pulmonary circulation Flashcards

1
Q

pulmonary embolism

A

-Complication of thrombus formation within the deep venous circulation

-US: estimated 100,000 deaths/year

-3rd leading cause of death among hospitalized patients

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2
Q

substances that can embolize to pulmonary circulation

A

-Thrombus*
-Air
-Amniotic fluid
-Fat
-Foreign bodies
-Parasite eggs
-Septic emboli
-Tumor cells

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3
Q

PE: thrombus

A

-MC
-Arises anywhere in venous circulation or heart
-Most often originates in deep veins of LE
-20% of calf vein thrombi propagate proximally to popliteal and ileofemoral veins
-May break off and embolize to pulmonary circulation

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4
Q

PE and DVT: risk factors

A

-PE and DVT are 2 manifestations of the same disease.
-70% patients with PE will have DVT on evaluation

-Same risk factors (Virchow’s triad)
-Venous stasis
-Injury to the vessel wall
-Hypercoagulability

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5
Q

what increases venous stasis

A

-immobility
-hyperviscosity
-increased central venous pressures

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6
Q

what damages vessels

A

prior thrombosis, orthopedic surgery, trauma

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7
Q

what causes hypercoagulability

A

-medications
-disease
-inherited genetic defects

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8
Q

pathophysiologic response to PE

A

-Pulmonary emboli are typically multiple, with the lower lobes* being involved in the majority of cases:
-Infarction - 2 circulation to to lungs so this is uncommon
-Abnormal gas exchange
-Cardiovascular compromise- right ventricular strain

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9
Q

PE acute/chronic

A

-Difficult to diagnose
-Depend on size of the embolus and the patient’s preexisting cardiopulmonary status

-Acute:
-develop symptoms and signs immediately after obstruction of pulmonary vessels
-Subacute:
-within days or weeks following the initial event
-Chronic
-slowly develop symptoms of pulmonary hypertension over many years (usually after PE that wasnt fully treated)

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10
Q

most common symptoms and signs of PE

A

-SYMPTOMS
-Dyspnea (rest or exertion) (73 percent)
-Pleuritic pain (44 percent)
-Calf or thigh pain (44 percent)
-Calf or thigh swelling (41 percent)
-Cough (34 percent)
->2-pillow orthopnea (28 percent)
-Wheezing (21 percent)

-SIGNS
-Tachypnea (54 percent)
-Tachycardia (24 percent)
-Rales (18 percent)
-Decreased breath sounds (17 percent)
-Accentuated pulmonic component of the second heart sound (15 percent)
-Jugular venous distension (14 percent)

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11
Q

hemodynamic stability

A

-Hemodynamically unstable PE is that which results in hypotension
-this is not good…
-Hypotension: systolic blood pressure <90 mmHg or
-Drop in systolic BP ≥40 mmHg from baseline for >15 minutes or
-Hypotension requiring vasopressors or inotropic support
-not due to other causes (sepsis, arrhythmia, LV dysfunction from acute myocardial ischemia or infarction, or hypovolemia)

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12
Q

PE-Wells criteria

A
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13
Q

PE dx tests and labs

A

-ECG abnormal (70%)
-Sinus tachycardia and nonspecific ST and T wave changes
-S1Q3T3 pattern

-ABG-Not diagnostic -> Usually hypoxemia, hypocapnia (low CO2), respiratory alkalosis

-Plasma D-dimer:
-sensitive but not specific test -> only helpful when its neg
-if its + it means nothing
-May be elevated in the presence of thrombus (non-specific)
-D-dimer <500 ng/ml has shown a sensitivity for absence of venous thromboembolism of 95–97%

-Leukocytosis, elevated ESR, LDH

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14
Q

PE imaging and special exams

A

-CXR:
-Exclude other common lung diseases
-Need for interpretation of V/ ˙Q scan
-Westermark’s sign-uncommon: A prominent central pulmonary artery with local oligemia
-Hampton’s hump-uncommon: Area of increased opacity that represent intraparenchymal infarct

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15
Q

lung scanning

A

-Perfusion scan:
-inject radiolabeled microaggregated albumin into the venous system, allowing the particles to embolize to the pulmonary capillary bed

-Ventilation scan:
-breathe a radioactive gas or aerosol while the distribution of radioactivity in the lungs is recorded.

-Both scans are interpreted together to give a high, low, or intermediate (indeterminate) probability that PE is the cause of the abnormalities

-look for places that are ventilated but not perfused

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16
Q

PE: lung scanning

A

-Normal perfusion scan: Excludes diagnosis of clinically significant PE

-High-probability scan:
-2 or more segmental perfusion defects in the presence of normal ventilation
-Sufficient for diagnosis of PE in most instances

-Most helpful: normal or high probability of PE

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17
Q

spiral CT pulmonary angiography

A

-MC evaluation
-has supplanted V˙ /Q˙ scanning as the initial diagnostic study
-Very sensitive: Thrombus in proximal pulmonary arteries
-Less sensitive: Distal arteries

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18
Q

pulmonary angiography

A

-Reference standard for the diagnosis of PE

-Definitive Dx:
-An intraluminal filling defect in more than one projection

-Secondary findings highly suggestive of PE:
-Abrupt arterial cutoff
-Asymmetry of blood flow—especially segmental oligemia

-Complications 5%

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19
Q

pulmonary angiography indications

A

-other testing is negative but high clinical suspicion
-Diagnosis of PE must be established with certainty
-Anticoagulation is contraindicated or placement of an inferior vena cava filter is contemplated

-Catheter Based Intervention- Catheter based extraction or thrombolysis

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20
Q

hemodynamically unstable PE that results in hypotension

A

-Hypotension: systolic blood pressure <90 mmHg or
-Drop in systolic BP ≥40 mmHg from baseline for >15 minutes or
-Hypotension requiring vasopressors or inotropic support not due to other causes (sepsis, arrhythmia, LV dysfunction from acute myocardial ischemia or infarction, or hypovolemia)

-look for right ventricle strian

21
Q

approach to PE tx flow chart

22
Q

tx-empiric therapy

A

-Supplemental oxygen: target an O2 sat ≥90%
-Mechanical ventilation
-Severe hypoxemia, hemodynamic collapse, or respiratory failure
-Assess bleeding risk to anticoagulate
-Low risk and stable: Empiric anticoagulation
-Moderate risk and stable: case by case
-High or absolute risk: no empiric therapy

23
Q

tx: PE confirmed

A

-Approach to anticoagulation is based on hemodynamic stability, risk and size of PE
-Stable, low risk, nonmassive: continue anticoagulation in hospital and anticoagulation as outpatient once discharged
-Stable, high risk, nonmassive or contraindication to anticoagulation: inferior vena cava filter
-Stable, mod risk, nonmassive: case by case

-Approach is based on hemodynamic stability, risk and size of PE
-Stable, intermediate risk, submassive: anticoagulated in hospital and monitor closely for deterioration, consider thrombolytic

-Unstable:
-Thrombolytic therapy followed by anticoagulation
-Thrombolysis is contraindicated, surgical or catheter directed embolectomy

24
Q

initial tx: anticoagulation

A

-Options for initial anticoagulation include the following:
-Low molecular weight (LMW) heparin- dosed by weight with no blood testing
-Fondaparinux

-Unfractionated heparin (UFH) - with extreme cases use this bc its backed with blood
-Oral factor 10a/Xa inhibitors or direct thrombin inhibitors -> Rivaroxabanandapixaban

25
long term tx
-Warfarin: -started after therapeutic for heparin/LMWH -affects hepatic synthesis of vitamin K–dependent coagulant proteins (ll, Vll, lX, X, protein C & S) -target INR is 2.5 (2.0 to 3.0) -warfarin is only used in mechanical heart valve pts really -affected by drugs and diet -> need to monitor -other oral anticoagulants Rivaroxaban (Xarelto) Apixaban (Eliquis) Dabigatran (Pradaxa) Edoxaban (Savaysa)
26
anticoagulant therapy duration
-At least 3 months after first episode when REVERSABLE risk factor -12 months after a first-episode idiopathic thrombus -6–12 months to indefinitely in patients with nonreversible risk factors or recurrent disease
27
thrombolytics
-(streptokinase, urokinase, rt-PA) -Patients at high risk for death -Rapid resolution may be lifesaving -Absolute contraindications: Active internal bleeding and stroke within past 2 months -Major contraindications: -Uncontrolled hypertension, surgery or trauma within the past 6 weeks
28
inferior vena cava filter
-Absolute contraindication to anticoagulation -Recurrent PE despite adequate anticoagulant therapy -Complication of anticoagulation -Hemodynamic or respiratory compromise where recurrent PE could be lethal -Done with surgical pulmonary thromboendarterectomy
29
pulmonary circulation is unique
-High blood flow -Low pressure -Low resistance -Ability to recruit and distend blood vessels to accommodate high blood flow with little resistance change
30
pulmonary hypertension
-Inappropriate pulmonary artery pressure for a given cardiac output -Pulmonary hypertension classification: -Mild: mean PA pressure is > 25 mm Hg -Moderate > 30 mm Hg MAP -Severe > 45 mm Hg MAP
31
causes of pulmonary hypertension
-1. MC cause is left heart disease (pulmonary venous hypertension PVH) -> back up into pulmonary circulation -left heart disease- systolic/diastolic dysfunction, valvular disease, congenital -2. chronic hypoxia -3. chronic thromboembolic pulmonary hypertension (CTEPH)- clots -4. pulmonary arterial hypertension- TREATABLE with pulmonary vasodilator (uncommon!)
32
pulmonary hypertension pathophysiology
-Idiopathic or identifiable (secondary) cause -Causes structural abnormalities in pulmonary vessels -Smooth muscle hypertrophy -Intimal proliferation -May stimulate atheromatous changes and in situ thrombosis -pulmonary artery problem -End result: narrows arterial bed and increases pressure
33
idiopathic (primary) Pulmonary HTN: signs and symptoms
-Typically young women, evidence of right heart failure that is usually progressive -> Leading to death in 2–8 years -Patients have manifestations of low cardiac output: -Weakness, Fatigue -Edema -Retrosternal CP -Ascites (advanced ds) -Peripheral cyanosis -Syncope
34
secondary pulmonary hypertension: signs and symptoms
-known cause -Difficult to recognize clinically in early stages -S/s primarily of underlying disease -May cause or contribute to: -Dyspnea -Chest pain -Fatigue and syncope
35
exam findings of pulmonary hypertension
-Expiratory splitting of S2 -Accentuation of pulmonary component of S2 -Advanced cases -tricuspid and pulmonary valve insufficiency -signs of right ventricular failure/cor pulmonale
36
classification of PH
just know general idea
37
pulmonary hypertension labs/dx test
-Polycythemia -Electrocardiographic changes: -Right axis deviation -Right ventricular hypertrophy -Right ventricular strain -Right atrial enlargement
38
pulmonary hypertension imaging
-Chest radiographs and high-resolution CT scans: -Diagnosis of pulmonary hypertension and determination of the secondary cause -In chronic disease: Dilation of the right and left main and lobar pulmonary arteries and enlargement of pulmonary outflow tract -In advanced disease: Right ventricular and right atrial enlargement
39
pulmonary hypertension echocardiography
-Secondary causes: Mitral stenosis, left atrial myxoma, and pulmonary valvular disease, shunt -Severity of ds: May reveal right ventricular enlargement and paradoxical motion of interventricular septum
40
pulmonary hypertension work up to rule out secondary causes
-LFTs -HIV test -Collagen-vascular serologic studies -Polysomnography -V/Q lung scanning, CTA -Surgical lung biopsy ****Right heart cath for definitive dx -pulmonary artery and left side of heart will be high
41
tx of idiopathic (primary) pulmonary hypertension
-Until recently has been lung transplantation -Currently, a variety of therapeutic options are now available and approved -Anticoagulation -Supplemental oxygen esp.night -Diuretics -Pulmonary Vasodilators****: only for true group 1 pulmonary arterial hypertension -Prostacyclines: epoprostenol, treprostinil, and iloprost, -PDE-5 Inhibitors: sildenafil, tadalafil -Endothelial antagonists: Bosentan, Ambrisentan, Macitentan -Calcium Channel Blockers
42
tx of secondary pulmonary hypertension
-Treat the underlying disorder -+/- O2 -+/- Anticoagulation -+/- Vasodilator therapy (? Benefits) -+/- Marked polycythemia tx -+/- Cor pulmonale tx -+/- Pulmonary thromboendarterectomy
43
cor pulmonale
-RV hypertrophy and eventual failure from pulmonary disease (group 3 PH) or from pulmonary hypertension -Most common causes: hypoxemia -Pulmonary hypertension -Chronic obstructive pulmonary disease -Idiopathic pulmonary fibrosis
44
cor pulmonale symptoms and signs
-Fatigue, lethargy, and exertional syncope -Exertional angina -Cough, hemoptysis, hoarseness -RUQ pain -Increased intensity of pulmonic component of S2 -RV heave or gallop -Cyanosis -Clubbing -Distended neck veins -Prominent lower sternal or epigastric pulsations -An enlarged and tender liver, and dependent edema
45
cor pulmonale tests
-CBC: Polycythemia -ABG: -Arterial oxygen saturation is often below 85% -PCO2 may or may not be elevated -ECG may show: -Right axis deviation and peaked P waves -Incomplete or complete RBBB -+/- RVH -Supraventricular arrhythmias
46
cor pulmonale imaging
-Chest radiograph: -Discloses presence or absence of lung disease -Prominent or enlarged RV and PA -PFT: May confirm underlying lung disease -Echocardiogram: Normal LV size and function BUT RV hypertrophyZ & RA dilation -Right Heart Catheterization: Gold standard: indicated when the necessary information cannot be obtained with echo
47
cor pulmonale tx
-Therapy is directed at the pulmonary process responsible for right heart failure -Oxygen -Salt and fluid restriction -Diuretic therapy
48
cor pulmonale tx
-Compensated cor pulmonale has same prognosis as the underlying pulmonary disease -Once congestive signs appear, average life expectancy is 2–5 years