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


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 “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 (<8.0 kPa). How it will be explained in this essay, John’s LVF caused hypoxemia due to pulmonary oedema.
Pulmonary oedema is the abnormal accumulation of fluid in the interstitial spaces surrounding alveoli, with possibly fluid exudation into alveolar air spaces and it results from two mechanisms: increased pulmonary capillary hydrostatic pressure (CHP) and/or abnormally increased capillary permeability (Hansen 1998, p492).
According to this definition, the author will describe the respiratory physiology related to the alveoli, its membrane, the capillaries and the mechanisms that occur during the gasses exchange.
The factors influencing the movement of O2 and CO2 across the respiratory membrane are:
Partial pressure gradients and gas solubility.
Matching of alveolar ventilation and pulmonary blood perfusion.
Structural characteristics of the respiratory membrane (Marieb 2004).
The amount of O2 or CO2 that dissolves in the plasma depends on pressure gradients and the solubility of the gas. Because solubility is constant, the primary determinant of gas exchange is the partial pressure gradient of the gas across the alveolar-capillary membrane. The gas laws (Henry, Boyle and Dalton) state that individual gases flow from regions of higher partial pressure to regions of lower partial pressure (Silverthorn 2001). This explains the reason why O2 passes from the alveoli (104 mmHg) to the capillaries (40 mmHg) until equilibrium is reached (104 mmHg). And the same occurs but in opposite direction with CO2, in the alveoli 40 mmHg and in the capillaries 45 mmHg – thus gaseous exchange occurs.
The amount of oxygen that can be transported to cells depends not only on the PaO2 provided by ventilation but also on the quantity of haemoglobin (Hb) and its affinity for oxygen (about 99% of O2 and 20% of CO2 is carried by the Hb). The oxygen-haemoglobin dissociation curve shows the relationship between the PaO2 and the percentage of haemoglobin-binding sites occupied by oxygen. A shift to the left indicates higher affinity (decreased oxygen release to the tissues) whereas a shift to the right demonstrates the opposite conditions (Marieb 2004). The graphic and the factors that can produce a shift to the left or right are shown in the appendix 1.
For gas exchange to be efficient there must be a close match between ventilation (amount of gas reaching the alveoli) and perfusion (the blood flow in pulmonary capillaries). In alveoli where ventilation is inadequate (low PO2) the terminal arterioles constrict and blood is redirected to respiratory areas where PO2 is high. In alveoli where ventilation is maximal, pulmonary arteries dilate, increasing blood flow into the associated pulmonary capillaries (Marieb 2003).
The walls of the alveoli and of the capillaries together form a very thin barrier for the gases to cross, estimated at not more than 0.5 micrometers thick (Thibodeau & Patton 1993).
To explain the capillaries exchange fluids in the lungs and the dynamics of pulmonary interstitial fluids work, it is necessary to mention some data:
The pulmonary capillary pressure is about 7 mmHg.
The interstitial fluid pressure is about -8 mmHg.
The alveolar walls are so thin that any positive pressure in the interstitial spaces greater than alveolar air pressure (0 mmHg) could force the fluid from the interstitial space into the alveoli.
The lower pressure that exists in the pulmonary capillaries and the pulmonary lymphatic system keep the alveoli dry by draining the extra fluid into the lung interstitium through the small openings between the alveolar epithelial cells and carried away through the pulmonary lymphatics or absorbed into the pulmonary capillaries (Guyton & Hall 2000, p448-449).

PATHOPHYSIOLOGY OF HYPOXEMIA RELATED TO PULMONARY OEDEMA

When the left ventricle fails in its function of pumping the blood through the systemic circulation while the right ventricle continues to function adequately, blood continues to reach the lungs pumped by the right ventricle, but the left ventricle is not able to accommodate such a return of blood. As a result, the mean pulmonary filling pressure rises because of a shift of large volumes of blood from the systemic circulation into the pulmonary circulation.
That large amount of blood in the lungs leads to an increase in pulmonary capillary pressure, and if this rises above a value equal to the colloid osmotic pressure of the plasma (28 mmHg), fluid begins to exudes into the interstitial spaces and alveoli, resulting in pulmonary oedema (Guyton & Hall 2000).
If the alveolar-capillary membrane is thickened by fluid, partial pressure gradients and gas solubility remain unaltered; however, mismatching of alveolar ventilation and pulmonary blood perfusion occurs. In addition, the structural characteristics of the respiratory membrane are compromised, thus gas diffusion is impaired resulting in hypoxemia. If fluid is third spaced into alveoli or into the intrapleural space, further detriment to gas exchange results from impaired ventilation. Due to the left ventricular failure, less blood arrives to the lungs and to all the organs, suffering hypoxemic effects associated with lack of both oxygenation and perfusion (Hansen 1998, p492-493).

MANAGEMENT

In this section the author will explain the management of John’s symptoms in respective sections – it is acknowledged that the actual management occurred simultaneously.
Hypoxemia:
On admission to the ICU, John had a SpO2 of 87% measured by pulse oxymetry and was receiving 10 litres of O2 via facial mask. He displayed clinical and physical signs of respiratory distress including ronchi and crackles on auscultation, tachypnoea and the use of accessory muscles when breathing. Initial assessment of these symptoms involved gaining accurate invasive baseline measurements – the ABG showed a SaO2 of 86% and a PaO2 of 7.8 kPa. Despite these observations clinically of hypoxemia, the decision was made at this stage to manage John’s symptoms without mechanical ventilation – oxygen therapy was increased to humidified oxygen at FiO2 of 50%, and later increased to 60% according with the PaO2 on the ABG. Webb et al (1999), acknowledge that in cases of hypoxemia one of the therapeutic priorities is raise PaO2 by O2 therapy in order to maintain PaO2 within the plateau range of the oxygen-haemoglobin dissociation curve. Webb et al (1999) concur with the incremental increase of FiO2, as seen in John’s management, stating the fraction of inspired oxygen should be carefully titrated upwards to achieve the target of PaO2. However, Masip et al (2000) and L’Her et al (2003) argue that early intervention of non-invasive mechanical ventilation, as opposed to conventional oxygen therapy alone, results in rapid improvement of the clinical signs of respiratory distress and gas exchange thus decreasing the occurrence of endotracheal intubation. However, these studies used small population samples and concluded no absolute evidence of decrease in morbidity or early mortality.
Furosemide IV was administered in an initial bolus of 40 mg; as a result, John’s urine output over the next two hours was 250ml and 160ml respectively. However, three hours post the initial diuretic bolus, John’s urine output again began to fall. A furosemide IV infusion was commenced at 10 mg/h, a therapy well recognized by Webb et al (1999) in the treatment of hypoxemia secondary to pulmonary oedema.
Furosemide is a loop diuretic that inhibits sodium and chloride reabsorption in the ascending limb of the loop of Henle, with a resulting increase in sodium and a decrease in free water clearance. When furosemide is administered IV, its action in respect to pulmonary oedema is complex; it reduces pulmonary vascular congestion and pulmonary venous pressure by causing a systemic venous dilation (Grahame-Smith & Aronson, 2002).
The European Society of Anaesthesia (2003) and Cottes et al (2001) recommend low dose diuretics and high dose nitrates to treat pulmonary oedema. In John’s case, the LVF and subsequent hypotension, prevented the use of these vasodilators.
To support John’s renal function in the presence of his low BP, dopamine IV was commenced at 3 µg/kg/min. Dopamine is a catecholamine precursor of noradrenaline and acts on dopaminergic, ?1 and ? receptors. Receptor activity is dose dependent. Dopamine is unique in low dosages (0.5 to 2µg/kg/min) because it acts mainly on dopaminergic receptors causing vasodilation of the renal and mesenteric arteries, increasing renal blood flow (Badcott 1998). In low to moderate dosages (2 to 10µg/kg/min) it acts directly on the ?1 receptors of the myocardium and indirectly by releasing noradrenaline. These actions increase myocardial contractility and stroke volume, thereby increasing cardiac output, but consequently increasing myocardial oxygen consumption (Kenry & Salerno, 2003). In higher dosages (>10µg/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

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