W15 PAH, PE, Anaphylaxis

Question 1

PH etiologies

Answer 1

type 1: pulmonary arterial hypertension
type 2: d/t left-sided heart disease
type 3: d/t lung disease and/or hypoxia
type 4: chronic thromboembolic pulmonary hypertension (CTEPH)

Question 2

PAH
Treatment
What are the three pathways

Answer 2

mechanistic goals of all agents is either/or
● prevent proliferation of endothelium
● vasodilation (or prevent vasoconstriction)

endothelin receptor antagonists (ERA)
—bosentan (Tracleer™), ambrisentan, macitentan
—pros: oral;
—cons: teratogenicity, edema, flushing, and other SE’s

phosphodiesterase-5 inhibitors (PD5i)
—⭐️sildenafil (Revatio™), tadalafil (Adcirca™)
—pros: oral;
—cons: headache, flushing, dyspepsia, and other SE’s, don’t use w/ nitrates, like we learned

prostanoids (prostaglandin/prostacyclin analogs, or PCA)
—epoprostenol (IV), treprostinil (IV/SQ/inh/oral), iloprost (inh)
cons: routes and frequent/continuous doses (IV pumps), only if PAH is severe

Answer 3

acute vasoreactivity test
● following short-acting vasodilator (inhaled NO
or PDE inhibitor), at least 10 mmHg decrease in PAP, PAP
≤40 mmHg, and no reduction in CO or increase in PCWP
● a minority of patients are vasoreactive and
qualify for high
-dose CCBs

supportive agents:
● oxygen supplementation to maintain >92%
● immunizations!
● diuretics (loop +/- thiazide)
● rate control agents for atrial arrhythmias
● anticoagulation? controversial
therapeutic goals
● improve 6-minute walking distance
● improve dyspnea
● improve hemodynamics
● delay clinical worsening

therapeutic goals
● improve 6-minute walking distance
● improve dyspnea
● improve hemodynamics
● delay clinical worsening

Question 4

anaphylaxis treatment

Answer 4

non-pharmacologic
● remove offending agent
● place patient in recumbent position w/ lower extremities elevated
● monitor vital signs every 2-5 minutes
● administer oxygen as needed (ie, hypoxia, bronchospasm, difficulty breathing)
pharmacologic
● epinephrine IM every 5-10 minutes
● diphenhydramine (Benadryl) IM or IV, consider ranitidine or famotidine IV for added antihistamine effect
● corticosteroid to prevent recurrence or protracted anaphylaxis
● if bronchospasm, give inhaled albuterol
● if hypotension, give fluids and IV vasopressors (ie, epinephrine)

— beta2 agonism helps with bronchoconstriction
—alpha 1
—(swollen tongue/lips/mucosal) alpha

Question 5

Antithrombotic Therapy for VTE Disease

Answer 5

subsegmental PE
● if low risk for recurrent VTE, surveillance > anticoagulation
● if high risk of recurrent VTE (incl +DVT), anticoagulation > surveillance

incidental finding of PE and asymptomatic
● treat like a symptomatic PE

acute PE
● give thrombolytic (fibrinolytic) only if hypotensive, as long as patient does not have a high bleeding risk
● can also give thrombolytic it patient deteriorates after starting on anticoagulation

low-risk PE: outpatient treatment > hospitalization as is reasonable (patient has access to medications, resources,
outpatient f/u, etc.)
● see Hestia Criteria for eligibility for home treatment
● evidence: no difference in long-term all-cause mortality, major bleeding, or recurrent PE

Question 6

PE locations and symptoms

Answer 6

more distal = less hemodynamic instability

higher clot burden doesn’t always correlate w/
more hemodynamic instability

RV dysfunction = submassive PE

● echo: RV dilation, strain, hypokinesis
● cardiac markers: ↑BNP or ↑trop
● thrombolysis may be considered

+hemodynamic instability = massive PE, definitely consider thrombolysis or thrombectomy ASAP

Question 7

thrombolytics / fibrinolytics - MOA video
alteplase/tPA, tenecteplase/TNK, reteplase

Answer 7

MOA: converts plasminogen to plasmin, including those within the thrombus
bleed risk is significantly higher than with other antithrombotics, be aware of contraindications; for example, for alteplase/tPA to treat MI or PE
● active internal bleeding
● history of recent stroke
● recent (within 3 months) intracranial or intraspinal surgery or serious head trauma
● presence of intracranial conditions that may increase the risk of bleeding
● bleeding diathesis
● current severe uncontrolled hypertension
● more contraindications exist for use in acute ischemic stroke

Q: If a patient goes into cardiac arrest from acute massive PE, what rhythm would you expect to see?
Q: In addition to sudden death, what other long-term consequences may result from untreated PE?