Bonnies exam Pulmonary embolism, Pulmonary Edema, Pulmonary hypertension

What structural changes occur in the lungs during pulmonary edema?

Alveolar wall and interstitial swelling, increased surface tension, atelectasis, frothy sputum.

What are the two major categories of pulmonary edema?

Cardiogenic and Noncardiogenic.

What is the most common cause of cardiogenic pulmonary edema?

Left-sided heart failure (Congestive Heart Failure).

What LVEF percentage is considered life-threatening?

Less than 35%.

What causes increased capillary permeability in noncardiogenic pulmonary edema?

Alveolar hypoxia, ARDS, toxic inhalation, infections, radiation, acute head injury.

What is decompression pulmonary edema?

Sudden removal of pleural effusion.

What are symptoms of chronic CHF?

Dyspnea, orthopnea, fatigue, muscle weakness, low LVEF, low BP, central sleep apnea.

What lab abnormalities are associated with left-sided heart failure?

Hyponatremia, hypochloremia, hypokalemia.

What biomarker confirms CHF diagnosis?

BNP (Brain Natriuretic Peptide).

What BNP level indicates severe CHF?

Above 900 pg/mL.

What chest x-ray findings indicate cardiogenic pulmonary edema?

Cardiomegaly, Kerley lines, Bat's wings, fluffy opacities.

What x-ray features distinguish noncardiogenic pulmonary edema?

No cardiomegaly, no pleural effusion, fluffy densities near hilum.

What is the initial treatment focus for noncardiogenic pulmonary edema?

Support ventilation and oxygenation.

What medications reduce preload in cardiogenic pulmonary edema?

Nitroglycerin, loop diuretics, morphine sulfate.

What medications reduce afterload

Captopril, Enalapril, Nitroprusside.

What are the three positive inotropic agents and their uses?

Dobutamine (mild hypotension),

Dopamine (moderate),

Norepinephrine (severe).

What medication treats bradycardia?

Atropine.

What medications treat tachycardia?

Digitalis,

procainamide,

metoprolol.

What is the FiO₂ range for nasal cannula

22-45%;

What is the FiO2 range for HFNC?

35-90%.

What therapy is indicated for impending ventilatory failure?

Lung expansion therapy (IS, CPAP, PEP, IPPB, HFNC).

How do you choose a ventilatory strategy based on ABG?

Determine if the issue is oxygenation (hypoxemia) or ventilation (hypercapnia).

What is a saddle embolus?

A large embolus lodged at the bifurcation of the pulmonary artery.

What is Virchow's Triad?

Venous stasis,

hypercoagulability,

endothelial injury.

What are non-blood sources of emboli?

Fat, air, amniotic fluid, bone marrow, tumor fragments.

What are risk factors for PE?

Inactivity, surgery, trauma, hypercoagulation disorders.

What tests diagnose PE?

D-dimer, ultrasound, CTPA, V/Q scan, angiogram, MRI/MRA.

What does an elevated D-dimer indicate?

Possible clot; normal level rules out PE.

What is the first-line test for PE?

CT Pulmonary Angiography (CTPA).

What lung sounds may be heard in PE?

Crackles, wheezes, pleural friction rub.

What ECG findings are associated with PE?

Sinus tachycardia, atrial arrhythmias, RBBB, P pulmonale.

What chest x-ray findings may indicate PE?

Increased density, hyperradiolucency, pulmonary artery dilation, edema, cor pulmonale.

Which heparin type is preferred for DVT prophylaxis?

Low molecular weight heparin.

What are the four thrombolytic agents?

Streptokinase, Urokinase, Alteplase, Reteplase.

What dietary advice is given to patients on Warfarin?

Avoid foods high in vitamin K (leafy greens, liver, grapefruit, green tea).

Are Greenfield filters recommended to prevent PE?

Yes, to prevent clots from reaching pulmonary circulation.

What defines pulmonary hypertension?

Mean pulmonary artery pressure > 25 mm Hg.

What are the five classifications of PH?

-PAH,
-PH due to left heart disease,
-PH due to lung disease/hypoxia,
-chronic thromboembolic PH,
-PH with unclear mechanisms.

What are common symptoms of PH?

Dyspnea, fatigue, chest pain, syncope, hemoptysis, hoarseness.

What therapies treat PH?

Diuretics, phosphodiesterase inhibitors, blood thinners, digoxin.

What are signs of right-sided heart failure?

JVD, peripheral edema, hepatomegaly, ascites, pitting edema.

What are signs of left-sided heart failure?

Crackles, orthopnea, frothy sputum, hypotension, cyanosis.

Pulmonary Edema

Produces a restrictive lung disorder characterized by swelling of alveolar walls and interstitial spaces due to fluid movement.

Atelectasis

Occurs as a result of increased surface tension due to swelling in pulmonary edema.

Frothy Sputum

Fluid that accumulates in the tracheobronchial tree, which may be white, blood-tinged, or pink.

Cardiogenic Pulmonary Edema

A type of pulmonary edema caused by left-sided heart failure leading to engorgement of capillaries.

Noncardiogenic Pulmonary Edema

A type of pulmonary edema not caused by heart failure.

Left Ventricular Ejection Fraction (LVEF)

A measurement where LVEF less than 40% may confirm heart failure, and less than 35% is life threatening.

Transudate

Refers to fluid that leaks from pulmonary capillaries into the alveoli due to lung damage and inflammation.

Increased Capillary Permeability

A condition that may lead to pulmonary edema caused by factors such as infection, hypoxia, and inhalation of toxic agents.

Decompression Pulmonary Edema

Occurs due to the sudden removal of a pleural effusion.

Symptoms of Congestive Heart Failure (CHF)

Include external dyspnea, orthopnea, fatigue, skeletal muscle weakness, and lower LVEF.

Hyponatremia

A possible abnormal lab result from left-sided heart failure, which may result from diuretic therapy or fluid retention.

Brain Natriuretic Peptide (BNP)

A biomarker that helps establish the diagnosis of CHF.

Severe CHF

Characterized by BNP levels above 900 pg/mL.

Moderate CHF

Characterized by BNP levels above 600 pg/mL.

Chest X-ray Features of Cardiogenic Pulmonary Edema

Includes pulmonary venous congestion, cardiomegaly, engorgement of pulmonary arteries, and Kerley A and B lines.

Fluffy Densities

Appear on chest x-ray in noncardiogenic pulmonary edema, often near the hilum.

Differences in Chest X-ray

Cardiogenic pulmonary edema shows cardiomegaly and pleural effusion, while noncardiogenic does not.

Treatment of Noncardiogenic Pulmonary Edema

Initial management focuses on supporting ventilation and oxygenation.

High-altitude pulmonary edema (HAPE)

Treated by returning the patient to a lower elevation or by supplemental oxygen and positive-pressure ventilation.

Cardiogenic treatment

Initial management includes agents such as digitalis, supplemental oxygen, assisted ventilation if necessary, and loop diuretics for volume overload.

Preload reducers

Reduce pulmonary venous return, decreasing pulmonary capillary hydrostatic pressure and fluid transudation into the pulmonary interstitium and alveoli.

Nitroglycerin

A very effective, predictable, and rapid-acting medication for preload reduction.

Loop diuretics

Considered cornerstone in the treatment of cardiogenic pulmonary edema, presumed to decrease preload through diuresis and direct vasodilation.

Morphine sulfate

May be used to reduce preload but has adverse effects such as nausea, vomiting, or respiratory depression.

Afterload reducers

Reduce systemic vascular resistance, increasing cardiac output and improving renal perfusion, allowing for diuresis.

Captopril

Prevents the conversion of angiotensin I to angiotensin II and is a potent vasodilator.

Enalapril (Vasotec)

A competitive angiotensin converting enzyme (ACE) inhibitor that reduces angiotensin II levels.

Nitroprusside (Nitropress)

A potent, direct, smooth muscle-relaxing agent that primarily reduces afterload and can mildly reduce preload.

Positive inotropic agents

Used for vasodilation effects and to increase myocardial contraction and cardiac output.

Dobutamine

Commonly used for patients with mild hypotension (systolic blood pressure 90 to 100 mm Hg).

Dopamine

Generally reserved for patients with moderate hypotension (systolic blood pressure 70 to 90 mm Hg).

Norepinephrine

Generally reserved for patients with severe hypotension (systolic blood pressure less than 70 mm Hg).

Antidysrhythmic agents

Atropine can be given to treat bradycardia.

Digitalis, procainamide, or metoprolol

Examples of medications that might be used to treat tachycardia.

Lung expansion therapy

Indicated for patients with pulmonary edema that have an ABG indicating impending ventilatory failure.

Ventilatory strategy decision questions

Consider whether the patient is having an oxygenation or ventilation issue.

Hypoxemic respiratory failure

Treated with various oxygen therapy modalities to manage patients' oxygenation status.

Hypercapnic respiratory failure

Treated with ventilatory support techniques that mechanically breathe for the patient to manage the PaCO2 level and acid-base status.

Continuous mechanical ventilation

Justified when acute ventilatory failure is thought to be reversible.

Alteplase

A fibrinolytic agent that dissolves blood clots.

Systemic agent

Commonly referred to as clot-busters, beneficial in treating acute pulmonary embolism.

Biventricular failure

Combination of left-sided and right-sided heart failure.

Cor Pulmonale

Right-heart failure.

d-dimer blood test

Also called fibrinogen test, used to check for an increased level of the protein fibrinogen, an integral component of the blood-clotting process.

Deep vein thrombosis (DVT)

Insidious disorder where most pulmonary blood clots originate or break away from sites of deep venous thrombosis in the lower part of the body.

Thrombus

A blood clot that forms and remains in a vein.

Embolus/embolism

A blood clot that becomes dislodged and travels to another part of the body.

Virchow Triad

Three primary factors associated with the formation of DVT: venous stasis, hypercoagulation, and injury to the endothelial cells.

Saddle embolus

When a large embolus detaches from a thrombus and passes through the right side of the heart, it may lodge in the bifurcation of the pulmonary artery.

Major structural changes of the lungs and heart associated with pulmonary embolism (PE)

Blockage of the pulmonary vascular system, pulmonary hypertension, right-heart failure, pulmonary infarction, alveolar atelectasis, alveolar consolidation, bronchial smooth muscle constriction.

Age group most likely to suffer sudden death from a massive pulmonary embolism

65+.

Common sources of pulmonary emboli

Blood clots, fat, air, amniotic fluid, bone marrow, tumor fragments.

Risk factors associated with PE

Venous stasis, surgical procedures, trauma, hypercoagulation disorders.

Example of venous stasis risk factor

Inactivity, prolonged bed rest, prolonged sitting, congestive heart failure, varicose veins, thrombophlebitis.

Example of surgical procedures risk factor

Hip surgery, pelvic surgery, knee surgery, certain obstetric or gynecologic procedures.

Example of trauma risk factor

Bone fractures, extensive injury to soft tissue, postop or postpartum states.

Example of hypercoagulation disorders risk factor

Oral contraceptives, pacemakers, pregnancy and childbirth, supplemental estrogen, family history of venous thromboembolism, smoking, malignant neoplasms, burns.