary blood flow

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6
Q

PAH classification

A
  1. pulmonary artery HTN 2. Left heart disease 3. PH with respiratory disease or hypoxia 4. chronic thromboembolic disease 5. unclear/multifactorial
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7
Q

what is PAH

A

one form of PH sustained elevation of mean pulmonary arterial pressure >25mmHg Mean pulmonary capillary wedge pressure (PCWP) and /or mean left ventricular end diastolic pressure <15 mmHg

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8
Q

normal blood pressure in pulmonary artery

A

12-16

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9
Q

multi hit hypothesis of pathogenesis of pulmonary arterial hypertension

A

primary genetic background modifier genes environmental trigger

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10
Q
A

normal pulmonary artery and alveolus

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11
Q
A

pulmonary artery remodeling

internal fibrosis

medial hypertrophy

adventitial proliferation

luminal obliteration

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12
Q

signs of pulmonary HTN

A

JVD

Edema

chest pain

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13
Q

what is prostacyclin

A

PGI2

activity through cAMP

Vasodilator

inhibits proliferation of vascular smooth muscle

Decreases platelet aggregation

decreased prostacyclin synthase in PAH

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14
Q

goals of PAH therapy

A

fell better

live longer

breath

prevent blood clots

decrease scarring/blocked pipes

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15
Q

supportive therapy for PAH

A

oxygen

coumadin

digoxin

diuretics

treatment of underlying/coexisting disease

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16
Q

spectrum of treatments for PAH

A

nothing

oral medicines

nebulized medicines

continuously infused medicines

gene therapy

lung transplant

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17
Q

classes of drugs for PAH

A

prostacycline

prostacycline analogues

Phosphodesterase inhibitors

endothelin receptor antagonists

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18
Q

oral therapies for PAH

A

sildenafil

tadalafil

riociguat

bosentan

ambrisentan

macitentan

treprostinil

selexipag

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19
Q

inhaled therapies for PAH

A

loloprost (6-9 inhalations daily)

Treprostinil (dosed QID up to 15 puffs)

20
Q

infusional therapies for PAH

A

Epoprostenol

Treprostinil

21
Q

how do thrombi form

A

blood stasis

hyper coagulable states

vessel wall abnormalities

22
Q

where do emboli originate

A

deep veins of lower extermities or pelvis

upper extremity veins

right heart chamber

SVC

23
Q

what happens when an embolus occur

A

decreased or total cessation of pulmonary blood flow to affected distal zone

physiologic dead space increased

bronchoconstriction

surfactnant production decreases (atelectasis)

arterial hypoxemia

24
Q

how does a PE cause increased PVR

A

50% occlusion necessary

dependant on amoutn of surface involved, underlying cardiopulmonary reserve and neurohormonal response

when mean PAP reaches >40 mmHg the RV will fail and collapse occurs

25
Q

what causes death in PE

A

from cardiovascular collapse rather than respiratory failure

26
Q

clinical symptoms of PE

A

pain or swelling of extremity is most common

dyspnea

pleuritic chest pain

cough

apprehension

hemoptysis

physical findings include tachycardia, tachypnea, hypoxia

27
Q
A

DVT

28
Q
A

PE

29
Q
A

PE

30
Q

how do you treat PE

A

prevent - DVT prophylaxis, anticoagulants, mechanical compression

acute - anticoagulation

31
Q

anticoagulant drugs

A

subQ heparin, warfarin, low MW heparin

32
Q

supportive therapy for PE

A

oxygen, fluids and vasopressors for hypotension, thrombolytic therapy only with shock/cardiac arrest, embolectomy

33
Q
A
34
Q

cardiogenic pulmonary edema

A

pressure related

LV problesm, left sided valve problems, pulmonary vein obstruction

35
Q

non cardiogenic pulmonary edema

A

leaky capillaries

ARDS, HAPE, neurogenic, opiate OD

36
Q

how do lungs protect themselves from excessive movement of fluid into interstitial spaces

A

lymphatic drainage aided by changes in intrathoracic pressure with normal respiration

37
Q

gel like matrix of hte lung is capabel of what

A

absorbing the additional fluid without affecting interstitial pressures

38
Q
A

pulmonary edema

39
Q
A

pulmonary edema

40
Q

pathophys of pulmonary edema

A

decreased lung compliance

decreased lung volume

increased airway resistance

increased work of breathing

V/Q mismatch

increased A-a gradient

hypoxemia

41
Q

clinical findings of mild pulmonary edema

A

dyspnea

orthopnea

few rales in bases

variable amount of peripheral edema

42
Q

clinical findings of acute pulmonary edema

A

prod cough of frothy blood tinged sputum

tachypnic

apprehensive

peripheral extremities cool, clammy, cyanotic

rales and wheezing

engorged neck veins

tachycardia

cardiac enlargement

43
Q
A

pulmonary edema

44
Q

managment of cardiogenic edema

A

improve cardiac function

afterload reduction, inotropes

eliminate excess fluid

oxygen/ventilatory support

advanced therapies - ECMO, LVAD, transplant

45
Q

managment of non cardiogenic edema

A

oxygen

ICU

advanced support

treat underlying disease

RC Test 4 (10 decks)

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