Pulmonary Hypertension Flashcards Preview

Respiratory 2 > Pulmonary Hypertension > Flashcards

Flashcards in Pulmonary Hypertension Deck (28):
1

CLinical features

Exertional dyspnea
Fatigue
Weakness

Advanced - severe dyspnea with exertional dizziness/light-headedness
Exertional syncoe

Honeymoon period following acute PE****

2

If you are worried about pulmonary HTN, the next step is

Good screening tool

May over or underestimate the PAP

3

Echo findings

RV much larger than the left

May compromise left ventricle filling

Can help you dx underlying left heart dz

4

PAH (precapillary)

Elevated mPAP, normal PCWP
Elevated TPP
Elevated PVR

5

Post-cap or pumonary venous hypertension

Elevated mPAP
Elevated PCWP
Normal TPP
Normal PVR though total resistance is elevated

6

Both PAH and post-capillary hypertension cause

Increased workload of the right ventricle leading to RV failure

7

PH vs. PAH

PH - means mean lumonary vasculary pressure is elevated

PAH - must be due to pre-cap

PH - mPAP over 25

PAH - mPAP over 25 plus PAWP less than 15 plus PVR over 3 wood units

8

PAH dz

Elevated mPAP and PVR leading to RV failure and premature death

9

Confirmatory dx

Right heart catheterization

MUST be done in all pts to establish dx

This can exlude congenital, differentiate between PAH and venous

Severity and prognosis

Tests vasodilator therapy

10

Vasodilator testing

SHould be evaled in every pt prior to tx

Done with iNO, prostacylin or adenosine

Decrease in mean PAP of at least 10 mmHg to a pressure of less than 40 mmHg WITH an increased or changed cardiac output is considered positive

11

Groups of pulm HTN

1 - PAH
2 - due to left heart dz (common venous cause)
3 - due to lung dz or hypoxia
4 - chronic thrombomboli
5 - other unclear mechs

12

Radiography

Peripheral markings
Enlarged PA shaodws
Loss of retrosternal

CT - more sensitive

13

PFTs

Usually normal

DLCO - may be normal, mild to moderate reduction common**

Oxygenation may be normal but dest with exercise

increased dead space (increased V/Q)

14

Exercise testing

6 minute walk test

Decrease in VO2 max, AT, O2 pulse, rate of increase, etc.

Correlates with functional class

15

CTEPH

Symptomatic PH (mPAP over 25)
Persistent perfusion defects
After adequate anticoagulation for 3-6 months

16

Screening for CTEPH

V/Q scan

17

Dx of CTEPH

Look for hx of PE or pulm HTN of unclear cause (detected by echo)

Then get chest CTA or V/Q lung scan

18

Pathogenesis

Unbalance between vasoconstrictors and dilators

LEads to dysfunction and injury

Leads to PAH

19

Disease pathways

Endothelin

Nitric oxide pathway

Prostacyclin pathway

20

Histopathology

Intimal fibrosis

increased medai lthickness

Pulmonary arteriolar occlusion

Plexiform lesions

21

Acute to chornic trnasition

Resistance ot lysis

Persistence of ligands

Abnormal clot structure

22

Acute to CTEPH progresion

PE specific factors
Chonirc medical conditions
Genetic factors
Thrombotic factors

23

Pathophysiology of CTEPH

2 ways

unaffected part of the lung (away from the blockage) gets increased amount of cardiac outflow...increased flow and pressure leads to stretch which leads to secondary changes

1) large mechanical compoennt

2) downstream changes due to the blockage

24

Funcational assemement

1 - wihout limitation
2 - slight
3 - marked
4 - inability

25

Txs

Diuretics

Anticoagulants

Digoxin

Supplemental O2

26

Calcium channel blockers

Only a small subset benefit from CCB

WHo show resonse ot vasoreactivity

27

Prostacyclin analogues

Vasodilators

Indicated for all functional

28

Pulmonary endarterectomy

Surgical tx of choice

EVERY pt should be evaluated for PEA at expert center