Left Ventricular Failure Causing Hypoxemia and Low Blood Pressure †Nursing Management Essay

Left Ventricular Failure Causing Hypoxemia and Low Blood Pressure – Nursing Management Essay Free Online Research Papers Left Ventricular Failure Causing Hypoxemia and Low Blood Pressure Nursing Management Essay In this essay the author will analyse the normal and pathologic physiology of left ventricular failure (LVF) and how this is related to hypoxemia and low blood pressure (BP). The nursing management will be discussed as well. John had two myocardial infarctions (MI) during the last five years and was waiting for coronary artery bypass graft (CABG) surgery. The angiogram showed severe triple vessels coronary artery disease with poor left ventricular (LV) function. John was admitted to critical care presenting low peripheral saturations, symptoms of respiratory distress and low blood pressure. Ten litres of oxygen were administered by nasal mask; a central venous catheter and an arterial line were inserted in order to continuously monitor John’s BP and central venous pressure (CVP), and to obtain arterial blood gases (ABG’s). John’s mean arterial pressure (MAP) was 55 mmHg and the ABG showed a Partial pressure of arterial oxygen (PaO2) of 7.8 kPa, a partial pressure of arterial carbon dioxide (PaCO2) of 5.5 kPa and an arterial oxygen saturation of haemoglobin (SaO2) of 86%. A urinary catheter was inserted and a chest X-ray was performed. Pulmonary oedema was diagnosed. The oxygen supplied was changed to humidified oxygen at 50% of inspired fraction of O2 (FiO2) and afterwards increased to 60% according to the ABG results; 40 milligrams (mg) of furosemide IV were given as a bolus and continuous intravenous infusion of dopamine was started at 3 micrograms/ kilogram/minute ( µg/kg/min). After 3 hours of treatment, an Intra-aortic Balloon Pump (IABP) was inserted and a furosemide infusion was started at 10 mg/h. PHYSIOLOGY OF BLOOD PRESSURE AND MYOCARDIUM. BP is defined as the force per unit area exerted on a vessel wall by the contained blood, and is expressed in millimetres of mercury (mmHg) (Marieb 2004). The mechanisms that are involved to regulate BP are: neural control of vasoconstriction and contractility, capillary fluid shift mechanism altering blood volume and renal excretory and hormonal mechanisms which alter blood volume and vasoconstriction (Adam Osborne 1997). Marieb (2004) and Thibodeau Patton (1993) state that the neural controls of peripheral resistance act by redistributing blood in respond to specific demands of the body and maintaining adequate MAP by altering blood vessels diameter. These changes are controlled by baroreceptors (located in the carotid sinusis, the aortic arch and in the large arteries of the neck and thorax) and chemoreceptors (activated by an increase in CO2 or decrease in O2 or pH). The renal regulation of BP acts altering blood volume by a direct mechanism, filtrating more or less water in the kidney tubules; or by an indirect mechanism called renin-angiotensin. If the BP drops, the kidneys release an enzyme called renin which triggers a series of reactions that produce angiotensin II (potent vasoconstrictor). It also stimulates the secretion of aldosterone by the adrenal cortex which enhances renal reabsorption of sodium, and stimulates the posterior pituitaria to release anti-diuretic hormone (ADH) which promotes more reabsorption (Marieb 2004, p725-729). During normal homeostasis, the above described physiology maintains normal BP. However, as a consequence of the myocardial infarction, John developed left ventricular failure (LVF) that resulted in low blood pressure. The normal physiology of the myocardium, left ventricular function and the terms related to it are stated below. The bulk of the heart wall is the thick, contractile, middle layer of specially constructed and arranged cardiac muscle cells called myocardium (Thibodeau Patton 1993). Although equal volumes of blood are pumped by the two ventricles, the workloads are totally different. The walls of the left ventricle are three times as thick as those of the right, and its cavity is more circular, this is because the left ventricle has to pump the blood through the systemic circuit and there is five times more resistance than in the pulmonary system. Myocardial function is determined by three factors: Preload: Refers to the amount of blood in the heart before contraction begins and it is the amount of stretch placed on a cardiac muscle fiber just before systole; is related to Starling’s law of the heart, which states that â€Å"the force of myocardial contraction is determined by the length of the muscle cell fibers† (Hudak, Gallo Morton 1998). Afterload: Is the pressure that must be overcome by the ventricles to eject blood (Marieb 2004). The most critical factor determining afterload is the resistance imposed by the vascular bed on blood flow. There are three sources of resistance: blood viscosity, vessel length and vessel diameter. Contractility: Is defined as an increase in contractile strength that is independent of muscle stretch and end diastolic volume (EDV) (Marieb 2004). The more vigorous contractions are a direct consequence of a greater calcium influx into the cytoplasm from the extracellular (EC) fluid and the sarcoplasmic reticulum (SR). PATHOPHYSIOLOGY OF LOW BLOOD PRESSURE John suffered two MI during the past 5 years, the changes that occur in the myocardium after a MI are very important to understand the mechanisms that lead to LVF, and consequently, to low BP. According to Gheorghiade Bonow (1998) recurrent episodes of myocardial ischemia, producing repetitive myocardial stunning, may contribute to the overall magnitude of LV dysfunction and heart failure symptoms. It has been shown (Woods et al, 1995) that changes in LV contractility and compliance precipitate sympathetic compensation by increasing the heart rate in order to maintain cardiac output and elevating the systemic vascular resistance (SVR) to sustain BP. Immediately after an infarction, blood flow ceases in the coronary vessels beyond the occlusion except for small amounts of collateral flow. Guyton Hall (2000) maintain that when the area of ischemia is large, some of the muscle fibers in the middle of the area die rapidly. Immediately around it is a non-functional area because there is nor contraction or is diminished. Extending circumferentially around the non-functional area is an area that is still contracting but that weakly. During the next days after the infarction, the borders of the non-functional area either become functional again or die, depending on the enlargement of the collateral arterial channels. In the meantime, fibrous tissue begins to develop among the dead fibers because the ischemia stimulates growth of fibroblasts; therefore, the dead muscle tissue is replaced by fibrous tissue. Finally, the heart gradually hypertrophies to compensate the loss of cardiac muscle. After a large myocardial infarction, the heart’s capability of pumping is permanently decreased below that of a healthy heart. LV failure due to inadequate contractility results in a decreased cardiac output leading to a poor tissue perfusion as well as to an increase in the volume remaining in the ventricle at the end of systole. That results in a low BP and high pressures in the left atrium that could cause pulmonary oedema (Hansen1998, p379). PHYSIOLOGY OF HYPOXEMIA RELATED TO PULMONARY OEDEMA Adam Osborne (1997) defined hypoxemia as a low concentration of oxygen in the blood (10 µg/kg/min) ? adrenergic receptors are stimulated increasing peripheral resistance, and therefore, increasing the BP (Kenry Salerno, 2003). The author recognizes the controversy of renal-dose dopamine, and on analyzing the literature, there is no conclusive evidence to support either one point of view or another. Vovan Brenner (2000) and Ichai et al (2000) defend the use of renal-dose dopamine and Friedrich (2001) and Bracco Parlow (2002) criticize its use. Both groups concur that further studies should be undertaken in order to clarify the true effect of renal-dose dopamine. Low blood pressure: When an arterial line was inserted, John’s MAP was 55 mmHg and the CVP was 14 mmHg. Initially, 250 ml of gelofusine was administered over 30 min. John’s BP increased to 62 mmHg. It is important to note that the CVP increased to 17 mmHg following the 250 ml of gelofusine. Because John was already in pulmonary oedema, doctors were cautious to not compromise his condition by administering further fluids and decided to wait, considering that John’s urine output was adequate despite his BP. At this point, it is relevant to emphasize the discussion that exists in the literature comparing crystalloids and colloids in fluid therapy. After a systematic review of 105 articles, Choi et al (1999) concluded that there are no apparent differences in pulmonary oedema, mortality or length of stay when using either crystalloid or colloid. Nonetheless, Cook (2003) argues that crystalloids increase hydrostatic pressure but decrease colloidal pressure and could enhance pulmonary oedema. After 3 hours, John’s BP decreased to 50 mmHg and his urine output diminished to 60 ml/h. How it has been mentioned in the pathophysiology chapter, John’s low BP was due to poor LV function, thus decreasing cardiac output (CO). Therefore, to resolve the hypotension it needs to be improved CO. Aggressive inotropic therapy would be unsuitable because the cause of John’s low BP could be masked behind the inotropes. Considering it, IABP therapy commenced, triggering the balloon 1:1 and on maximum augmentation. The IABP consists of a 25cm balloon that is inserted, via the femoral artery, in the descending aorta with its tip at the distal aortic arch. Inflation and deflation is synchronized to John’s cardiac cycle (Overwalder 1999). The IABP is set to inflate at the beginning of diastole displacing blood above the balloon (forcing the blood up and into the coronary arteries, improving myocardial perfusion and oxygen supply) and below the balloon (the blood is forced into the systemic circulation). When the balloon deflates, it creates a relative space to accommodate the blood before systole, resulting in a full load ejection. With less resistance to pump against, the heart requires less oxygen to function (Metules 2003). Summing up, when IABP therapy is started an increase in MAP, CO, and ejection fraction, along with a decrease in heart rate, pulmonary artery diastolic and capillary wedge pressure should be observed (Metules 2003). Upon IABP therapy, John’s BP increased to 65 mmHg during the first 30 min, and to 75 after 90 min of treatment. In addition, renal perfusion was improved and the urine output was observed to increase, as well as a decrease in John’s heart rate (from 100 beats per minute (bpm) to 85 bpm). John didn’t have a pulmonary artery catheter in situ, it is therefore inaccurate to comment on any suspected change in CO, SVR or pulmonary artery wedge pressure (PAWP). Overwalder (1999) states that IABP therapy is not exempt from complications such as artery injury perforation, aortic perforation, femoral artery thrombosis, peripheral embolization and limb ischemia. Nursing care involved the evaluation of John’s skin colour and temperature on the legs, and the presence of infection, pain or bleeding. Pedal pulses were recorded every two hours in order to avoid limb ischemia, which can occur because of a reduced blood flow to the leg, thrombosis formed around the catheter or arterial spasm (Metules 2003). CONCLUSION The author has analysed how John’s LVF caused hypoxemia and low BP. The therapy and treatment provided (although not always supported by the literature) was effective in resolving John’s low PaO2 and low BP. It may have been beneficial to provide John with a higher concentration of FiO2 (80%) humidified oxygen via facial mask or using non-invasive mechanical ventilation on admission, instead of 40% humidified oxygen that was administered, in order to correct as quickly as possible John’s hypoxemia. IABP seems a very aggressive therapy to correct John’s low BP, taking into account the risks and complications inherent to this therapy; perhaps increasing the dopamine to a cardiac dose could have been an option in order to increase John’s BP. However, the insertion of a pulmonary artery catheter would have been useful to monitor the haemodynamic status (CO, SVR, PAWP), guiding the treatment. The author has achieved a better understanding of both physiology and pathophysiology whilst analysing in detail the treatment administered and other possible interventions that could improve John’s care. REFERENCE LIST Adam S Osborne S (1997) Critical care nursing science practice. Bath: Oxford. Badcott S. (1998) Inotropes- choosing the right agent for the right job. MKCPA Critical Care Group study day. September 29th. Bracco D Parlow JL (2002) Prevention: dopamine does not prevent death, acute renal failure, or need for dialysis. Canadian journal of anesthesia 49:417-419. Chadda K .et al (2002) Cardiac and respiratory effects of continuous positive airway pressure and non-invasive ventilation in acute cardiac pulmonary edema. Critical Care Medicine. Nov; 30(11):2457-61. 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San Francisco: Pearson. Thibodeau G Patton K (1993) Anatomy physiology. 2nd ed. St. Louis: Mosby Vovan T Brenner M (2000) Controversy: Is there a â€Å"renal dose† dopamine? Critical care medicine April 28(4):1220. Webb A, Shapiro M, Singer M and Sutter P (1999). Oxford textbook of critical care. Oxford: Oxford. Woods S. L. et al (1995) Cardiac nursing. 3rd ed. Pennsylvania: J.B. Lippincott. BIBLIOGRAPHY Hobsley M Imms FJ (1992) Physiology in surgical practice. 1st ed. London: Edward Arnold. Mattera C (2000) Heart failure and pulmonary edema. Jems May 25(5): 36-47. Schierhoud G Roberts I (1998) Fluid resuscitation with colloid or crystalloid solutions in critically ill patients: a systematic review of randomised trials. BMJ March 316: 961-964. Stevenson LW (2003) Clinical use of inotropic therapy for heart failure: looking backward or forward? Part I: Inotropic infusions during hospitalization. Circulation July 22: 367-372. Kellum JA Bellomo R (2000) Low-dose dopamine: What benefit? 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