Supraventricular tachycardia (SVT) is a heart condition where the heart beats irregularly due to electrical abnormalities. It is fairly common, especially in children and women, yet unfamiliar to most people who are not diagnosed with it. There are three types of SVT: atrioventricular nodal re-entry tachycardia, atrial tachycardia, and Wolff-Parkinson-White syndrome. All three types have the same symptoms during episodes, which can last from seconds to hours and include palpitations, fatigue, dizziness, etc. However, the three types have different causes, all of which are unknown. To detect this condition an electrocardiograph is typically used. It compares the waves of the patient’s heart to a normal heart’s waves. Vagal maneuvers are …show more content…
This obviously excludes exercise, stress, or a high fever as a reason for the spike in heart rate, but includes abnormal electrical impulses sent from the natural pacemaker of the heart.
The most common type of SVT is atrioventricular nodal re-entry tachycardia (AVNRT). In AVNRT there is an abnormal "shortcut" the impulses can take in the AV node to go forward and backwards at the same time, triggering an extra heart beat. This means the impulses travel continuously and speed the heart rate to 150-250 beats per minute. Patients are born with the extra pathway in the AV node however the cause of this extra pathway is still unknown (Atrioventricular, 2016).
The second and less common type of SVT is atrial tachycardia. In this type of SVT the SA node gets overpowered by an area of tissue in the atria that starts to develop and control the rate of the heart. Generally this area of tissue creates a faster rate than the SA node would. Again, the cause of the overpowering tissue that causes atrial tachycardia is unknown (Kenny,
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An electrocardiograph (ECG) is a common test that tracks impulses through the heart. Sensors are placed on the body to pick up impulses and the ECG will illustrate the time each impulse takes to get from the upper chambers to the lower chambers of the heart by showing three waves. The "P wave" is the first wave that originates from the atria, followed by the "QRS complex" that comes from the ventricles, and lastly the "T wave" that shows when the ventricles are at rest again (Electrocardiogram, 2015). Doctors will time the waves to see if the timing is correct or if they are too fast or too slow (Figures 3 and 4). They will also measure the impulse to see if one part of the heart has too much electrical activity than it is able to handle. This test can also be done with a miniature portable ECG recorder that can be worn for a period of time to actually catch an episode of SVT, which is usually more successful because episodes are so unpredictable. These portable ECGs can also be called Holt monitors and event recorders and also have sensors that get tape on specific areas of the chest (Electrocardiogram, 2015). Another more specialized test for those already diagnosed with SVT but want to locate the exact cause of abnormal heart beats is an electrophysiologic test. Doctors insert catheters with electrical sensors on them in a vein in the arm or upper thigh. The doctor moves the catheter around in the heart, with the help
There are several different heart problems that show up as an abnormal EKG reading. For example, a heart block can occur when there is a delay in the signals coming from the SA node, AV node, or the Purkinje fibers. However, clinically the term heart block is used to refer to an AV block. This delays or completely stops communication between the atria and the ventricles. AV block is shown on the EKG as a delayed or prolonged PR interval. The P wave represents the activity in the atria, and the QRS complex represents ventricular activity. This is why the PR interval shows the signal delay from the AV node. There are three degrees of severity, and if the delay is greater than .2 seconds it is classified as first degree. Second degree is classified by several regularly spaced P waves before each QRS complex. Third degree can be shown by P waves that have no spacing relationship to the QRS complex. Another type of blockage is bundle branch block. This is caused by a blockage in the bundle of His, creating a delay in the electrical signals traveling down the bundle branches to reach the ventricles. This results in a slowed heart beat, or brachycardia. On an EKG reading this is shown as a prolonged QRS complex. A normal QRS is about .8-.12 seconds, and anything longer is considered bundle branch block. Another type of abnormal EKG reading is atrial fibrillation, when the atria contracts very quickly. On the EKG this is shown by no clear P waves, only many small fibrillating waves, and no PR interval to measure. This results in a rapid and irregular heartbeat. On the other hand, ventricular fibrillation is much more serious and can cause sudden death if not treated by electrical defibrillation.
In this lab, I took two recordings of my heart using an electrocardiogram. An electrocardiogram, EKG pg. 628 Y and pg. 688 D, is a recording of the heart's electrical impulses, action potentials, going through the heart. The different phases of the EKG are referred to as waves; the P wave, QRS Complex, and the T wave. These waves each signify the different things that are occurring in the heart. For example, the P wave occurs when the sinoatrial (SA) node, aka the pacemaker, fires an action potential. This causes the atria, which is currently full of blood, to depolarize and to contract, aka atrial systole. The signal travels from the SA node to the atrioventricular (AV) node during the P-Q segment of the EKG. The AV node purposefully delays
“Ebstein’s anomaly is a rare cardiac anomaly that occurs in approximately one in 20,000 live births and accounts for less than 1% of all congenital heart disease (Ebstein’s anomaly in adults)”. The goal of this paper is to examine Ebstein’s Anomaly - to understand what it is, how it affects the heart, possible presenting symptoms, and other possible complications associated with this anomaly. Diagnosis of this anomaly is key in treating patients, thus echocardiographic as well as other test modalities are vital in assessing what the treatment options are available, as well as discerning what the prognosis may be. Advancing test modalities have helped distinguish Ebstein’s Anomaly with other differential diagnoses. Developments with testing modalities coupled with comprehensive calculations, formulas, and measurements have facilitated correctly diagnosing, and therefore properly treating cardiac patients.
Cardiomyopathy, by definition, means the weakening of the heart muscle. The heart is operated by a striated muscle that relies on the autonomic nervous system to function. Cardiomyopathy is diagnosed in four different ways based on what caused the illness and exactly what part of the heart is weakened. The four main types of cardiomyopathy are dilated cardiomyopathy, hypertrophic cardiomyopathy, restrictive cardiomyopathy, and arrhythmogenic right ventricular dysplasia. One other category of cardiomyopathy that is diagnosed is “unclassified cardiomyopathy.” Unclassified cardiomyopathy is the weakening of the heart that does not fit into the main four categories.
Two heart sounds are normally heard through a stethoscope on the chest wall, "lab" "dap". The first sound can be described as soft, but resonant, and longer then the second one. This sound is associated with the closure of AV valves (atrioventricular valves) at the beginning of systole. The second sound is louder and sharp. It is associated with closure of the pulmonary and aortic valves (semilunar valves) at the beginning of diastole. There is a pause between the each set of sounds. It is a period of total heat relaxation called quiescent period.
This syndrome increase blood flow causes the heart to pump blood to the lungs at an increasing rate and destroys the blood vessels in the lungs. Several Heart defects that causes disorder is ventricular septal defect (VSD), atrial septal defect (ASD), Patent ductus arteriosus (PDS), and Atrioventricular canal defect (ACD) (Mayo Clinic,2016) This hole usually causes symptoms that include blue or gray skin pigments, shortness of breath, extreme fatigue, chest pains, racing or skipped heart beats, and dizziness. Other symptoms include coughing up blood, swelling in the abdominal region, and numb and/or enlarged fingers and toes. Some of the way ER syndrome can be diagnosed are Chest X-ray are used for heart and pulmonary artery enlargement. Electrocardiogram (ECG) electrical activity of the heart that help test for heart defect that are caused by ES, Echocardiogram is normally used for listing to sound of the heart during, but during ER testing it helps to see if the patient have a heart defect, Magnetic resonance imaging (MRI) is used to take images of blood vessels and lungs and blood test is use to check blood count, which ES would make it
In a normal strip, one can clearly identify a P wave before every QRS complex, which is then followed by a T wave; in Atrial Fibrillation, the Sinoatrial node fires irregularly causing there to be no clear P wave and an irregular QRS complex (Ignatavicius & Workman, 2013). Basically, it means that the atria, the upper chambers of the heart, are contracting too quickly and no clear P wave is identified because of this ‘fibrillation’ (Ignatavicius & Workman, 2013). Clinical Manifestations and Pathophysiology A normal heart rhythm begins at the sinoatrial node and follows the heart's conduction pathway without any problems. Typically the sinoatrial node fires between 60-100 times per minute (Ignatavicius & Workman, 2013).
An electrocardiogram (ECG) is one of the primary assessments concluded on patients who are believed to be suffering from cardiac complications. It involves a series of leads attached to the patient which measure the electrical activity of the heart and can be used to detect abnormalities in the heart function. The ECG is virtually always permanently abnormal after an acute myocardial infarction (Julian, Cowan & Mclenachan, 2005). Julies ECG showed an ST segment elevation which is the earliest indication that a myocardial infarction had in fact taken place. The Resuscitation Council (2006) recommends that clinical staff use a systematic approach when assessing and treating an acutely ill patient. Therefore the ABCDE framework would be used to assess Julie. This stands for airways, breathing, circulation, disability and elimination. On admission to A&E staff introduced themselves to Julie and asked her a series of questions about what had happened to which she responded. As she was able to communicate effectively this indicates that her airways are patent. Julie looked extremely pale and short of breath and frequently complained about a feeling of heaviness which radiated from her chest to her left arm. The nurses sat Julie in an upright in order to assess her breathing. The rate of respiration will vary with age and gender. For a healthy adult, respiratory rate of 12-18 breaths per minute is considered to be normal (Blows, 2001). High rates, and especially increasing rates, are markers of illness and a warning that the patient may suddenly deteriorate. Julie’s respiratory rates were recorded to be 21 breaths per minute and regular which can be described as tachypnoea. Julies chest wall appeared to expand equally and symmetrical on each side with each breath taken. Julies SP02 levels which are an estimation of oxygen
The study of cardio physiology was broken up into five distinct parts all centering on the cardiovascular system. The first lab was utilization of the electrocardiogram (ECG). This studied the electrical activities of the heart by placing electrodes on different parts of the skin. This results in a graph on calibrated paper of these activities. These graphs are useful in the diagnosis of heart disease and heart abnormalities. Alongside natural heart abnormalities are those induced by chemical substances. The electrocardiogram is useful in showing how these chemicals adjust the electrical impulses that it induces.
Hypertrophic cardiomyopathy is an inherited disease that affects the cardiac muscle of the heart, causing the walls of the heart to thicken and become stiff. [1] On a cellular level, the sarcomere increase in size. As a result, the cardiac muscles become abnormally thick, making it difficult for the cells to contract and the heart to pump. A genetic mutation causes the myocytes to form chaotic intersecting bundles. A pathognomonic abnormality called myocardial fiber disarray. [2,12] How the hypertrophy is distributed throughout the heart is varied. Though, in most cases, the left ventricle is always affected. [3] The heart muscle can thicken in four different patterns. The most common being asymmetrical septal hypertrophy without obstruction. Here the intraventricular septum becomes thick, but the mitral valve is not affected. Asymmetrical septal hypertrophy with obstruction causes the mitral valve to touch the septal wall during contraction. (Left ventricle outflow tract obstruction.) The obstruction of the mitral valve allows for blood to slowly flow from the left ventricle back into the left atrium (Mitral regurgitation). Symmetrical hypertrophy is the thickening of the entire left ven...
The second beat is the semilunar valve opening to allow blood into the aorta or pulmonary trunk. The cardiac cycle is composed of five stages. These stages are atrial systole, early ventricular systole, late ventricular systole, early ventricular diastole, and late ventricular diastole. In order for atrial systole to occur, the blood that has been flowing between the atrium and ventricle via the opened atrioventricular valves must be deposited into the ventricles. The SA node is responsible for the contraction of the atrial myocardium.
Individuals with AN keep their body in a state of starvation. Their body must function without the sustenance that it needs to continue functioning. Bradycardia is the most common heart arrhythmia for individuals with this disorder. As a result of the caloric deficit, the body tries to decrease cardiac work by reducing cardiac output. (Casiero & Frishman, 2006). The baroreceptor reflex is the body’s mechanism to regulate blood pressure through use of baroreceptors, which then transmits information to the brainstem. The vagal nerve receives this information, then sends impulses to the sinus node to slow the beat of the heart. (Kollai et al, 1994) A study published in the Oxford Heart Journal measured cardiac va...
Most often the disease starts in the left ventricle, and then often spreads to both the atrium and right ventricle as well. Usually there will also be mitral and tricuspid regurgitation, due to the dilation of the annuli. This regurgitation will continue to make problems worse by adding excessive volume and pressure to the atria, which is what then causes them to dilate. Once the atria become dilated it often leads to atrial fibrillation. As the volume load increases the ventricles become more dilated and over time the myocytes become weakened and cannot contract as they should. As you might have guessed with the progressive myocyte degeneration, there is a reduction in cardiac output which then may present as signs of heart failure (Lily).
When you have Tachycardis your heart rate is above 100 beats per minute. Tachycardis is caused by heart injuries from past times. Tachycardis usually occurs months or years after a heart attack. A treatment for Tachycardis can be inserting a device called a defibrillator. A defibrillator will detect and treat abnormally fast heart rhythms.
Oxygen was first admitted to the client with chest pain over 100 years ago (Metcalfe, 2011). Chest pain is a large bracket that can contain many different conditions, but for the purpose of this analysis it is focused manly upon a myocardial infarction. A myocardial infarction is mainly referred to as a heart attack, and occurs when one or more coronary arteries leading to the heart reduce or completely stop blood flow (Tuipulotu, 2013 ). Administering high concentrations of oxygen to patients with chest pain is now embedded in guidelines, protocols and care pathways, even with a lack of clear supporting evidence (Nicholson, 2004 ). High concentration of oxygen means that up to 60% is administered (Knott, 2012). More recent research has suggested that the use of oxygen in this scenario is unnecessary and can lead to unwanted side effects, especially in normoxic cardiac patients (Moradkham & Sinoway, 2010 ). The aim of this comparative analysis is to dismantle and understand both the benefits and risks of the commonly known practice of administration of oxygen to the client with chest pain. Through completing this analysis using recent and appropriate evidence a more improved practice can be given and understood.