Electrolyte and metabolic ECG abnormalities
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This document discusses various electrolyte abnormalities and their ECG manifestations. Hyperkalemia causes widened and low amplitude P-waves, widened QRS complex with potential fusion of the QRS-T segment and loss of the ST segment, and tall tented T-waves. Hypokalemia results in ST depression and flattened T-waves and possible negative T-waves. Hypercalcemia speeds repolarization, causing tall peaked T-waves at mild levels and extremely wide QRS complex with low R-waves and disappearance of P-waves at severe levels. Hypocalcemia causes a narrowed QRS complex, reduced PR interval, flattened and inverted T-waves, and prolonged QT and ST intervals. Hypomag
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electrolyte.pdf
1. Hypokalemia is defined as a serum potassium level below 3.5 mEq/L. It can cause weakness, paralysis, and ECG changes. Treatment involves oral or IV potassium supplementation as well as treating the underlying cause.
2. Hyperkalemia is defined as a serum potassium above 5.5 mEq/L. It can cause muscle weakness, arrhythmias, and ECG changes like peaked T waves. Treatment focuses on stabilizing the heart with calcium, driving potassium into cells with insulin/glucose or beta-agonists, and removing potassium from the body with cation exchange resins or dialysis.
3. Severe cases may require higher doses administered more quickly via
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This document discusses myocardial ischemia and injury as seen on electrocardiograms (ECGs). It notes that ischemia is caused by a mismatch between blood supply and demand in the heart muscle. If blood flow is restored before glycogen is depleted, the cells can resume contraction, but if depletion occurs, the cells become "stunned" or can die off, leading to infarction. ECG changes like T wave inversion or ST segment depression reflect ischemia or injury and confer prognostic significance, as around 20% of patients with these changes may experience future cardiac events. The document outlines specific patterns of ST segment depression and elevation seen in ECGs that indicate myocardial injury.
Bundle branch blocks
Bundle branch blocks occur when the left or right bundle branch is blocked, preventing normal conduction of electrical impulses through the ventricles. Right bundle branch block is usually benign but can worsen prognosis in acute myocardial infarction by indicating occlusion of the proximal left anterior descending artery. Left bundle branch block is more serious as it can mask signs of myocardial infarction and worsen prognosis in acute infarction. The Sgarbossa criteria can help diagnose myocardial infarction in the presence of left bundle branch block. Left anterior and posterior hemiblocks involve conduction abnormalities localized to one side of the ventricles.
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The document discusses constrictive pericarditis, providing details on:
1) The pathology of constrictive pericarditis which involves thickening and scarring of the pericardium leading to loss of elasticity.
2) The pathophysiology of constrictive pericarditis where the inelastic pericardium constrains cardiac filling and prevents adaptation to volume changes.
3) Key diagnostic features of constrictive pericarditis seen on echocardiogram include septal bounce, rapid early diastolic mitral inflow, and increased mitral annular velocities that rise with inspiration.
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Localising MI with ECG is a clinical skill. The culprit artery involved can be identified with ECG even without coronary angiography.
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Dr. Awadhesh Kumar Sharma is a consultant cardiologist who has extensive training and experience in cardiology. The goal of this session is to provide a basic understanding of ECG waves and intervals, ECG interpretation, and the clinical application of ECGs. The document then discusses the history of ECGs, the fundamentals of how they work, normal ECG components including intervals, leads, and rhythms, as well as how to interpret ECGs and some common abnormalities.
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This document provides an overview of ECG interpretation including:
- The anatomy of the heart's conduction system and how ECG leads are attached
- How to read an ECG strip and calculate heart rate
- Normal P, QRS, and T waves along with intervals like PR and QT
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- Electrolyte imbalances that can affect the ECG tracing
It concludes with examples of ECG strips and questions to test the reader's understanding.
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This document provides an overview of electrocardiography (ECG) basics for technicians. It discusses the heart's conduction system and how ECGs work to record electrical activity. The 12 standard ECG leads and their placements are described. Key aspects of normal ECG waveforms and intervals like P waves, QRS complex, T waves, and QT interval are explained. Common abnormalities that can cause changes in axis or abnormal complexes are also summarized. The document concludes with tips on interpreting ECGs and the important aspects to include in an ECG report.
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This document discusses left ventricular hypertrophy (LVH) and right ventricular hypertrophy (RVH). It defines LVH as an increase in left ventricle mass due to increased wall thickness or cavity size. There are two types of LVH - systolic overload from conditions like hypertension which compromise the left ventricle during systole, and diastolic overload from things like valvular diseases which compromise it during diastole. The document outlines ECG criteria for diagnosing LVH including Sokolov-Lyon and Cornell voltage criteria. It also discusses RVH manifestations on ECG like right axis deviation, tall R waves in right precordial leads, and an S1S2S3 pattern.
Atrial enlargement
Biatrial enlargement is diagnosed when criteria for both right and left atrial enlargement are present on the same ECG.
The diagnosis of biatrial enlargement requires criteria for LAE and RAE to be met in either lead II, lead V1 or a combination of leads.
Ecg
This document provides a 100 step guide to electrocardiogram (ECG) interpretation written by Dr. S. Aswini Kumar. It begins with basic definitions of an ECG, the machine used to record it, and how the paper is formatted. It then explains how to analyze various aspects of the ECG including heart rate, rhythm, electrical axis, P wave, PR interval, QRS duration, ST segment, T wave, and conditions like myocardial infarction. The document provides criteria for interpreting abnormalities and identifying conditions. It concludes with examples of analyzing ECG findings and providing an impression.
Treadmill test (TMT)
Exercise testing is a noninvasive tool to evaluate the cardiovascular system's response to stress from exercise. During exercise, the body's metabolic rate and cardiac output increase substantially, placing high demands on the cardiopulmonary system. This makes exercise an effective way to assess cardiac function and perfusion. Various protocols exist for exercise testing using treadmills, bicycles, or other devices, with different protocols suited for evaluating patients with different cardiovascular conditions or exercise capacities. Careful analysis of electrocardiogram changes during and after exercise can provide information about myocardial ischemia.
Approach to a patient with T wave abnormality in ECG
A 45 years old lady presented with generalized weakness and palpitations. She is a diagnosed case of chronic renal failure with Diabetes mellitus and Hypertension. Her serum K+ level is 6.8 meq/L. She had the following ECG.
Case; A 54 years old gentleman complained of chest discomfort on exertion for the last 5 months. He is smoker for 10 years, diabetic for 5 years and hypertensive for 3 years. He had the following ECG.
Case: A 25 years old gentleman presented with chest pain and fever .He was normotensive, non-smoker and non-diabetic. His pulse 128b/min and BP-130/80 mm Hg. Troponin I was normal.
Case: A 58 years old gentleman complained of severe central chest pain with excessive sweating 5 days back. He is smoker for 7 years, diabetic for 5 years and hypertensive for 4 years. His BP-90/70 mm Hg. He had the following ECG.
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This document discusses various non-coronary causes of ST-elevation on electrocardiograms (ECGs) including ventricular aneurysms, pericarditis, early repolarization patterns, left ventricular hypertrophy, left bundle branch block, hypothermia, cardioversion, intraventricular hemorrhage, hyperkalemia, Brugada pattern, type 1C antiarrhythmic drugs, hypercalcemia, pulmonary embolism, hypothermia, myocarditis, and tumor invasion of the left ventricle. It then discusses left ventricular aneurysms, early repolarization, acute pericarditis, hyperkalemia, hypothermia, increased intracranial pressure, Brugada syndrome, Tak
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The document discusses Long QT Syndrome (LQTS), an inherited heart condition characterized by an abnormally prolonged QT interval on electrocardiograms. It describes the causes and types of LQTS, including LQT1, LQT2 and LQT3, which are associated with different genetic mutations and ECG patterns. The main symptoms of LQTS are syncope and cardiac arrest, typically in children or teenagers. Diagnosis involves measuring the QT interval and identifying risk factors. Treatment focuses on beta-blockers, lifestyle changes and implantable cardioverter-defibrillators for high-risk patients.
ECG in Emergency Department - Advances in ACS ECG
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Transesophageal echocardiography
Trans-esophageal echocardiography (TEE) uses ultrasound to obtain high-quality images of the heart and surrounding structures. It involves inserting a probe with an ultrasound transducer at the tip through the mouth and esophagus. TEE provides clearer images than transthoracic echocardiography as the esophagus is directly behind the heart. A TEE exam involves systematically imaging the heart in various planes as the transducer is advanced and manipulated. Standard views include the mid-esophageal four-chamber, two-chamber, aortic, and RV inflow-outflow views. Real-time 3D TEE can provide en face views of structures.
Left Bundle Branch Block (LBBB)
- Left bundle branch block (LBBB) is caused by conditions that damage the left bundle branch, such as hypertension, dilated cardiomyopathy, and ischemic heart disease.
- LBBB is diagnosed based on criteria including a QRS duration of over 120ms and abnormal ST segment and T wave patterns.
- The prognosis of LBBB depends on any underlying heart conditions, with LBBB increasing the risk of mortality. LBBB may resolve temporarily following a premature ventricular contraction due to resetting of the conduction system.
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Approach to a patient with T wave abnormality in ECG
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Electrolyte imbalance
This document discusses electrolyte imbalances, specifically hypokalemia, hyperkalemia, and magnesium imbalance. It outlines the causes, clinical manifestations, and treatment considerations for anesthesia for each condition. Key points include decreased cardiac contractility and arrhythmias with hypokalemia, skeletal muscle weakness and cardiac effects with hyperkalemia, and uses of magnesium for conditions like preeclampsia and tetanus. Treatment involves oral or IV potassium replacement, calcium or sodium bicarbonate for hyperkalemia, and magnesium supplementation. Anesthetic implications are also addressed.
electrolyte.pdf
1. Hypokalemia is defined as a serum potassium level below 3.5 mEq/L. It can cause weakness, paralysis, and ECG changes. Treatment involves oral or IV potassium supplementation as well as treating the underlying cause.
2. Hyperkalemia is defined as a serum potassium above 5.5 mEq/L. It can cause muscle weakness, arrhythmias, and ECG changes like peaked T waves. Treatment focuses on stabilizing the heart with calcium, driving potassium into cells with insulin/glucose or beta-agonists, and removing potassium from the body with cation exchange resins or dialysis.
3. Severe cases may require higher doses administered more quickly via
Effect of electrolytes on cardiac rhythm
Electrolyte imbalances can cause cardiac arrhythmias by disrupting the normal ionic balance across cardiac cell membranes. Common electrolyte disorders include hyperkalemia, hypokalemia, hypocalcemia, hypercalcemia, hypomagnesemia, and hypermagnesemia. Each has distinct ECG patterns - for example, hyperkalemia causes tall peaked T waves while hypokalemia causes ST depression and flattened T waves. Treatment involves replacing the deficient electrolyte or removing excess electrolytes.
Effect of electrolytes on cardiac rhythm
Electrolyte imbalances can cause cardiac arrhythmias by disrupting the normal ionic balance across cardiac cell membranes. The key electrolytes involved are potassium, magnesium, and calcium. Hypokalemia causes ST depression and flattened, inverted T waves. Hyperkalemia results in peaked T waves, PR prolongation, and widened QRS complexes. Hypocalcemia and hypomagnesaemia lead to prolonged QT intervals and ST segment changes, while their hyper counterparts cause conduction delays. Diagnosis relies on identifying these characteristic ECG patterns, and treatment focuses on replacing the deficient electrolyte or removing excesses.
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This document discusses the effects of changes in electrolyte concentrations on the heart. It summarizes that:
1. Distribution of electrolytes like sodium, potassium, and calcium are responsible for the electrical activity of tissues including the heart. Changes in the concentration of these electrolytes can alter cardiac electrical activity and the electrocardiogram (ECG).
2. Hypokalemia and hyperkalemia affect the heart's resting membrane potential and excitability, causing changes to the ECG like tall/tented T waves or merger of QRS and T waves respectively.
3. Hypocalcemia reduces cardiac excitability and prolongs the ST segment and QT interval on ECG, while
Hyperkalemia
Hyperkalemia can be caused by high potassium intake, redistribution of potassium from cells, or low renal potassium excretion. It may be drug-induced or related to decreased renal function, hypoaldosteronism, decreased circulating volume, or pseudohyperkalemia. Clinical manifestations range from weakness to cardiac arrhythmias. Emergent therapy includes calcium to stabilize membranes, insulin with glucose to shift potassium into cells (unless glucose is over 175 mg/dL), and potassium-binding resins. Additional workup may include ECG, chemistry panel, creatinine kinase, TTKG, and hemodialysis for severe cases.
Hyperkalemia
Hyperkalemia can be caused by high potassium intake, redistribution of potassium from cells, or low renal potassium excretion. It may be drug-induced or related to decreased renal function, hypoaldosteronism, decreased circulating volume, or pseudohyperkalemia. Clinical manifestations range from weakness to cardiac arrhythmias. Emergent therapy includes calcium to stabilize membranes, insulin with glucose to shift potassium into cells (unless glucose is over 175 mg/dL), and potassium-binding resins. Additional workup may include ECG, chemistry panel, creatinine kinase, TTKG, and hemodialysis for severe cases.
Electrolytes imbalance and ECG changes presentation 2005
1) The document discusses various electrolyte imbalances including hyperkalemia, hypokalemia, hypercalcemia, hypocalcemia, and the effects of digitalis and hypothermia on the ECG.
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Hypokalaemia.pptx
Potassium is the most abundant intracellular cation, with only about 2% located in the extracellular fluid. Intracellular potassium is responsible for maintaining cell volume and the resting membrane potential. Hypokalemia is defined as a plasma potassium concentration below 3.5 mmol/L and can cause neuromuscular problems like weakness, cardiac issues like arrhythmias, and impaired renal function. Hypokalemia results from decreased intake, shifting into cells, renal wasting, or extrarenal losses such as diarrhea or medications. Management involves treating the underlying cause, replacing potassium orally or intravenously while monitoring the ECG, and adjusting intravenous infusion rates based on severity.
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This document discusses ECG changes that occur due to electrolyte imbalances. It begins by introducing Arrhenius' theory of electrolyte dissociation, which established that electrolytes produce electricity when dissolved in water and dissociate into ions. It then discusses how various electrolytes like sodium, potassium, calcium normally distribute in the cardiac cell and influence the cardiac action potential. The main part provides details on ECG changes seen in hyperkalemia, hypokalemia, hypercalcemia, and hypocalcemia. It examines the electrophysiological effects of these electrolyte disturbances and includes illustrations of ECG patterns. The document emphasizes the importance of evaluating the QT interval and looking for arrhythmias in cases of electrolyte imbalance
Alterations of-potassium-metabolism
This document discusses alterations in potassium metabolism, including hypokalemia and hyperkalemia. It covers the physiological considerations of potassium regulation in the body, with 98% located intracellularly and serum levels normally between 3.5-5 mEq/L. Rapid regulation of potassium involves the sodium-potassium pump and hormones like insulin and catecholamines. Causes, clinical presentations, and treatments are described for both hypokalemia and hyperkalemia. Hypokalemia can result from excessive losses or intracellular shifts, while hyperkalemia involves a positive potassium balance or rapid extracellular shifts. Treatments aim to correct the underlying cause, stabilize cardiac function, shift potassium intracellularly, and promote excretion.
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This document discusses hypokalemia and hyperkalemia. It defines normal potassium levels and factors that influence potassium levels. Hypokalemia is defined as a potassium level below 3.5 mEq/L and can be caused by decreased intake, shifts of potassium into cells, or increased excretion. Hyperkalemia is a potassium level above 5.5 mEq/L and can result from increased intake, decreased excretion, or shifts of potassium out of cells. Clinical features and treatment approaches are described for both hypokalemia and hyperkalemia.
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Hyperkalemia and its management
This document discusses hyperkalemia, including its definition, causes, clinical manifestations, and treatment. It provides details on potassium regulation and homeostasis in the body. The main causes of hyperkalemia are a shift of potassium from intracellular to extracellular space, excessive potassium intake, and decreased renal potassium excretion. Symptoms range from weakness to cardiac arrhythmias. Treatment involves calcium gluconate for cardiac issues, insulin with glucose to shift potassium intracellularly, sodium bicarbonate for acidosis, and diuretics or dialysis to increase renal excretion.
Effects of hypo & hyper kalemia
The document discusses hyperkalemia, its effects on the electrocardiogram (ECG), and the role of calcium gluconate in reversing these effects. Hyperkalemia is a potentially lethal condition defined as a serum potassium level above 5 mEq/L. It can cause abnormal heart rhythms and cardiac arrest. On ECG, hyperkalemia presents as tall, peaked T waves and prolonged PR interval. Calcium gluconate works by antagonizing the effects of potassium at the cellular level and restoring the normal threshold potential, allowing action potentials to occur and reestablishing normal cardiac conduction. By rapidly shifting potassium into cells, calcium gluconate can quickly reverse the ECG changes and cardiac effects caused by hyperkalemia
Anti arrhythmic drugs
Anti-arrhythmic drugs can be used to terminate or prevent arrhythmias. They work by blocking ion channels involved in cardiac action potentials. Class 1 drugs block sodium channels, prolonging the action potential. Class 1A drugs like procainamide and quinidine prolong the action potential. Class 1B drug lidocaine has rapid sodium channel blocking kinetics. Class 2 drugs like esmolol are beta blockers that reduce automaticity. Class 3 drugs like amiodarone and dofetilide block potassium channels, prolonging the action potential. Calcium channel blockers like verapamil are Class 4 drugs that suppress arrhythmias by blocking calcium channels, especially in the SA and AV nodes. Choice of drug depends
HYPOKALEMIA .pptx
This document discusses the physiology and pathophysiology of hypokalemia. It covers the normal distribution and regulation of potassium in the body, as well as causes of hypokalemia including decreased intake, extrarenal losses, and renal losses. Types of renal tubular acidosis that can cause hypokalemia are described. The approach to hypokalemia involves considering underlying causes like Bartter syndrome, Gitelman syndrome, Liddle's syndrome, and hypomagnesemia. Treatment principles for correcting hypokalemia are provided.
Channelopathy
1. Channelopathies are diseases caused by defects in ion channels that regulate the movement of ions across cell membranes.
2. Ion channels can be voltage-gated or ligand-gated and mutations can lead to loss or gain of channel function.
3. Periodic paralysis is a rare neuromuscular disorder related to defects in muscle ion channels, causing episodic weakness. The main types are hypokalemic and hyperkalemic periodic paralysis.
4. Other channelopathies include long QT syndrome, Brugada syndrome, and other cardiac channelopathies that affect cardiac electrophysiology and can cause arrhythmias.
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Electrolyte and metabolic ECG abnormalities
- 1. Electrolyte and metabolic ECG abnormalities Mr. Aby Thankachan,M.Sc(N), Ph.D (N) Asst Professor HICON, CBE
- 2. HYPERKALEMIA Normal range - 3.6 to 5.2 millimoles per liter (mmol/L) ECG characteristics of hyperkalemia, high blood potassium: • P-waves are widened and of low amplitude due to slowing of conduction • QRS complex: – QRS widening – fusion of QRS-T
- 3. – loss of the ST segment • Tall tented T waves The initial part of the QRS complex is often spared as purkinje fibers are less sensitive to hyperkalemia. These changes can also occur in acidosis (via the same mechanism) and during Class IC anti- arrhythmic intoxication. • At concentrations > 7.5 mmol/L atrial and ventricular fibrillation can occur.
- 6. ECG 1
- 7. ECG 2
- 9. Potassium of 9.4 mmol/L
- 10. Hypokalemia Hypokalemia, low blood potassium, results in: • ST depression and flattening of the T wave • Negative T waves • A U-wave may be visible
- 14. Potassium level of 1.5
- 16. Hypercalcemia Normal Range 8.5 to 10.5 milligrams per deciliter (mg/dL) Hypercalcemia, high blood calcium, speeds repolarization. Characteristics of hypercalcemia: • Mild: broad based tall peaking T waves • Severe: extremely wide QRS, low R wave, disappearance of p waves, tall peaking T waves.
- 18. Calcium – 4.6 mmol/L
- 19. Hypocalcemia ECG-characteristics of hypocalcemia, low blood calcium: • Narrowing of the QRS complex • Reduced PR interval • T wave flattening and inversion • Prolongation of the QT-interval • Prominent U-wave • Prolonged ST and ST-depression
- 21. Hypocalcaemia prolongs the ST segment causing QT prolongation
- 22. Hypermagnesaemia • The normal range for blood magnesium level is 1.7 to 2.2 mg/dL (0.85 to 1.10 mmol/L).
- 24. Hypomagnesaemia • ECG changes in isolated hypomagnesaemia – Prolonged PR interval – Prolonged QT interval