Respiratory - Status Asthmaticus, PE, Pulm HTN

status asthmaticus - what is it?

• airway hyperactivity that produces severe airway narrowing that is refractory to aggressive bronchodilator therapy, which may result in respiratory failure

status asthmaticus - PATHOPHYSIOLOGY

• extrinsic OR intrinsic TRIGGER → bronchial smooth muscle spasm, bronchial mucosa inflammation/edema, thickened secretions (extremely tenacious) → AIRWAY OBSTRUCTION → DECREASED VENTILATION → airtrapping (increased PaCO2, hyperinflation → decreased venous return, decreased CO, CARDIOPULMONARY ARREST); hypoxemia

status asthmaticus - clinical presentation

• dyspnea, tachypnea

• cough/chest tightness

• accessory muscle use

• wheezing → decreased breath sounds → absent breath sounds → OMINOUS SIGN

• V/Q mismatch

• CXR may have flattened diaphragm (sign of airtrapping)

• tachycardia

• pulsus paradoxus > or = to 15mmHg (severe is greater than 18)

• anxiety → DECREASED LOC

• may have elevated WBC, eosinophils

• peak flow rate < 80% of predicted, <50% is severe

• history of previous intubations (higher mortality)

status asthmaticus - ABG progression (on room air)

• STAGE 1 - normal PaO2, respiratory alkalosis (decreased PaCO2)

• STAGE 2 - mild hypoxemia, respiratory alkalosis (decreased PaCO2)

• STAGE 3 - worsening hypoxemia, normalization of pH and PaCO2

• STAGE 4 - severe hypoxemia, respiratory acidosis (INCREASED PaCO2)

status asthmaticus - management

• measure peak flow rate (PFR) (the MAXIMUM speed at which air can be exhaled after a full inspiration)

  • admit to hospital if 50-70%; admit to ICU if <50%

• bronchodilator: short-acting beta-2 agonists (such as albuterol)

• anticholinergics (such as ipratropium)

• corticosteroids (systemic) (such as methylprednisolone, prednisone)

• O2, pulse ox

• hydration (to prevent thickened secretions)

• avoid sedation agents

• intubation (if respiratory acidosis, severe hypoxemia, silent chest, or change in LOC occur)

  • if intubated/sedated, AVOID paralytics because when combined with steroids it can increase incidences of neuropathy

status asthmaticus - VENTILATOR MANAGEMENT

• use low rate to INCREASE exhalation time

• use low tidal volumes to prevent auto-PEEP

• increase inspiration/expiration (I/E) ratio, often greater than 1:3-4, to allow time for optimal exhalation and to prevent auto-PEEP

pulmonary embolism - what is it?

• a partial or complete obstruction of the pulmonary capillary bed by a blood clot or another substance such as fat, air, amniotic fluid, or a foreign material, with a disruption of blood flow to an area of the lung

  • MASSIVE: >50% occlusion

  • SUBMASSIVE: <50% occlusion

  • 80-90% result from DVT

Venous Thromboembolism - RISK FACTORS

• Strong - Fracture (hip or leg), hip or knee replacement, major trauma, spinal cord injury

• Moderate - arthroscopic knee surgery, central lines, chemotherapy, HF/respiratory failure, hormone replacement therapy, malignancy, oral contraceptives, stroke, pregnancy/postpartum, previous VTE

• Weak - bed rest >3 days, prolonged sitting, increasing age, laparoscopic surgery, obesity, pregnancy/antepartum, varicose veins

pulmonary embolism - PATHOPHYSIOLOGY

• clot in pulmonary vasculature → decreased perfusion of blood → LOCAL RELEASE OF BIOCHEMICAL SUBSTANCES (local lung constriction, atelectasis, pulmonary infarction) AND V/Q MISMATCH (decreased pulmonary perfusion, INCREASED PAP, RV failure, decreased CO (MAY BE FATAL))

pulmonary embolism - signs and symptoms (most, massive)

• MOST

  • dyspnea/tachypnea

  • tachycardia/CP

  • right sided S3/S4 sounds

  • anxiety

  • cough/hemoptysis/crackles

  • syncope

  • petechiae (FAT EMBOLI)

  • low-grade fever

  • respiratory alkalosis

  • positive D-Dimer

• MASSIVE

  • hypoxemia

  • hypotension

  • EKG changes - RBBB, right axis deviation on EKG, tall peaked P-waves in lead II, RV strain pattern, ST elevation in V1 and V2

  • cardiopulmonary arrest (PEA)

  • elevated BNP (due to RV wall stress)

pulmonary embolism - TYPES

• venous thromboembolism (DVT)

• fat emboli (long-bone, pelvic fractures)

• air emboli (surgery, IV lines)

• catheter embolization

• RA/LA or RV embolus (a-fib/flutter); LA leading to stroke is more common

• amniotic fluid embolism (amniocentesis, abruptio placenta, abortion)

• tumor emboli (malignancy causes an increase in thrombin)

• septic emboli (bacterial/viral)

pulmonary embolism - diagnosis

• pulmonary angiography (GOLD STANDARD)

• V/Q scan (not definitive)

• high-speed CT scan

• D-dimer (good rule out test; if positive, it means that a clot is present in the body; not DEFINITIVE of it’s in the lungs)

• venous doppler (helps with identifying the source)

pulmonary embolism - how does it affect alveolar dead space? why?

• a PE will INCREASE ALVEOLAR DEAD SPACE, meaning that the volume of air that DOES NOT participate in gas exchange increases, as there is no blood flow past alveoli in that area of pulmonary circulation

pulmonary embolism - prevention (mechanical vs. pharmacological)

• mechanical - graduated compression stockings and/or intermittent pneumatic compression (USE CONTINUOUSLY EXCEPT WHILE AMBULATING)

• pharmacological - low-molecular-weight heparin (enoxaparin (Lovenox) DAILY); low-dose unfractionated heparin TID (rivaroxaban (Xarelto) DAILY); apixaban (Eliquis) BID

pulmonary embolism - treatments

• maintain adequate airway, ventilation, and oxygenation

• fluids

• anticoagulation (heparin; low-molecular-weight heparin; coumadin (on the first day of treatment), MAY REQUIRE LONG-TERM ANTICOAGULATION)

• fibrinolytic therapy (for all patients with hemodynamic compromise with low risk for bleeding)

• maintain CO (inotropes, fluids)

• analgesics (for pain)

pulmonary hypertension - what is it?

• defined as a MEAN PAP greater than 25 at rest and a PAOP that is less than 16 at rest with secondary right heart failure

  • NORMAL mean PAP is about 20; since the RV normal pumps into a low-pressure system, the wall of the RV is THIN compared to that of the LV; pulmonary HTN results in cor pulmonale and RV failure

pulmonary hypertension - 5 groups

• group 1 - pulmonary arterial HTN (PAH); sporadic and hereditary due to localized small pulmonary muscular arterioles (such as collagen vascular diseases, drug/toxin induced)

• group 2 - pulmonary HTN (PH) due to left heart disease, such as LV failure or valvular (mitral or aortic) disease

• group 3 - PH due to lung diseases or hypoxemia

• group 4 - PH due to chronic thromboembolic problems

• group 5 - PH that has unclear factors or is multifactorial (such as sarcoidosis)

pulmonary hypertension - signs and symptoms

• exertional dyspnea, lethargy, and fatigue due to an inability to increase cardiac output with activity

• progression to RV failure, chest pain, syncope with exertion, and peripheral edema

• passive hepatic congestion may cause anorexia and ABD pain

• Ortner’s syndrome (cough, hemoptysis, hoarseness)

• systolic ejection murmur, increased intensity of pulmonic component of S2 heart sound, diastolic pulmonic regurgitation murmur, right sided murmurs, and gallops are augmented with inspiration

• RV hypertrophy, elevated JVD, hepatomegaly, ascites, pleural effusion

pulmonary hypertension - TREATMENT

• treat the underlying cause as able

• each “group” has specific treatments based on the cause

• all regimens should consider diuretics, oxygen, anticoagulants, digoxin, and exercise training

• use dilators, which include calcium channel blockers, or phosphodiesterase-5 inhibitors (such as sildenafil (Viagra), tadalifil (Cialis), or treprostinil (Remodulin)

• for patients who are refractory to all medical interventions- LUNG TRANSPLANTATION (bilateral or heart-lung transplant) or possible atrial septostomy (right to left shunt)