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MS2 Respiratory > 9/23- Pulmonary Vascular Diseases > Flashcards

9/23- Pulmonary Vascular Diseases Flashcards

1
Q

What are the systolic/diastolic/mean BP for pulmonary arteries?

Characteristics of pulmonary circulation?

A

Pulmonary circulation is high flow, low pressure, highly compliant system (low resistance)

  • Systolic: 30 mmHg
  • Diastolic: 10 mmHg
  • Mean: 15 mmHg
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2
Q

What regulates vascular tone in pulmonary circulature?

A

Vascular endothelium

  • NO (dilator)
  • Endothelin (constrictor)

Autonomic nervous system

  • a1 adrenergic receps (constriction)
  • B2 adrenergic receps (dilation)
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3
Q

What is the mechanism of NO dilation of vasculature?

A
  • Secreted by endothelial cells
  • Activates guanylate cyclase (GC) to increase cGMP levels
  • Also activates Ca dependent K channels in vascular smooth muscle
  • Dilates both venous > arterial
  • NO is a gas, which can be inhaled to result in primary pulmonary vasodilation
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4
Q

What are the determinants of pulmonary artery pressure?

A
  • Blood volume
  • Rate of fluid flow through system (CO, viscosity, vessel size)
  • Pressure inhibiting flow across cap bed (left atrial pressure)
  • PAP = CO x (PVRa + PVRcaps + PVRv)
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5
Q

What are some pulmonary vascular disorders?

A
  • Pulmonary hypertension
  • Pulmonary embolism
  • Pulmonary vasculitides
  • Pulmonary arteriovenous malformation
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6
Q

What is the cutoff for pulmonary HTN?

A

Mean PA pressure > 25 mmHg

(recall, normal is 15 mmHg)

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7
Q

How is Pulmonary HTN classified?

A

1. Pulmonary arterial hypertension (PAH)

  • Toxin/drug use
  • HIV
  • Portal hypertension, liver cirrhosis
  • Sickle Cell Disease
  • Group 1 disease have specific targeted treatments*

2. Left heart disease

3. Lung diseases and/or hypoxia

  • Obstructive
  • Restrictive
  • Chronic hypoxemia

4. Chronic thromboembolic pulmonary HTN (CTEPH)

  • Persistent elevation of pulmonary P -> symptoms and heart failure

5. Unclear multifactorial mechanisms

  • Sarcoidosis
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8
Q

What are the structural and functional changes in pulmonary HTN?

A

Increased PVR

  • Sustained vasoconstriction (muscle layer hypertrophy and permeation into other layers)
  • Vascular remodeling
  • In-situ thrombosis
  • Increased arterial wall stiffness
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9
Q

What is idiopathic Pulmonary Arterial HTN?

  • Epidemiology
  • Pathology
A

Epidemiology

  • Uncommon
  • More in women
  • Mean age = 50 yo

Pathology

  • Hypertrophy/fibrosis vascular bed
  • In situ thrombosis
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10
Q

What is the prognosis for idiopathic Pulmonary Arterial HTN?

A
  • Variable
  • Mean survival 2-3 yrs from time of diagnosis
  • Depends on severity, cardiac function, exercise tolerance, response to vasodilators
  • Non-responders: 9-18 months
  • Responders w/ preserved function:- >50% for 5 yrs
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11
Q

What are the clinical features of PAH?

A
  • Shortness of breath
  • Atypical chest pain
  • Palpitations
  • Cough
  • Syncope (if advanced; developing RHF)
  • Hemoptysis
  • Hypotension
  • Tachycardia
  • Atrial arrhythmias

- Loud P2

- Tricuspid regurgitation murmur

  • JVD
  • Signs and symptoms of cor pulmonale (RHF)
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12
Q

Case)

  • 45 yo female with worsening SOB
  • Chest pain, orthopnea, PND What is seen on her CXR?
A
  • Don’t see infiltrate, pneumonia, fibrosis
  • Preserved lung structure/anatomy

Heart seems somewhat abnormal:

  • Large pulmonary artery indicative of pulmonary HTN
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13
Q

What is seen of echocardiogram of pulmonary HTN?

A
  • Small LV cavity; normal LV ejection fraction
  • Severe RV dilatation, severely reduced RV global systolic function
  • PA systolic pressure estimate 105-110 mmHg
  • No interatrial septal defect
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14
Q

What does the evaluation of suspected pulmonary HTN look like?

A
  • ECHO to screen for PH and r/o primary cardiac disease
  • PFT to r/o primary lung disease (esp. COPD) and restrictive lung disease
  • Spiral CT (possible angiogram) to r/o pulmonary vascular disease (thromboembolic disease, vasculitis)
  • Right heart cath: Pulmonary artery pressure, PCWP, hemodynamics
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15
Q

What is the treatment for PAH (pulmonary HTN in general?) ?

A
  • Optimize therapy for related diseases
  • Supportive (O2, anticoagulation, diuretics, digoxin)
  • Targeted therapy - Surgical
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16
Q

What are targeted therapies for PAH?

A
  • Prostacyclins
  • Endothelin receptor antagonist
  • NO pathway drugs
  • Soluble guanylate cyclase stimulators
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17
Q

What are characteristics of prostacyclins for PAH treatment?

Examples (probably don’t need to name)?

A

Vasodilatory, antiplatelet, antiproliferative

  • Berapost (PO)
  • Epoprostenol (IV)
  • Iloprost (inhaled)
  • Treprostinil (SQ, IV, inhaled, PO)
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18
Q

What are characteristics of endothelin receptor antagonists for PAH treatment?

Examples (probably don’t need to name)?

A

Blocks receptor for ET-1, a potent vasoconstrictor and mitogen

  • Bosentan (PO)
  • Ambrisentan (PO)
  • Sitaxsentan
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19
Q

What are examples of NOs for PAH treatment (probably don’t need to name)?

A
  • Phosphodiesterase inhibitors: Sildenafil/Tadalafil
  • Inhaled NO
  • Dipyridamole
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20
Q

Name soluble guanylate cyclase stimulators (probably don’t need to name)?

A

Riociguat

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21
Q

What are surgical therapies for PAH?

A

Lung transplantation

  • Double lung transplantation typically
  • Heart-lung if PAH secondary to congenital heart disorders

Atrial septostomy

  • Reduces RVEDP, improves cardiac index at expense of decreased PaO2
  • Bridge to transplantation

Pulmonary endarterectomy for CTEPH

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22
Q

What is cor pulmonale?

  • Cause
  • Signs
A
  • RV hypertrophy (and ultimately resulting in right heart failure) 2ndary to increased PVR
  • Most commonly results from chronic pulmonary diseases (esp. COPD) that affect pulmonary vasculature.
  • Signs:
  • Hepatojugular reflux
  • Lower extremity edema
  • Pulsatile liver
  • Tricuspid regurgitation
  • Ascites
23
Q

What is the treatment for cor pulmonale?

A
  • Treat underlying cause(COPD, etc.)
  • Minimize vasoconstriction, vasodilate (O2),
  • Improve cardiac output w/rhythm control and contraction
24
Q

Epidemiology of PE/DVT?

A
  • Venous thromboembolism is a major medical problem
  • > 5 million DVT cases annually
  • Of these, 650,000 develop pulmonary embolism (PE)
  • Of pts with PE, 100,000 die annually
  • Not uncommon cause of death in acute care hospital setting
  • > 70% of pts that die of PE are not suspected before death; maintain a high index of suspicion and pursue the diagnosis when warranted
25
Q

What are causes of pulmonary embolism?

A
  • Thrombus
  • Fat (occurs in long bone fractures)
  • Tumors
  • Trophoblast
  • Air (catheter placement, scuba diving)
  • Amniotic fluid
26
Q

What is VIrchow’s triad?

A
  1. Venous stasis
  2. Intimal injury
  3. Altered coagulation
27
Q

What are the risk factors for thrombosis?

A
  • Age > 70 yo
  • Obesity
  • Sedentary/Bed rest
  • Trauma
  • Chronically ill
  • Pelvic surgery/trauma
  • Prolonged anesthesia (>1 hour)
  • Surgery of lower extremities
  • Hip fracture/replacement
  • Pregnancy/postpartum
  • Right ventricular failure
  • Oral contraceptives (5-10 fold increase)
  • Underlying malignancy (Trousseau’s syndrome)
  • Inherited/acquired deficiency of naturally
  • occurring anticoagulants:resistance to activated protein C (Factor V Leiden)
  • Prothrombin gene mutation
  • protein C deficiency
  • protein S deficiency
  • Antiphospholipid antibody syndrome
  • Anti-thrombin III deficiency
  • Hyperhomocysteinemia
28
Q

What are symptoms of DVT?

A
  • Pain
  • Tenderness
  • Swelling
  • (+) Homan’s sign: dorsiflexion of foot/ankle -> pain
29
Q

What are the symptoms and findings of pulmonary embolism?

A

Symptoms

  • Dyspnea
  • Impending doom
  • Palpitations (tachycardia)
  • Hemoptysis and pleuritic chest pain are signs of infarction (uncommon, 20% of patients with significant cardiopulmonary disease)

Findings

  • Tachypnea
  • Tachycardia
  • Low grade fever
  • With massive embolism
  • fixed split of S2, and S3 or S4, dilated neck veins, and cyanosis, hypotension
30
Q

What is the diagnostic process of DVT?

A

- Contrast venography: Gold standard, only accurate method in asymptomatic individuals.

- IPG: Serial negative IPG or US is comparable in accuracy to negative venography in patients with suspected DVT

- Compression ultrasonagraphy*: Often the diagnostic modality of choice. The sensitivity and specificity approach 97%-98% for symptomatic patients.

  • MRI: High sensitivity and specificity, expensive

- D-dimer: Low levels of plasma D-dimer (under 500 ng/mL) by ELISA technique may have a high negative predictive value

31
Q

T/F: You can get DVT in upper extremity veins?

A

True!

32
Q

What is seen on CXR for someone with DVT?

A
  • Localized oligemia -> Westermark sign:
  • Hampton’s hump
  • Consolidation (infarct)
  • Usual report is “normal”
33
Q

What is seen on EKG for someone with DVT?

A
  • Tachycardia
  • Right axis deviation (right sided strain)
  • New onset atrial fib
34
Q

What is S1Q3T3?

A

The classic finding; “not common, but always talked about”

35
Q

What are the diagnostic tests on PE of someone with DVT?

A

ABG’s: increased A-a difference;

Pa02 may be above 80;

C02 usually decreased

Remember to calculate the A-a diff

  • A-a difference is usually increased
  • Alveolar gas equation
  • [FIO2(PB-PH20) – PaC02/R] – Pa02
  • [150-PaC02/0.8] - Pa02
36
Q

What is the Wells Diagnostic Scoring? Considerations?

A

Predicts clinical likelihood of PE

  • Signs/symptoms of DVT (3)
  • Another diagnosis less likely than DVT (3)
  • HR > 100 (1.5)
  • Immobilization/surgery within 4 wks (1.5)
  • Previous DVT/PE (1.5)
  • Hemotpysis (1)
  • Malignancy (active or treated within 6 mo) (1)

Pre test probability: ≤ 2 low; 2-6 Moderate; >6 High

37
Q

What is the diagnostic approach?

A
  • Chest CT with contrast, PE protocol
  • Less commonly VQ scan
  • Rarely, pulmonary angiogram
  • If negative or inconclusive and clinical suspicion present….

–>further diagnostic testing

  • Evaluate for DVT or perform other diagnostic test.
38
Q

Pros/cons of diagnosing PE with helical/spiral CT?

A

Helical/spiral CT:

Advantages

  • Specificity
  • Availability
  • Safety
  • Relatively rapid
  • Other diagnosis
  • Advancing technology

Limitations:

  • Expense
  • Not portable
  • Need contrast
  • Poor visualization in some areas
  • Contraindication: renal insufficiency/allergy
  • Reader expertise
39
Q

What is a ventilation perfusion scan (VQ scan)?

A
  • Nuclear medicine test to evaluate ventilation (V) and perfusion (Q)
  • “Matched” defects
  • non-diagnostic, compare to x-ray
  • “Unmatched” defects
  • suggestive of perfusion abnormality
40
Q

Describe Pulmonary Angiogram

  • Process
  • Purpose
  • Commonality
A
  • Intra-arterial dye
  • Directly assesses vasculature
  • Rarely used now
41
Q

What do each of these gross pictures show?

A

1- Embolus with infarct

2- Saddle embolus

3- Infarct

42
Q

How can DVT be prevented?

A

Based on level of risk and risk of bleeding

  • Low: (under 10% VTE without prophylaxis) early ambulation only
  • Moderate: (risk of VTE 40%): most general surgical pts or med pts at bedrest; give LMWH, LDUH, fondaparinux or mechanical if bleeding risk high
  • High: orthopedic, major trauma, spinal cord injury; give LMWH, fondaparinux, rivoroxaban, Vit K antagonist; mechanical if bleeding risk high
43
Q

How to treat PE?

A

Anticoagulation

  • Acute
  • Weight-adjusted heparin IV
  • LMWH
  • Long term
  • Warfarin
  • Oral factor XA inhibitors
  • LMWH Thrombolysis

Embolectomy

IVC Filter

44
Q

What is HIT?

  • Mechanism
  • Labs
A

Heparin Induced Thrombocytopenia

  • Immune-mediated drug reaction
  • Results in platelet removal -> thrombocytopenia (most common, 90%)
  • Results in platelet aggregation and release of procoagulant microparticles (thrombosis)
  • Defined by presence of heparin-reactive antibodies to platelet factor 4 (HIT Abs)
45
Q

What are complications of HIT?

A
  • Deep vein thrombosis
  • Pulmonary embolism
  • Myocardial infarction
  • Occlusion of limb arteries (possibly resulting in amputation)
  • Cerebrovascular accidents (stroke, TIA)
  • Skin necrosis
  • End-organ damage (e.g., adrenal, bowel, spleen, gallbladder or hepatic infarction; renal failure)
  • Death
46
Q

What is Warfarin?

  • Mechanism
  • Dynamics/activity
  • Metabolism
  • ASEs
  • Management
  • Reversal
A
  • Antagonizes Vitamin K dependent factors (Factors 2, 7, 9, and 10 as well as protein C and protein S)
  • Delayed effect based on the shortest 1/2 life (Factor 7: 6 hrs); 18-24 hrs
  • Crosses placenta; CONTRAINDICATED in pregnancy
  • Numerous drug-drug, drug-disease (liver), and drug-food (Vit K) interactions
  • Careful monitoring of INR (standardized msmt of PT); usual targeted range is 2-3
  • Reversal with Vitamin K (mild) or FFP
47
Q

What things diminish Warfarin effect? INR level?

A

INR level will be low

  • Inhibits drug absorption: Cholestyramine
  • Increases metabolism (enhance p450): Barbiturates, Carbamazepine, Phenytoin, Rifampin
  • Vitamin K: foods, esp leafy greens
48
Q

What things enhance Warfarin effect? INR level?

A

INR will be high

- Displaces from albumin: choral hydrate

- Decreased metabolism (inhibits p450): Amiodarone, clopidogrel, ethanol, fluconazole, fluoxetine, metronidazole, sulfamethoxazole

- Eliminate gut bacteria and decrease K: Broad-spectrum antibiotics

49
Q

What should the duration of therapy be for ?? (HIT?) (PE?)

A
  • 3 months in patients with transient risk factors
  • May be life long in patients with recurrent thrombosis or continued risk factors (e.g. malignancy, hypercoagulable state)
50
Q

What is an IVC filter? What is it used to treat?

A

IVC filter: treatment of PE

  • Patients with massive PE who could not tolerate a recurrence
  • Patients with contraindications to anticoagulation
  • Recommended for repeat PE despite anticoagulation or when anticoagulation is contraindicated
  • Filter is a wire apparatus inserted through a catheter in the inferior vena cava to prevent PE
  • Filter may be removed
51
Q

What are other therapies for PE?

A
  • Thrombolytic: reserved for patients with massive PE (clinically severe, severe cardio pulmonary compromise, i.e. hemodynamic instability, hypoxemia, RV dysfunction despite resuscitative efforts).
  • Embolectomy
52
Q

Summary of Pulmonary HTN

A
  • Various causes and important to classify based on WHO grouping
  • Treatment will be guided by etiology
  • Progressive shortness of breath, loud P2
  • Idiopathic Pulmonary Arterial HTN pathology is medial hypertrophy and intimal fibrosis
  • Treatment with pulmonary vasodilators and lung transplant
53
Q

Summary of DVT/PE

A
  • Risk factors of prolonged immobility, hypercoagulable states etc.
  • Symptoms of leg swelling, pain in DVT
  • Sudden onset SOB+- pleuritic chest pain with hypoxemia in PE
  • DVT diagnosed with venous compression ultrasonography
  • PE diagnosed by spiral CT or V/Q scan
54
Q

Summary of Pulmonary Vascular Disorders

A
  • Treatment with anticoagulation (UFH, LMWH or Warfarin); Less commonly IVC filter, thrombolysis, embolectomy
  • Major complications of heparin is Heparin induced thrombocytopenia
  • Major complication of Warfarin is drug-drug interactions

MS2 Respiratory (26 decks)

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