B4.067 - Pulmonary Vascular Disease Flashcards
3 major diseases of pulmonary vessels
Pulmonary embolism Pulmonary hypertension Pulmonary edema
what is the swan ganz catheter
invasive hemodynamic measurement of pulmonary artery pressures
which part of the heart has the lowest pressure
right atrium
SVR calculation (systemic vascular resistance)
SVR = 80 x (MAP - RAP)/ (CO)
calculation of pulmonary vascular resistance (PVR)
PVR = 80 x (MAP - LAP)/Pulmonary blood flow
PAH classification
- pulmonary artery HTN 2. Left heart disease 3. PH with respiratory disease or hypoxia 4. chronic thromboembolic disease 5. unclear/multifactorial
what is PAH
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
normal blood pressure in pulmonary artery
12-16
multi hit hypothesis of pathogenesis of pulmonary arterial hypertension
primary genetic background modifier genes environmental trigger
normal pulmonary artery and alveolus
pulmonary artery remodeling
internal fibrosis
medial hypertrophy
adventitial proliferation
luminal obliteration
signs of pulmonary HTN
JVD
Edema
chest pain
what is prostacyclin
PGI2
activity through cAMP
Vasodilator
inhibits proliferation of vascular smooth muscle
Decreases platelet aggregation
decreased prostacyclin synthase in PAH
goals of PAH therapy
fell better
live longer
breath
prevent blood clots
decrease scarring/blocked pipes
supportive therapy for PAH
oxygen
coumadin
digoxin
diuretics
treatment of underlying/coexisting disease
spectrum of treatments for PAH
nothing
oral medicines
nebulized medicines
continuously infused medicines
gene therapy
lung transplant
classes of drugs for PAH
prostacycline
prostacycline analogues
Phosphodesterase inhibitors
endothelin receptor antagonists
oral therapies for PAH
sildenafil
tadalafil
riociguat
bosentan
ambrisentan
macitentan
treprostinil
selexipag
inhaled therapies for PAH
loloprost (6-9 inhalations daily)
Treprostinil (dosed QID up to 15 puffs)
infusional therapies for PAH
Epoprostenol
Treprostinil
how do thrombi form
blood stasis
hyper coagulable states
vessel wall abnormalities
where do emboli originate
deep veins of lower extermities or pelvis
upper extremity veins
right heart chamber
SVC
what happens when an embolus occur
decreased or total cessation of pulmonary blood flow to affected distal zone
physiologic dead space increased
bronchoconstriction
surfactnant production decreases (atelectasis)
arterial hypoxemia
how does a PE cause increased PVR
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
what causes death in PE
from cardiovascular collapse rather than respiratory failure
clinical symptoms of PE
pain or swelling of extremity is most common
dyspnea
pleuritic chest pain
cough
apprehension
hemoptysis
physical findings include tachycardia, tachypnea, hypoxia
DVT
PE
PE
how do you treat PE
prevent - DVT prophylaxis, anticoagulants, mechanical compression
acute - anticoagulation
anticoagulant drugs
subQ heparin, warfarin, low MW heparin
supportive therapy for PE
oxygen, fluids and vasopressors for hypotension, thrombolytic therapy only with shock/cardiac arrest, embolectomy
cardiogenic pulmonary edema
pressure related
LV problesm, left sided valve problems, pulmonary vein obstruction
non cardiogenic pulmonary edema
leaky capillaries
ARDS, HAPE, neurogenic, opiate OD
how do lungs protect themselves from excessive movement of fluid into interstitial spaces
lymphatic drainage aided by changes in intrathoracic pressure with normal respiration
gel like matrix of hte lung is capabel of what
absorbing the additional fluid without affecting interstitial pressures
pulmonary edema
pulmonary edema
pathophys of pulmonary edema
decreased lung compliance
decreased lung volume
increased airway resistance
increased work of breathing
V/Q mismatch
increased A-a gradient
hypoxemia
clinical findings of mild pulmonary edema
dyspnea
orthopnea
few rales in bases
variable amount of peripheral edema
clinical findings of acute pulmonary edema
prod cough of frothy blood tinged sputum
tachypnic
apprehensive
peripheral extremities cool, clammy, cyanotic
rales and wheezing
engorged neck veins
tachycardia
cardiac enlargement
pulmonary edema
managment of cardiogenic edema
improve cardiac function
afterload reduction, inotropes
eliminate excess fluid
oxygen/ventilatory support
advanced therapies - ECMO, LVAD, transplant
managment of non cardiogenic edema
oxygen
ICU
advanced support
treat underlying disease
