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Nursing - Mechanics of pulmonary ventilation - Effects of smoking on cardiovascular system - Assessment Answer

November 13, 2018
Author : Andy Johnson

Solution Code: 1DAB

Question: Mechanics of Pulmonary ventilation - Effects of Smoking Cardiovascular system

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Nursing Assignment

Assignment Task

Task 1: Describe the mechanics of pulmonary ventilation in a resting healthy person?

Task 2: Cardiovascular health is a National Health Priority with smoking identified as having a negative effect on the health of the cardiovascular system. Describe one smoking-related structural change to the cardiovascular system and the consequences to cardiovascular system function

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Answer : Pulmonary ventilation defines exchange of gases between lungs alveoli and air. It happens because of difference between pressure in the lungs alveoli and atmospheric air. A pressure gradient develops due to changes in lung volume which results from thoracic wall movement. There are two phases of ventilation (inspiration and expiration) happens rhythmically with a respiratory rate of 12-16 cycles/minute. This rate is defined in terms of respiratory cycles occurring per minute and varies according to age, sex and physical activity. Resting person generally has a rate of 12-16 c/min while it increases up to 40 c/min during physical activity (McLafferty et al, 2013). Two different terms are used to define the respiratory rate- tachypnea and bradypnea. Tachypnea is known as higher rate than the normal and bradypnea is the lower rate than the normal rate.

Thoracic cavity constitutes a rigid structure for the protection of vital organs. In contrast to this, pulmonary ventilation requires flexibility during respiration process for inspiration and expiration process (Seeley, Stephens & Tate, 2003). Force provided by inspiratory muscles helps ribs for the extension for inspiration and returns it to the normal stage. Due to lack of muscles, lungs cannot start their movement process hence follow chest movement to which they are attached by pleural system. Intercostal muscles (external and internal muscles) play an important for pulmonary ventilation. External intercostal muscles and diaphragm both contracts during resting inspiration.

A signal generated within medulla oblongata provides stimulus to motor neurons for contraction of inspiratory muscles. It results into entry of atmospheric air into the lungs as the outside pressure (760 mmHg) is higher than inner intrapulmonary pressure which is 759 mmHg (McLafferty et al, 2013). During resting phase, intrapulmonary pressure reduces by 2-3 mmHg for inspiration in comparison with atmospheric air. In reverse, intrapulmonary pressure increases by 2-3 mmHg for expiration during resting phase (Seeley, Stephens & Tate, 2003).

Abdominal cavity is separated from the chest cavity through diaphragm having convex structure towards the chest cavity. During inhalation, diaphragm moves downward by 2 cm in resting phase. Contraction allows introduction of air into the lungs known as tidal volume.

Pulmonary ventilation is based upon Boyle’s law which denotes an inverse relationship between volume and pressure. The volume of thoracic cavity increases due to contraction of diaphragm and external intercostal muscle. This results into decreased pressure within the thoracic cavity as per the Boyle’s law and the process of inspiration takes place.

In contrast to inspiration, expiration is a passive process and thoracopulmonary cavity return to its actual position. According to the Boyle’s law Reduction in volume of thoracic cavity because of muscle relaxation increases the intrapulmonary pressure (761 mmHg) that acts as a driving force for elimination of air containing carbon di oxide from lungs to the atmosphere (Seeley, Stephens & Tate, 2003).

Answer: Smoking is known as an independent risk factor for cardiovascular diseases. It has a direct impact on the mechanism of lipid transport by altering enzymes involved in high density lipoprotein (HDL) metabolism. Cigarette smoking lowers the activity of cholesterol acyltransferase (LCAT), cholesterol ester transfer protein (CETP) and hepatic lipase (He, Zhao & Peng, 2013).

Smoking is associated with decreased level of apolipoprotein A-1 (apoA-1) which in turn impairs HDL synthesis (He, Zhao & Peng, 2013). Synthesis of nascent HDL particles involves formation of apoA-1 followed by interaction with free cholesterol from hepatic tissues. Esterification of this cholesterol occurs in the presence of LCAT enzyme. Cigarette smoking is known for lowering of LCAT plasma concentration. Reduced activity of LCAT affects HDL maturation and also induces clearance of newly formed HDL from the circulatory system.

LCAT, hepatic lipase and CETP are involved in HDL metabolism within plasma and arterial wall. Large HDL particles (HDL2) are generated through LCAT which are redistributed by CETP into smaller particles (HDL3) followed by hydrolysis process through lipase enzyme. Smoking reduced concentration of HDL2 sub fraction but does not have any impact on HDL3. It is also evident that second hand smoke also lowers HDL2 concentration significantly (Barnoya & Glantz, 2005).

Oxidants are capable of modification of HDL and impairs athero-protective properties of HDL. Oxidised HDL increases the disease severity and also increases vascular inflammation process (He, Zhao & Peng, 2013).

Endothelial dysfunction is associated with cardiovascular diseases. Research studies indicates that various types of risk factors triggers an inflammatory process that results into loss of antithrombotic properties of endothelium. Smoking appears as an important modifiable risk factors associated with abnormal endothelial physiology (Tousoulis, Charakida, & Stefanadis, 2006). Dysrhythmia can occurs due to various reasons for example, hormonal changes, electrolyte changes within blood stream etc. Abnormal heart beat is the one of the main symptoms associated with heart diseases.

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