Pulmonary HTN

Question 1

:) What are the 5 broad categories within the classification of pulmonary hypertension?

Answer 1

1. pulmonary artery HTN (eg. idiopathic)
2. pulmonary HTN due to L) heart disease
3. Pulmonary HTN due to lung diseases/hypoxia
4. chronic thromboembolic pulmonary HTN
5. pulmonary HTN with unclear multifactorial mechanisms (eg. myeloproliferative disorders, splenectomy, sarcoid, renal failure)

Question 2

:) Which treatments improve survival in pulmonary HTN?

Answer 2

Supplemental O2
diuretics
digoxin
anticoagulation

Question 3

:) What are some pulmonary vasodilators?

Answer 3

oral endothelin antagonists: bosentan, ambrisentan
PDE-5 inhibitors: sildefanil
prostacyclin analogue (inhaled iloprost & IV epoprostenol are synthetic analogues of PGI2)
iNOS
Home O2

Question 4

:) What are some signs of RHF?

Answer 4

parasternal heave
S4 (movement of blood during diastole into a stiff ventricle) & loud S2 (particularly with increased intensity of P2 with pulmonary HTN)
Palpable pulmonic tap (felt in L) ICS)
Bad TCR (with murmur of tricuspid insufficiency), possibly pulm insufficiency
Canon V waves
elevated JVP
pulsatile liver
hepatosplenomegaly
ascites
peripheral oedema

Question 5

:) What’s TAPSE & what’s it useful for?

Answer 5

Tricuspid annular plane systolic excursion (TAPSE) describes apex-to-base shortening (tricuspid annulus in relation to RV apex)
>=1.7cm considered normal
Best evaluated in the 4-chamber view in M-mode echocardiography or cardiac MRI
Reflects RV longitudinal function, correlates closely with the RVEF
Both highly specific and easy to measure
Useful for measuring prognosis in pulm HTN, IHD particularly inferior MI, CCF

Question 6

:) What drugs are available to acutely drop PVR intra-op?

Answer 6

inhaled NO
prostacyclin analogues (epoprostenol infusion, inhaled iloprost)
IV or inhaled PDE-5 inhibitor (milrinone- inhaled complex ++ setup)

Question 7

:) What are the best vasodilators/inotropes for pulm HTN?

Answer 7

milrinone= inodilator

vasopressin incr SVR but not PVR

Question 8

:) What’s the main method of periop decompensation in pulm HTN?

Answer 8

R) heart failure

Question 9

:) What are some causes of primary pulmonary HTN?

Answer 9

idiopathic

due to CTD (hereditary, drug-induced, HIV, portal HTN, veno-occlusive disease)

Question 10

:) Are there manageable/reversible risk factors in management of primary pulmonary HTN?

Answer 10

No

Question 11

:) What’s the main risk issue with pulmonary HTN during anaesthesia?

Answer 11

anaesthesia may precipitate acute RV failure (impairing LV output hence CO & O2 delivery), dysrhythmia & death
respiratory failure accounts for 60% of cases of periop mortality in pulm HTN.

Question 12

:) What are the general goals of anaesthesia with pulmonary HTN?

Answer 12

avoid precipitating RV failure by:

• avoiding increases in PVR (avoiding hypoxaemia, hypercarbia, acidosis, hypothermia, drugs increasing PAP (N2O, ketamine), high or low lung volumes (use PEEP but not excessive volumes), SNS stimulation (eg. inadequate analgesia, blunting of response to laryngoscopy))
• protecting RV perfusion0 avoid sudden drops in preload (aim to maintain pts normal haemodynamics- HR, BP)

Question 13

:) What are signs of R) heart strain on ecg?

Answer 13

deep S wave in lead I
Q wave in lead III
TWI in lead III (this S1Q3T3 pattern seen in 12% of pts with PE)

RV dilation may lead to R)-sided conduction delays (incomplete or complete R) BBB), R)-axis deviation)

ST depression & TWI particularly in leads V1-3, inferior leads (II, III, aVF but particularly III as this is the most R)-facing)

poor R wave progression

Signs of RVH: R) axis deviation, dominant R wave in V1, dominant S wave in V5,6

Question 14

:) Which patients with pulmonary HTN are managed with vasodilators?

Answer 14

Specifically for primary PAH: Those who’ve even identified as “vasoactive responders” on R) heart Cath- given a CCB, they get a 20% reduction in their pulmonary pressures
Sustained response is rare

Question 15

:) How manage “vasoactive responders”? do patients with PAH respond?

Answer 15

high-dose CCBs generally, other options= oral endothelin antagonists (Bosentan, ambrisentan) & PDE-5 inhibitors (sildefanil)

<20% response in PAH

Question 16

:) How decide when the pt perfusing their heart? and how may this help with BP targets?

Answer 16

CPP=ASP-RVSP in systole
CPP=ADP-RVDP in diastole
whichever the widest difference likely most perfusion, support their BP to optimise coronary perfusion (ie. if focussing on diastolic, ensure not rapid HR & ensure DBP at least 60)
coronary blood flow through left coronary is phasic (more in diastole), through right is pulsatile (forward flow in both phases but slightly more in systole)

Question 17

:) How manage regional for severe AS vs pulm HTN?

Answer 17

AS: art line in pre-induction, vasopressor running, aim to support L) heart blood flow by maintaining afterload & volume to the preload-dependent ventricle
Pulm HTN: issue is use of alpha agonists will raise pulm pressures too so may not improve R) heart perfusion pressures, also with the regional technique the pulm pressures not likely to drop as much as the systemic pressures so losing RV perfusion yet not significant reduction in it’s afterload. Vasopressin likely the most appropriate drug to run under the guidance of a cardiac anaesthetist.

Question 18

:) On R) heart Cath, what’s R) atrial pressure usually? RV? PA? PCWP? LA pressure?
how does PCWP usually compare to pulmonary artery diastolic pressure? What’s measuring a surrogate for LA pressure useful for & in which conditions may LA pressure be elevated? At what point is pulmonary oedema likely to occur?

Answer 18

<5/0mmHg
25/0mmHg
PA: 25/10mmHg(due to pulmonary valve closure @ beginning of diastole)
PCWP normally 5-10mmHg mean (similar to RAP), >20 is pathological. Shows a, c & v waves as on the CVP trace.
CVP: (atrial contraction), c (TCV closure/elevation into atrium) & v (back-pressure from blood filling RA) waves. X descent (downward movement of contracting/emptying ventricle), Y descent (TCV opens).

LA <8mmHg

Mean PCWP is approximately 0–5 mmHg lower than the pulmonary artery diastolic pressure, unless there is increased pulmonary vascular resistance.

(from Gemma lecture: The PCWP is supposedly a surrogate for LA pressure but can’t tell whether it’s a pulmonary capillary, pulmonary venous or LA problem. If the wedge is high, it’s heart disease or pulmonary venous disease. If the PA pressures are high but wedge pressure is normal, acute dyspnoea, may be PE). PVR is measured distal to the wedge.

High LA pressure in:
MS
MR
AS, AR
LV failure, hypertrophy, restrictive cardiomyopathy, LVOTO
pericarditis/cardiac tamponade
evaluation of pulmonary HTN

Pulmonary oedema likely when LAP >20mmHg