Open Lung Ventilation And Its Impact On The Cardiovascular System - Research Paper Example

Open Lung Ventilation And Its Impact On The Cardiovascular System Abstract Positive pressure ventilation is a very common procedure that is used to establish respiration in a critically ill patient. Infact it is the commonest form of mechanical ventilation. The pressures delivered to the airways and lungs through this form of ventilation are radically different from those encountered in regular respiration. While in most of the settings, these differences in pressure pose no threat especially when the positive pressure ventilation is delivered for a short duration of time, in some situations differences in pressure gradients lead to adverse effects on the hemodynamics of the lungs, heart and other organs. These aspects have to be kept in mind while instituting artificial respiration to a patient. This assignment aims at identifying the negative effects of positive pressure ventilation on the cardiovascular system. Introduction Positive pressure ventilation or PPV is a method of forcing air or oxygen into the lungs of a patient (most often who has respiratory difficulty or failure or is unable to breathe) by either using bag and mask or by means of a mechanical ventilator. In PPV, since air is forced into the lungs of the patient, the pressure inside the airways is always higher than the atmospheric pressure outside the body. PPV is the main form of mechanical ventilation. Mechanical ventilation is indicated in many conditions like respiratory arrest, acute respiratory distress syndrome, acute lung injury, respiratory muscle fatigue, coma, obtundation and neuromuscular disease. It also initiated in tachypnea, in lung conditions where vital capacity is less than 15 ml/kg and minute ventilation of more than 10 litres per minute. PaO2 of less than 55mmHg and PaCO2 of more than 50mmHg with pH less than 7.25 are laboratory indicators for mechanical ventilation (1). PPV is a departure from the normal physiology of spontaneous respiration. PPV is a life-saving therapy but not without the risk of other significant problems. In the first place, it is not easy to deliver artificial ventilation without expertise. Secondly, it requires a costly set up. Thirdly, it can be associated with other complications which can be life- threatening too. These complications include barotrauma, volutrauma, problems of oxygen toxicity like absorptive atelectasis, diffuse alveolar damage, tracheobronchitis and hypercarbia, ventilator-associated pneumonia, auto-PEEP and detrimental cardiovascular effects (1). This literature review aims at studying negative effects of PPV on cardiovascular system. Detrimental effects of PPV on cardiovascular system 1. Decreased venous return to the heart During normal breathing, there is negative pressure in the thorax during inspiration. This negative pressure helps in venous return to the heart and increases blood flow through the pulmonary capillaries by alleviating pressure on them. But in positive pressure ventilation, during inspiration, the intrathoracic pressure increases. This increase causes decrease in venous return to the heart which in turn decreases the right ventricular output and also the pulmonary blood flow. There may be a paradoxical reduction in right ventricular output and this probably offsets the venous return decrease (2). As PEEP increases, return to left ventricle decreases due to decrease in right ventricular outflow. The increased intrathoracic-extrathoracic gradient that assists the left ventricular output partially offsets the decreased return to the left ventricle (3). During normal expiration, the intrathoracic pressure returns to zero. This increases venous return to the heart. PEEP during expiration continues to inhibit venous return to the heart and this results in venous stasis. Venous stasis can be seen as reduced collapsibility of inferior vena cava (3). Venous return in positive pressure ventilation can be increased by administering fluids, but this is not recommended because the increase is at the cost of increase in central venous pressure. Increased central venous pressure results in increased end-capillary pressures in all the organs including lungs and hence is not good. 2. Fluid retention Because of decreased venous return, there is reduced atrial distension which increases the secretion of antidiuretic hormone and atrial natriuretic peptide. Both these hormones cause salt water retention (4). 3. Perfusion-ventilation mismatch Mean capillary pressure is the gradient between pulmonary artery pressure and venous outflow pressure in the pulmonary vein. It is usually 7- 10mmHg. Intrathoracic pressure usually does not influence the gradient. Normal breathing pressures in the interstitium and the alveoli are small relative to the capillary perfusion pressure. It is because of this low pressure that fluid and substrate movement between the compartments is facilitated by the hydrostatic and oncotic pressures. The low pressure system does not influence capillary flow. There are some areas in the lung which are different. Lung areas higher than atria have lower pressure gradients and lung areas in the dependent regions have lung tissue pressing on capillaries. However these effects are small and transient in normal people. But in those suffering from COPD, the lungs are hyperinflated and during expiration there is high intrathoracic pressure. This high pressure compresses the interstitium and the capillaries. This in turn results in increased capillary resistance, thus modifying blood flow. When positive pressure ventilation is delivered to such patients, even minimal peak inspiratory pressures increase the interstitial pressures considerably beyond capillary pressure. The increase in interstitial pressures compress the capillaries and impede blood flow. After a certain degree of rise in interstitial pressures, reflex hypoxic vasoconstriction, a method of diversion of blood flow at low pressures in spontaneous breathing will be offset. All these result in perfusion-ventilation mismatch (4). Positive pressure ventilation leads to high venous pressures which adversely affect pressure gradients. This in turn affects Starling's forces and encourages fluid flux. All these amount to interstitial fluid retention which further contributes to ventilation-perfusion mismatch (4) In case of critically ill patients in whom positive pressure ventilation is most often delivered, the integrity of capillary endothelium is damaged by persistently high venous pressures resulting in 'capillary stress failure.' This further aggravates ventilation-perfusion mismatch (4). 3. Increased risk of myocardial infarction Non-invasive PPV alleviates symptoms in congestive heart failure and acute pulmonary edema by improving left ventricular function and oxygenation. However some researchers doubt the safety of this application because of increased risk of myocardial infarction. (5) 4. Splanic hypoperfusion The decrease in venous return as a result of PPV results in decreased cardiac output and hypotension in some patients. This is more commonly seen in patients with high PEEP. The resultant decrease in mean arterial pressures combined with increased resistance in gastrointestinal vascular bed lead to splanic hypoperfusion. Since gut mucosa shunts oxygen, hypoxia at the tip of villi ensues easily in splanic hypoperfusion. Splanic perfusion is further contributed by vasoconstriction and redistribution of blood to vital organs as a result of raised catecholamines either because of raised plasma-renin-angiotensin aldosterone activity or due to iatrogenic catecholamines. Splanic perfusion produced thus can cause ileus, mucosal damage or even worse reperfusion injury (6). 5. Decreased venous return from the head Since continuous positive pressure in the heart leads to decreased venous return from the head, intracranial pressure can rise and worsen delirium and agitation (1). Conclusion Though PPV is a useful procedure for initiating and maintaining artificial respiration, it has many side effects and is not without hazardous risks. PPV has detrimental effects on the cardiovascular system because of alteration of hemodynamics by the varying pressure gradients. The most important side effect is decreased venous return to the heart. Hence it is wise to apply this procedure after careful patient selection and proper evaluation. References 1. Byrd, R.P. and Kosseifi, S.G. (2008). Ventilation, Mechanical. Emedicine from WebMD. Retrieved on 14th April 2009 http://emedicine.medscape.com/article/304068-overview 2. Miranda, D.R., Klompe, L., Mekel, J., et al. (2006). Open lung ventilation does not increase right ventricular outflow impedance: an echo-Doppler study. Crit Care Med, 34, 2555-60. 3. Mitaka, C., Nagura, T., Sakanishi, N., Tsunoda, Y., Amaha, K. (1989). Two-dimensional echocardiographic evaluation of inferior vena cava, right ventricle, and left ventricle during positive-pressure ventilation with varying levels of positive end-expiratory pressure. Crit Care Med, 17, 205-10. 4. Soni, N., and Williams, P. (2008). Positive Pressure Ventilation: What is the Real Cost? Medsacpe Pediatrics. Retrieved on 14th April 2009 http://www.medscape.com/viewarticle/581344_1 5. Nadar, S., Prasad, N., Taylor, R., and Lip, G. (2006). Positive pressure ventilation in the management of acute and chronic cardiac failure: a systematic review and meta-analysis. International Journal of Cardiology, 99(2), 171-185. 6. Mutlu, G.M., Mutlu, E.A., Factor, P. (2001). GI Complications in Patients Receiving Mechanical Ventilation. Chest, 119(4), 1222- 1241. Read More