Patho-Physiological Mechanisms of Acute Pulmonary Oedema - Assignment Example

Running Head: Case Study A Mr Smith Student’s Name: Instructor’s Name: Course Code and Name: University: Date Assignment is due: Case Study A Mr Smith Question One a) Outline the patient preparation/education required to perform a 12 lead ECG. Your answer needs to include the rationale for patient positioning for an ECG. Explain why the ECG is called a 12 lead ECG. A 12 lead ECG is a medical technology used to record the electrical impulse activity of the human heart. This has otherwise been referred to as the depolarisation and or repolarisation of the heart’s myocardium (Corrado1 et al., 2009). In contemporary practice, a 12 lead ECG is done by monitoring the patient’s heart rhythm and rate (Singh, Connolly & Crowns, 2007; Scott, 2008). Many doctors are currently using the procedure to evaluate a patient’s response to such medications as anti-dysrhythmics (Goldfinch, 2006). Again, the 12 lead ECG is used to obtain the baseline recordings of the heart before any surgical procedure is initiated (Corrado1 et al., 2009). It is also used in the evaluation of the effects and impacts of a disease or injury that has impacted on the heart’s functionality (Cecil, Bennett & Plum, 2005). Finally, the 12 lead ECG is used in the detection of ischemia presence or of any functionality damage (Singh, Connolly & Crowns, 2007). The 12 lead reference captures the notion that the examination interacts with the heart at 12 distinct points. There are 12 areas of the human heart’s anatomy through which an examiner gains access to the human heart (Cecil, Bennett & Plum, 2005). Each one of these is called a leads. The 12 lead ECG views most of the surfaces on the left ventricle from a whopping 12 distinct angles (Cecil, Bennett & Plum, 2005). This explains why the procedure is called a 12 lead ECG. There are six different limb leads and six distinct chest leads. The limb leads include, avR (at the base of the right arm). AvL (at the base of the left arm) avF (at the base of the left foot), I (measuring the electrical impulse potential between the left and the right arm), II (measuring the electrical impulse potential between the left and the right leg) and III (measuring the electrical impulse potential between the left arm and the left leg) (Davis, 2005). The chest leads include, V1 (the fourth right intercostals), V2 (the fourth left intercostals), V3 (the space between then fourth left intercostals and the mid-clavicular), V4 (mid-clavicular or mid-collarbone), V5 (the fifth intercostals space/ anterior axillary line) and V6 (fifth intercostals/midaxillary line) (Corrado1 et al., 2009). Positioning of the patient is of a cardinal importance because the leads used as explained above are the eyes of the examiner (Cecil, Bennett & Plum, 2005). The positive electrode is the one that ‘sees’ the heart. As such, the position that an examiner places the positive electrode on a patient’s body necessarily determines the particular area of the patient’s heart that the examiner can see via a particular lead (Cecil, Bennett & Plum, 2005). The appropriate patient preparation/education required to perform a 12 lead ECG includes about 9 steps. The first step is to explain the entire procedure to the patient so that he or she can understand what they will be going through and what you intend to find out. This also gives you the opportunity to obtain the consent from the patient (Cecil, Bennett & Plum, 2005). The next step is to check for any allergies in the patient (Das, 2010). The third step is to ensure that all the cables have been connected in the 12 lead points as appropriate (Das, 2010). The fourth step is to check whether the patient’s body surface is dry and clean. The fifth step in the procedure is to ensure that the electrodes are all in an intimate/close contact with the patient’s skin (Corrado1 et al., 2009). The sixth step is to enter the patient’s data and then to wait until the patient’s tracing has no artefact, before proceeding to request that the patient lie on the table perfectly still. The last step (ninth) is then to push the button of the apparatus which then initiates the tracing of heart impulses (Das, 2010). b) Calculate the heart rate (a trial and ventricular) on the ECG. Outline the methods available to calculate the heart rate from a 12 lead ECG and briefly discuss. The three methods ECG ruler Six second strip 30 second squares division by 300 The heart rate is a time function. For one to measure the heart rate therefore, one needs an ECG rhythm strip. The ECG paper provides a precise scale that is used to measure time in cycles of 1 second usually measured in 25 mm of the ECG paper scale made up of small boxes and grids (Corrado, 2010). The ECG ruler therefore, is the paper strip that has a scale with markings placed 25 mm apart, each 25mm representing a single second of the heart rate (Corrado, 2010). The ruler also includes hash marks placed at both the bottom and top of the graph-like paper to indicate the intervals of one second and or three seconds (Cecil, Bennett & Plum, 2005). Contemporary procedures have three distinct methods of calculating the human heart rate (Davis, 2005). The three include the six-second count, the calliper method and finally the triplicate calculation method (Das, 2010). The most common method in hospitals across the world is the six-second count mainly because it is easy and straight forward. The method involves a multiplication of a factor of 10 by the total QRS complexes number divided by six seconds (Cecil, Bennett & Plum, 2005). This gives the QRS complexes of the heart within a single minute (60 second duration). This method works very well regardless of whether the heart rhythm is irregular and or regular. The 6-second count is adequate in measuring either fast or slow rhythms (Das, 2010). The count of six seconds on the ECG ruler is what is called a six-second strip. As such, the six-second strip refers to a single count of QRS complexes. In our case study, the number of QRS occurring in a count of six seconds is 15 (Davis, 2005). This is then multiplied by 10 to get a heart rate of 150 QRS per minute as the heart rate (Corrado et al., 2010). The triplicate calculation method is mainly employed to measure the heart rates within short periods such as in less than three seconds. It is also used to calculate the heart rates accruing from rapid tachycardia (Das, 2010). While being a very quick method of calculating the heart rate, the triplicate method is not as accurate as the 6-count method (Cecil, Bennett & Plum, 2005). Again, for the triplicate method to be effective and reliable, the heart rhythm must also be very regular and consistent, called consistent R-R intervals, even though for a short duration (Corrado1 et al., 2009). In using the triplicate method, one needs to allocate the calculation area of the ECG paper as a large square measuring 0.20 seconds which translates to 5mm (Cecil, Bennett & Plum, 2005). The first step is to establish the R wave falling on the thicker vertical line and then to measure how the preceding R waves occur subsequently and at what length apart. In this understanding for instance, a single QRS after every one fifth of a second will equal to 5 QRS per second or 300 QRS per minute (Goldich, 2006). A popular term in this calculation is division by 300, referring to the number of QRS complexes occurring in every minute (Corrado, 2010). A single GRS is that a division of the minute by 300 in the example given above. Given that the multiplication is by a factor of 10, then the rate can be given by an area of 300/10 resulting to 30 second squares (Das, 2010). This means that the recorded number of R waves in the 30 large squares will equal to 6 seconds and the rate is then given when the 30 seconds squares are multiplied by 10 (Corrado1 et al., 2009). The third method of calculating heart rate is the calliper method used when one wants an accurate number of millimetres occurring in an R-R interval. Since the ECG paper usually records at speed of 25mm/second, the total millimetres will be 1500 which is then divided the R-R interval to get the QRS number in every minute (Cecil, Bennett & Plum, 2005). Given the explanation given above, one can use the markings plotted on the ECG paper to accurately calculate events occurring within a patient’s cardiac cycle (Davis, 2005). The horizontal axis has large blocks of 0.2 seconds each and small blocks of 0.04 seconds each (Cecil, Bennett & Plum, 2005). On the vertical axis, which represents the voltage (electrical energy), has each vertical millimetre representing 0.1 millivolts of electrical energy. The deflections are however typically referred to as millimetres and not millivolts (Cecil, Bennett & Plum, 2005). c) You have Identify the rhythm in Figure 1 is called Atria fibrillation (AF). Concisely outline what criteria it meets to confirm this label. One example would be no p waves The rhythm identified in the case study is indeed atrial fibrillation, a common abnormal heart rhythm involving the two atria (upper chambers of a human heart) (Fox, Parise & D'Agostino, 2005). The name atria is derived from the quivering/fibrillating of heart muscles in the atria which is abnormal since normally there are supposed to be coordinated contractions (Das, 2010). When the pulse is measured and the heartbeats are counted and they seem not to occur at near-regular intervals, then there is a notable abnormality (Fox, Praise & D'Agostino, 2005). Whenever there is a coordinated atrial contraction in the initial track of each heart beat is indicative of AF (Cecil, Bennett & Plum, 2005). The strongest indicator of the condition in the case study is the absence of P waves on the ECG paper (Davis, 2005). A normal atrial depolarization has the core electrical vector directed away from SA nodes towards AV nodes and also spreading from right atrium towards left atrium. This is what is referred to as the ECG P wave. A normal P wave must be upright at leads aVF, II and III since the normal electrical activity moves towards positive electrodes in these leads. It must then be inverted at aVR since the electrical activity is moving away from positive electrode for the aVR lead (Levy, 2005). Given that P waves must always be upright when at the II and aVF leads and then inverted at the aVR lead, the case study ECG paper shows that the patient has no p waves, thus having an AF (Cecil, Bennett & Plum, 2005). Question Two Explain the patho-physiological mechanisms of Acute Pulmonary Oedema. Importantly, acute pulmonary Oedema must be conceived as a common medical emergency, one that is overly life-threatening. In its intervention, nursing care must aim at making an early diagnosis immediately the condition is suspected to prevent the condition become too severe to treat (Davis, 2005). Acute pulmonary Oedema can simply be defined as a set of signs and or symptoms grossly representing a transference of body fluids (i.e. blood) from the intravascular compartment and onto the interstitial before reaching the alveoli (Anterior & Kit, 2007). Both the cardiac and the non-cardiac condition can produce a pulmonary Oedema and the nursing care provided needs to understand the underlying conditions precipitating the Oedema (Levy, 2005). It is s complicated clinical problem whose patients frequently experience cardiac and or pulmonary disturbances concurrently (Angerio & Kot, 2007). In practice, the physiopathology of the acute pulmonary Oedema is alike to that of subcutaneous tissues such as when there is an imbalance in the Starling Forces leading to fluid accumulation within the alveolus and the interstitial. The simple explanation is where brokage at one end of a pipe may cause pressure to rise behind such brokage until the pipe bursts or forces the liquid behind the brokage to push into any available space (Davis, 2005). The mechanism responsible for keeping the alveolus dry include the plasma oncotic pressure of about 25mm/Hg, which is higher than the pulmonary capillary pressure of 7-12 mm/Hg (Luna, Fiol-Sala & Antman, 2007). Secondly, the connective tissue as well as cellular barriers, which are relatively impermeable to most plasma proteins is also involved just as the extensive lymphatic system, in keeping the alveolus and the interstitial dry (Levy, 2005). When the normal mechanisms of keeping lungs dry are overwhelmed by excessive fluids or malfunction in any other way, the Oedema accumulates in very predictable sequential steps/stages. The first stage is an increment of fluid transfer into the lung’s interstitium. This is because the lymphatic flow increases while there is no equivalent increase in the interstitial volume (Davis, 2005). The second stage occurs when the capacity of a patient’s lymphatic system to drain any excess fluid is grossly exceeded. Body liquids begin to accumulate within interstitial spaces surrounding the lung vasculature and the bronchioles. This is what causes roentgenographic patterns of the interstitial pulmonary Oedema (Angerio & Kot, 2007). The third and final stage of the process accrues when the body fluid continues to accumulate and thus increase the pressure. This causes the fluid to push into the interstitial space surrounding the alveoli. Again, the pressure and liquid flow disrupts most of the tight junctions normally found along alveolar membranes. These fluids build up initially within the alveolar capillary membranes periphery before ultimately flooding the alveoli (Cecil, Bennett & Plum, 2005). Notably it is within the third stage that the roentgenographic picture obtainable of the alveolar pulmonary Oedema becomes possible (Luna, Fiol-Sala & Antman, 2007). Again the gas exchange process becomes critically impaired. Another important thing to note is that the processes occurring as detailed above not only occur at the alveolus sites. Gravity also exerts a considerable amount of influence on fluid mechanics within the lung. Again, blood is normally heavier/denser than both the air and the air-containing tissue (Angerio & Kot, 2007). The net effect of this gravitational pressure is most pronounced on either lung. During normal circumstances, a greater level of perfusion accrues at lung bases on either side, and not just at either location apices. When the pressures at the pulmonary venous rise or when the fluids begin to grossly accumulate at both lung bases, the patient’s blood flow also begins a pattern redistribution towards the apices (Angerio & Kot, 2007). Question Three a) Identify the nursing goals of care, interventions and evaluation for managing this situation. Your answer must include scientific rationales for action Nursing care in cases of pulmonary Oedema primarily require early diagnosis so as to establish the early pathophysiology of the condition before it becomes irreversible and then helping the patient recover through a variety of interventions (Panhuyzen-Goedkoop, 2009). Once the condition has been treated, the nursing care then moves on to evaluation and management of the condition until full recovery is achieved (Cecil, Bennett & Plum, 2005). The procedure of nursing care begins with the care giver studying and asking about the patient’s previous history in relation to cardiac and or pulmonary diseases as well as any previous episodes of a pulmonary Oedema incidence (Saffitz, 2006). Any previous instance of cardiac failure or current use of prescription medicine should be noted (Cecil, Bennett & Plum, 2005). Nursing care then proceeds to physical examination which is done with the aim of establishing any signs of a ventricular failure, a manifestation of dyspnoea, a sign or signs of a hypoxia development and finally the presence of fluids in any of the lungs (Sweeney, Bank & Nsah, 2007). In these diagnostic stages, the care giver also conducts a series of laboratory tests as well as image exams with the aim of establishing any malfunction and or abnormality. Such tests and exams target diagnosis and assessment of cardiac, renal and respiratory functions (Levy, 2005). There are seven standard tests and exams conducted during the normal diagnostic care stages for many pulmonary Oedema patients beginning with blood studies where the CBC is tested differential status, electrolyte states, the BUN, the concentration levels of serum protein and creatinine (Luna, Fiol-Sala & Antman, 2007). Secondly, there is a urinalysis as well as microscopic urine examination which enables proteinuria detection (Drezner, 2009). The third test is the room-air arterial test for blood gas concentration. If the test notes a decrease in the PCO2 and PO2 levels, or a reduction of PO2 and increase of PCO2, then there is a severe incidence of the Oedema and an urgent need of mechanic ventilation (Cecil, Bennett & Plum, 2005). The fourth test available is the PA plus the lateral chest scan which is useful in detecting early signs of the pulmonary Oedema (Levy, 2005). Kerley B lines and presence of horizontal lines detectible laterally within the lower zones which are contradictory to blood vessel contours shows a progressing Oedema (Cecil, Bennett & Plum, 2005). With progress, the alveolar Oedema can be observed with a butterfly pattern, normally characterized by central predominance of a series of shadows with clear zones at the periphery lobes. This test also helps in detecting abnormal cardiac enlargement (Luna, Fiol-Sala & Antman, 2007). The fifth test is the ECG (electrocardiograph) which is done to confirm or as a follow up to any detection of cardiac abnormality (Jahangir, 2007). The ECG usually works best in diagnosing the factors causing the Oedema. There are other tests available test for selected patients, most of which are targeted at identifying the underlying cause of an Oedema when such is not outrightly clear (Drezner, 2009). One such test is the right heart catheterization, used to measure the pulmonary capillary’s wedge pressure. Any variation from the universally elevated level of less than 25 mmHg (Boaco & Ward, 2005) and an abnormal one indicative of cardiac pulmonary Oedema that is over 25 mmHg. Another test is the echocardiography, which is used to show any existing valvular lesions and or cardiomyophaty (Cecil, Bennett & Plum, 2005). Other tests include blood cultures, pulmonary function tests and many other less common tests (Dublin, 2005). During intervention, nursing care should ensure that an acute pulmonary Oedema occurrence is a very dynamic medical emergency such that treatment arrangements need to be made soonest the diagnosis is confirmed or even suspected (Uren, 2005). The patient requires frequent examinations. In treatment, patients must necessarily be placed in sitting positions with their legs dangling over a bed side so as to make the respiration process easier (Cecil, Bennett & Plum, 2005). When rapid ventricular response and or atrial fibrillation is attributed as a cause, 0.25 mg of Dioxin should be administered in a slow push IV push to total up to 1 - 1.5 mg in 24 hours (Drezner, 2009). b) Identify the mechanism of action and desired effect of Frusemide, GTN, Morphine and oxygen therapy in the treatment of Acute Pulmonary Oedema. Frusemide, GTN, Morphine and oxygen therapy are all used in the treatment of acute pulmonary Oedema. To begin with, oxygen therapy involves providing 100% oxygen (pure oxygen) to a patient delivered via a mask so as to aid in the abnormal respiratory mechanisms of the patient (Drezner, 2009). The process ensures that the patient has sufficient oxygenation despite having fluids in the lungs. Secondly, the Morphine administration is used to help the patient reduce the level of anxiety during treatment, to decrease the sympathetic outflow and to trigger venodilation (Panhuyzen-Goedkoop, 2009). Morphine is also used to decrease preload, which in turn helps to relieve the effects of pulmonary Oedema (Cecil, Bennett & Plum, 2005). Morphine should however, never be administered to patients who have a decreased sensorium or an increased respiratory drive since it may cause respiratory arrests. Whenever such arrests are noted 0.8 - 2.0 mg of naloxone IV bolus can help reverse it (Drezner, 2009). The ideal initial dosage of Morphine should be 2 - 5 mg of IV bolus, repeated severally to a maximum level of 15 mg (Jahangir, 2007). For Frusemide, a 40 - 100 mg of IV bolus is usually administered to patients with the aim of causing instant venodilation so as to create diuresis that mobilizes fluid to move out of the lungs and into circulation (Bosco & Ward, 2005). When such happens, the urine is expelled from the system to reduce venous return. Finally, Nitro-glycerine can and should be administered to patients in o.4 mg IV drip and or in sublingual tablets to relieve pulmonary Oedema (Hussar, 2006). Nitro-glycerine is used primarily aimed to produce venodilation and also to dilate the epicedial coronaries. When this happens, it becomes a treatment for ischemia cases by itself, notably important ischemia is the underlying cause of pulmonary Oedema (Drezner, 2009). 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