Pulmonary HTN Flashcards
Discuss strategies for resuscitation, intubation, and ventilation of a patient with pulmonary hypertension. (Pure alpha)
RV failure patients are very sensitive to hypoxia and hypercapnea due to associated pulmonary arterial vasoconstriction and resultant increase in RV pressure.
Deliver high flow (15L) oxygen via a non-rebreather and/or High flow oxygen via nasal cannula concomitantly may further increase your Fi02 (optimizing preoxygenation).
If this is not sufficient, non-invasive positive pressure ventilation (NIPPV) may be an option.
Because these patients are very sensitive to increase pulmonary artery pressures, you should start NIPPV at the lowest pressure possible and monitored closely for decompensation.
Does this patient need more IV fluids?
No. In a patient with hypotension and a normal RV, 1-2 L of NS bolus will often be adequately tolerated and will likely be beneficial. In a patient with acutely decompensated RV function, large fluid boluses will worsen RV dilatation, cause further compression of the left ventricle precipitating decreased cardiac output and cardiovascular collapse.
On physical exam, this patient has pitting edema and signs of volume overload. Bedside ultrasound is often an excellent tool to assess fluid tolerance in the shock patient, but in this case will likely not be helpful in assessment of volume status, as PAH patients will almost always have a dilated IVC due to elevated right ventricular pressures.
Patients with right heart failure have a RV:LV > 1 (normal is < 0.6) and there will often be a thickened right ventricular wall secondary to chronic pulmonary hypertension.
The ideal hemodynamic agent would increase cardiac output, maintain SVR and decrease pulmonary vascular resistance (PVR). This agent does not exist. Most experts advocate starting with a vasopressor then adding an inotrope, given that most inotropes can cause decrease SVR (which will decrease right ventricular perfusion).
Vasopressors
Norepinephrine
norepinephrine is becoming the universal first line agent for shock, especially undifferinated shock . It will increase systemic vascular resistance, which will increase right ventricular perfusion and has some Beta-1 effect that can provide some augmentation of inotropy. Unfortunately, it will also increase pulmonary vascular resistance. However, if there is any component of distributive shock, such as in this patient where sepsis is a consideration, norepinephrine would be a sound first line choice.
Vasopressin
Often used as an adjunct to increase SVR following norepinephrine, vasopressin could be used as a first line pressor in right heart failure patients as it will increase SVR but decrease pulmonary vascular resistance by a nitric oxide mechanism.
Phenylephrine
Essentially contra-indicated due its potent pulmonary vasoconstriction effects.
Inotropes
Dobutamine
While an excellent Beta-1 agonist that will increase cardiac output, dobutamine can cause tachycardia and systemic vasodilation. As such, it should not be started until a vasopressor is running.
Milrinone
A phosphodiesterase inhibitor, milrinone will increase contractility and peripheral arterial and venous vasodilation. As such, it has similar properties to dobutamine.
Epinephrine
Epinephrine’s strong Beta-1 stimulation will increase cardiac output and will not cause systemic vasodilation. However, it may be more likely to cause tachydysrythmias, which are poorly tolerated in right heart failure due to their effect on ventricular filling time.
How will proceed with intubation in this patient with pulmonary hypertension?
In pulmonary hypertension with RV failure, intubation must be seen as an absolute last resort.
This is because:
Sedatives used for RSI will cause hypotension which worsen RV ischemia
Transient hypoxia and hypercapnea will worsen pulmonary vasoconstriction, increase pulmonary artery pressure and RV ventricular pressures
Positive pressure ventilation will further increase pulmonary artery pressures and right ventricular pressure
The combination of the above factors can precipitate almost immediate decline in cardiac output and cardiac arrest.
Some experts will advocate for an awake intubation to prevent the systemic hypotension from sedative medications as well as the hypercapnea that may result from the apneic period. Alternatively, ketamine can be considered without the use of a paralytic as it will maintain respiratory drive. If RSI is to be used, avoid propofol due to risk of hypotension and instead consider etomidate in addition to a paralytic agent.
What is your ventilation strategy in the patient with pulmonary hypertension?
Given the drawbacks of increased intrathoracic pressure, you should aim for low tidal volumes (6-8 ml/kg ideal body weight) and low plateau pressures (< 30 mmHg). Minimal PEEP should be used (< 12 cm H20). Unlike an ARDS protocol for ventilation, these patients cannot tolerate permissive hypercapnea and hypoxia due to pulmonary vasoconstriction.
Discuss the indications of inhaled vs systemic epoprostenol.
Inhaled Epoprostenol: indicated for the management of pulmonary arterial hypertension (PAH) in 6 years of age and older. It is used to reduce pulmonary artery pressure, improve exercise capacity, and reduce dyspnea. 6 and older Systemic is for 12 and older.
Additionally, systemic epoprostenol is also indicated for the treatment of primary pulmonary hypertension (PPH) in patients 6 years of age and older.
