Structure Of The Respiratory System Biology Essay


The structure of the respiratory system is made up into two parts; the upper respiratory tract and the lower respiratory tract. The upper respiratory tract contains the external nose, nasal cavity, the pharynx (nasopharynx, oropharynx, and the laryngopharynx) and the larynx. These structures are lined with a ciliated mucosa which warms and humidifies air taken in, and filters out foreign particles from this air. The lower respiratory tract contains the trachea, which branches down into two main bronchi (airways) at the carina. The right and left bronchi then connect to the left and right lungs and further down to the bronchioles and alveoli. This system protects the body from invading organisms and exchange gases between the air inhaled and the blood. (Huether & McCance, 2008)

There are three steps in the process of the exchanging of gases between the outside air and the blood. These three steps are ventilation, diffusion, and perfusion. Ventilation is the movement of air into and out of the lungs. Diffusion is the movement of gases between air spaces in the lungs and the bloodstream. Perfusion is the movement of blood into and out of the capillary beds of the lungs to body organs and tissues. (Huether & McCance, 2008)

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In heart failure, the heart cannot contract forcefully enough during systole to eject adequate amounts of blood into the circulation. When this happens the ejection fraction drops when the ventricle dilates. As this decreases, oxygen reaching the tissues decreases and blood accumulates in the pulmonary vessels. Cardiac output decreases and causes fluid to back up into the pulmonary system. When hydrostatic pressure (the force water pressing against the confining walls of a space) builds up in the pulmonary venous system, the alveoli (where gas exchanges of oxygen and carbon dioxide occur) become fluid filled. This increase of fluid in the pulmonary system also causes an increase in pulmonary venous pressure. Manifestations include symptoms of inadequate tissue perfusion and pulmonary and systemic congestion. Respiratory symptoms that can occur are a hacking cough (early manifestation of heart failure), dyspnea or feelings of breathlessness, crackles or wheezes in the lungs, frothy, pink-tinged sputum (life-threatening sign of pulmonary edema), and tachypnea. (Ignatavicius & Workman, 2010) Obesity can also have an impact on the respiratory system. With AH being categorized as obese this increases the workload of the system in attempt to supply adequate oxygen to all vital tissues.

AH had many of these respiratory symptoms. She had complaints of shortness of breath with activity, fatigue, weak non-productive cough, and diminished breath sounds in her lower lobes bilaterally. Her respirations were between 16 to 20 breaths per minute and her oxygen saturation was around 94% on room air. She did not show any use of accessory muscle use. AH did have to utilize rest periods with activity such as ambulation and eating. When she arrived to the emergency department, AH complained of shortness of breath, fatigue, and presented with crackles upon auscultation. No supplemental oxygen or respiratory agents were administered during her admission, but coughing and deep breathing were encouraged throughout the day. AH’s Hemoglobin and Hematocrit values were in normal ranges indicating that there is adequate oxygen in the blood and not over-diluted from fluid retention and CO2 values was high indicating that there is increased carbon dioxide in the blood as a complication from the her heart failure. Labs are shown previously in the table.


The renal system is composed of two kidneys, blood vessels, two ureters, bladder, and the urethra. The kidneys maintain a stable environment for optimal cell and tissue metabolism by balancing solute and water transport, excreting metabolic waste products, conserving nutrients, and regulating acids and bases. The kidneys also have endocrine functions by secreting hormones (renin, erythropoietin, dihydrooxyvitamin D3, erythrocyte production, and calcium metabolism). The formation of urine is achieved through the process of glomerular filtration, and tubular reabsorption, and secretion within the kidney. The ureters deliver the urine produced by the kidney to the bladder. The bladder stores the urine that it receives by the ureters. Then urine is released from the bladder through the urethra. (Huether & McCance, 2008).

Infections of the urinary tract and kidneys are common among women. When collecting information on past medical history for AH, reoccurring urinary tract infections were listed. Urinary tract infections are common in women due to the fact of their short urethra (3 to 4 cm) compared to a male urethra (18 to 20 cm) and the closeness of the urethra to the anus. (Huether & McCance, 2008). A urinary tract infection is an inflammation of the urinary epithelium usually caused by bacteria. It may occur anywhere along the urinary tract but acute cystitis (inflammation of the bladder) is the most common site. AH is at risk for this infection because of female gender, elderly age, treatment with antibiotics, and indwelling catheter. Generally these infections are mild and result without any complications. Manifestations of cystitis include frequency, urgency, dysuria (painful urination), and suprapubic and low back pain. Hematuria, cloudy urine, and flank pain are more serious symptoms. Elderly patients may by asymptomatic or demonstrate confusion or vague abdominal discomfort. (Huether & McCance, 2008). AH did not demonstrate any of these manifestations during her hospital stay. Her recurrent infections and other concurrent illness put her at a greater risk of mortality. These infections are diagnosed by urine cultures of specific microorganisms. A single large dose of antibiotics or a three to seven-day course are most common treatments. Antibiotics are chosen from past experience, sensitivity, and resistance. AH had a urine culture obtained on February 08, 2012 and showed small amounts of bacteria present. Her urine was clear yellow and specific gravity was 1.030. AH was prescribed Ciprofloxacin (Cipro) 250 MG tab BID. Cipro is a fluoroquinolone antibiotic.

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Heart failure is a condition that may contribute to acute renal failure. Heart failure causes poor perfusion to the kidneys and can cause a decrease in oxygen delivery and cause cell injury (Ignatavicius & Workman, 2010). When there is low renal blood flow, the kidneys activate the renin-angiotension-aldosterone system. Renin assists in regulating blood flow, glomerular filtration rate, and blood pressure. Renin is secreted when blood pressure or blood volume changes are sensed. Renin then converts angiotensinogen into angiotensin I. Angiotensin converting enzyme (ACE) converts angiotensin I to form angiotensin II. Angiotensin II is a potent vasoconstrictor that increases peripheral vascular resistance (dilation or constriction) to maintain vascular tone when there are low perfusion states, as in heart failure. Angiotensin II also has sympathetic (fight or flight) stimulation causing the adrenal cortex to release aldosterone. Aldosterone is responsible for sodium and water retention and excretion of potassium in the kidneys. Angiotensin II also has cellular effects that can cause overgrowth and hypertrophy of vascular smooth muscle cells and cardiac fibroblasts (responsible for remodeling process of heart structure). This compensatory mechanism is meant to protect all organs during low cardiac output states, but overtime, has negative effects than further worsens heart failure. (Ignatavicius & Workman, 1991/2010) This is why angiotension converting enzymes are a common medication given to these patients. It stops angiotension I from converting to angiotension II, which stops the vasoconstricting affects.

When the kidneys do not receive enough oxygen, they are not able to perform optimally. “Pre-renal azotemia is acute renal failure caused by poor blood flow to the kidneys” (Ignatavicius & Workman, 2010). The results of pre-renal azotemia can be reversed if the patients cardiac output cardiac output increases or returns back to their normal functioning for that individual. Diuretics can be prescribed to promote renal blood flow. AH is at an increased risk for complications of ARF because of having heart failure and also being put on fluid restrictions. AH was only able to receive 1.5 liters of fluid per 24 hours. This fluid restriction decreases the workload of the heart but contributes to a decrease in urine production and increased concentration of the urine, which is harder on the already affected kidneys. AH did not report any abnormality in urine characteristics or amount. AH was producing the adequate amount of urine at least 30ml/hour which was measured by her indwelling catheter. AH’s blood urea nitrogen and creatinine values were all high and the glomular filtration rate was at a normal value. These values indicate that the kidneys are being overworked. Labs are all shown previously in the table.

There is also another compensatory mechanism that occurs in the renal system. Natriuretic peptides are neurohormones that work by encouraging vasodilation and diuresis through sodium loss in the renal tubules. The B-type natriuretic peptide (BNP) is made and released by the ventricles when a patient has fluid overload as a result of heart failure. This number increases with age and has a greater concentration in women. With AH having congestive heart failure, this number will be increased in her lab work. A BNP level can help with the diagnosis and severity of congestive heart failure. The body does this to try and help the heart, but can actually make it worse in the end.