PE + Pulmonary HTN + Cor Pulmonale Flashcards
pulmonary embolism def + description
Definition: A result of a thrombus formation within deep venous circulation traveling into pulmonary circulation
Description:
-3rd leading cause of death among hospitalized patients
- most pts will have PE and DVT on evaluation
- PE typically present in multiples!!!!
- Often affects LOWER LOBES- Lobes of greater perfusion
substances that can embolize to pulmonary circulation
-Thrombus* (MC) -> most pts have DVT and PE
-Air
-Amniotic fluid
-Fat
-Foreign bodies
-Parasite eggs
-Septic emboli
-Tumor cells
PE and DVT: risk factors
Risk factors = Virchow’s triad
-Venous stasis
-Injury to the vessel wall
-Hypercoagulability
what increases venous stasis
-immobility** * (pts in bed)
-hyperviscosity
-increased central venous pressures
bloodflow through veins slows down when you dont move at all, blood is too thick, when you have a condition that causes too much blood in veins (HF, obese)
what damages vessels
- prior thrombosis
- orthopedic surgery
- trauma
what causes hypercoagulability
-medications
-disease
-genetic defects
pathophysiologic response to PE
PE are typically multiple, with lower lobes being involved in majority of the cases
–Abnormal gas exchange
- Cardiovascular compromise: right ventricular strain
- infarction (rare)
Infarction - RARE
- 2 circulations to lungs so rare
- need large PE
PE typically present as ______.
PE affects which lobes?
- PE typically present in multiples!!!!
- Often affects LOWER LOBES- Lobes of greater perfusion
PE signs and symptoms
-Difficult to diagnose
-Depend on size of the embolus and the patient’s preexisting cardiopulmonary status
MC:
- dyspnea (on rest or exertion)
- SOB
- CALF/THIGH PAIN or SWELLING
- Orthopnea: >2 pillows at night
PE presentation: acute vs subactue vs chronic
Acute
- S/S present IMMEDIATELY after obstruction of pulmonary vessels
Subacute
- S/S present within DAYS or WEEKS following initial event
Chronic
S/S slowly develop over many YEARS
most signs of PE
Signs:
-Tachypnea (MC)
-Tachycardia (24 percent)
-Rales (18 percent)
-Decreased breath sounds (17 percent)
-Accentuated pulmonic component of the second heart sound (ddx with PHTN)*
-JVD (14 percent)
hemodynamically unstable PE
PE 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
PE-Wells criteria
How to determine Probability of Pulmonary Embolism:
“DA PITCH”
- DVT signs + synmptoms: 3
-Alternative Dx not likely: 3 - Previous DVT/PE: 1.5
- Immobilization > 3 days: 1.5
- Tachycardia: 1.5
- Cancer with active tx: 1
- Hemoptysis: 1
If < 4 Pts = PE Unlikely
If > 4 Pts = PE Likely
PE: abg
ABG: NOT diagnostic
- hypoxemia
- hypocapnia (low CO2)
- respiratory ALKALOSIS -> tachypnea
PE EKG
Abnormal in 70%!!!
-Sinus tachycardia and nonspecific ST and T wave changes
-S1Q3T3 pattern
Plasma D-dimer: PE
Very sensitive but non specific: ONLY HELPFUL IF ITS NEGATIVE!!!!
-May be elevated in the presence of thrombus (non-specific)
- D-dimer is used to r/o diagnosis of PE if <500 ng/mL
–
PE: lab values
-Leukocytosis: increase WBC
- elevated ESR: inflammation
- LDH: nonspecific tissue damage
PE CXR
-Excludes other common lung diseases
-Need for interpretation of V/ ˙Q scan
-Westermark’s sign
-Hampton’s hump: uncommon
Westermark’s sign
Prominent central pulmonary artery [black arrow] with local oligemia (Decrease in lung markings) [white arrow]
Hampton’s Hump
PE sign:
Increased opacity that represents intraparenchymal infarct
Hard to differentiate from consolidation in Pn
Ventillation-perfusion (V/Q) scan
Perfusion scan:
- Inject radiolabeled albumin into the venous system
- normal scan: exclude dx of clinically significant PE
- > 2 segmental perfusion defects with normal ventilation is highly suggestive of PE
Ventilation scan:
- Breathe a radioactive gas/ 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.
spiral CT pulmonary angiography
MC evaluation: GOLDEN STANDARD
- Very sensitive in proximal pulm arteries
- Less sensitive in distal arteries
- normal chest CT not adequate to exclude PE
“spiral-> more important for center and the ends not as sensitive”
pulmonary angiography
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
pulmonary angiography indications
-Other testing is negative, but high clinical suspicion
-Anticoagulation is contraindicated
- Placement of IVC filter is contemplated
- Catheter based extraction or thrombolysis
PE tx-empiric therapy: o2, vent, anticoagulate
-Supplemental oxygen: target an O2 sat ≥90%
Mechanical ventilation
-Severe hypoxemia
- hemodynamic collapse
- 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 tx, wait till CT angiography
PE confirmed tx: stable pt, nonmassive, and varied risk what is the anticoagulation tx
Approach to anticoagulation is based on hemodynamic stability, risk, and size of PE
Stable, low risk, nonmassive:
- Empiric Anticoagulation
- continue anticoagulation in hospital and anticoagulation as outpatient once discharged
Stable, mod risk, nonmassive: - case by case
Stable, high risk, nonmassive or contraindication to anticoagulation:
- No empiric therapy, wait till CT angiography
- IVC filter
PE: Stable, intermediate risk, submassive tx
Stable, intermediate risk, SUBMASSIVE:
- anticoagulated in hospital and monitor closely for deterioration
- consider thrombolytic
PE: unstable PE tx
-Thrombolytic therapy followed by anticoagulation
-if thrombolysis is contraindicated: surgical/catheter directed embolectomy
initial tx: anticoagulation
Low molecular weight (LMW) heparin*
- Longer Half-life = Harder to control
-dosed by weight with no blood testing
Fondaparinux*
Oral factor Xa inhibitors or direct thrombin inhibitors
– Rivaroxaban
- apixaban
Unfractionated heparin (UFH): rarely
long term anticoagulant tx
WARFARIN/coumadin:
-start after LMW Heparin
-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 usually
-affected by drugs and diet -> need to monitor
Other oral anticoagulants
Rivaroxaban (Xarelto)
Dabigatran (Pradaxa)
Edoxaban (Savaysa)
anticoagulant therapy duration for PE
At least 3 months:
- first episode with REVERSIBLE risk factor
12 months:
- first episode of idiopathic thrombus
6–12 months to indefinitely:
- nonreversible risk factors
- recurrent disease
thrombolytics indications and drug names
Indication:
- unstable PE
-Patients at high risk for death
-Rapid resolution may be lifesaving
-stable, moderate risk, submassive (consider)
Drug names:
- Streptokinase
- Urokinase
- rt-PA
thrombolytics absolute CI and major CI
Absolute CI:
-Active internal BLEEDING and STROKE within past 2 MONTHS
Major contraindications:
-Uncontrolled HTN
- surgery or trauma within the past 6 weeks
inferior vena cava filter
Purpose: Prevent DVT from traveling to lungs; physical filter catches emboli
Indications:
- Recurrent PE despite anticoagulant therapy
- pts cannot tolerate anticoagulation therapy
- Hemodynamic/Respiratory compromise where a recurrent PE can be lethal
Surgery name to insert IVC filter:
- pulmonary thromboendarterectomy
pulmonary circulation is unique
-High blood flow:
-LOW pulmonary artery pressure
-LOW vascular resistance: blood can flow easily for efficient gas exchange
-Ability to recruit and distend blood vessels to accommodate high blood flow with little resistance change
pulmonary hypertension + scale (mild, mod, severe)
Definition:
- Inappropriate pulmonary artery pressure for a given CO
Pulmonary hypertension classification:
-Mild: mean pulmonary arterial pressure is > 25 mm Hg
-Moderate > 30 mm Hg MAP
-Severe > 45 mm Hg MAP
——-
mild: 25
mod: 30
severe: 45
Classification of P HTN
1) PHTN
- pre-capillary issue with pulmonary arteries
2) PHTN + LEFT heart ds (MC!! 75%)*
- Post capillary back up increase pressure
3) PHTN + LUNG ds or hypoxia *
4) PHTN + Chronic THROMBOTIC or EMBOLIC ds -> chronic clots
5) miscellaneous
pulmonary hypertension pathophysiology of group 1
A STRUCTURAL abnormalities in pulmonary vessels
- could be idiopathic or secondary cause
-Smooth muscle hypertrophy from increased pressure
-Intimal proliferation
-May stimulate formation of plaque within the arteries changes and clot formations within vessels
End result: NARROW arterial bed and increases pressure!!! -> possible R heart failure (cor pulmonale)
idiopathic Pulmonary HTN: presentation and symptoms
-Typically young women,
- evidence of progressive right HF (peripheral edema) that is usually progressive -
- Leading to death in 2–8 years
SX of low CO:
-Weakness, Fatigue
-Edema
-Retrosternal CP
-Ascites (advanced ds)
-Peripheral cyanosis
-Syncope
secondary pulmonary hypertension: signs and symptoms
Difficult to recognize clinically in early stages
-S/s primarily of UNDERLYING disease
May cause or contribute to basic sx:
-Dyspnea
-Chest pain
-Fatigue and syncope
exam findings of pulmonary hypertension
-Expiratory splitting of S2
-Accentuation of pulmonary component of S2 (DDx with PE)
Advanced cases
-tricuspid and pulmonary valve insufficiency
-signs of right ventricular failure/cor pulmonale
——-
Splitting of S2 heart sound: suggests abnormal delay in pulmonary valve closure
tricuspid and pulmonary valve insufficiency: backflow worsens R HF signs
WHO classification of PH: functional classification
Class 1 : Without limitations
Class 2: Slight Limitation
Class 3:Significant Limitation
Class 4: Severe Limitation
pulmonary hypertension labs + EKG
POLYCYTHEMIA: increase in RBCs from chronic hypoxia
EKG: basically R hypertrophy
-Right axis deviation
-Right ventricular + atrial hypertrophy
-Right ventricular strain
pulmonary hypertension CXRAY and HRCT
CXR & HRCT:
- Used to diagnosis PH and determine secondary cause
Chronic disease:
- Dilation of right & left main and lobar pulmonary arteries
Advanced disease:
- Right ventricular & right atrial enlargement
pulmonary hypertension echocardiography
Secondary causes:
- Mitral stenosis
- left atrial myxoma: heart tumor
- pulmonary valvular disease
- left to right shunt
Severity of ds:
- right ventricular enlargement
- paradoxical motion of interventricular septum
Definitive dx of PHTN
**Right heart catheterization for definitive dx
-pulmonary artery and left side of heart will be high
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
tx of idiopathic (primary) pulmonary hypertension
-Until recently has been lung transplantation
Pulmonary Vasodilators**: only for true group 1 PHTN
-Prostacyclines: epoprostenol, treprostinil, and iloprost,
-PDE-5 Inhibitors: sildenafil, tadalafil
-Endothelial antagonists: Bosentan, Ambrisentan, Macitentan
-Calcium Channel Blockers
other tx:
-Anticoagulation
-Supplemental oxygen esp.night
-Diuretics
tx of secondary pulmonary hypertension
Treat the underlying disorder: left heart ds + PHTN
-+/- O2
-+/- Anticoagulation
-+/- Vasodilator therapy (? Benefits)
-+/- Marked polycythemia tx
-+/- Cor pulmonale tx
-+/- Pulmonary thromboendarterectomy
cor pulmonale definition and causes
Definition:
- RV hypertrophy causing RIGHT heart failure due to pulmonary ds (group 3 PHTN) or from pulmonary hypertension
- lung ds or HTN -> increased pressure from pulmonary arteries -> RV hypertrophy -> Right HF
Most common causes: hypoxemia
-Pulmonary HTN
-Chronic obstructive pulmonary disease
-Idiopathic pulmonary fibrosis
cor pulmonale symptoms
Sx due to underlying pulmonary conditions:
-Cough
-hemoptysis
Sx due to right HF:
- exertional syncope*
-Exertional angina *
-RUQ pain*
- Fatigue, lethargy
- hoarseness from compression of enlarged R atrium
cor pulmonale signs
-Increased intensity of pulmonic component of S2
-RV heave or gallop: R ventricle hypertrophy
-Prominent lower sternal or epigastric pulsations: R ventricle hypertrophy
-Cyanosis
-Clubbing: lung ds
-Distended neck veins (HF)
-enlarged/ tender LIVER* (HF)
cor pulmonale EKG
EKG:
-Right axis deviation and peaked P waves
-Incomplete or complete RBBB
- SVT arrhythmias
-+/- RVH
cor pulmonale CBC, ABG, PFT
CBC: Polycythemia- High hemoglobin/RBCs
ABG: Hypoxemia, PCO2 may be elevated
PFT: May confirm underlying lung disease
cor pulmonale chest xray and echo
Chest xray:
-Discloses presence or absence of lung disease
-enlarged RV and pulmonary artery
Echocardiogram:
- RV hypertrophy & RA dilation
- Normal LV size and function
Right Heart Catheterization: cor pulmonale
Gold standard!!!:
-Indicated when echo cannot provide sufficient info
cor pulmonale tx
- Treat pulmonary process causing Right HF
- O2
- Salt/Fluid Restriction = ↓ CO
- Diuretic therapy
cor pulmonale prognosis
-Compensated cor pulmonale has same prognosis as the underlying pulmonary disease
-Once congestive signs appear, average life expectancy is 2–5 years
when is right heart catherization the most definitive dx
Cor pulmonale:
- when echo doesn’t provide sufficient information
Pulmonary HTN:
- the most definitive dx of PHTN
