test 6 pulmonary arterial hypertension- PAH Flashcards
Pulmonary Arterial Hypertension-PAH defined by and surgical mortality
- Mean pulmonary pressure >25 mmHg at rest or >30 mmHg during exercise
- Surgical mortality higher for patients with PAH
* 4-24%
Pulmonary Arterial Hypertension-PAH caused by
- Congenital abnormalities
- Valve disorders
- Volume excess
- LV dysfunction
- Idiopathic
Hemodynamics of Pulmonary Arterial Hypertension
- RV failure leads to ↓ pulmonary blood flow
- ↓ pulmonary blood flow leads to hypoxia
- Hypoxia leads to ↑ PVR
- ↑ PVR leads to ↑ strain on RV
- ↓ RV SV= ↓ LV output= ↓ coronary blood flow
- Cardiac arrest
Hemodynamic Treatment of Pulmonary Artery Hypertension in the OR Setting Goals
- Avoid elevations in PVR
- Maintain SVR
- Avoid myocardial depressants and maintain contractility
- Maintain chronic prostaglandin therapy without altering dosage
- Use low-pressure mechanical ventilation when possible
Pharmacologic Treatment of Pulmonary Artery Hypertension in the OR Setting
- Prostacyclin Analogs
- Nitroso Dilators
- Inhaled Nitric Oxide (iNO)
Prostacyclin Analogs
- Prostacyclin analogs are potent, effective pulmonary vasodilators
- Significantly reduce PVR
- Short half life
Prostacyclin Analogs improve
- Exercise tolerance
- Breathing
- Hemodynamics
- Survival
Nitric oxide (Endothelial Derived Relaxation Factor (EDRF)) and how it works
- Produced in the endothelial cells via nitric oxide synthase
- diffuses from the endothelial cells to the vascular smooth muscle where it increases cGMP and reduces intracellular Ca2+
- results in smooth muscle relaxation
Nitroso Dilators
- IV
- Reduce PA pressures, but may reduce CO and SVR
- Beneficial for moderate PAH and RV dysfunction
- Not for severe RV dysfunction
Nitroprusside (Nipride)
• Direct-acting vasodilator
• Nitrate group converted into NO in vascular smooth muscle
• Increased cGMP -> vasodilation
• Short duration (1-2 min)
• Possible cyanide and thiocyanite toxicity
• Metabolic acidosis
• ↑ mixed venous PO2
-Light sensitive
- Light breaks down the cyanide and not as protected
Inhaled Nitric Oxide (iNO)
• Selective pulmonary vasodilator
• Devoid of systemic actions
• Favorably affects lung V/Q relationships because it vasodilates lung regions that are well ventilated
- Unobstructed alveoli diffuse iNO to vasodilate capillaries with high vascular resistance
Inhaled Nitric Oxide (iNO) Therapeutic Uses
- Pulmonary hypertension
- Persistent pulmonary hypertension of the newborn
- Adult respiratory distress syndrome
Inhaled Nitric Oxide (iNO)
- Administered by blending dilute NO into the ventilator inlet gas
- Concentrations range from 0.05-80 ppm
- Onset of action 1-2 minutes
- Low toxicity with safety precautions
Inhaled Nitric Oxide (iNO) Possible Adverse Effects
• Depend on dosage and concentration • Combines with O2 to form NO2 • NO2 > 10ppm may cause • Cell damage • Hemorrhage • Pulmonary edema • Death • Methemoglobinemia may occur due to NO inactivation process (blood levels monitored daily)
ITC AVOXimeter Systems Measure Hemoglobin
- ITC AVOXimeter
* Total hemoglobin
* Oxyhemoglobin
* Carboxyhemoglobin
* Methemoglobin