There was a particular case study which I came across when I was on my clinical rotation. The case study involved a man who was called Mr. Curtis. He was 74 years old and the man had actually been admitted due to a routine cholecystectomy. He had a medical history of high blood pressure as well as the cardiac myocardial infarctions over a period of the last one year.
While performing my routine observation through an electrocardiogram, I realized that the patient had an irregular heart rate (HR).The results of the cardiogram were as shown in the picture below:
Based on the above electrocardiogram, it is very clear that the patient has what is known as an irregular heart rate. A regular or rather a normal cardiac rhythm is characterized by a P wave, a QRS and finally the T wave.
|
WAVE/INTERVAL |
VALUES |
|
QT Interval |
0.36-0.44 Seconds. |
|
P wave |
Amplitude:2-3 mm high Deflection:+ in I,II,AVF,V2-V6 Duration:0.06-0.12 seconds |
|
T wave |
Amplitude: 0.5 mm in limb hills. Deflection:I,II,V3-V6 Duration:0.1-0.25 seconds |
|
ST segment |
0.08-0.12 seconds. |
|
QRS complex |
Amplitude:5-0 mm High Deflection: + in I, II, III, AVL, AVF, and V4-V6. Duration:0.06-0.1 seconds |
|
PR Interval |
0.012-0.2 seconds |
The above table and image illustrate a normal electrocardiogram .If we actually compare the results from the patient and the standard, we realize that there are a lot of discrepancies both in the P wave, the QRS complex, The QT interval, the ST segment and finally the T wave.
Based on the above results, the patient might be suffering from cardiac arrhythmia. This is a condition which is also known as irregular heartbeat and is simply a group of different conditions of the heart with irregular heartbeats. The heartbeats can either be too slow or too fast .The results from Mr. Curtis clearly shows that his heartbeat is very fast and that is typical of cardiac arrhythmia. A fast heartbeat is known as tachycardia .Even though majority of arrhythmias are not very serious, they can eventually lead to stroke.
The heart has an electrical system which when falters in any manner, leads to what is known as cardia arrhythmia. An electrical stimulus is usually generated by the sinoatrial node which is a mass or tissue that is found in the right atrium of the human heart (Kunisek, 2012). The sinus node generates an electrical stimulus which travels through conduction pathways downwards. Therefore, the potential reasons for such an arrhythmias involves anything that alters the electrical system of the heart. Such reasons include stress, certain medications and substances like nicotine and caffeine.
Even though treatment of cardiac arrhythmias is not necessary, it should be carried whenever the condition is causing significant or serious signs and symptoms. That is, it should be treated whenever it is posing a health risk to the patient. As previously discussed, cardiac arrhythmias might be either slow heartbeats or fast heartbeats. The treatment option for both also differ but not that much.
In the treatment of slow heartbeats, doctors usually use what is known as a pacemaker since no study has established any form of medications that can cause the hear increase its beats. A pacemaker is a device that is usually or rather implanted in the body near the collarbone. This pacemaker has wires with electrodes that are spread in the blood vessels to the heart and their function is to sense and send signals to the heart to increase heartbeats whenever it slows down.
Doctors usually prescribe a variety of drugs to counter cardiac arrhythmias. The drugs that are used to treat cardiac arrhythmias are known as Antiarrhythmic. The most common Antiarrhythmic are Amiodarone which is also called Cordarone. Others include Flecainide, Procainamide and finally the sotalol. Besides these drugs, there are two other classes of drugs and they include Beta-blockers and the calcium channel blockers. Examples of beta blockers include metoprolol or Toprol XL. These drugs work by reducing the work rate of the heart. Calcium channel blockers on the other hand include verapamil and calan which are used to lower the heart rate.
Beta blockers and calcium channel blockers both have different mechanisms of action. Beta blockers work by blocking the actions of a hormone known as epinephrine or adrenaline. Since calcium usually narrows blood vessels, the calcium channel blockers work by blocking the action of calcium so that the blood vessels can relax and widen thus reducing the heart beats or heart rate.
Antiarrhythmic drugs have several side effects and they include swelling of legs, blurry vision, dizziness, light headedness and fainting also happens sometimes. One can also lose appetite, experience a metallic taste in mouth and being sensitive to light as well. Finally, one can experience diarrhea and constipation.
Disturbances in equilibrium in electrolytes leads to cardiac arrhythmias. The major electrolytes that play a role in cardiac arrhythmia are potassium. The level of potassium in blood plasma should always be maintained at 3.5 and 5.2 mmol /L. Whenever the level of potassium reduce or increase, the overall effects are on the myocardium or the heart muscles which either leads to fast or slow heartbeats .In management of the cardiac arrhythmias, it is therefore necessary to ensure that the resting membrane potential which is defined by the ratio of ICF to that of ECF, is maintained at the required or the recommended levels.
Besides medication and electrolyte management, monitoring is another method in which cardiac arrhythmias can be well assessed and treated. There are various monitoring procedures that can be used. Electrocardiogram, Holter Monitor and finally event monitor are some of the monitoring procedures that are commonly used.
An event monitor is a device the patient wears whenever he or she is on her daily activities. This device is used to monitor those cardiac arrhythmias that are not frequent. It has electrodes that are placed on the patient’s chest then the wires from the electrodes are then attached to the box which is then worn on a belt. Whenever there are any symptoms, a certain button is pressed and activates recording. The monitor would then record the readings One minute before the button was pressed and 40 seconds after the occurrence of the arrhythmia.
A Holter Monitor is another device that can be used to monitor patients. It also has electrodes that are placed on the chest. The device record electrical signals from the heart and then stored by the same device. The patient is then advised on recording his or her activities as well as symptoms like dizziness and the rapid heartbeats.
An Electrocardiogram is also used to monitor the electrical activity of the heart. It has electrodes that are placed on the chest, arms and legs then connected to the machine which eventually produce a graph of the rhythm of the heart.
The following were the results from Mr. Curtis.
|
|
ABG |
Normal range |
|
PH |
7.32 |
7.35-7.45 |
|
PaO2 |
64 |
80-100 mmHg |
|
PaCO2 |
55 |
35-45 mmHg |
|
HCO3- |
26 |
22-28 mmol/L |
|
SaO2 |
91% |
95-100% |
From the results, it is clear that the PH of the blood is below the normal ranges.PaO2 is also below the normal values while PaCO2 is higher the normal values.SaO2 is also below the normal values but the HCO3 is normal .The basic reason as to why there is an imbalance in the blood gases is due to the fact that the alveoli are congested thus there is no balance in the uptake of oxygen and the expulsion of carbon dioxide. The blood pressure increase as the heart tends to work more.
The pathophysiology of acute pulmonary edema can be briefly summarized in the flow chart below
According to McCance, abnormalities in hydrostatic pressure, capillary oncotic pressures, capillary permeability and finally the lymphatic drainage eventually leads to Acute Pulmonary edema. The condition might as well be due to either systolic or diastolic heart failure. Systolic heart failure refers to a condition whereby the left ventricles begin to weaken thus making them unable to sustain an adequate cardiac output. Diastolic heart failure on the other hand refers to a condition in which the left ventricles fail to relax or dilate fully between contractions and this leads to what is known ventricular filling which also eventually result into decreased output. There are several factors or rather conditions that can lead to heart failure. The most common include high blood pressure, cardiomyopathy, coronary artery diseases and finally the valve dysfunction.
Compensatory mechanisms are always stimulated whenever there is reduced cardiac output that arise from heart failure. The compensatory mechanisms include vasoconstriction and fluid retention. Inadequate oxygen in tissues also stimulate the sympathetic nervous system that leads to vasoconstriction through the release of noradrenaline. Reduced flow of blood in the kidneys also stimulates what is known as the renin angiotensin system that leads to systemic vasoconstriction. In summary, all these factors improves on the general cardiac output.
Vasoconstriction always leads to elevated afterload which usually makes the cardiac function very weak .Increased pressure as well as volume in the pulmonary circulation leads to movement of the intravascular fluid in the alveolar cells and the interstitial spaces. It is the congestion of the fluids in the lungs that makes them unable to function properly in terms of gaseous exchange and this eventually leads to respiratory distress or Acute Pulmonary edema.
For a patient suffering from Acute Pulmonary edema, the core objective for treatment is to maximize the functioning of the heart through reducing cardiac work as well as the intravascular volume .There are several form of treatment that are utilized. The treatments are meant to reduce intrapulmonary pressures and allowing the lymphatic system to expel fluids within the alveolar spaces.
Drugs like furosemide, nitroglycerin, nitroprusside, morphine and oxygen are the most commonly used to treat flash pulmonary edema. Furosemide usually acts as a vasodilator and a diuretic. Nitroglycerin on the other hand works as a vasodilator with the aim of reducing preload and when taken in large doses, leads to decreased afterload thus improving on the general cardiac output.
Nitroprusside is usually used as venous and arterial dilator which reduce both the preload and the after load hence reducing blood pressure. Morphine on the other hand reduce pulmonary edema and blood pressure by venous dilation (Obrowski, 2016). However, morphine can lead to respiratory depression hence should be used with a lot of care and caution.
The nursing interventions for patients with acute pulmonary Edema include the titration with oxygen the nasal cannula so as to keep the oxygen saturation within the 92-100% per MD order. The patient will also be given the Lasix 60mg IV BID per MD order and will also be weighed on a daily basis .The patient is also supposed to be placed on the 1500 ml fluid restricted diet per MD order and both the intake and output will be monitored then calculated for each shift.
Components of HDU patient assessment.
There are several components of the HDU assessment and they include airway, breathing, circulation, disability, specialing. All the above components have set standards which the nurses will have to compare against the patient so that they can tell or know how to effectively handle the patient.
Respiratory symptoms of APO and why they occur
There are different signs and symptoms for acute respiratory edema. The most common however include rapid and irregular heartbeats, Blue tinged lips, and a cold and clammy skin, there is also wheezing or gasping for breath. Some patients will also have a feeling of suffocation or drowning which get worse when the patient lies down. There is also coughs which produce sputum that is frothy and may have spots of blood as well. Anxiety, restlessness and a sense of apprehension are also common. Dyspnea is also common and it gets worse whenever the patient lies down.
References
Kunisek, J. (2012). Influence of Patern and Degree of Left Ventricular Hypertrophy on Cardiac Arrhythmias. Cardiac Arrhythmias – New Considerations. doi:10.5772/38133
Obrowski, M. (2016). Deadly High Altitude Pulmonary Disorders: Acute Mountain Sickness (AMS); High Altitude Pulmonary Edema (HAPE) and High Altitude Cerebral Edema (HACE): A Clinical Review. International Journal of Pulmonary & Respiratory Sciences, 1(1). doi:10.19080/ijoprs.2016.01.555553
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