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Shock and Burns Modules...

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Modules Week 4 and Week 6 Module In this week, you will learn the principles of hemodynamic monitoring and the importance of interpreting the data to help guide treatment for a critically ill patient. Additionally, we will discuss shock, the manifestations of different types of shock, and the planning of appropriate nursing care of individuals experiencing shock. Shock is a life-threatening condition and is closely related to hemodynamics in terms of monitoring for adequate tissue perfusion. During shock, acute kidney injury can occur if tissues are not getting adequate oxygenation; if kidney injury is not caught early, it may result in potential life-threatening outcomes. In addition, shock can result in irreversible cell damage and cell death, which can eventually lead to multiple organ dysfunction syndrome (MODS) if the condition is prolonged. Therefore, the goal of nursing care is early recognition and collaborative treatment.

HEMODYNAMICS: The Why and What of Invasive Monitoring Hemodynamics is the term we use to describe circulation and the intravascular pressure and flow that occurs as blood moves through the vascular system. We use hemodynamic monitoring within the ICU to help more closely evaluate a critically ill patient. For example, in a patient who has cardiogenic shock, we may want to evaluate the heart's ability to pump. In a patient with a severe congestive heart failure exacerbation, we may want to evaluate the total blood volume. We also may want to monitor the pressure the heart is working against and interpret the vascular resistance the heart is working to overcome with each beat. If you are working in the ICU and setting up or preparing for a patient to have hemodynamic monitoring, you will need to get familiar with several pieces of equipment. First, the transducer will allow the pressure generated by the blood flow to convert to an electrical signal that you will see in a numeric value on the bedside monitor. Pressure tubing is used with a device on the tubing that allows us to flush the line and maintain patency of the catheter tip. Flushing the pressure tubing is important in order to remove air bubbles and to fill the line with fluid after obtaining blood samples to prevent potential clotting. We connect the pressure tubing to a 1,000 ml or 500 ml bag of normal saline. The tubing is then connected to another bag to maintain a pressure of 300 mm Hg to prevent arterial blood from backing up into the pressure tubing. In the ICU setting, we use several different types of lines to monitor our patient's hemodynamic status. Any time your patient has an invasive line for hemodyamic monitoring, it is important to understand why he or she has it and what you need to be on the lookout for. Let's explore some more of those examples below. So your patient has an arterial line? This is a consistent way that we can monitor what is happening with our patient's arterial blood pressure. This is great news if you have a patient who is on vasoactive medications or who has a dangerously high or low blood pressure! Arterial lines not only give us an accurate picture of the blood pressure, but we can also obtain arterial blood sampling from the pressure tubing. If we think back to Week 2, our ARDS patients are one

group of ICU patients that need frequent ABG evaluation. Arterial lines are catheters similar to peripheral IVs but are located in the radial or brachial artery. Before insertion, it is important that collateral blood flow is verified. Now let's think back to how we manage vascular access devices. We will need to care for the arterial line in a similar way. For instance, we will need to utilize a sterile dressing and be sure to change the flush bag and tubing every 72 hours. As with any invasive line, there are always some risks. Thrombosis is the leading risk for arterial lines, as well as catheter-related bloodstream infections, skin breakdown under the transducer, bleeding if the system itself is disconnected, or air embolism. When the arterial line is removed, pressure must be held for at least 5 minutes and until the bleeding stops. Your patient has a line for central venous pressure (CVP) measurement? Great! Now we have a very accurate way to evaluate fluid status. We know from our reading that central venous pressure is a measurement taken in the right atrium. This gives us a much clearer picture of current blood volume and fluid balance. In fact, CVP is most often measured in patients with a tenuous fluid balance who require very close monitoring. Normal CVP readings are 2 to 6 mm Hg. What does it mean when these values are not within the normal range? Well, if your patient has a decreased CVP, this would indicate low circulating volume. If you were caring for a patient with an increased CVP, the patient most likely has fluid overload. The CVP catheter is inserted through the internal jugular or subclavian vein. However, in either case, the tip of the catheter resides in the superior vena cava. Pressure tubing is attached to the distal port of a multilumen central venous catheter. Even more so than an arterial line, this type of invasive monitoring presents the highest risk for catheter-associated bloodstream infection. When caring for your patient, make sure to keep the entire system closed, utilize a sterile dressing, and cap off all ports. Ensure that tubings are changed in recommended intervals. If drawing blood from the central line, make sure to use sterile technique. Some other risks to be mindful of include pneumothorax on insertion, excessive bleeding, and air or catheter embolism. Cardiac complications can also arise, and these include dysrhythmias and cardiac tamponade. Oftentimes the healthcare provider will ask for assistance when removing the central line. We can assist the physician by instructing our patient to "bear down" and take a big breath in and blow out. Then the provider will remove the catheter as the patient exhales. Can you think of the reason why this is the procedure for CVP removal? Don't overinflate with excitement! It's just a pulmonary artery catheter (PAC)! Our text is a great resource for the ins and outs of PA catheters. But the short version is that a PA catheter is a catheter with several functions allowing us the ability to measure CVP, the pressure in the pulmonary artery, and pressure in the left atrium. A PA line gives us information to calculate cardiac output, cardiac index, and systemic vascular resistance (SVR). You will find out how important these numbers can be with our shock patient population. The PA catheter can be inserted even at the bedside in some critical care settings. A single-lumen introducer is placed within the internal jugular or subclavian vein. The PA catheter is then threaded all the way through the right atrium, right ventricle and reaches the final destination in the pulmonary artery. Different from some of the other monitoring devices we discussed, the nurse has a specific intervention with this catheter in order to get the desired measurement. In order to obtain readings, the nurse will need to inflate a small balloon at the tip of the catheter. Inflating this balloon will obtain pressure values that allow us to assess the functioning of the left atrium

of the heart. The balloon is inflated by using the small syringe that is attached to one port. When the balloon is inflated by inserting a small amount of air into the catheter, it allows the tip of the catheter to float from the pulmonary artery into a pulmonary capillary. This process is known as “wedging." When the catheter tip floats as far as it can, the pulmonary capillary wedge pressure (PCWP) can be obtained. As soon as this measurement is completed, we must deflate the balloon to make sure the catheter is not still wedged. As exciting as all this monitoring can be, there are still risks involved. Immediately after insertion, we will always want to obtain a chest X-ray to confirm PA catheter placement. This will also rule out the other major complication, a pneumothorax. We discussed several complications of invasive hemodynamic monitoring above, and these catheters are no different. Remember to always cover the insertion site with a sterile dressing. Utilize caps, and change your pressure tubings and dressings within 72 hours to decrease the risk for infection. Patients with multilumen catheters are also at risk for hemothorax, cardiac dysrhythmia (especially when the catheter is advanced through the right ventricle), air embolism, pulmonary artery rupture, and balloon rupture. As a critical care nurse, the more you understand about hemodynamic monitoring catheters the more helpful you will be to patients and know what treatments to anticipate! Arterial lines and CVP lines are more frequently used in the critical care and step-down settings than the PA catheter. Although PA line use is often reserved for the most critically ill patients, it is still important to understand the why's and what's of hemodynamic monitoring!

Shock! What Does It All Mean? Shock is a life-threatening condition resulting from an imbalance between the supply and demand of oxygen. As a result, hypoxia occurs, leading to inadequate cellular function, which can eventually lead to organ failure and even death. In the ICU, the nurse will care for patients with all different types of shock. But ultimately, any type of shock will lead to hypoxia and organ dysfunction or failure. Our patients may arrive to the ICU with an injury, infection, myocardial infarction, GI bleed, or even an allergic reaction, but in each of these cases shock can develop and be potentially life threatening. We classify shock as one of three basic types: hypovolemic, cardiogenic, and distributive. Distributive shock, although a basic type of shock, also has three different types within its own category: neurogenic, anaphylactic, and septic shock. Additionally, each of these types of shock can have four distinct stages—initial, compensatory, progressive, and refractory. Hypovolemic shock is the result of reduced intravascular blood volume. A patient you are caring for with hypovolemic shock will have decreased cardiac output, resulting in inadequate tissue perfusion and a shift from aerobic to anaerobic metabolism. Anaerobic metabolism will result in the accumulation of lactic acid and cause metabolic acidosis. Hypovolemic shock can be caused by trauma, burns, GI bleeding, acute pancreatitis, dehydration, diarrhea, and vomiting, to name a few. Initially, the nurse may only notice subtle changes in clinical signs; as the patient moves into the compensatory stage of shock, the fightor-flight mechanisms kick in (i.e., the cardiac contractility increases, heart rate goes up, blood glucose levels increase, and the urine output decreases). If hypovolemic shock is not corrected with fluid resuscitation and identification and treatment of the underlying

cause is not determined promptly, the patient will begin to exhaust the compensatory mechanisms and will exhibit signs and symptoms of the progressive stage of shock. The patient will show significant changes, as demonstrated by the following clinical manifestations: hypotension; paleness with cool, clammy skin; a change in mental status; and irregular tachyarrhythmias. If the shock progresses to the refractory stage, impending death will occur. Cardiogenic shock is often the result of an acute myocardial infarction and results in the reduction in cardiac output despite adequate circulating blood volume. If you are a nurse caring for patients in the cardiac intensive care unit, this will be a type of shock that you see frequently. The primary goal, as discussed in Week 3, is revascularization. If this does not occur following an AMI, the outcome is usually fatal. The clinical manifestations of cardiogenic shock are similar to hypovolemic shock; however, these patients usually deteriorate much more quickly. When the left ventricle becomes damaged, it is unable to pump efficiently and cardiac output decreases. In an effort to compensate, the nonischemic areas of the myocardium contract even more forcefully. This mechanism raises the oxygen demands and increases the workload of the heart. To treat cardiogenic shock, the focus is on revascularization of the myocardium, improved oxygenation to decrease cardiac demand, managing pulmonary edema, and providing supportive care using inotropic medications and vasodilators to improve the efficiency of the heart while reducing left ventricular afterload. Intra-aortic balloon pumps may be used to prolong coronary artery perfusion during diastole. Left ventricular assist devices are a final treatment option that may be used in a cardiothoracic intensive care unit as the patient awaits a heart transplant. Distributive shock is categorized into three different types of shock: neurogenic shock, anaphylactic shock, and septic shock. Sepsis is a frequent cause of death in patients being cared for in the intensive care unit, and patients who develop septic shock have a mortality rate estimated at around 40–50%. Septic shock is the result of a widespread infection that leads to an inflammatory response. As critical care nurses, it will be our diligence that protects our patients from potential hospitalacquired infections. If an infection that results in sepsis does occur, the condition may result in profound hypotension, altered coagulation, impaired circulation, anaerobic metabolism, and multisystem organ dysfunction syndrome (MODS). Prevention of sepsis is promoted through meticulous infection control practices. Additionally, the nurse plays an essential role in identifying early changes and facilitating immediate interventions to prevent full-blown septic shock. The nurse should be aware of possible causes of infections, such as hospital-acquired pneumonia, urinary tract infections, and central line infections. Timely identification of the causative organism and the initiation of antibiotics improve survival of patients with sepsis or septic shock. Neurogenic shock can occur with disease or injury to the upper spinal cord, spinal anesthesia, and in patients with vasomotor depression. What occurs with this type of shock is a disturbance in the nervous system that inhibits the vasomotor center, thereby inhibiting sympathetic stimulation of nerve fibers that travel down the spinal cord. The disruption in the impulse results in a blockage of the sympathetic outflow, resulting in vasodilation, inhibition of

baroreceptor response, and impaired thermoregulation. Management of neurogenic shock focuses on treating the cause, immobilization of spinal injuries, IV fluids to treat hypotension, and treatment and management of bradycardia and hypothermia. Anaphylactic shock is a severe allergic reaction that can precipitate from a foreign substance when someone is sensitive to an antigen-antibody response. With an initial exposure, the patient may not be sure of the symptoms; however, with additional exposure, the antigen may cause an anaphylactic reaction. The clinical presentation of shock includes flushing, pruritus, and angioedema. Upper and lower airway obstruction is of big concern, because the patient may not be able to ventilate if the swelling is severe enough. The goal of treatment is to remove the antigen and to treat with epinephrine, which promotes bronchodilation and vasoconstriction. Multiple organ dysfunction syndrome (MODS) is the progressive dysfunction of organ systems as a result of an uncontrolled inflammatory response. This condition is associated with mortality rates as high as 80% when three or more organ systems fail. The most common cause of MODS is sepsis and septic shock; however, MODS can occur after any severe injury or disease process that has a massive systemic inflammatory response, including any of the classifications of shock. Management is focused on prevention and support. The initial source of inflammation must be eliminated or controlled, and support for each organ must be provided along with adequate nutrition and metabolic support. The expected outcome for the patient experiencing shock or with MODS is improved tissue perfusion.

Burns: The Thick of the Matter Burns have often been noted as one of the most lethal forms of trauma. A burn is said to have occurred when the skin or other tissues are destroyed by heat, cold, electricity, radiation, or chemicals. When a burn covers over 50% of the total body surface area (TBSA), a significantly high morbidity and mortality rate can occur. This statistic becomes even more significant with older adult and very young patients as a smaller percentage of burned area results in a greater mortality risk. As with the trauma patient, the initial management of the burn patient will have a dramatic impact on the long-term outcome of the patient. Caring for the patient with a burn injury will require fluid resuscitation, early excision and closure of the wound, tissue debridement and healing, respiratory support, metabolic demand management, and intense microbial surveillance and infection control practices. Understanding the depth of the burn injury the patient has experienced will also help predict wound care treatment requirements, the need for skin grafting, and overall cosmetic and functional outcomes. Burns generally are classified as superficial, partial-thickness, or full-thickness burns. If your patient has a superficial burn, it is a burn that destroys the epidermis only. Your assessment will show skin that is pink or red. This type of burn can be very painful and can even occur with a sunburn. A superficial burn usually heals within 3–5 days. When caring for a patient who has a superficial partial-thickness burn, the burn does not just involve the epidermis but also extends into a limited portion of the dermis. Upon

assessment, you will note skin that appears moist, pink, or mottled red, and the patient will report a great deal of pain. Deep partial-thickness burns result in the destruction of the epidermis and most of the dermis, with only some of the skin appendages remaining. The skin will appear pale, pearly red, or white and can actually even be less painful, because more destruction of sensory nerves has occurred. These wounds will most likely need to be excised and grafted to achieve better function and decrease the length of healing time. Finally, if you are caring for a patient who has a full-thickness burn, we know from our reading that it is the destruction of all the layers of the skin down to or even past the subcutaneous fat, fascia, muscles, or bone. A leathery eschar, or nonelastic layer of necrotic tissue, is created that does not blanch with pressure. The nerves are destroyed and the injury will require skin grafting to achieve permanent wound closure. Another important assessment in addition to the depth of the injury in the burn patient is the extent of the injury. To describe the extent or size of the burn, we estimate the TBSA that has been burned. The quickest way to initially calculate the percentage of TBSA is to utilize the rule of nines. The technique divides the TBSA into areas representing 9% or multiples of 9%, allowing a rapid estimation for the provider of TBSA burned. Another approach often used by nurses is to use the palms of his or her hands to estimate TBSA. The palm of the hand is equivalent to 1% body surface area. The Lund and Browder chart is another, more accurate assessment that incorporates body surface area with age-related proportions. Accurate assessment of TBSA burned is critical for fluid resuscitation calculations required for the treatment of the burn patient. A precise way of determining the amount of fluid replacement is the use of the Parkland formula. The calculation estimates the approximate amount of lactated ringers fluid to be given over 24 hours with the following formula: Total amount = 4 mL per kg per %TBSA burned in adult patients, with half of the total volume infused in the first 8 hours and the second half given over the next 16 hours. For example, an adult weighing 80 kg with a 65% TBSA from a house fire would result in the following: 4 ml × 80 kg × 65% TBSA = 20,800 mL of LR to be infused over 24 hours. The patient will receive 10,400 mL in the first 8 hours at a rate of 1300 mL ...