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

A
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
Q

long term tx

A

-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
Q

anticoagulant therapy duration

A

-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
Q

thrombolytics

A

-(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
Q

inferior vena cava filter

A

-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
Q

pulmonary circulation is unique

A

-High blood flow
-Low pressure
-Low resistance
-Ability to recruit and distend blood vessels to accommodate high blood flow with little resistance change

30
Q

pulmonary hypertension

A

-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
Q

causes of pulmonary hypertension

A

-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
Q

pulmonary hypertension pathophysiology

A

-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
Q

idiopathic (primary) Pulmonary HTN: signs and symptoms

A

-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
Q

secondary pulmonary hypertension: signs and symptoms

A

-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
Q

exam findings of pulmonary hypertension

A

-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
Q

classification of PH

A

just know general idea

37
Q

pulmonary hypertension labs/dx test

A

-Polycythemia

-Electrocardiographic changes:
-Right axis deviation
-Right ventricular hypertrophy
-Right ventricular strain
-Right atrial enlargement

38
Q

pulmonary hypertension imaging

A

-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
Q

pulmonary hypertension echocardiography

A

-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
Q

pulmonary hypertension work up to rule out secondary causes

A

-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
Q

tx of idiopathic (primary) pulmonary hypertension

A

-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
Q

tx of secondary pulmonary hypertension

A

-Treat the underlying disorder
-+/- O2
-+/- Anticoagulation
-+/- Vasodilator therapy (? Benefits)
-+/- Marked polycythemia tx
-+/- Cor pulmonale tx
-+/- Pulmonary thromboendarterectomy

43
Q

cor pulmonale

A

-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
Q

cor pulmonale symptoms and signs

A

-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
Q

cor pulmonale tests

A

-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
Q

cor pulmonale imaging

A

-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
Q

cor pulmonale tx

A

-Therapy is directed at the pulmonary process responsible for right heart failure
-Oxygen
-Salt and fluid restriction
-Diuretic therapy

48
Q

cor pulmonale tx

A

-Compensated cor pulmonale has same prognosis as the underlying pulmonary disease
-Once congestive signs appear, average life expectancy is 2–5 years