Pulmonary Vascular and Sleep Disorders
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1
What is pulmonary hypertension (PH)?
Mean pulmonary artery pressure (mPAP) >20 mmHg
2
What was the historical diagnostic threshold for PH?
≥25 mmHg
3
Why was the mPAP threshold lowered?
Earlier detection and intervention improve prognosis.
4
What type of circulatory system is pulmonary circulation?
Low-pressure system
5
What causes pulmonary hypertension?
Remodeling and constriction of pulmonary vasculature
6
What happens when pulmonary arteries constrict?
Increased pulmonary vascular resistance and pressure
7
What is the most common cause of pulmonary hypertension?
Left-sided heart disease
8
What is the other common cause of PH?
Primary lung disease
9
What is the most common symptom of PH?
Dyspnea
10
What other symptoms occur in PH?
Chest pain and syncope
11
What is pulmonary arterial hypertension (PAH)?
A distinct PH subtype characterized by narrowing of pulmonary arteries
12
What was PAH formerly called?
Primary pulmonary hypertension
13
What is the usual nature of idiopathic PAH?
Idiopathic
14
What cellular changes occur in pulmonary vascular cells in PH?
Apoptosis resistance; cell proliferation; dysregulated metabolism; increased oxidant stress
15
What cells undergo pathological changes in PH?
Pulmonary vascular cells and adventitial fibroblasts
16
What type of remodeling occurs in distal pulmonary arterioles?
Hypertrophic, fibrotic, and plexogenic remodeling
17
What happens to vascular compliance in PH?
Decreased vascular compliance
18
What is vascular compliance?
Ability of a structure to distend
19
What does decreased vascular compliance cause?
Vascular stiffness and difficulty expanding
20
What happens to blood flow when pulmonary vessels become stiff?
Only a small volume passes despite high pressure.
21
What thrombotic complication occurs in PH?
In situ thrombosis
22
What happens to the pulmonary artery media and intima in PH?
Thickening
23
What is a plexiform lesion?
A complex vascular lesion associated with pulmonary arterial hypertension
24
What happens to the right ventricle in PH?
It enlarges and weakens due to increased workload.
25
Why does right ventricular hypertrophy develop in PH?
The RV works harder against increased pulmonary vascular resistance.
26
What is the function of the right ventricle?
Pumps blood to the lungs for oxygenation
27
What happens when the left ventricle is weak?
Blood congestion increases pulmonary vascular pressure.
28
What is the most common presentation of PH?
Dyspnea and/or fatigue
29
What symptoms suggest advanced PH?
Edema; chest pain; syncope
30
What causes right ventricular failure in PH?
Difficulty pumping blood through narrowed pulmonary arteries
31
What are signs of right ventricular failure?
Elevated JVP; pedal edema; ascites
32
What causes generalized edema in RV failure?
Blood flow stasis and increased preload
33
What is the normal cardiothoracic ratio?
$0.5$
34
What does an increased cardiothoracic ratio suggest?
Ventricular hypertrophy
35
What other chest X-ray finding may occur in PH?
Blunting of the costophrenic recess
36
What does 2D echocardiography directly measure in PH?
It does not directly measure mPAP; it measures sPAP.
37
What sPAP suggests pulmonary hypertension in the lecture?
>35 mmHg
38
What right ventricular finding may be visible on echocardiography?
RV dilation
39
What is the gold standard for diagnosing PH?
Right heart catheterization (RHC)
40
What does right heart catheterization directly measure?
Mean pulmonary artery pressure
41
What mPAP confirms PH on RHC?
>20 mmHg
42
What is the general catheter pathway in RHC?
Femoral or subclavian access → jugular vein → tricuspid valve → RV → pulmonary artery
43
What happens in clinical Stage A PH?
Vascular histopathological changes without hemodynamic changes; asymptomatic
44
What happens in clinical Stage B PH?
PVR, PAP, and RAP increase while CO begins to decline.
45
What happens in clinical Stage C PH?
Further increases in PVR and RAP with decreasing CO due to decompensation
46
What does CO stand for?
Cardiac output
47
What does PAP stand for?
Pulmonary artery pressure
48
What does PVR stand for?
Pulmonary vascular resistance
49
What does RAP stand for?
Right atrial pressure
50
What is the significance of declining CO in advanced PH?
It may eventually cause PAP to decrease.
51
What is pulmonary function testing in PH?
Nonspecific; may show obstructive or restrictive disease
52
How is diffusing capacity assessed in the lecture?
Controlled inhalation of carbon monoxide followed by measurement of absorption
53
What does DLCO measure?
Diffusing capacity of the lungs for carbon monoxide
54
What is the characteristic pulmonary function test finding in PAH?
Isolated reduction in DLCO
55
Can FEV1 be normal in PAH?
Yes
56
What CT finding suggests PH?
Enlarged main pulmonary artery
57
What is the normal CT relationship between the MPA and ascending aorta?
Typically similar in size
58
What is WHO Group 1 PH?
Pulmonary arterial hypertension (PAH)
59
What was WHO Group 1 formerly called?
Primary pulmonary hypertension
60
What is idiopathic PAH (IPAH)?
Progressive disease that can lead to right heart failure and early mortality
61
What is the main pathological problem in Group 1 PH?
Thickening and narrowing of pulmonary arteries
62
What congenital condition is associated with Group 1 PAH?
Congenital heart disease
63
What is the prognosis of PAH associated with surgically corrected congenital heart disease?
Generally favorable
64
What connective tissue disease is associated with PAH?
Systemic sclerosis
65
What infection is associated with PAH?
HIV
66
What mnemonic identifies WHO Group 1?
PRIMARY = ONE
67
What is WHO Group 2 PH?
Pulmonary hypertension associated with left heart disease
68
What is the most common etiology of PH?
WHO Group 2: left heart disease
69
What conditions cause Group 2 PH?
LV systolic dysfunction; aortic or mitral valve disease; HFpEF
70
What does HFpEF mean?
Heart failure with preserved ejection fraction
71
What does an ejection fraction above 50% indicate?
Preserved ejection fraction
72
What does an ejection fraction below 50% indicate?
Reduced ejection fraction
73
What is the primary mechanism of Group 2 PH?
Backward transmission of pressure from left heart dysfunction
74
Are pulmonary arteries as thick and stiff in Group 2 as in Group 1?
No
75
What mnemonic identifies Group 2 PH?
IT TAKES TWO PEOPLE TO FALL IN LOVE
76
What is WHO Group 3 PH?
Pulmonary hypertension associated with lung disease
77
What is the second most common etiology of PH?
WHO Group 3: lung disease
78
What are the specific etiologies of Group 3 PH?
COPD and interstitial lung disease
79
What does COPD stand for?
Chronic obstructive pulmonary disease
80
What does ILD stand for?
Interstitial lung disease
81
How severe is PH typically in Group 3?
Modest
82
What causes pulmonary vasoconstriction in Group 3 PH?
Alveolar hypoxia
83
Why do pulmonary arteries constrict in alveolar hypoxia?
To divert blood toward better-oxygenated lung segments
84
What does hypoxic pulmonary vasoconstriction optimize?
Ventilation-perfusion matching and systemic oxygen delivery
85
What mnemonic identifies Group 3 PH?
OXY HAS 3 LETTERS
86
What is WHO Group 4 PH?
Chronic thromboembolic pulmonary hypertension (CTEPH)
87
What percentage of patients develop CTEPH after pulmonary embolism according to the lecture?
Around 3–7%
88
What percentage of CTEPH patients have no history of pulmonary embolism?
25%
89
How does CTEPH develop?
Persistent clots form scar tissue that obstructs pulmonary blood flow.
90
What surgery can potentially cure CTEPH?
Pulmonary thromboendarterectomy (PTE)
91
What does PTE remove?
Chronic obstructive pulmonary clots
92
What mnemonic identifies Group 4 PH?
CLOT HAS 4 LETTERS
93
What is WHO Group 5 PH?
Miscellaneous diseases affecting the pulmonary vasculature
94
What diseases are associated with Group 5 PH?
Sarcoidosis; sickle cell disease; schistosomiasis
95
How does sarcoidosis cause PH?
Granulomatous inflammation of pulmonary vessels
96
How do sickle cells contribute to PH?
Abnormally shaped RBCs obstruct blood vessels.
97
What mechanisms contribute to PH in sickle cell disease?
Hemolysis; hypoxemia; thromboembolism; chronically high CO; chronic liver disease
98
What is a globally common cause of PH in Group 5?
Schistosomiasis
99
What condition is associated with schistosomiasis-related PH?
Hepatosplenic disease in portal hypertension
100
What are prostanoids used for in PAH?
Pulmonary vasodilation
101
What are examples of prostacyclin analogues?
Epoprostenol; treprostinil; selexipag
102
What is the mechanism of prostacyclin analogues?
Activate adenylate cyclase, increasing cAMP and causing vasodilation.
103
What does PGI2 stand for?
Prostacyclin
104
What are endothelin receptor antagonists (ERAs)?
Drugs that block endothelin receptors to cause vasodilation
105
What are examples of nonselective ERAs?
Bosentan and macitentan
106
Which ERA is ETA-selective?
Ambrisentan
107
What is endothelin-1 (ET-1)?
A vasoconstrictor and vascular smooth muscle mitogen
108
Which receptors mediate endothelin-1 effects?
ETA and ETB
109
What happens when endothelin receptors are activated?
Phospholipase C activation and calcium mobilization cause vasoconstriction.
110
What is the effect of ERAs on the endothelin pathway?
Inhibition of vasoconstriction and promotion of vasodilation
111
What are examples of PDE-5 inhibitors used in PAH?
Sildenafil and tadalafil
112
What is the mechanism of PDE-5 inhibitors?
Prevent hydrolysis and inactivation of cGMP
113
What was sildenafil originally developed for according to the lecture?
Pulmonary hypertension
114
What is the effect of riociguat?
Increases bioactive cGMP
115
What is the nitric oxide pathway in PAH?
NO activates soluble guanylyl cyclase → cGMP activation → vasodilation
116
What is the therapeutic goal of nitric oxide pathway effectors?
Upregulate nitric oxide
117
What is pulmonary thromboembolism?
Obstruction of pulmonary arteries by an embolus
118
What does venous thromboembolism encompass?
Deep vein thrombosis and pulmonary embolism
119
Where do most pulmonary emboli originate?
Deep veins of the legs
120
How does a DVT cause pulmonary embolism?
Clot dislodges → travels to heart → lodges in pulmonary artery
121
What can pulmonary embolism damage?
Lung parenchyma
122
What cardiac defect may allow an embolus to bypass the pulmonary circulation and reach the brain?
Patent foramen ovale (PFO)
123
What is Virchow's triad?
Venous stasis, hypercoagulability, and endothelial damage
124
What are the two most common autosomal dominant prothrombotic mutations?
Factor V Leiden and prothrombin gene mutation
125
What is the mechanism of Factor V Leiden mutation?
Resistance to activated protein C
126
What is the normal role of activated protein C?
Anticoagulant that inactivates clotting factors V and VIII
127
What does prothrombin gene mutation cause?
Increased plasma prothrombin concentration
128
What is antiphospholipid antibody syndrome (APAS)?
An acquired prothrombotic state
129
What clinical history is associated with APAS?
Recurrent spontaneous abortions
130
What are clinical risk factors for pulmonary thromboembolism?
Cancer; obesity; smoking; vaping; long-haul travel; hypertension; COPD; CKD; estrogen; pregnancy; surgery; trauma; coronavirus
131
How does smoking and vaping increase thrombotic risk?
Vasoconstriction promotes a prothrombotic state.
132
Why does long-haul air travel increase PE risk?
Prolonged seating causes venous stasis in the legs.
133
How can travelers reduce venous stasis?
Stand up occasionally and use medical-grade compression socks.
134
Why does surgery increase PE risk?
Prolonged immobility
135
Why does coronavirus increase PE risk?
It promotes a procoagulant state.
136
What is the normal relationship between alveolar ventilation and capillary perfusion?
They are normally matched.
137
What happens to perfusion in a pulmonary artery obstructed by a clot?
Decreases
138
What happens to ventilation in the affected region during PE?
It is maintained relative to reduced perfusion.
139
What does pulmonary embolism cause in gas exchange?
Ventilation-perfusion mismatch
140
What happens to blood flow in unaffected lung regions?
More blood flow relative to ventilation can also cause V/Q mismatch.
141
What percentage of PE cases are massive or high-risk?
5–10%
142
What defines massive pulmonary embolism in the lecture?
Extensive thrombosis affecting at least half of pulmonary vasculature
143
What is a saddle embolism?
An embolus lodged at the pulmonary artery bifurcation
144
What are the hallmarks of massive PE?
Hypotension; cyanosis; dyspnea; syncope
145
Which finding differentiates massive PE from other PE types?
Hypotension
146
What percentage of PE cases are submassive?
20–25%
147
What defines submassive PE?
RV dysfunction despite normal systemic arterial pressure
148
Is hypotension present in submassive PE?
No
149
What percentage of PE cases are low-risk?
65–75%
150
Which PE category is most common?
Low-risk pulmonary embolism
151
What is the prognosis of low-risk PE?
Excellent; it usually resolves on its own.
152
What organization issued the 2026 acute PE guidelines?
American Heart Association (AHA) and American College of Cardiology (ACC)
153
What is the purpose of the 2026 acute PE classification?
Assess disease severity
154
What characterizes Group A acute PE?
Subclinical; incidental and asymptomatic
155
What characterizes Group B acute PE?
Symptomatic with low clinical severity score
156
What characterizes Group C acute PE?
Symptomatic with elevated clinical severity score
157
What characterizes Group D acute PE?
Incipient cardiopulmonary failure with transient hypertension responsive to treatment
158
What characterizes Group E acute PE?
Cardiopulmonary failure with persistent hypertension despite management
159
What is PE called in the West because of its nonspecific symptoms?
The Great Masquerader
160
What is commonly called the Great Masquerader in the Philippines?
Pulmonary tuberculosis
161
What is the most common symptom of PE?
Unexplained breathlessness
162
What Wells score indicates high likelihood of DVT?
≥3
163
What Wells score indicates high likelihood of PE?
≥4
164
What clinical history should be considered when evaluating PE?
Signs or history of DVT
165
What is Homan's sign associated with?
Deep vein thrombosis
166
What is non-thrombotic pulmonary embolism?
Pulmonary vascular obstruction by material other than a blood clot
167
What are the types of non-thrombotic pulmonary embolism?
Fat; tumor; air; amniotic fluid; hydatid cyst; septic embolism
168
What causes fat embolism?
Bone marrow entering the circulation after pelvic or long-bone fracture
169
How much air is described as relatively safe in the lecture?
Up to 100 cc
170
What causes D-dimer elevation?
Breakdown of fibrin by plasmin
171
What does elevated D-dimer indicate?
Endogenous thrombolysis
172
What is the main clinical use of D-dimer in suspected PE?
Rule out pulmonary embolism
173
Can a high D-dimer confirm PE?
No; other diseases can also elevate it.
174
What does a low or normal D-dimer suggest according to the lecture?
PE is unlikely.
175
What is the classic ECG sign of PE?
McGinn–White sign (S1Q3T3)
176
What does the S1 component of S1Q3T3 indicate?
Prominent S wave in lead I
177
What does the Q3 component indicate?
Q wave in lead III
178
What does the T3 component indicate?
Inverted T wave in lead III
179
What other ECG finding may occur in PE?
Tachycardia
180
Does every patient with PE show S1Q3T3?
No
181
What is Westermark's sign?
Focal oligemia due to reduced pulmonary blood volume
182
What does the affected lung look like in Westermark's sign?
Reduced or absent lung markings
183
What is Hampton's hump?
Pleural-based opacity representing hemorrhage and necrotic lung tissue
184
What is Palla's sign?
Enlarged right descending pulmonary artery
185
What is the principal imaging test for PE?
Chest CT scan with IV contrast
186
Is echocardiography reliable for diagnosing PE?
No
187
What is commonly seen on 2D echocardiography in PE?
Normal findings in most patients
188
What is McConnell's sign?
RV free-wall hypokinesis with normal or hyperkinetic RV apex motion
189
What treatment is sufficient for a hemodynamically stable patient with normal RV function?
Anticoagulation alone
190
What is the mechanism of unfractionated heparin (UFH)?
Binds to and accelerates antithrombin activity
191
How is UFH administered?
Continuous intravenous drip
192
What monitoring is needed with UFH?
Constant monitoring of blood parameters
193
What are low-molecular-weight heparins (LMWH)?
Fragments of UFH with greater bioavailability
194
What are advantages of LMWH?
Predictable dose response; longer half-life; convenient administration
195
What are examples of LMWH?
Enoxaparin and tinzaparin
196
How are LMWH administered?
Subcutaneously
197
What is fondaparinux?
An anti-Xa pentasaccharide
198
Does fondaparinux cause HIT?
No
199
How is fondaparinux administered?
Subcutaneously
200
What is HIT?
Heparin-induced thrombocytopenia
201
What is an advantage of direct oral anticoagulants?
They do not cause HIT.
202
Which drugs are listed as anti-Xa DOACs in the lecture?
Dabigatran; rivaroxaban; apixaban
203
Which drug is listed as an anti-thrombin DOAC in the lecture?
Edoxaban
204
What is a disadvantage of DOACs?
They are expensive.
205
Which anticoagulants are sufficient for Group A and B acute PE?
DOACs
206
Which anticoagulants are recommended for Group C and D acute PE?
LMWH
207
What is recommended for Group E acute PE?
LMWH and consideration of UFH
208
What is pulmonary embolectomy?
Surgical removal of a pulmonary embolus
209
When is pulmonary embolectomy considered?
As a last resort for Group D and E patients
210
What is the most common form of in-hospital PE prophylaxis?
Low-dose UFH or LMWH
211
Which hospitalized patients may receive low-dose UFH or LMWH prophylaxis?
Patients with malignancy, immobility, or trauma history
212
What is the goal of in-hospital anticoagulant prophylaxis?
Prevent DVT and potential PE
213
What is obstructive sleep apnea (OSA)?
Airway obstruction causing cessation of breathing during sleep
214
What are the two bases of OSA diagnosis?
Symptoms and overnight polysomnography
215
What are the major nocturnal symptoms of OSA?
Snoring; snorting; gasping; breathing pauses
216
What are the major daytime symptoms of OSA?
Sleepiness and fatigue despite adequate sleep opportunity
217
What does AHI stand for?
Apnea-hypopnea index
218
What is the formula for AHI?
$\frac+\text}}$
219
What is the minimum frequency of obstructive events used in the lecture's OSA sleep-study criteria?
≥5 episodes per hour
220
What is apnea?
Complete cessation of breathing for ≥10 seconds
221
Is ventilatory effort present during obstructive apnea?
Yes, despite blocked airflow
222
What is hypopnea?
≥30% reduction in airflow with ≥3% oxygen desaturation, lasting ≥10 seconds
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