Influence of Mean Airway Pressure on Cardiovascular Performance Research Paper

  • Length: 9 pages
  • Subject: Anatomy
  • Type: Research Paper
  • Paper: #88942822

Excerpt from Research Paper :

Airway Pressure on Cardiovascular Performance


The Influence of Mean Airway Pressure on Cardiovascular Performance

Breathing, also known as pulmonary ventilation, is the basic connection between the heart and lungs (Williams & Whitney, 2006). The connection allows air between the lungs and the atmosphere and the exchange of gases between the air and the alveoli in the lungs. Body receptors can detect changes involved in the movement of air and the pressure that accompanies it. These receptors can either increase or decrease breathing rate. They encourage slower breathing when blood pressure rises and faster breathing rate if the blood pressure goes down. Meanwhile, an exchange of gases between body tissues and capillaries is needed to maintain life. It brings in the gases living tissues need for survival. Blood carries oxygen molecules when leaving the heart and distributes it throughout the body. Very small capillaries coordinate in the flow and distribution of oxygen. The exchange of gases happens in the capillaries. Blood flows through them to bring nutrients to the cells. At the same time, it carries metabolic waste products away. It is, therefore, the job of capillaries to feed the living tissues of the body with nutrients. The heart, lungs and the network of blood vessels together keep the circulatory system healthy and functional in sustaining lie. They interact interdependently. The heart pumps blood, the lungs bring in oxygen from the atmosphere for the blood to carry and the blood vessels distribute the nutrients carried by the blood to all living body tissues (Williams & Whitney).

If the heart-lung coordinated system fails to deliver enough oxygen for the body's metabolic needs, anaerobic metabolism occurs (Meliones, 2000). This can lead to acidosis and, ultimately, organ dysfunction. A critical balance must, therefore, be struck between oxygen supply and oxygen demand. The goal of managing the combined systems is to optimize the relationship between the systems and to avoid abnormalities in the failure of the relationship (Meliones). The average pressure generated during one breathing or respiratory cycle is referred to as mean airway pressure (Marini & Ravenscraft, 1992). It closely reflects mean alveolar pressure. Under conditions of passive inflation, mean airway pressure reflects alveolar ventilation, arterial oxygenation, hemodynamic performance, and barotraumas (Meliones).

Mechanical Ventilation and PEEP

Mechanical Ventilation

This is a closed system or a box, which resembles the lungs (Daoud, 2007). It delivers air and oxygen by electrical or pneumatic power through a tube inserted into a patient's airway. The physician or health care provider determines and sets the control panel of the ventilator for the pattern of delivery of gases into the lungs. The modes of ventilation include assist/control, auto-flow, auto-PEEP, bi-level positive airway pressure, and continuous positive airways pressure or CPAP. Most of the current ones are positive-pressure ventilators. A pressure gradient makes gas flow into the lungs similar to natural breathing. Air is released when the respiratory muscles are passively relaxed (Daoud).

Mechanical ventilation is usually indicated for bradypnea or apnea with respiratory arrest, acute lung injury and acute respiratory distress syndrome, tachypnea, vital capacity of less than 15 mL/kg, minute ventilation greater than 10 L/min, respiratory muscle fatigue, coma, hypotension and neuromuscular disease (Byrd & Mosinefar, 2010).

Positive End-Expiratory Pressure or PEEP

This is a process. The expiratory valve in the ventilator closes when it inspires, thus bringing the flow of oxygen and air into the lungs (Daoud, 2007). It opens to allow natural exhaling and pressure on the lungs to return to baseline. While allowing these, the ventilator can also apply positive pressure during exhalation. This limits the ability of the lungs to expel. This increases functional residual capacity or FRC. And FRC increases the mean airway pressure on the lungs. This process is called PEEP (Daoud).

PEEP improves oxygenation through another process, called alveoli recruitment (Daoud, 2007). Alveoli are air sacs in the lungs. Through positive pressure, the flow of gas into the lungs recruits the alveoli to absorb the oxygen from the flow. The PEEP process keeps the alveoli open for a longer period and recruits more alveoli. These actions allow better oxygenation (Daoud).

Airway Pressure Release

Airway pressure release ventilation or APRV was first introduced to clinical practice more than 20 years ago as an alternative to mechanical ventilation (Daoud, 2007). But it was only recently that it caught attention as an effective and safe alternative for patients with acute lung injury or ALI or acute respiratory distress syndrome or ARDS. Among its major attractions is reducing ventilator-induced lung injury through the use of lung protective strategies. APRV was first described by Stock and Downs in 1987 as a continuous positive airway pressure or CPAP with an intermittent release phase. It has demonstrated advantageous effects on oxygenation, hemodynamics, regional blood flow and organ perfusion and on sedation and neuromuscular blockades usage. There is spontaneous breathing through better gas distribution and better VQ matching to the poorly aerated dorsal area of the lungs and higher mean airway pressure. This is the chief advantage over conventional ventilation or the "open-lung" approach (Daoud).

Two research teams compared the hemodynamic effects of APRV on ALI/ARDS patients with inverse ratio PCV (Daoud, 2007). Both teams found that the patients had significantly higher cardiac index, oxygen delivery, saturation of oxygen in the blood vessels, and urine output while on APRV. Another research team, headed by Hering, experimented on the use of APRV on 12 pigs with ALI. In a similar study, this team found that APRV improved blood flow to the stomach, duodenum, ileum and colon in the pigs. Kaplan and his team also found significantly improved urine output and glumerular filtration rate in respondents who were placed on APRV. APRV also yielded a 70% decrease in the need for neuromuscular blockades and approximately 40% use of sedation as compared with conventional mechanical ventilation. These decreased usages suggest decreased length of mechanical ventilation and stay at the ICU (Daoud).

These investigations provide evidence of the simplicity, safety and effectives of APRV for patients with ALI/ARDS at present (Daoud, 2007). No mortality has resulted from its use. However, evidence of its superiority to other ventilatory methods in oxygenation, hemodynamics, regional blood flow, comfort and length of mechanical ventilation. A large human study is needed to compare it with conventional mechanical ventilation using lung-protective strategies in order to make a final conclusion on its worth. In the meantime, APRV is a present recommended only for carefully selected patients. Consultation with specialists or respiratory therapists adequately knowledgeable with APRV is needed (Daoud).

Positive Pressure Ventilation

This can improve cardiovascular performance in patients with increased struggle to breath, pulmonary edema, upper airway obstruction and impaired left ventricle pump function (Williams & Whitney, 2006). Un-aided or spontaneous breathing can develop negative intra-thoracic pressure swings, which increase venous return and left ventricle afterload. These can further lead to pulmonary edema. Pulmonary edema and heart failure can lead to a worsening of the edema and hypoxia (Williams & Whitney).

Its progenitor, the negative pressure machine or iron lung, was a metal cylinder that hung around the patient's neck (Byrd & Mosenifar, 2010). The vacuum pump created negative pressure that expands the chest. This reduces intrapulmonary pressure and brings ambient air into the patient's lungs. The negative pressure drops to zero when the vacuum is terminated. The Drinker and Shaw tank-type was among the first machines for mechanical ventilation, introduced in 1929. This is now used only in a few situations. The use of PPV became popular in the United States and Scandinavia in the 50s during the onslaught of the polio epidemic. In those days in Copenhagen, 50% of the air needed by patients with polio and respiratory paralysis was manually forced continuously by as many a 1,400 medical students. This huge requirement and the decrease of death rate from 80% to 25% led to the preference for positive-pressure machines in the operating room for use in the ICU (Byrd & Mosenifar).

PPV applies airway pressure at the patient's airway through an endotracheal or tracheostomy tube (Byrd & Mosenifar, 2010). It leads the flow of gas until the end of the ventilator breath. As the airway falls to zero, an elastic recoil of the chest pushes the tidal volume out by passive exhalation. With the introduction of computer feedback systems, modern ventilators enable fine adjustments in tidal volume, airway pressures, and timing of the respiratory cycle. The goal is to improve ventilator-patient interaction and to limit ventilator-induced lung injury. Newer methods are based on attractive physiologic hypotheses and worth trying out. Current evidence, however, has yet to prove that alternative methods are better than conventional mechanical ventilation, specifically on tidal volume. So far, most clinicians use them only when conventional mechanical ventilation fails (Byrd & Mosenifar).

Cardio-respiratory System, Interventions and Interactions

The function of this system is to provide enough oxygen that will meet the metabolic demands of the body as well as eliminate the CO2 generated (Meliones, 2000). Fulfilling this function consists of many interactions between the cardiovascular and respiratory system. When it…

Cite This Research Paper:

"Influence Of Mean Airway Pressure On Cardiovascular Performance" (2011, August 19) Retrieved January 18, 2017, from

"Influence Of Mean Airway Pressure On Cardiovascular Performance" 19 August 2011. Web.18 January. 2017. <>

"Influence Of Mean Airway Pressure On Cardiovascular Performance", 19 August 2011, Accessed.18 January. 2017,