This document provides an overview of various types of arrhythmias including their definitions, characteristics, causes, clinical effects, and treatment approaches. It begins with objectives and descriptions of normal cardiac physiology and the mechanisms that can lead to arrhythmias. It then defines different types of arrhythmias according to the WHO/ISFC classification system and provides detailed descriptions, characteristics, and management considerations for various specific arrhythmias including sinus tachycardia, premature atrial contractions, atrial fibrillation, various types of heart block, ventricular tachycardia, ventricular fibrillation, and more. The goal is to educate on arrhythmia diagnosis and clinical management.
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.
Wolff–Parkinson–White syndrome (WPW) is one of several disorders of the conduction system of the heart that are commonly referred to as pre-excitation syndromes. WPW is caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles. Electrical signals traveling down this abnormal pathway (known as the bundle of Kent) may stimulate the ventricles to contract prematurely, resulting in a unique type of supra-ventricular tachycardia referred to as an atrio-ventricular reciprocating tachycardia.
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.
Wolff–Parkinson–White syndrome (WPW) is one of several disorders of the conduction system of the heart that are commonly referred to as pre-excitation syndromes. WPW is caused by the presence of an abnormal accessory electrical conduction pathway between the atria and the ventricles. Electrical signals traveling down this abnormal pathway (known as the bundle of Kent) may stimulate the ventricles to contract prematurely, resulting in a unique type of supra-ventricular tachycardia referred to as an atrio-ventricular reciprocating tachycardia.
cardiac arrhythmias are abnormal heart rhythms that occur when the electrical signals controlling the heart beat are not working properly.
these can include tachycardia ,Bradycardia,atrial fibrillation and more.
Basavarajeeyam is an important text for ayurvedic physician belonging to andhra pradehs. It is a popular compendium in various parts of our country as well as in andhra pradesh. The content of the text was presented in sanskrit and telugu language (Bilingual). One of the most famous book in ayurvedic pharmaceutics and therapeutics. This book contains 25 chapters called as prakaranas. Many rasaoushadis were explained, pioneer of dhatu druti, nadi pareeksha, mutra pareeksha etc. Belongs to the period of 15-16 century. New diseases like upadamsha, phiranga rogas are explained.
micro teaching on communication m.sc nursing.pdfAnurag Sharma
Microteaching is a unique model of practice teaching. It is a viable instrument for the. desired change in the teaching behavior or the behavior potential which, in specified types of real. classroom situations, tends to facilitate the achievement of specified types of objectives.
Title: Sense of Smell
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the primary categories of smells and the concept of odor blindness.
Explain the structure and location of the olfactory membrane and mucosa, including the types and roles of cells involved in olfaction.
Describe the pathway and mechanisms of olfactory signal transmission from the olfactory receptors to the brain.
Illustrate the biochemical cascade triggered by odorant binding to olfactory receptors, including the role of G-proteins and second messengers in generating an action potential.
Identify different types of olfactory disorders such as anosmia, hyposmia, hyperosmia, and dysosmia, including their potential causes.
Key Topics:
Olfactory Genes:
3% of the human genome accounts for olfactory genes.
400 genes for odorant receptors.
Olfactory Membrane:
Located in the superior part of the nasal cavity.
Medially: Folds downward along the superior septum.
Laterally: Folds over the superior turbinate and upper surface of the middle turbinate.
Total surface area: 5-10 square centimeters.
Olfactory Mucosa:
Olfactory Cells: Bipolar nerve cells derived from the CNS (100 million), with 4-25 olfactory cilia per cell.
Sustentacular Cells: Produce mucus and maintain ionic and molecular environment.
Basal Cells: Replace worn-out olfactory cells with an average lifespan of 1-2 months.
Bowman’s Gland: Secretes mucus.
Stimulation of Olfactory Cells:
Odorant dissolves in mucus and attaches to receptors on olfactory cilia.
Involves a cascade effect through G-proteins and second messengers, leading to depolarization and action potential generation in the olfactory nerve.
Quality of a Good Odorant:
Small (3-20 Carbon atoms), volatile, water-soluble, and lipid-soluble.
Facilitated by odorant-binding proteins in mucus.
Membrane Potential and Action Potential:
Resting membrane potential: -55mV.
Action potential frequency in the olfactory nerve increases with odorant strength.
Adaptation Towards the Sense of Smell:
Rapid adaptation within the first second, with further slow adaptation.
Psychological adaptation greater than receptor adaptation, involving feedback inhibition from the central nervous system.
Primary Sensations of Smell:
Camphoraceous, Musky, Floral, Pepperminty, Ethereal, Pungent, Putrid.
Odor Detection Threshold:
Examples: Hydrogen sulfide (0.0005 ppm), Methyl-mercaptan (0.002 ppm).
Some toxic substances are odorless at lethal concentrations.
Characteristics of Smell:
Odor blindness for single substances due to lack of appropriate receptor protein.
Behavioral and emotional influences of smell.
Transmission of Olfactory Signals:
From olfactory cells to glomeruli in the olfactory bulb, involving lateral inhibition.
Primitive, less old, and new olfactory systems with different path
Lung Cancer: Artificial Intelligence, Synergetics, Complex System Analysis, S...Oleg Kshivets
RESULTS: Overall life span (LS) was 2252.1±1742.5 days and cumulative 5-year survival (5YS) reached 73.2%, 10 years – 64.8%, 20 years – 42.5%. 513 LCP lived more than 5 years (LS=3124.6±1525.6 days), 148 LCP – more than 10 years (LS=5054.4±1504.1 days).199 LCP died because of LC (LS=562.7±374.5 days). 5YS of LCP after bi/lobectomies was significantly superior in comparison with LCP after pneumonectomies (78.1% vs.63.7%, P=0.00001 by log-rank test). AT significantly improved 5YS (66.3% vs. 34.8%) (P=0.00000 by log-rank test) only for LCP with N1-2. Cox modeling displayed that 5YS of LCP significantly depended on: phase transition (PT) early-invasive LC in terms of synergetics, PT N0—N12, cell ratio factors (ratio between cancer cells- CC and blood cells subpopulations), G1-3, histology, glucose, AT, blood cell circuit, prothrombin index, heparin tolerance, recalcification time (P=0.000-0.038). Neural networks, genetic algorithm selection and bootstrap simulation revealed relationships between 5YS and PT early-invasive LC (rank=1), PT N0—N12 (rank=2), thrombocytes/CC (3), erythrocytes/CC (4), eosinophils/CC (5), healthy cells/CC (6), lymphocytes/CC (7), segmented neutrophils/CC (8), stick neutrophils/CC (9), monocytes/CC (10); leucocytes/CC (11). Correct prediction of 5YS was 100% by neural networks computing (area under ROC curve=1.0; error=0.0).
CONCLUSIONS: 5YS of LCP after radical procedures significantly depended on: 1) PT early-invasive cancer; 2) PT N0--N12; 3) cell ratio factors; 4) blood cell circuit; 5) biochemical factors; 6) hemostasis system; 7) AT; 8) LC characteristics; 9) LC cell dynamics; 10) surgery type: lobectomy/pneumonectomy; 11) anthropometric data. Optimal diagnosis and treatment strategies for LC are: 1) screening and early detection of LC; 2) availability of experienced thoracic surgeons because of complexity of radical procedures; 3) aggressive en block surgery and adequate lymph node dissection for completeness; 4) precise prediction; 5) adjuvant chemoimmunoradiotherapy for LCP with unfavorable prognosis.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
These simplified slides by Dr. Sidra Arshad present an overview of the non-respiratory functions of the respiratory tract.
Learning objectives:
1. Enlist the non-respiratory functions of the respiratory tract
2. Briefly explain how these functions are carried out
3. Discuss the significance of dead space
4. Differentiate between minute ventilation and alveolar ventilation
5. Describe the cough and sneeze reflexes
Study Resources:
1. Chapter 39, Guyton and Hall Textbook of Medical Physiology, 14th edition
2. Chapter 34, Ganong’s Review of Medical Physiology, 26th edition
3. Chapter 17, Human Physiology by Lauralee Sherwood, 9th edition
4. Non-respiratory functions of the lungs https://academic.oup.com/bjaed/article/13/3/98/278874
ARTIFICIAL INTELLIGENCE IN HEALTHCARE.pdfAnujkumaranit
Artificial intelligence (AI) refers to the simulation of human intelligence processes by machines, especially computer systems. It encompasses tasks such as learning, reasoning, problem-solving, perception, and language understanding. AI technologies are revolutionizing various fields, from healthcare to finance, by enabling machines to perform tasks that typically require human intelligence.
Explore natural remedies for syphilis treatment in Singapore. Discover alternative therapies, herbal remedies, and lifestyle changes that may complement conventional treatments. Learn about holistic approaches to managing syphilis symptoms and supporting overall health.
Report Back from SGO 2024: What’s the Latest in Cervical Cancer?bkling
Are you curious about what’s new in cervical cancer research or unsure what the findings mean? Join Dr. Emily Ko, a gynecologic oncologist at Penn Medicine, to learn about the latest updates from the Society of Gynecologic Oncology (SGO) 2024 Annual Meeting on Women’s Cancer. Dr. Ko will discuss what the research presented at the conference means for you and answer your questions about the new developments.
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Ve...kevinkariuki227
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
TEST BANK for Operations Management, 14th Edition by William J. Stevenson, Verified Chapters 1 - 19, Complete Newest Version.pdf
2. OBJECTIVES
• Normal Physiology of cardiac impulse
formation and conduction.
• Pathophysiology / Haemodynamics
• WHO/ISFC classification of arrhythmias
• ECGs
• Clinical manifestations
• Principles of management of arrhythmias
2
M3 LECTURE
3.
4. Mechanism of Arrhthmogensis
1. Disorder of impulse formation.
a) Automaticity.
b) Triggered Activity.
1) Early after depolarization.
2) Delayed after depolarization.
2. Disorder of impulse conduction.
a) Block – Reentry.
b) Reflection.
3. Combined disorder.
8. WHO/ISFC DEFINITIONS
DEFINITIONS TYPES
Arrest Cessation of electrical activity of the heart or part of it Sinus; ventricular
Block Delay or failure of propagation Sinus; AV; BB
Bradycardia ≥3 consecutive impulses the same PM at rate slower
than the intrinsic rate of that PM
Sinus;AV;Ventri
Escape 1 or 2 consecutive impulses from the same or several
PMs due to delay in formation or arrival of the expected
impulse from the prevailing rhythm
AV;Ventricular
Escape Rhythm ≥ 3 consecutive escape beats AV; Ventricular
Extrasystoles A premature impulse ( occasionally 2 consec ones) Atrial;AV;Ventr
Fibrillation Rapid and irregular Atrial; Ventr
Flutter Rapid and regular (usually ≥ 250/min Atrial; Ventr
Tachycardia ≥ 3 consecutive impulses from the same PM at a rate
greater than 100/min
Atrial;AV; Ventr
8
M3 LECTURE
10. Haemodynamics
Determinants:
• Myocardial chronotropy and regularity;
• Diastolic filling time
• Myocardial inotropy and Frank-Sterling effect
• Stroke volume and cardiac output
• Peripheral resistance, blood flow and BP
All these are inter-related and subject to neuro-
humoral influences
10
M3 LECTURE
12. CLINICAL EFFECTS OF
ARRHYTHMIAS
Effect Extrasystoles Tachyarrhythmias Bradyarrhythmias
Asymptomatic Occasional Occasional Occasional
Palpitation Very common Occasional Occasional
Dizziness Common Very common Very common
Syncope None Very common Very common
Hypotension/Shock None Very common Very common
Pulmonary oedema None Very common None
Embolic
Phenomenon
None Common None
Sudden death None Very common Very common
M3 LECTURE 12
13. Arrhythmia Assessment
• ECG
• 24h Holter monitor
• Echocardiogram
• Stress test
• Coronary angiography
• Electrophysiology study
14. Principles of Management
• To eliminate symptoms
• To prevent imminent death
• To reduce possible risks other than the direct
effects of the arrhythmias e.g stroke in AFib
M3 LECTURE 14
16. SINUS TACHYCARDIA
• Rate: 101-160/min
• P wave: sinus
• QRS: normal
• Conduction: normal
• Rhythm: regular or slightly irregular
• The clinical significance of this dysrhythmia depends on the
underlying cause. It may be normal.
• Underlying causes include:
increased circulating catecholamines
CHF
hypoxia
PE
increased temperature
stress
response to pain
• Treatment includes identification of the underlying cause and
correction.
17.
18. SINUS BRADYCARDIA
• Rate: 40-59 bpm
• P wave: sinus
• QRS: Normal (.06-.12)
• Conduction: P-R normal or slightly prolonged at slower rates
• Rhythm: regular or slightly irregular
• This rhythm is often seen as a normal variation in athletes, during
sleep, or in response to a vagal maneuver. If the bradycardia becomes
slower than the SA node pacemaker, a junctional rhythm may occur.
• Treatment includes:
treat the underlying cause,
atropine,
isuprel, or
artificial pacing if patient is hemodynamically compromised.
19.
20. SINUS ARRHYTHMIA
• Rate: 45-100/bpm
• P wave: sinus
• QRS: normal
• Conduction: normal
• Rhythm: regularly irregular
• The rate usually increases with inspiration and decreases with
expiration.
• This rhythm is most commonly seen with respiration due to
fluctuations in vagal tone.
• The non respiratory form is present in diseased hearts and sometimes
confused with sinus arrset (also known as "sinus pause").
• Treatment is not usually required unless symptomatic bradycardia is
present.
21.
22. PREAMATURE ATRIAL
CONTRACTIONS
• Rate: normal or accelerated
• P wave: usually have a different morphology than sinus P waves
because they originate from an ectopic pacemaker
• QRS: normal
• Conduction: normal, however the ectopic beats may have a different
P-R interval.
• Rhythm: PAC's occur early in the cycle and they usually do not have
a complete compensatory pause.
• PAC's occur normally in a non diseased heart.
• However, if they occur frequently, they may lead to a more serious
atrial dysrhythmias.
• They can also result from CHF, ischemia and COPD.
23.
24. SINUS PAUSE, ARREST
• Rate: normal
• P wave: those that are present are normal
• QRS: normal
• Conduction: normal
• Rhythm: The basic rhythm is regular. The length of the pause is not a
multiple of the sinus interval.
• This may occur in individuals with healthy hearts. It may also occur
with increased vagal tone, myocarditis, MI, and digitalis toxicity.
• If the pause is prolonged, escape beats may occur.
• The treatment of this dysrhythmia depends on the underlying cause.
If the cause is due to increased vagal tone and the patient is symptomatic,
atropine may be indicated.
25.
26. PAROXYSMAL ATRIAL
TACHYCARDIA
• Rate: atrial 160-250/min: may conduct to ventricles 1:1, or 2:1, 3:1,
4:1 into the presence of a block.
• P wave: morphology usually varies from sinus
• QRS: normal (unless associated with aberrant ventricular conduction).
• Conduction: P-R interval depends on the status of AV conduction
tissue and atrial rate: may be normal, abnormal, or not measurable.
• PAT may occur in the normal as well as diseased heart.
It is a common complication of Wolfe-Parkinson-White syndrome.
• This rhythm is often transient and doesn't require treatment.
However, it can be terminated with vagal maneuvers.
Digoxin, antiarrhythmics, and cardioversion may be used.
27.
28. ATRIAL FIBRILLATION
• Rate: atrial rate usually between 400-650/bpm.
• P wave: not present; wavy baseline is seen instead.
• QRS: normal
• Conduction: variable AV conduction; if untreated the ventricular
response is usually rapid.
• Rhythm: irregularly irregular. (This is the hallmark of this
dysrhythmia).
• Atrial fibrillation may occur paroxysmally, but it often becomes
chronic. It is usually associated with COPD, CHF or other heart
disease.
• Treatment includes:
Digoxin to slow the AV conduction rate.
Cardioversion may also be necessary to terminate this rhythm.
29.
30.
31. FIRST DEGREE A-V HEART
BLOCK
• Rate: variable
• P wave: normal
• QRS: normal
• Conduction: impulse originates in the SA node but has prolonged
conduction in the AV junction; P-R interval is > 0.20 seconds.
• Rhythm: regular
• This is the most common conduction disturbance. It occurs in both
healthy and diseased hearts.
• First degree AV block can be due to:
inferior MI,
digitalis toxicity
hyperkalemia
increased vagal tone
acute rheumatic fever
myocarditis.
• Interventions include treating the underlying cause and observing for
progression to a more advanced AV block.
32.
33. SECOND DEGREE A-V BLOCK
MOBITZ TYPE I (WENCKEBACK)
• Rate: variable
• P wave: normal morphology with constant P-P interval
• QRS: normal
• Conduction: the P-R interval is progressively longer until one P wave
is blocked; the cycle begins again following the blocked P wave.
• Rhythm: irregular
• Second degree AV block type I occurs in the AV node above the
Bundle of His.
• It is often transient and may be due to acute inferior MI or digitalis
toxicity.
• Treatment is usually not indicated as this rhythm usually produces no
symptoms.
34.
35. SECOND DEGREE A-V BLOCK
MOBITZ TYPE II
• Rate: variable
• P wave: normal with constant P-P intervals
• QRS: usually widened because this is usually associated with a bundle
branch block.
• Conduction: P-R interval may be normal or prolonged, but it is
constant until one P wave is not conducted to the ventricles.
• Rhythm: usually regular when AV conduction ratios are constant
• This block usually occurs below the Bundle of His and may progress
into a higher degree block.
• It can occur after an acute anterior MI due to damage in the bifurcation
or the bundle branches.
• It is more serious than the type I block.
• Treatment is usually artificial pacing.
36.
37. THIRD DEGREE (COMPLETE)
A-V BLOCK
• Rate: atrial rate is usually normal; ventricular rate is usually less than 70/bpm.
The atrial rate is always faster than the ventricular rate.
• P wave: normal with constant P-P intervals, but not "married" to the QRS
complexes.
• QRS: may be normal or widened depending on where the escape pacemaker is
located in the conduction system
• Conduction: atrial and ventricular activities are unrelated due to the complete
blocking of the atrial impulses to the ventricles.
• Rhythm: irregular
• Complete block of the atrial impulses occurs at the A-V junction, common
bundle or bilateral bundle branches.
• Another pacemaker distal to the block takes over in order to activate the
ventricles or ventricular standstill will occur.
• May be caused by:
digitalis toxicity
acute infection
MI and
degeneration of the conductive tissue.
• Treatment modalities include:
external pacing and atropine for acute, symptomatic episodes and
permanent pacing for chronic complete heart block.
38.
39. RIGHT BUNDLE BRANCH BLOCK
• Rate: variable
• P wave: normal if the underlying rhythm is sinus
• QRS: wide; > 0.12 seconds
• Conduction: This block occurs in the right or left bundle branches or
in both. The ventricle that is supplied by the blocked bundle is
depolarized abnormally.
• Rhythm: regular or irregular depending on the underlying rhythm.
• Left bundle branch block is more ominous than right bundle branch
block because it usually is present in diseased hearts. Both may be
caused by hypertension, MI, or cardiomyopathy. A bifasicular block
may progress to third degree heart block.
• Treatment is artificial pacing for a bifasicular block that is associated
with an acute MI.
40.
41.
42. PVC BIGEMNY
• Rate: variable
• P wave: usually obscured by the QRS, PST or T wave of the PVC
• QRS: wide > 0.12 seconds; morphology is bizarre with the ST segment and the T wave
opposite in polarity. May be multifocal and exhibit different morphologies.
• Conduction: the impulse originates below the branching portion of the Bundle of His;
full compensatory pause is characteristic.
• Rhythm: irregular. PVC's may occur in singles, couplets or triplets; or in bigeminy,
trigeminy or quadrigeminy.
• PVCs can occur in healthy hearts. For example, an increase in circulating
catecholamines can cause PVCs. They also occur in diseased hearts and from
drug (such as digitalis) toxicities.
• Treatment is required if they are:
associated with an acute MI,
occur as couplets, bigeminy or trigeminy,
are multifocal, or
are frequent (>6/min).
• Interventions include:
lidocaine,
pronestyl, or
quinidine.
43.
44. VENTRICULAR TACHYCARDIA
• Rate: usually between 100 to 220/bpm, but can be as rapid as 250/bpm
• P wave: obscured if present and are unrelated to the QRS complexes.
• QRS: wide and bizarre morphology
• Conduction: as with PVCs
• Rhythm: three or more ventricular beats in a row; may be regular or irregular.
• Ventricular tachycardia almost always occurs in diseased hearts.
• Some common causes are:
CAD
acute MI
digitalis toxicity
CHF
ventricular aneurysms.
• Patients are often symptomatic with this dysrhythmia.
• Ventricular tachycardia can quickly deteriorate into ventricular fibrillation.
Electrical countershock is the intervention of choice if the patient is
symptomatic and rapidly deteriorating.
Some pharmacological interventions include lidocaine, pronestyl, and
bretylium.
45.
46. TORSADE DE POINTES
• Rate: usually between 150 to 220/bpm,
• P wave: obscured if present
• QRS: wide and bizarre morphology
• Conduction: as with PVCs
• Rhythm: Irregular
• Paroxysmal –starting and stopping suddenly
• Hallmark of this rhythm is the upward and downward deflection of the QRS
complexes around the baseline. The term Torsade de Pointes means "twisting
about the points."
• Consider it V-tach if it doesn’t respond to antiarrythmic therapy or treatments
• Caused by:
drugs which lengthen the QT interval such as quinidine
electrolyte imbalances, particularly hypokalemia
myocardial ischemia
• Treatment:
Synchronized cardioversion is indicated when the patient is unstable.
IV magnesium
IV Potassium to correct an electrolyte imbalance
Overdrive pacing
47.
48. VENTRICULAR FIBRILLATION
• Rate: unattainable
• P wave: may be present, but obscured by ventricular waves
• QRS: not apparent
• Conduction: chaotic electrical activity
• Rhythm: chaotic electrical activity
• This dysrhythmia results in the absence of cardiac output.
• Almost always occurs with serious heart disease, especially acute MI.
• The course of treatment for ventricular fibrillation includes:
immediate defibrillation and ACLS protocols.
Identification and treatment of the underlying cause is also needed.
49.
50. IDIOVENTRICULAR RHYTHM
• Rate: 20 to 40 beats per minute
• P wave: Absent
• QRS: Widened
• Conduction: Failure of primary pacemaker
• Rhythm: Regular
• Absent P wave
Widened QRS > 0.12 sec.
Also called " dying heart" rhythm
Pacemaker will most likely be needed to re-establish a normal heart rate.
• Causes:
– Myocardial Infarction
– Pacemaker Failure
– Metabolic imbalance
– Myoardial Ischemia
• Treatment goals include measures to improve cardiac output and establish a normal
rhythm and rate.
• Options include:
– Atropine
– Pacing
• Caution: Supressing the ventricular rhythm is contraindicated because that rhythm
protects the heart from complete standstill.
51.
52. VENTRICULAR STANDSTILL
(ASYSTOLE)
• Rate: none
• P wave: may be seen, but there is no ventricular response
• QRS: none
• Conduction: none
• Rhythm: none
• Asystole occurs most commonly following the termination of atrial,
AV junctional or ventricular tachycardias. This pause is usually
insignificant.
• Asystole of longer duration in the presence of acute MI and CAD is
frequently fatal.
• Interventions include:
CPR,
artificial pacing, and
atropine.