PE + Pulmonary HTN + Cor Pulmonale Flashcards

1
Q

pulmonary embolism def + description

A

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

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2
Q

substances that can embolize to pulmonary circulation

A

-Thrombus* (MC) -> most pts have DVT and PE

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

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3
Q

PE and DVT: risk factors

A

Risk factors = Virchow’s triad
-Venous stasis
-Injury to the vessel wall
-Hypercoagulability

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4
Q

what increases venous stasis

A

-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)

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5
Q

what damages vessels

A
  • prior thrombosis
  • orthopedic surgery
  • trauma
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6
Q

what causes hypercoagulability

A

-medications
-disease
-genetic defects

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7
Q

pathophysiologic response to PE

A

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

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8
Q

PE typically present as ______.

PE affects which lobes?

A
  • PE typically present in multiples!!!!
  • Often affects LOWER LOBES- Lobes of greater perfusion
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9
Q

PE signs and symptoms

A

-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

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10
Q

PE presentation: acute vs subactue vs chronic

A

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

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11
Q

most signs of PE

A

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)

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12
Q

hemodynamically unstable PE

A

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

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13
Q

PE-Wells criteria

A

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

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14
Q

PE: abg

A

ABG: NOT diagnostic
- hypoxemia
- hypocapnia (low CO2)
- respiratory ALKALOSIS -> tachypnea

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15
Q

PE EKG

A

Abnormal in 70%!!!
-Sinus tachycardia and nonspecific ST and T wave changes
-S1Q3T3 pattern

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16
Q

Plasma D-dimer: PE

A

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

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17
Q

PE: lab values

A

-Leukocytosis: increase WBC
- elevated ESR: inflammation
- LDH: nonspecific tissue damage

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18
Q

PE CXR

A

-Excludes other common lung diseases
-Need for interpretation of V/ ˙Q scan
-Westermark’s sign
-Hampton’s hump: uncommon

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19
Q

Westermark’s sign

A

Prominent central pulmonary artery [black arrow] with local oligemia (Decrease in lung markings) [white arrow]

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20
Q

Hampton’s Hump

A

PE sign:

Increased opacity that represents intraparenchymal infarct
Hard to differentiate from consolidation in Pn

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21
Q

Ventillation-perfusion (V/Q) scan

A

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.

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22
Q

spiral CT pulmonary angiography

A

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”

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23
Q

pulmonary angiography

A

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

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24
Q

pulmonary angiography indications

A

-Other testing is negative, but high clinical suspicion
-Anticoagulation is contraindicated
- Placement of IVC filter is contemplated
- Catheter based extraction or thrombolysis

25
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
26
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
27
PE: Stable, intermediate risk, submassive tx
Stable, intermediate risk, SUBMASSIVE: - anticoagulated in hospital and monitor closely for deterioration - consider thrombolytic
28
PE: unstable PE tx
-Thrombolytic therapy followed by anticoagulation -if thrombolysis is contraindicated: surgical/catheter directed embolectomy
29
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
30
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)
31
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
32
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
33
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
34
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
35
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
36
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
37
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
38
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)
39
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
40
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
41
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
42
WHO classification of PH: functional classification
just know general idea -- Class 1 : Without limitations Class 2: Slight Limitation Class 3:Significant Limitation Class 4: Severe Limitation
43
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
44
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
45
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
46
Definitive dx of PHTN
**Right heart catheterization for definitive dx -pulmonary artery and left side of heart will be high
47
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
48
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
49
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
50
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
51
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
52
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)
53
cor pulmonale EKG
EKG: -Right axis deviation and peaked P waves -Incomplete or complete RBBB - SVT arrhythmias -+/- RVH
54
cor pulmonale CBC, ABG, PFT
CBC: Polycythemia- High hemoglobin/RBCs ABG: Hypoxemia, PCO2 may be elevated PFT: May confirm underlying lung disease
55
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
56
Right Heart Catheterization: cor pulmonale
Gold standard!!!: -Indicated when echo cannot provide sufficient info
57
cor pulmonale tx
- Treat pulmonary process causing Right HF - O2 - Salt/Fluid Restriction = ↓ CO - Diuretic therapy
58
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
59
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