Pulmonary vascular resistances

The units for PVR are dyne.s. cm 5 and 80 is used as a conversion factor to account for the different units used within the equation 

Serotonin (5-hydroxytryptamine) Increased peak airway pressure 

High or low lung volume Volatile anaesthetic agents 

The point to demonstrate is that resistance is lowest around the FRC. The curve rises at low lung volumes as there is direct compression of the vessels. At high lung volumes, the vessels are overstretched, which alters the flow dynamics and increases resistance further. The curve will be moved up or down by those other factors (above) which increase or decrease PVR. 

The V/Q term describes the imbalance between ventilation (V) and perfusion (Q) in different areas of the lung. Given that alveolar ventilation is 4.5 l.min and pulmonary arterial blood flow is 5.0 l.min 1, the overall V/Q ratio is 0.9. Both ventilation and perfusion increase from top to bottom of the lung, but perfusion by much more than ventilation. 

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The relationship for pulmonary vascular resistance is very non-linear owing to the effect of recruitment and distension of vessels in the pulmonary vascular bed in response to increased pulmonary blood flow. The PVR is usually around 10 times lower than the systemic vascular resistance, at 50-150 dyne.s.cm-5. 

Theophylline reduces contractile activity of smooth musculature, widens bronchi and blood vessels, reduces pulmonary vascular resistance, stimulates the respiratory center, and increases the frequency and power of cardiac contractions. It is used for bronchial asthma, preventing attacks, and systematic treatment. Theophylline is also used for symptomatic treatment of bronchospastic syndrome of a different etiology (chronic obstructive pulmonary disease, chronic bronchitis, and pulmonary emphysema). A large number of combined drags are based on theophylline. Synonyms of theophylline are adophyllin, asthmophyllin, theocin, and many others. 

Some ACEIs have demonstrated a beneficial effect on the severity of heart failure and an improvement in maximal exercise tolerance in patients with heart failure. In these patients, ACEIs significantly decrease peripheral (systemic vascular) resistance, BP (afterload), pulmonary capillary wedge pressure (preload), pulmonary vascular resistance and heart size and increase cardiac output and exercise tolerance time. 

Since Kantrovitz et al. described the concept of counterpulsation in 1968 [3], the lABP has been the mainstay for temporarily augmenting the cardiac output and improving hemodynamics in acutely decompensated refractory HF [4, 5]. lABP use has been shown to reduce heart rate, left ventricular end-diastolic pressure, mean left atrial pressure, afterload, and myocardial oxygen consumption by at least 20-30%. The lABP also modestly increases coronary perfusion pressure and decreases the right atrial pressure, pulmonary artery pressure, and pulmonary vascular resistance [6]. 

Esmolol decreases arterial pressure, heart rate, ventricular contractility, and pulmonary vascular resistance. 

Other reported side effects include vomiting, salivation, lacrimation, shivering, skin rash, and an interaction with thyroid preparations that may lead to hypertension and tachycardia. Ketamine also may raise intracranial pressure and elevate pulmonary vascular resistance, especially in children with trauma or congenital heart disease. Increases in intraocular pressure also may occur, and vigilance is required if ketamine is used in ocular surgery. 

Assess for a fherapeuf ic response as evidenced by decreased chest pain, dyspnea on exertion, fatigue, pulmonary arterial pressure, pulmonary vascular resistance, and syncope, and improved pulmonary function... 

Mecfianism of Action A prostaglandin that dilates systemic and pulmonary arterial vascular beds, alters pulmonary vascular resistance, and suppresses vascular smooth muscle proliferation. Therapeutic Effect Improves symptoms and exercise tolerance in patients with pulmonary hypertension delays deterioration of condition. Pharmacokinetics Protein binding 60%. Metabolized in liver. Primarily excreted in urine minimal elimination in feces. Half-life 20-30 min. 

There is a dose-dependent decrease in systemic blood pressure during isoflurane anaesthesia. This is mainly the result of a marked reduction in peripheral vascular resistance. In contrast, the decrease in arterial blood pressure during halothane anaesthesia appears to be mainly the result of a reduction in myocardial contractility. Isoflurane, in common with other volatile agents, has little effect on pulmonary artery pressure or pulmonary vascular resistance. 

Nitrous oxide has both a direct depressant and sympthomimetic effect on the myocardium. In healthy patients these tend to counterbalance each other, the resultant effect being minimal cardiovascular depression. In patients with car-diovascular disease or who are taking conconcurrent medication with, e.g. 3 blockers, its depressant effect may be more obvious. Nitrous oxide supplementation of high-dose opioid-based anaesthesia may result in a reduction in cardiac output and heart rate although the mechanism of this is unclear. Nitrous oxide may have a venoconstrictor effect resulting in increased pulmonary vascular resistance, particularly in the presence of pulmonary hypertension. 

NO activates soluble guanylyl cyclase to elevate cGMP levels in vascular smooth muscle Vasodilator relaxes other smooth muscle inhalation of NO leads to increased blood flow to parts of the lung exposed to NO and decreased pulmonary vascular resistance Hypoxic respiratory failure and pulmonary hypertension Inhaled gas Toxicity Methemoglobinemia... 

McLaughlin VV, Genthner DE, Panella MM, Rich S. Reduction in pulmonary vascular resistance with long-term epoprostenol (prostacyclin) therapy in primary pulmonary hypertension. N Engl J Med 1998 338(5) 273-7. 

Ribeiro PA, al Zaibag M, Abdullah M. Pulmonary artery pressure and pulmonary vascular resistance before and after mitral balloon valvotomy in 100 patients with severe mitral valve stenosis. Am Heart J 1993 125(4) I I 10-1114. 

Cardiac output can be measured using dye- or thermal-dilution techniques or by placement of an electromagnetic flow probe around the pulmonary artery. Insertion of a pressure transducer or fluid-filled catheter into the pulmonary artery and pulmonary vein allows for the calculation of pulmonary vascular resistance. The measurement of flow through the proximal aorta may also be useful but does not include coronary blood flow and as such is not equivalent to... 

Other experimental reproductive effects. Human systemic effects by inhalation pulmonary vascular resistance changes, cough, dyspnea, and other pulmonary changes. Mutation data reported. Violent reaction with cyclohexane, F2, formaldehyde, alcohols, nitrobenzene, petroleum, toluene. When heated to decomposition it emits toxic fumes of NOx. See also NITRIC OXIDE. 

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