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MD2 Respiratory > Pulmonary Vascular Disease > Flashcards

Pulmonary Vascular Disease Flashcards

1
Q

Normal ABGs

A

pH 7.35-7.45
PaCO2 35-45 mmHg
PaO2 80-100 mmHg
22-26 HCO3

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2
Q

Define shock

A

Hypotension despite 500mL IV fluid and persisting >15min

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3
Q

What is the effect of respiration on CO?

A

Pooling of blood occurs on inspiration; this decreases venous return to the left heart and in turn decreases CO and SBP (a decrease >10mmHg is termed “pulsus paradoxus”)

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4
Q

What changes occur to the pulmonary pressures with exercise?

A

CO increases but pulmonary pressures do not due to dilatation and recruitment of pulmonary vessels

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5
Q

List 3 causes of pulmonary HTN

A

Increased LAP
Increased pulmonary blood flow
Increased pulmonary vascular resistance (vasoconstriction, obstruction or obliteration)

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6
Q

List 3 causes of increased LAP which may result in pulmonary HTN

A

Mitral stenosis
LVF
Diastolic dysfunction

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7
Q

List 3 causes of increased pulmonary blood flow

A

Left to right shunt
High flow states
Excess central volume

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8
Q

List a cause of pulmonary vasoconstriction which may result in increased pulmonary vascular resistance and therefore pulmonary HTN

A

Low alveolar O2 (including hypoventilation)

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9
Q

List 2 causes of pulmonary vasculature obstruction which may result in increased pulmonary vascular resistance and therefore pulmonary HTN

A

PE

Primary pulmonary HTN

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10
Q

List 3 causes of pulmonary vasculature obliteration which may result in increased pulmonary vascular resistance and therefore pulmonary HTN

A

Arteritis
Emphysema
Pulmonary fibrosis

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11
Q

What might be the physiological consequences of increased resistance at the pre-capillary level in the pulmonary circulation? What might happen to gas exchange?

A

Pulmonary HTN leads to RV dilatation and hypertrophy
RV changes lead to increased systemic venous pressure and decreased CO
Increased systemic venous pressure leads to extravasation of fluid into tissues and the peritoneal and pleural spaces
Gas exchange is reduced, leading to hypoxaemia, particularly with exertion

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12
Q

What is the definition of pulmonary HTN?

A

Mean PA pressure >25 mmHg

PVR >3 Woods units

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13
Q

What are Woods units?

A

System for measuring PVR that uses increments of pressure

PVR = (pulmonary arterial pressure - pulmonary capillary wedge pressure)/CO

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14
Q

List 7 symptoms of pulmonary vascular disease

A 
SOB
Syncope/collapse
Lethargy
Swelling of ankles
Cough
Haemoptysis
Chest pain (often pleuritic)
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15
Q

List 3 signs of pulmonary HTN

A

RV heave
Loud P2 with 4th heart sound
Prominent “v” wave in the JVP

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16
Q

List 3 signs of RHF

A

Elevated JVP +/- v waves
TR (with pulsatile liver)
SOA, ascites

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17
Q

26 year old women presents with sudden episode of collapse
At presentation she has a reduced conscious state
O/E: HR 120, BP 70/50, SaO2 90% on RA, RR 35, normal chest sounds, JVP 5cm, heart sounds normal (?3rd heart sound)
ECG: sinus tachycardia and RV strain pattern
CXR: clear
ABG: pH 7.48, PaCO2 30mmHg, PaO2 55mmHg, HCO3- 24
Assess the patient’s current state

A

Evidence of severe physiological compromise: shock with reduced conscious state, RV strain/failure, severe type 1 respiratory failure

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18
Q

26 year old women presents with sudden episode of collapse
At presentation she has a reduced conscious state
O/E: HR 120, BP 70/50, SaO2 90% on RA, RR 35, normal chest sounds, JVP 5cm, heart sounds normal (?3rd heart sound)
ECG: sinus tachycardia and RV strain pattern
CXR: clear
ABG: pH 7.48, PaCO2 30mmHg, PaO2 55mmHg, HCO3- 24
What findings might you expect in the case of cardiac tamponade or constrictive pericarditis? What about this presentation makes these diagnoses less likely?

A

Muffled heart sounds +/- pericardial rub
Pulsus paradoxus
In tamponade there may be signs of LHF as well
Would not expect such profound hypoxaemia (primary cardiac problems usually do not cause this)

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19
Q

List 4 causes of PE

A

Detached DVT from leg (most common)
Fat (e.g. post-trauma, classically long bone fractures)
Air (e.g. post-laparoscopic surgery)
Amniotic fluid (rare but catastrophic)

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20
Q

What is the % mortality of untreated PE?

A

30%

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21
Q

What % of acute treated PE are a result of chronic thromboembolic disease?

A

4%

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22
Q

Describe risk factors for thrombus formation within the framework of Virchow’s triad

A

Stasis: inpatient stay, after some surgical procedures, prolonged immobility
Hypercoagulable state: genetic abnormalities, factor deficiencies, malignancy, polycythaemia, pregnancy, medication
Abnormal vessels: trauma

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23
Q

What clinical features might help you make a diagnosis of PE? How might the clot burden influence this?

A 
Collapse and hypoxaemia
Widened A-a gradient of unclear cause
Pleuritic chest pain with no clear cause
Unexplained breathlessness
Evidence of pulmonary HTN
Evidence of a DVT (calf pain and swelling)
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24
Q

Describe the difference in presentation between a patient with a medium clot burden and a patient with repeated small emboli

A

Medium clot burden (clots tend to travel more distally): dyspnoea, pleuritic chest pain, cough, haemoptysis, fever, tachypnoea, tachycardia, pleural rub/effusion
Repeated small emboli: often unrecognised, pulmonary capillary bed is gradually eroded leading to progressive exertional dyspnoea

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25
Q

Outline Wells’ criteria for making a PE diagnosis

A 
Modified Wells criteria:
Clinical symptoms of DVT (leg swelling, pain with palpation) 3.0
Other diagnosis less likely than PE 3.0
HR >100 1.5
Immobilisation (≥3 days) or surgery in the previous 4 weeks 1.5
Previous DVT/PE 1.5
Haemoptysis 1.0
Malignancy 1.0

Probability high if >6.0, moderate if 2.0-6.0, low if 4.0
PE unlikely if

26
Q

What diagnostic tests are available for suspected PE?

A

D-dimer
ECG
V/Q scan
CTPA (diagnostic test of choice)

27
Q

What is D-dimer?

A

A fibrin degradation product

28
Q

What is the sensitivity and specificity of D-dimer? What is its NPV?

A

Sensitivity good (>95% with ELISA)
Low specificity
NPV excellent when low clinical probability of PE

29
Q

Is ECG useful in evaluating a potential PE?

A

Yes; may be abnormal in up to 70% of patients

BUT not specific

30
Q

What ECG changes are suggestive of PE?

A

Sinus tachycardia +/- right axis deviation, RBBB
S1Q3T3 (less common)
RV strain pattern

31
Q

Is a V/Q scan useful for diagnosing PE?

A

Combined with a high clinical probability, a high probability V/Q confers a 95% likelihood of having a PE
Normal (“low probability”) scan virtually rules out PE
Many patients fall into the intermediate group so more tests are required

32
Q

What are the strengths of a CTPA in suspected PE?

A

May detect other pulmonary abnormalities
Very good NPV (low risk of PE if negative; 2% over 3 months)
96% of patients with high clinical probability had PE

33
Q

What other Ix may be performed in suspected PE?

A

Echo
Venous U/S (not routine)
Pulmonary angiography (gold standard but rarely performed)

34
Q

In what % of patients with PE are abnormalities detected on echo?

A

30-40%

35
Q

When is echo more helpful in a case of suspected PE?

A

In massive PE (helpful for risk stratification; allows you to determine if there is RV strain if not obvious on ECG)

36
Q

5 therapies for treatment of PE

A 
Respiratory support
Haemodynamic support
Thrombolytic therapy
IVC filter
Anticoagulation
37
Q

When is thrombolytic therapy indicated in PE?

A

Most severe cases (major haemorrhage, haemodynamically unstable and unresponsive to aggressive fluid resuscitation and supportive care)

38
Q

When is an IVC filter used?

A

If there is failure of or contraindication to anticoagulation, or if further PE might be lethal

39
Q

Is there a clear mortality benefit with use of an IVC filter?

A

No

40
Q

What is the effect of anticoagulation on mortality from PE?

A

Mortality drops from ~30% to 2-8%

41
Q

When should anticoagulation be given in the case of PE?

A

ASAP (when safe)

42
Q

What is the most common duration of warfarin therapy following PE?

A

3-6 months is standard (indefinite if recurrent problem)

43
Q

What other anticoagulants are approved for treatment of PE/DVT?

A

Rivaroxaban

Dabigatran

44
Q

What INR should you aim for post-PE in a warfarinised patient?

A

2-3

45
Q

65 year old man with known COPD presents with 2/52 of worsening SOB and associated ankle swelling
O/E: SaO2 88% on RA, normal BP and HR/rhythm, RR 22 with clear use of accessory muscles, chest examination shows signs of hyperinflation, JVP 5cm with SOA ++
What is the diagnosis?
What Ix would you request?
What should be the management?

A

Dx: COPD causing RHF (cor pulmonale)
Ix: basic bloods (FBE, UEC, LFT), ABGs, 6MWT, CXR, lung function, ?sleep study, echo
Mx: cease smoking (if he hasn’t already), O2 (how much?), pulmonary rehab, bronchodilator therapy, diuretics

46
Q

6MWT protocol

A

6 Minute Walk Test

??

47
Q

24 year old women presents 3/52 after the delivery of her first child
Having episodes of syncope and is SOB on minimal exertion (has been feeling SOB for about 6/12)
O/E: RV heave, loud P2, prominent v wave in JVP, SaO2 93% on RA, otherwise normal
What do you think is going on?
What would you do next?

A

Has signs of pulmonary HTN

Important to order a CXR, CTPA

48
Q

Findings on CXR in pulmonary HTN

A 
Prominent hilar regions due to enlarged pulmonary arteries
RV enlargement (+/- cardiomegaly)
49
Q

Findings on CTPA in pulmonary HTN

A

Grossly dilated central pulmonary arteries
Normal lung parenchyma
No acute PE

50
Q

24 year old women presents 3/52 after the delivery of her first child
Having episodes of syncope and is SOB on minimal exertion (has been feeling SOB for about 6/12)
O/E: RV heave, loud P2, prominent v wave in JVP, SaO2 93% on RA, otherwise normal
Findings on CXR and CTPA suggestive of pulmonary HTN
Why might she have this?

A

Primary pulmonary HTN is usually a disease affecting the young
Long duration of breathlessness
Worse during pregnancy due to changes in blood volume and circulation

51
Q

What are the 5 diagnostic categories of PAH?

A

1) PAH
2) PH with left heart disease
3) PH with chronic lung disease/hypoxaemia
4) PH due to chronic thrombotic and/or embolic disease
5) Miscellaneous

52
Q

What are the different 5 types of primary PAH?

A

Idiopathic PAH
Familial PAH
Related to connective tissue diseases, HIV, portal HTN, anorexigens, congenital heart diseases
PPHN (persistent pulmonary HTN in neonates)
PAH with venule/capillary inversion (pulmonary veno-occlusive disease, PVOD)

53
Q

What kinds of left heart disease can cause pulmonary HTN?

A

Atrial or ventricular

Valvular

54
Q

List 4 chronic lung diseases which may cause pulmonary HTN

A

COPD
Interstitial lung diseases
Sleep-disordered breathing
Developmental abnormalities

55
Q

List 3 types of chronic thrombotic and/or embolic disease which mayy cause pulmonary HTN

A

TE obstruction of proximal PA
TE obstruction of distal PA
Non-thrombotic PE

56
Q

Give an example of a miscellaneous cause of PAH

A

Sarcoidosis

57
Q

What is the mortality of untreated PAH?

A

50% at 2 years from diagnosis

58
Q

Describe the principles of general care for PAH

A

Oral anticoagulants +/- diuretic +/- O2 +/- digoxin

59
Q

How should PAH be treated if the patient is positive on acute vasoreactivity testing?

A

Oral Ca2+ channel blocker

60
Q

How should PAH be treated if the patient is negative on acute vasoreactivity testing?

A

Endothelian receptor antagonist or PDE-5 inhibitor or prostanoid analogue
If severe, no improvement, or deterioration: consider atrioseptostomy +/- lung transplantation

MD2 Respiratory (9 decks)

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