Congestive heart failure (CHF) is the result of insufficient output because of cardiac failure, high resistance in the circulation or fluid overload. Left ventricle (LV) failure is the most common and results in decreased cardiac output and increased pulmonary venous pressure. In the lungs LV failure will lead to dilatation of pulmonary vessels, leakage of fluid into the interstitium and the pleural space and finally into the alveoli resulting in pulmonary edema. Right ventricle (RV) failure is usually the result of long standing LV failure or pulmonary disease and causes increased systemic venous pressure resulting in edema in dependent tissues and abdominal viscera. In the illustration on the left some of the features, that can be seen on a chest-film in a patient with CHF. Increased pulmonary venous pressure is related to the pulmonary capillary wedge pressure (PCWP) and can be graded into stages, each with its own radiographic features on the chest film (Table).
In daily clinical practice however some of these features are not seen in this sequence and sometimes may not be present at all.
This can be seen in patients with chronic heart failure, mitral valve disease and in chronic obstructive lung disease. Views of the upper lobe vessels of a patient in good condition (left) and during a period of CHF (right). In a normal chest film with the patient standing erect, the pulmonary vessels supplying the upper lung fields are smaller and fewer in number than those supplying the lung bases. The pulmonary vascular bed has a significant reserve capacity and recruitment may open previously non-perfused vessels and causes distension of already perfused vessels. First there is equalisation of blood flow and subsequently redistribution of flow from the lower to the upper lobes.
The term redistribution applies to chest x-rays taken in full inspiration in the erect position. In daily clinical practice many chest films are taken in a supine or semi-erect position and the gravitational difference between the apex and the lung bases will be less. In the supine position, there will be equalisation of blood flow, which may give the false impression of redistribution.
Normally the vessels in the upper lobes are smaller than the accompanying bronchus with a ratio of 0.85 (3). At the level of the hilum they are equal and in the lower lobes the arteries are larger with a ratio of 1.35. When there is redistribution of pulmonary blood flow there will be an increased artery-to-bronchus ratio in the upper and middle lobes. Stage II of CHF is characterized by fluid leakage into the interlobular and peribronchial interstitium as a result of the increased pressure in the capillaries.
When fluid leaks into the peripheral interlobular septa it is seen as Kerley B or septal lines. Kerley-B lines are seen as peripheral short 1-2 cm horizontal lines near the costophrenic angles.
When fluid leaks into the peribronchovascular interstitium it is seen as thickening of the bronchial walls (peribronchial cuffing) and as loss of definition of these vessels (perihilar haze). There is an increase in the caliber of the pulmonary vessels and they have lost their definition because they are surrounded by edema.
The lateral view nicely demonstrates the increased diameter of the pulmonary vessels and the hazy contours. Subtle ground glass opacity in the dependent part of the lungs (HU difference of 100-150 between the dependent and non-dependent part of the lung). In a patient with a known malignancy lymphangitic carcinomatosis would be high in the differential diagnostic list. Ground glass opacity is the first presentation of alveolar edema and a precursor of consolidation. This stage is characterized by continued fluid leakage into the interstitium, which cannot be compensated by lymphatic drainage.
This eventually leads to fluid leakage in the alveoli (alveolar edema) and to leakage into the pleural space (pleural effusion).
After treatment we can still see an enlarged cardiac silhouette, pleural fluid and redistribution of the pulmonary blood flow, but the edema has resolved.
On the left another patient with alveolar edema at admission, which resolved after treatment.
When you scroll through the images and go back and forth, you will notice the difference in vascular pedicle width and distribution of pulmonary flow.
Both on the chest x-ray and on the CT the edema is gravity dependent and differences in density can be measured.
This is not seen when the consolidations are the result of exsudate due to infection, blood due to hemorrhage or when there is a capillary leak like in ARDS. A possible explanation for this phenomenon could be, that the patient had been lying on his right side for a while before the x-ray was taken. The cardiothoracic ratio (CTR) is the ratio of the transverse diameter of the heart to the internal diameter of the chest at its widest point just above the dome of the diaphragm as measured on a PA chest film.
An increased cardiac silhouette is almost always the result of cardiomegaly, but occasionally it is due to pericardial effusion or even fat deposition. An increase in left ventricular volume of at least 66% is necessary before it is noticeable on a chest x-ray.
Other signs of CHF are visible, such as redistribution of pulmonary flow, interstitial edema and some pleural fluid. On a supine film the cardiac silhouette will be larger due to magnification and high position of the hemidiafragms. Exact measurements are not that helpful, but comparison to old supine films can be of value.
Because of the recent cardiac surgery, the possibility of pericardial effusion was taken into account, which is nicely demonstrated on the CT-image. On the left another patient with a large cardiac silhouette on the chest x-ray due to pericardial effusion. There has to be at least 175 ml of pleural fluid, before it will be visible on a PA image as a meniscus in the costophrenic angle.
If pleural effusion is seen on a supine chest film, it means that there is at least 500 ml present. A subpulmonic effusion may follow the contour of the diaphragm making it tricky to discern.


In these cases, the only way to detect pleural effusion, is when you notice that there is an increased distance between the stomach bubble and the lung.
The stomach is normally located directly under the diaphragm, so, on an erect PA radiograph, the stomach bubble should always appear in close proximity to the diaphragm and the lung. At first glance you might get the impression that there is a high position of the diaphragm.
However when you notice the increased distance of the stomach air bubble to the lung base, you realize that there is a large amount of pleural fluid on both sides (arrow).
The vascular pedicle is bordered on the right by the superior vena cava and on the left by the left subclavian artery origin (6). A vascular pedicle width less than 60 mm on a PA chest radiograph is seen in 90% of normal chest x-rays. An increase in width of the vascular pedicle is accompanied by an increased width of the azygos vein. The VPW is best used as a measure to compare serial chest x-rays of the same patient, as there is a wide range of values for the VPW. Dilation of the azygos vein is a sign of increased right atrial pressure and is usually seen when there is also an increase in the width of the vascular pedicle. The difference of the azygos diameter on an inspiration film compared to an expiration film is only 1mm. This means that the diameter of the azygos is a valuable tool whether or not there is good inspiration.
RV failure is most commonly caused by longstanding LV failure, which increases the pulmonary venous pressure and leads to pulmonary arterial hypertension, thus overloading the RV. The indication for ultrasound examination in many of these patients is abnormal liver function tests.
It is therefore important to consider the possibility of RV failure when a patient presents with liver enzyme abnormalities.
These changes in caliber can be attributed to variations in blood flow in the IVC in accordance with the respiratory and cardiac cycles.
Pulmonary artery-bronchus ratios in patients with normal lungs, pulmonary vascular plethora, and congestive heart failure. Pulmonary hypertension secondary to left-sided heart disease: a cause for ventilation-perfusion mismatch mimicking pulmonary embolism.
Total mass of the indicator after distribution in the compartment is the same as the mass before distribution. Most commonly, infants and children sustain cardiac arrest as a result of respiratory failure. Rhythm disturbances seen before pediatric cardiac arrest differ compared to adults and differ by age (see Table 1). The survival rate of children after cardiac arrest is higher than that of adults, but remains poor. The post-cardiac arrest syndrome consists of four general processes: anoxic brain injury, post-arrest myocardial dysfunction, systemic ischemia and reperfusion injury, and persistent precipitating pathophysiology. Consider the pediatric assessment triangle (PAT) in the evaluation of children to help identify symptoms and signs that may be harbingers of cardiac arrest. Respiratory distress, failure, and, ultimately, arrest are the most common precipitating causes of cardiac arrest in children. Cardiopulmonary resuscitation focuses on the early management of airway, breathing, and circulation. The defined heart rate at which a child is deemed to be bradycardic dependson a child’s age. The management of bradycardia focuses primarily on identifying and treating the underlying etiology. Risk factors for the development of VF include cardiac ectopy, hypertrophic cardiomyopathy, dilated cardiac myopathy, prior cardiac arrest, severe valvular disease, long QT syndrome, and Brugada syndrome. In the unstable patient, wide complex tachycardias are treated as VT until proven otherwise. Post-resuscitation care should be instituted once return of spontaneous circulation is achieved to prevent secondary organ injury and preserve neurologic function. Supraventricular tachycardia is a rapid rhythm originating above the ventricles as a result of either a re-entry mechanism or automaticity.
SVT is the most common significant arrhythmia in pediatric patients.The majority of cases occur in structurally normal hearts. For stable SVT that does not convert with vagal maneuvers, anti-arrhthymic drug administration is indicated.
Each year about 40% of myocardial infarctions are fatal, of which more than half of deaths occur in the emergency room or before reaching the hospital.
The main cause of both unstable angina and myocardial infarction is coronary artery disease. Pain may be accompanied by other signs: dizziness, fainting, nausea, vomiting, sweating, choking, anxiety, nervousness, palpitations (not all of these clinical signs occur in every acute myocardial infarction). Kulick received his undergraduate and medical degrees from the University of Southern California, School of Medicine. Ben Wedro practices emergency medicine at Gundersen Clinic, a regional trauma center in La Crosse, Wisconsin.
Charles "Pat" Davis, MD, PhD, is a board certified Emergency Medicine doctor who currently practices as a consultant and staff member for hospitals. While fatigue is a sensitive indicator of possible underlying congestive heart failure, it is obviously a nonspecific symptom that may be caused by many other conditions. Overall, the survival rate to hospital discharge following in-hospital (ICU) pediatric cardiac arrest is 22%.
Hypoxic ischemic encephalopathy is the most important cause of morbidity and mortality following resuscitation. Pulseless electrical activity (PEA) refers to any cardiac rhythm other than asystole in which there is electrical activity within the heart, but there is no palpable or perfusing pulse present. Management includes high-quality CPR, airway and respiratory support, and possible vasoactive medication administration. Ventricular tachycardia (VT) is a series of three or more consecutive ectopic beats originating from within ventricles rather than atria of the heart.
A brief history, including medication and family histories, may reveal the etiology of the tachyarrhythmia.


All pediatric patients who suffer cardiac arrest should be transferred to a higher level of care once stabilized. It is a narrow complex tachycardia at a rate of 150-300 bpm with 1:1 AV conduction and a fixed RR interval. Higher survival rates among younger patients after pediatric intensive care unit cardiac arrests. Out-of-hospital cardiac arrests in children and adolescents: Incidences, outcomes, and household socioeconomic status. Conventional and chest-compression-only cardiopulmonary resuscitation by bystanders for children who have out-of-hospital cardiac arrests: A prospective, nationwide, population-based cohort study. The process of atherosclerosis can be slowed by reducing these risk factors, thus reducing the risk of death or disability by myocardial infarction. Prevention of acute myocardial infarction is the best thing and it is never too late to change habits that can harm your heart.
He performed his residency in internal medicine at the Harbor-University of California Los Angeles Medical Center and a fellowship in the section of cardiology at the Los Angeles County-University of Southern California Medical Center. His background includes undergraduate and medical studies at the University of Alberta, a Family Practice internship at Queen's University in Kingston, Ontario and residency training in Emergency Medicine at the University of Oklahoma Health Sciences Center. Learn the causes, symptoms, treatments, testing, and procedures for coronary artery disease. Work of Breathing may also range from normal to bradypnea and apnea or tachypnea and respiratory distress immediately prior to arrest. These include respiratory or extra-pulmonary infections, upper or lower airway obstruction, tension pneumothorax, pulmonary edema, disorders of the chest wall trauma or thoracic cavity, central neurologic system (CNS) dysfunction, and metabolic, endocrine, or hematologic crises.
However, the 2010 AHA guidelines for cardiopulmonary resuscitation recommend a Circulation-Airway-Breathing (CAB) sequence.
Chest compressions are performed at a rate of at least 100 per minute with minimal interruptions. For simplicity, the American Heart Association (PALS) defines bradycardia as a heart rate < 60 bpm. In the child with a heart rate < 60 bpm and signs of poor perfusion or shock, chest compressions should be initiated. A 12-lead EKG and pediatric cardiology consultation may help differentiate VT from SVT with aberrancy or other arrhythmias.
If the patient is hemodynamically compromised but has palpable pulses, synchronized cardioversion should be performed. Therapeutic hypothermia (32o-34oF) may be considered for children who remain comatose after resuscitation from cardiac arrest.
Common symptoms of SVT include respiratory distress, shortness of breath, chest pain, palpitations, poor feeding, syncope, pallor or irritability. When there is total cessation of blood flow to an area (usually by a blood clot formation) results in a myocardial infarction. Chest pain that reaches maximum intensity within seconds can be a sign of another disease, aneurysm of aorta. Asphyxia begins with a variable period of systemic hypoxemia, hypercapnea, and acidosis that progresses to bradycardia, hypotension and, ultimately, cardiac arrest. Ominous circulation findings, such as delayed capillary refill and mottled and cyanotic skin, are clues that cardiac output and perfusion are may be compromised and cardiac arrest may be imminent.
Primary pediatric cardiac arrest is rare in otherwise healthy children and is most commonly associated with conditions such as viral myocarditis, pericarditis, dysrhythmias, and congenital heart disease. Positive pressure ventilations are delivered initially with bag-valve-mask device during brief pauses in chest compressions.
The most common vagal maneuver used in infants and young children is an ice pack applied to the face for 15-30 seconds. While performing the abdominal exam to rule out incarcerated hernia, the femoral pulses are noted to be fast. Elevated cholesterol, hypertension and smoking damages your arteries and contributes to plaque formation. He is a Clinical Professor (retired) in the Division of Emergency Medicine, UT Health Science Center at San Antonio, and has been the Chief of Emergency Medicine at UT Medical Branch and at UTHSCSA with over 250 publications. Cardiopulmonary arrest can be thought of as the ultimate shock state, resulting in markedly impaired oxygen delivery and extraction, endothelial activation, systemic inflammation, multi-organ failure and death.
Primary myocardial infarction, the most common cause of cardiac arrest in adult populations, is rare in children. An advanced airway (endotracheal tube or laryngeal airway) may be inserted, as long as chest compressions are only briefly interrupted.
Primary VF occurs in proarryhthmic conditions that affect the right ventricular outflow tract. Pediatric cardiology should be consulted to aid with further management in the intensive care setting.
Amiodarone or procainamide are additional drug therapy options if SVT persists despite adenosine administration.
Further, in children who sustain a cardiac cause, convention CPR is non-inferior to compression-only CPR.3 Therefore, conventional CPR is recommended for all pediatric cardiac arrest patients except when performed by basic life support (BLS) bystanders. Once an advanced airway is established, ventilation is delivered at a rate of 1 breath every 6 to 8 seconds (about 8 to 10 breaths per minute) without interrupting compressions. Atropine is reserved for arrest secondary to increased vagal tone or primary atrioventricular block.
Etiologies include primary electrical disease (long QTc syndrome), pulmonary hypertension, structural heart disease such as tetralogy of Fallot (TOF), and postoperative congenital heart disease. Secondary VF refers to VF that develops in the context of myocardial infarction, shock, or congestive heart failure. Which feature of this most common dysrhythmia distinguishes it from other tachydysrhythmias?
Other causes include myocarditis, Brugada syndrome, hypoxemia, arrhythmogenic right ventricular dysplasia, electrolyte imbalance (hyperkalemia), and ingestions (tricyclics, digoxin). Symptoms of ventricular tachycardia include chest pain, lethargy, syncope, hypotension, palpitations and sudden death with hemodynamic collapse.



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