Overview of Acquired Heart Diseases

Okay, next we're going to discuss acquired heart diseases. These are things that happen after birth. Your book highlights quite a few. In this lecture, we will focus on some of the more common acquired heart diseases. So cardiac dysrhythmias. So please make sure you watch the pediatric cardiac rhythm presentation. It'll help you understand a little bit more about rhythms and dysrhythmias. As a nurse, you must be familiar with the standards of normal heart rate for each age group. An initial nursing responsibility is recognition of abnormal heartbeat, either in rate or in rhythm. When a dysrhythmia is suspected, the apical rate is counted for one full minute and compared with the radial rate, which may be lower because not all apical beats are felt. Consequently, high or low heart rates should be regarded as suspicious. So if we have a low heart rate, bradycardia, this could be a heart block. Again, we need to know the normal to understand the abnormal. That's why you must be familiar with the heart rate for each age group. And then tachycardia, we're going to discuss our supraventricular tachycardia. So going right into our supraventricular tachycardia, if you want to look more about our bradycardia or our heart blocks, that's in the pediatric cardiac rhythm. So our supraventricular tachycardia. This is the most common tachydysrhythmia found in children and refers to a rapid regular heart rate of about 200 to 300 beats per minute. Could you imagine listening to something that's going that fast? As many as 1 in 250 children experience SVT. The onset of SVT is often sudden. The duration is variable and the rhythm may end abruptly and convert back to normal sinus rhythm. Clinical signs. and our infants and young children are poor feeding, extreme irritability, and paler. Children may also experience palpitations, dizziness, chest pain, and diaphoresis. So what's our treatment? Our treatment of SVT depends on the degree of compromise imposed on the dysrhythmia. In some cases, vagal maneuvers such as applying ice to the face for 15 to 30 seconds or having an older child perform a Valsalva maneuver, which could be exhaling against a closed glottis, blowing on the thumb as if it were a trumpet for about 30 to 60 seconds. This can terminate SVT. If vagal maneuvers fail or the child is hemodynamically unstable, adenosine, which is a drug that impairs AV conduction, may be used. So adenosine brings the heart rate down. That's AD, the D in adenosine brings the heart rate down. Adenosine is given by a rapid IV push. Again, adenosine is given by a rapid IV push and followed with a saline bullet immediately after the drug because it is a very short half-life. You want to give adenosine in the closest vessel to the heart. So if you have a PICC line in or if you have a, say, if you have a IV that's in the wrist and then you have an IV that's in the AC, you want to give it to the one that is closest to the heart. Again, the half-life of this medication is very short. You give that med real quick, rapid IV push, and then you give that saline bolus real quick. If adenosine is unsuccessful or cardiac output is compromised, esophageal overdrive pacing or synchronized cardioversion, which delivers an electrical shock to the heart, synchronized, can be used in intensive care settings. Sedation is needed for both procedures. Cardioversion should never be done on a conscious patient. Kawasaki disease. This is an acute systematic vascularitis of an unknown cause. It occurs in every racial group with 76% of the cases occurring in children younger than the age of five. The peak incidence is in the toddler age group. The acute disease is self-limited. However, with treatment, approximately 20 to 25% of children develop coronary artery dilation or aneurysm formulation. Infants younger than one year old are at the greatest risk for heart involvement. Although an increased incidence has been reported in older children, perhaps because of the later diagnosis in many. So what are our classic Kawasaki disease criteria? This includes a fever for five calendar days, along with four of the five clinical criteria below. Diagnosis may be made on day four of fever. by an experienced... clinician in children with fever, and more than four clinical criterion. So there's changes in the extremities. In the acute phase, edema or erythema of the palms and soles. In the subacute phase, peeling of the hands and feet. Bilateral conjunctival injection or inflammation without exudate. Changes in the oral mucosal membrane, such as erythema, cracking of the lips, oral field and gerodin, or strawberry tongue. really common. A rash, maculopapilla, diffused erythrodema, or erythromultiform-like rash may occur. Cervical lymphodempathy. These are all things, these are some of the criteria. The strawberry tongue and peeling of the hands, along with the fever for five calendar days, is something that is diagnosed for Kawasaki disease. So what's our current treatment? The current treatment of children with Kawasaki disease includes administration of high-dose IVIG along with cell estate therapy or aspirin therapy. IVIG has been demonstrated to be effective in reducing the incidence of coronary artery abnormalities when given within the first 10 days of the illness and ideally within the first seven days. Aspirin has been used historically to control fever and symptoms of inflammation. I know aspirin isn't commonly given to children. But in this case, it is the recommended therapy. So again, I'd remember about the high-dose IVIG for treatment of Kawasaki. So highlight that. MIS-C. So little is known about the pathophysiology of MIS-C. And it's felt that MIS-C is a consequence of immune-mediated injury triggered by COVID-19. The treatment is very similar to Kawasaki disease. Your book doesn't... may not have much information about it, but this information on this slide is from the CDC in 2020, and it describes MIS-C in children less than 21 years of age using the following criteria, a fever greater than 38 degrees for 24 hours or a subjective fever lasting longer than 24 hours. Laboratory evidence of inflammation, including but not limited to, one of the following, elevated CRP, ESR, fibrinogen, procalcitonin, D-dimer, ferritin, lactate acid dehydrogenase, interleukin-6, elevated neutrophils, reduced lymphocytes, and low albumin. Evidence of clinically severe illness requiring hospitalization with multi-system greater than two organ involvement would be cardiac, renal, respiratory, hematological, gastrointestinal, dermatological, or neurological. No alternative possible diagnosis. Positive for recurrent or recent COVID-19 infection. Documented by reverse transcupidase polymers chain reaction, RT-PCR. Serology or antigen test or COVID-19 exposure within the four weeks prior to the onset of symptoms. Positive for current or recent COVID-19 infection documented by RT-PCR. serology or antigen tests, or COVID-19 exposure within four weeks prior to the onset of symptoms. Again, treatment is very similar to Kawasaki disease. Rheumatic heart disease. Acute rheumatic fever is a result of an abnormal immune response to a group A strep infection, usually pharyngitis, a genetically susceptible host. It occurs most often in late school-age children and adolescents and is rare in adults. Acute rheumatic fever is a self-limiting illness that involves the joints, skin, brain, and heart. The cardiac valve damage, which is referred to as rheumatic heart disease, the most significant complication of acute rheumatic fever, occurs in more than half the cases. The mitral valve is most often affected. Upper respiratory infections, or URIs, with... Group A strep support a relationship with acute rheumatic fever, usually within two to six weeks. Untreated group A strep infection may cause damage to the heart valves. Repeated or recurrent infections cause cumulative valve damage. Acute rheumatic fever clinical manifestation. Carditis is seen in about 50 to 70 percent of cases. The most significant manifestations of acute rheumatic fever is carditis. Cardiasis is the only manifestation of acute rheumatic fever that leads to permanent damage. So signs could be tachycardia out of proportion to the degree of fever. cardiomegaly, new murmurs or changes to pre-existing murmurs, muffled heart sounds, pericardial friction realm, chest pain, changes in the ECG, especially a prolonged PR interval. Polyarthritis occurs in about 35 to 66 percent of cases. This includes swollen and hot red painful joints. After one to two days, different joints can be affected. Favors large joints such as the knees, elbows, hips, shoulders, and wrists. Subcutaneous nodules occurs in less than 10% of cases. Non-tender swelling located over bony provinces may persist for some time and then gradually resolve. Erythema margintum is less than 6%. Erythema macules with clear center and wavy, well-demarcated border, non-puretic, primarily affects the trunk and extremities. Children suspected of having acute rheumatic fever are tested for streptococcal antibodies. The most reliable and best standardized test is an elevated or rising antistreptolysin or ASO titer. Knowing that the child may have had a complication for a recent group A streptococcal infection, an ASO titer would be the best to order. So I would write that down. If a child is suspected of having acute rheumatic fever, on their tested for streptococcal antibodies and the best standardized test would be that ASO titer. Penicillin is the drug of choice for antibiotic treatment of acute rheumatic fever. Treatment for acute rheumatic fever is antibiotics, anti-inflammatory therapy, and supportive care. Children who have acute rheumatic fever are susceptible to recurrent infections that are likely to result in rheumatic heart disease. Anaphylaxis. I think we all have hopefully heard about anaphylaxis. What is it? Anaphylaxis is the acute clinical syndrome resulting from the interaction of an allergen and a patient who is hypersensitive to the allergen. When the antigen enters the circulatory system, a generalized reaction rapidly takes place and chemical substances, primarily histamine, are released from mast cells and cause vasodilation, bronchoconstriction, and increased capillary permeability. This is a life-threatening. Severe reactions are an immediate onset, an often life-threatening, and frequent involve multi-systems, primarily the cardiovascular, respiratory, gastrointestinal, and integumentary systems. Exposure to an antigen may be ingested, inhalation, skin contact, or injection. Examples of common allergens associated with anaphylaxis include drugs, antibiotics, chemotherapy agents. radiological contrast media, latex, foods, venom from bees or snakes, and biological agents. The onset of clinical symptoms usually occurs within seconds or minutes to the exposure of the antigen, and the rapid, rapidly of the reaction is directly related to the, its intensity. The sooner the onset, the more severe the reaction. So what are our signs and symptoms? Usually begins with uneasiness, restlessness, irritability, severe anxiety, headache, dizziness, paresthesia, and disorientation. We move to our bronchial constriction may follow. Causing narrowing of the airway, pulmonary edema, and hemorrhage may also occur. Laryngeal edema with severe acute upper airway obstruction may be life-threatening and requires rapid intervention. Shock occurs as a result of the mediator-induced vasodilation, which causes capillary permeability and loss of intravascular fluid. into the interstitial space. Sudden hypotension and impaired cardiac output with poor perfusion are seen. So what do we want to do? How do we want to treat this? Well, early recognition. We need to know the signs and symptoms. If you have done any school nursing, this might be the place that their diet might be seen with an anaphylactic reaction to an allergen. And epinephrine is the treatment of choice. This is the intermittent. muscular administration of epinephrine, usually up to 0.3 milligrams, is the first-line therapy. The administration should never be delayed. Two pre-mixed preparations are available, EpiPen Jr. for our smaller kids, for children that are 8 to 25 kilograms, and then our EpiPen for children over 25 kilograms. As in any shock state, the airway is our first concern, followed by assessment of the breathing and circulation. So shock. Shock or circulatory failure. is a complex clinical syndrome characterized by inadequate tissue perfusion to meet the metabolic demands of the body, resulting in cellular dysfunction and eventual organ failure. Although the causes are different, the physiological consequences are the same and include hypotension, tissue hypoxia, and metabolic acidosis. Circulatory failure in children is a result of hypovolemia, altered peripheral vascular resistance, or pump failure. Compensated shock. What is that? It's when vital organ function is maintained by intrinsic mechanisms and the child's ability to compensate is effective. Cardiac output and systematic arterial blood pressure are usually normal or increased. However, blood flow is generally uneven or maldistributed in the microcirculation. Early clinical signs are subtle and include apprehension, irritability, normal blood pressure, narrowing pulse pressure, thirst, paler, and diminished urinary output. What is a hypotensive or decompensated uncompensated shock? As our shock progresses, the body is not able to compensate anymore. Pifresian in the microcirculation becomes marginal despite compensatory adjustments, and the signs are more obvious and indicate early decompensation. These signs are tachypnea, moderate metabolic acidosis, ulceria, full paler extremities with decreased skin turgor and poor capillary filling. Hypotensive shock may be differentiated from compensated shock by evaluating blood pressure. The child in a hypotensive shock will have a low blood pressure. The hypotension is a late finding. So the child in hypotensive shock will have a low blood pressure, but hypotension in shock is a late finding. Another clinical sign of hypotensive shock is a change in the level of consciousness as brain perfusion declines. So what are our types of shock? We have our hypovolemic, so that's pretty, I feel, self-explanatory. We have our low blood volume or low volume, often due to hemorrhage or fluid shifting out of the vasculature. We have our distributive, which is blood vessel dilation or septic shock. Our cardiogenic, the heart is not pumping adequately. obstructive. This is a physical block of the blood flow. How do we treat this? Well, they're all about the same. Treatment of shock consists of three major interventions, oxygenation and ventilation, always number one. We want to make sure they're oxygenated and ventilated. Then we want to administer those fluids and then we want to improve the pumping action of the heart. So how can we do that? We got to increase our cardiac output. A lot of times this is our vasopressor support. So increasing that contractility. The child's already trying to increase that heart rate. If they're decompensated shock, they may not be compensating with heart rate anymore. Again, priority is to establish an airway and administer oxygen. After the airway is insured, circulatory stabilization is the major concern. You want to establish an adequate IV access, ideally with a minimum multilumen central lines. It's essential to deliver fluids and medications. All right, our last little bit of our cardiac lecture will be our case study. So I'm going to pause this now and we'll get started on that case study next.

Okay, next we're going to discuss acquired heart diseases. These are things that happen after birth. Your book highlights quite a few.

In this lecture, we will focus on some of the more common acquired heart diseases. So cardiac dysrhythmias. So please make sure you watch the pediatric cardiac rhythm presentation.

It'll help you understand a little bit more about rhythms and dysrhythmias. As a nurse, you must be familiar with the standards of normal heart rate for each age group. An initial nursing responsibility is recognition of abnormal heartbeat, either in rate or in rhythm. When a dysrhythmia is suspected, the apical rate is counted for one full minute and compared with the radial rate, which may be lower because not all apical beats are felt. Consequently, high or low heart rates should be regarded as suspicious.

So if we have a low heart rate, bradycardia, this could be a heart block. Again, we need to know the normal to understand the abnormal. That's why you must be familiar with the heart rate for each age group. And then tachycardia, we're going to discuss our supraventricular tachycardia.

So going right into our supraventricular tachycardia, if you want to look more about our bradycardia or our heart blocks, that's in the pediatric cardiac rhythm. So our supraventricular tachycardia. This is the most common tachydysrhythmia found in children and refers to a rapid regular heart rate of about 200 to 300 beats per minute.

Could you imagine listening to something that's going that fast? As many as 1 in 250 children experience SVT. The onset of SVT is often sudden. The duration is variable and the rhythm may end abruptly and convert back to normal sinus rhythm.

Clinical signs. and our infants and young children are poor feeding, extreme irritability, and paler. Children may also experience palpitations, dizziness, chest pain, and diaphoresis.

So what's our treatment? Our treatment of SVT depends on the degree of compromise imposed on the dysrhythmia. In some cases, vagal maneuvers such as applying ice to the face for 15 to 30 seconds or having an older child perform a Valsalva maneuver, which could be exhaling against a closed glottis, blowing on the thumb as if it were a trumpet for about 30 to 60 seconds.

This can terminate SVT. If vagal maneuvers fail or the child is hemodynamically unstable, adenosine, which is a drug that impairs AV conduction, may be used. So adenosine brings the heart rate down. That's AD, the D in adenosine brings the heart rate down.

Adenosine is given by a rapid IV push. Again, adenosine is given by a rapid IV push and followed with a saline bullet immediately after the drug because it is a very short half-life. You want to give adenosine in the closest vessel to the heart. So if you have a PICC line in or if you have a, say, if you have a IV that's in the wrist and then you have an IV that's in the AC, you want to give it to the one that is closest to the heart.

Again, the half-life of this medication is very short. You give that med real quick, rapid IV push, and then you give that saline bolus real quick. If adenosine is unsuccessful or cardiac output is compromised, esophageal overdrive pacing or synchronized cardioversion, which delivers an electrical shock to the heart, synchronized, can be used in intensive care settings.

Sedation is needed for both procedures. Cardioversion should never be done on a conscious patient. Kawasaki disease. This is an acute systematic vascularitis of an unknown cause. It occurs in every racial group with 76% of the cases occurring in children younger than the age of five.

The peak incidence is in the toddler age group. The acute disease is self-limited. However, with treatment, approximately 20 to 25% of children develop coronary artery dilation or aneurysm formulation.

Infants younger than one year old are at the greatest risk for heart involvement. Although an increased incidence has been reported in older children, perhaps because of the later diagnosis in many. So what are our classic Kawasaki disease criteria? This includes a fever for five calendar days, along with four of the five clinical criteria below. Diagnosis may be made on day four of fever.

by an experienced... clinician in children with fever, and more than four clinical criterion. So there's changes in the extremities. In the acute phase, edema or erythema of the palms and soles.

In the subacute phase, peeling of the hands and feet. Bilateral conjunctival injection or inflammation without exudate. Changes in the oral mucosal membrane, such as erythema, cracking of the lips, oral field and gerodin, or strawberry tongue. really common.

A rash, maculopapilla, diffused erythrodema, or erythromultiform-like rash may occur. Cervical lymphodempathy. These are all things, these are some of the criteria.

The strawberry tongue and peeling of the hands, along with the fever for five calendar days, is something that is diagnosed for Kawasaki disease. So what's our current treatment? The current treatment of children with Kawasaki disease includes administration of high-dose IVIG along with cell estate therapy or aspirin therapy. IVIG has been demonstrated to be effective in reducing the incidence of coronary artery abnormalities when given within the first 10 days of the illness and ideally within the first seven days.

Aspirin has been used historically to control fever and symptoms of inflammation. I know aspirin isn't commonly given to children. But in this case, it is the recommended therapy. So again, I'd remember about the high-dose IVIG for treatment of Kawasaki. So highlight that.

MIS-C. So little is known about the pathophysiology of MIS-C. And it's felt that MIS-C is a consequence of immune-mediated injury triggered by COVID-19.

The treatment is very similar to Kawasaki disease. Your book doesn't... may not have much information about it, but this information on this slide is from the CDC in 2020, and it describes MIS-C in children less than 21 years of age using the following criteria, a fever greater than 38 degrees for 24 hours or a subjective fever lasting longer than 24 hours. Laboratory evidence of inflammation, including but not limited to, one of the following, elevated CRP, ESR, fibrinogen, procalcitonin, D-dimer, ferritin, lactate acid dehydrogenase, interleukin-6, elevated neutrophils, reduced lymphocytes, and low albumin. Evidence of clinically severe illness requiring hospitalization with multi-system greater than two organ involvement would be cardiac, renal, respiratory, hematological, gastrointestinal, dermatological, or neurological.

No alternative possible diagnosis. Positive for recurrent or recent COVID-19 infection. Documented by reverse transcupidase polymers chain reaction, RT-PCR.

Serology or antigen test or COVID-19 exposure within the four weeks prior to the onset of symptoms. Positive for current or recent COVID-19 infection documented by RT-PCR. serology or antigen tests, or COVID-19 exposure within four weeks prior to the onset of symptoms.

Again, treatment is very similar to Kawasaki disease. Rheumatic heart disease. Acute rheumatic fever is a result of an abnormal immune response to a group A strep infection, usually pharyngitis, a genetically susceptible host.

It occurs most often in late school-age children and adolescents and is rare in adults. Acute rheumatic fever is a self-limiting illness that involves the joints, skin, brain, and heart. The cardiac valve damage, which is referred to as rheumatic heart disease, the most significant complication of acute rheumatic fever, occurs in more than half the cases.

The mitral valve is most often affected. Upper respiratory infections, or URIs, with... Group A strep support a relationship with acute rheumatic fever, usually within two to six weeks. Untreated group A strep infection may cause damage to the heart valves.

Repeated or recurrent infections cause cumulative valve damage. Acute rheumatic fever clinical manifestation. Carditis is seen in about 50 to 70 percent of cases. The most significant manifestations of acute rheumatic fever is carditis.

Cardiasis is the only manifestation of acute rheumatic fever that leads to permanent damage. So signs could be tachycardia out of proportion to the degree of fever. cardiomegaly, new murmurs or changes to pre-existing murmurs, muffled heart sounds, pericardial friction realm, chest pain, changes in the ECG, especially a prolonged PR interval.

Polyarthritis occurs in about 35 to 66 percent of cases. This includes swollen and hot red painful joints. After one to two days, different joints can be affected.

Favors large joints such as the knees, elbows, hips, shoulders, and wrists. Subcutaneous nodules occurs in less than 10% of cases. Non-tender swelling located over bony provinces may persist for some time and then gradually resolve.

Erythema margintum is less than 6%. Erythema macules with clear center and wavy, well-demarcated border, non-puretic, primarily affects the trunk and extremities. Children suspected of having acute rheumatic fever are tested for streptococcal antibodies.

The most reliable and best standardized test is an elevated or rising antistreptolysin or ASO titer. Knowing that the child may have had a complication for a recent group A streptococcal infection, an ASO titer would be the best to order. So I would write that down.

If a child is suspected of having acute rheumatic fever, on their tested for streptococcal antibodies and the best standardized test would be that ASO titer. Penicillin is the drug of choice for antibiotic treatment of acute rheumatic fever. Treatment for acute rheumatic fever is antibiotics, anti-inflammatory therapy, and supportive care.

Children who have acute rheumatic fever are susceptible to recurrent infections that are likely to result in rheumatic heart disease. Anaphylaxis. I think we all have hopefully heard about anaphylaxis.

What is it? Anaphylaxis is the acute clinical syndrome resulting from the interaction of an allergen and a patient who is hypersensitive to the allergen. When the antigen enters the circulatory system, a generalized reaction rapidly takes place and chemical substances, primarily histamine, are released from mast cells and cause vasodilation, bronchoconstriction, and increased capillary permeability.

This is a life-threatening. Severe reactions are an immediate onset, an often life-threatening, and frequent involve multi-systems, primarily the cardiovascular, respiratory, gastrointestinal, and integumentary systems. Exposure to an antigen may be ingested, inhalation, skin contact, or injection.

Examples of common allergens associated with anaphylaxis include drugs, antibiotics, chemotherapy agents. radiological contrast media, latex, foods, venom from bees or snakes, and biological agents. The onset of clinical symptoms usually occurs within seconds or minutes to the exposure of the antigen, and the rapid, rapidly of the reaction is directly related to the, its intensity.

The sooner the onset, the more severe the reaction. So what are our signs and symptoms? Usually begins with uneasiness, restlessness, irritability, severe anxiety, headache, dizziness, paresthesia, and disorientation.

We move to our bronchial constriction may follow. Causing narrowing of the airway, pulmonary edema, and hemorrhage may also occur. Laryngeal edema with severe acute upper airway obstruction may be life-threatening and requires rapid intervention. Shock occurs as a result of the mediator-induced vasodilation, which causes capillary permeability and loss of intravascular fluid. into the interstitial space.

Sudden hypotension and impaired cardiac output with poor perfusion are seen. So what do we want to do? How do we want to treat this? Well, early recognition. We need to know the signs and symptoms.

If you have done any school nursing, this might be the place that their diet might be seen with an anaphylactic reaction to an allergen. And epinephrine is the treatment of choice. This is the intermittent. muscular administration of epinephrine, usually up to 0.3 milligrams, is the first-line therapy.

The administration should never be delayed. Two pre-mixed preparations are available, EpiPen Jr. for our smaller kids, for children that are 8 to 25 kilograms, and then our EpiPen for children over 25 kilograms. As in any shock state, the airway is our first concern, followed by assessment of the breathing and circulation.

So shock. Shock or circulatory failure. is a complex clinical syndrome characterized by inadequate tissue perfusion to meet the metabolic demands of the body, resulting in cellular dysfunction and eventual organ failure. Although the causes are different, the physiological consequences are the same and include hypotension, tissue hypoxia, and metabolic acidosis. Circulatory failure in children is a result of hypovolemia, altered peripheral vascular resistance, or pump failure.

Compensated shock. What is that? It's when vital organ function is maintained by intrinsic mechanisms and the child's ability to compensate is effective. Cardiac output and systematic arterial blood pressure are usually normal or increased. However, blood flow is generally uneven or maldistributed in the microcirculation.

Early clinical signs are subtle and include apprehension, irritability, normal blood pressure, narrowing pulse pressure, thirst, paler, and diminished urinary output. What is a hypotensive or decompensated uncompensated shock? As our shock progresses, the body is not able to compensate anymore.

Pifresian in the microcirculation becomes marginal despite compensatory adjustments, and the signs are more obvious and indicate early decompensation. These signs are tachypnea, moderate metabolic acidosis, ulceria, full paler extremities with decreased skin turgor and poor capillary filling. Hypotensive shock may be differentiated from compensated shock by evaluating blood pressure. The child in a hypotensive shock will have a low blood pressure. The hypotension is a late finding.

So the child in hypotensive shock will have a low blood pressure, but hypotension in shock is a late finding. Another clinical sign of hypotensive shock is a change in the level of consciousness as brain perfusion declines. So what are our types of shock? We have our hypovolemic, so that's pretty, I feel, self-explanatory.

We have our low blood volume or low volume, often due to hemorrhage or fluid shifting out of the vasculature. We have our distributive, which is blood vessel dilation or septic shock. Our cardiogenic, the heart is not pumping adequately.

obstructive. This is a physical block of the blood flow. How do we treat this?

Well, they're all about the same. Treatment of shock consists of three major interventions, oxygenation and ventilation, always number one. We want to make sure they're oxygenated and ventilated. Then we want to administer those fluids and then we want to improve the pumping action of the heart.

So how can we do that? We got to increase our cardiac output. A lot of times this is our vasopressor support. So increasing that contractility.

The child's already trying to increase that heart rate. If they're decompensated shock, they may not be compensating with heart rate anymore. Again, priority is to establish an airway and administer oxygen.

After the airway is insured, circulatory stabilization is the major concern. You want to establish an adequate IV access, ideally with a minimum multilumen central lines. It's essential to deliver fluids and medications. All right, our last little bit of our cardiac lecture will be our case study. So I'm going to pause this now and we'll get started on that case study next.

Transcript for:Overview of Acquired Heart Diseases

Transcript for:
Overview of Acquired Heart Diseases