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
Q

PE tx-empiric therapy: o2, vent, anticoagulate

A

-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
Q

PE confirmed tx: stable pt, nonmassive, and varied risk what is the anticoagulation tx

A

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
Q

PE: Stable, intermediate risk, submassive tx

A

Stable, intermediate risk, SUBMASSIVE:
- anticoagulated in hospital and monitor closely for deterioration
- consider thrombolytic

28
Q

PE: unstable PE tx

A

-Thrombolytic therapy followed by anticoagulation
-if thrombolysis is contraindicated: surgical/catheter directed embolectomy

29
Q

initial tx: anticoagulation

A

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
Q

long term anticoagulant tx

A

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
Q

anticoagulant therapy duration for PE

A

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
Q

thrombolytics indications and drug names

A

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
Q

thrombolytics absolute CI and major CI

A

Absolute CI:
-Active internal BLEEDING and STROKE within past 2 MONTHS

Major contraindications:
-Uncontrolled HTN
- surgery or trauma within the past 6 weeks

34
Q

inferior vena cava filter

A

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
Q

pulmonary circulation is unique

A

-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
Q

pulmonary hypertension + scale (mild, mod, severe)

A

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
Q

Classification of P HTN

A

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
Q

pulmonary hypertension pathophysiology of group 1

A

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
Q

idiopathic Pulmonary HTN: presentation and symptoms

A

-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
Q

secondary pulmonary hypertension: signs and symptoms

A

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
Q

exam findings of pulmonary hypertension

A

-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
Q

WHO classification of PH: functional classification

A

Class 1 : Without limitations
Class 2: Slight Limitation
Class 3:Significant Limitation
Class 4: Severe Limitation

43
Q

pulmonary hypertension labs + EKG

A

POLYCYTHEMIA: increase in RBCs from chronic hypoxia

EKG: basically R hypertrophy
-Right axis deviation
-Right ventricular + atrial hypertrophy
-Right ventricular strain

44
Q

pulmonary hypertension CXRAY and HRCT

A

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
Q

pulmonary hypertension echocardiography

A

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
Q

Definitive dx of PHTN

A

**Right heart catheterization for definitive dx
-pulmonary artery and left side of heart will be high

47
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

48
Q

tx of idiopathic (primary) pulmonary hypertension

A

-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
Q

tx of secondary pulmonary hypertension

A

Treat the underlying disorder: left heart ds + PHTN

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

50
Q

cor pulmonale definition and causes

A

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
Q

cor pulmonale symptoms

A

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
Q

cor pulmonale signs

A

-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
Q

cor pulmonale EKG

A

EKG:
-Right axis deviation and peaked P waves
-Incomplete or complete RBBB
- SVT arrhythmias
-+/- RVH

54
Q

cor pulmonale CBC, ABG, PFT

A

CBC: Polycythemia- High hemoglobin/RBCs

ABG: Hypoxemia, PCO2 may be elevated

PFT: May confirm underlying lung disease

55
Q

cor pulmonale chest xray and echo

A

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
Q

Right Heart Catheterization: cor pulmonale

A

Gold standard!!!:
-Indicated when echo cannot provide sufficient info

57
Q

cor pulmonale tx

A
  • Treat pulmonary process causing Right HF
  • O2
  • Salt/Fluid Restriction = ↓ CO
  • Diuretic therapy
58
Q

cor pulmonale prognosis

A

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

59
Q

when is right heart catherization the most definitive dx

A

Cor pulmonale:
- when echo doesn’t provide sufficient information

Pulmonary HTN:
- the most definitive dx of PHTN