Need a 500 words Content map regarding Nursing and Biology
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Severe dyspnoea is the sudden and severe shortness of breath or having difficulties in breathing. It is exists as one of the common reasons why patients visit the accident and emergency department in a hospital. After an exercise, breathlessness is considered to be a normal condition. However, after rest this usually should resolve.
If a patient is experiencing breathlessness that comes suddenly and unexpectedly, it may be a major warning or sign of a fundamental medical condition associated with the heart or in the lungs (Diller, G. P., et.al. 2007). Besides exercise, severe dyspnoea can be caused by factors like panic attacks, anxiety, obesity etc. In our case an examination on the ECG monitor showed atrial fibrillation a symptom of Heart attacks and which is associated to the severe dyspnoea along with chest pain.
Heart failure causes difficulty in the heart pumping out blood to the body organs and into the lungs for cleansing. This causes a build-up of water inside the lungs and makes breathing extra difficult and leads to dyspnoea. Therefore the shortness of breath may have been caused by atrial fibrillation or supraventricular tachycardia.
Respiratory rate of 24 breaths/minute for the 78 years old female seems quite at the normal range. The typical respiratory rate for a healthy elder person above sixty five years at rest is 12–28 breaths per minute. The average rate of respiratory at rest by age from birth to age of 80 years is 30-40 breaths per minute.
SpO2 85%, on room air. Fundamentally, a saturation of 97% of all the haemoglobin in a human body is filled with oxygen molecules. When the saturation range is 96% to 100%, this is generally considered normal. A saturation below 90% could lead to life threatening problems. The boundary between a healthy saturation level (95-98%) and respiratory failure (usually 85-90%) is narrow. When oxy-haemoglobin is below 90% it is considered low and in our case the old woman has a saturation of 85% meaning that insufficient amounts of oxygen reaches the body cells a situation that could damage some of her organs.
When resting, the normal heart rate is generally between 60 and 100 beats per minute. A person who is fit may have a lower heart rate, although it is considered abnormal if your resting heart rate is faster. Therefore a pulse rate of 120 beats per minute clearly is not a threat but shows that all is not right in the body.
Auscultation of lungs identifies bilateral basal crackles which means there is airway irritation and inflammation with increased mucus production. It will be wise to go ahead and examine if Mrs Brown has some other common symptoms like a wet cough, fever and relate to the shortness of breath to know why the crackles are there.
The pathogenesis causing the clinical manifestations with which Mrs Brown presented. Looking at the Respiratory rate of 24 breaths/minute, blood pressure 170/95mmHg, and bilateral basal crackles, Mrs Brown is developing lung complications, which could be pulmonary edema. This condition is frequently caused by heart failure a condition that was evident form the ECG monitor that showed atrial fibrillation. When the heart cannot pump blood to the body efficiently, blood backs up into the veins which take blood through the lungs to the left side of the heart (Ware, L. B., et.al. 2005).
Even as the pressure in these blood vessels rises, fluid is pushed into the air spaces called alveoli in the lungs. The fluid decreases normal oxygen movement through the lungs. This combined with the increased pressure can lead to shortness of breath. From the observations carried out, even if the breaths per minute seem okay in the patient, something is not right with the bilateral basal crackles inside the lungs and the high blood pressure (Ware, L. B., et.al. 2005). However to confirm if the pathogenesis is correct, together with all the tests done including the ECG, others tests and observations like pale or blue skin colour, blood chemistries, complete blood count, echocardiogram should be carried out to just as a support.
The first stage in managing patients with cardiogenic pulmonary edema is to address the issue of resuscitation that includes taking care of the airway, breathing, and circulation. It will be wise to administer oxygen to Mrs Brown to keep oxygen saturation at greater than 90%, because arrhythmia could be devastating to some body organs like the brain.
We can use a face mask, non-invasive pressure-support ventilation, or intubation and mechanical ventilation as safe procedures of oxygen. The chosen method will depend on Mrs Brown’s level of consciousness, or the presence of hypoxemia and acidosis. Intubation and mechanical ventilation is necessary when there is stubborn hypoxemia, acidosis, or altered mental status.
After administration of Oxygen medical treatment follows and it focuses to reduce the pulmonary venous return, reduction of systemic vascular resistance, inotropic support. Conducting a preload reduction is important so as to decrease pulmonary capillary hydrostatic pressure as well as lessens fluid transudation into the pulmonary interstitium and alveoli (Ware, L. B., et.al. 2005). Also, afterload reduction will increase cardiac output and improve renal perfusion allowing easy diuresis when the patient has fluid overload. If Mrs Brown remains hypoxic despite complementary oxygenation or still have severe breathing distress she will require ventilatory support to add to the medical therapy.
Patients with acute valvular disorders may not tolerate medications to reduce their preload and afterload and inotropic support is necessary in this subset of patients, to uphold adequate blood pressure. Besides these nursing strategies, ultrafiltration to remove the fluid is equally important particularly if the patient has renal dysfunction and diuretic resistance. Also Intra-aortic balloon pumping may be employed to achieve hemodynamic stabilization in the patient before definitive therapy (Ware, L. B., et.al. 2005). This decreases afterload as the pump deflates; during diastole, the pump inflates to improve coronary blood flow. Lastly will be Mrs Brown should be given a low-salt diet to minimize fluid retention.
IV Furosemide mechanism of action is blocking the absorption of sodium, chloride, and water from the filtered fluid in the kidney tubules, causing a profound increase in the output of urine (diuresis). The onset of action after oral administration is within one hour, and the diuresis lasts about 6-8 hours.
Direct acting vasodilator is useful in the preload and afterload to increase the cardiac output and reduce pulmonary vascular resistance. Sublingual glyceryl trinitrate is a vasodilating agent used for the relaxation of vascular smooth muscle. It produces dilation of both arterial and venous beds. Dilation of the post capillary beds, including large veins, promotes peripheral pooling of blood and decreases venous return to the heart reducing left ventricular and end diastolic pressure while arteriolar relaxation reduces systemic vascular resistance.
Reference
Ware, L. B., & Matthay, M. A. (2005). Acute pulmonary edema. New England Journal of Medicine, 353(26), 2788-2796.
Diller, G. P., & Gatzoulis, M. A. (2007). Pulmonary vascular disease in adults with congenital heart disease. Circulation, 115(8), 1039-1050.
