• What normally causes the presentation? – Syncope
– Palpitations
– Light-headedness
– Cardiac Arrest
– ?shortness of breath, fatigue, and chest pain
Presenter
Presentation Notes
Dysrhythmia is the American term..means the same, and is gaining in the literature! These are the common symptoms of arrhythmias … need to diagnose with ECG. There are MANY arrhythmias! We will look at only a few here! This is advanced cardiac stuff!
Identification by Location
• Arrhythmias by location – Supraventricular
– Nodal (Junctional)
– Ventricular
Location? Supraventricular? Could be SA node • SA node is not coordinated……
Look at the trace… note no definite p wave...just a lot of squiggle…….. So lost the atrial kick (30%) of filling……. So CO must be down….so less Oxygen going to brain ..fainting!
Atrial Arrhythmias • Atrial fibrillation
– >400bpm
– Not immediately fatal
– But… embolisation highly likely
• Premature atrial contraction (PAC) – “Skips”
– Caffeine, stress
• SVT – Can be genetic, short spurts of rapid beats
Presenter
Presentation Notes
Types of Atrial Arrhythmias��Atrial fibrillation. The electrical signal that circles uncoordinated through the muscles of the atria (the upper chambers of the heart), causing them to quiver (sometimes more than 400 times per minute) without contracting. The ventricles (the lower chambers of the heart) do not receive regular impulses and contract out of rhythm, and the heartbeat becomes uncontrolled and irregular. It is the most common atrial arrhythmia, and 85 percent of people who experience it are older than 65 years.��Atrial fibrillation can cause a blood clot to form, which can enter the bloodstream and trigger a stroke. Underlying heart disease or hypertension increases the risk of stroke from atrial fibrillation as does age even without heart disease or hypertension.��Premature atrial contraction (PAC or premature atrial impulses). A common and benign arrhythmia, a PAC is a heartbeat that originates away from the sinus node, which sends electrical signals through the upper chamber. It typically occurs after the sinus node has initiated one heartbeat and before the next regular sinus discharge. A PAC can cause a feeling of a skipped heartbeat. Use of caffeine, tobacco, and/or alcohol, or stress can bring on PACs or increase their frequency.��Supraventricular tachycardia (SVT). Characterized by a rapid heart rate that ranges between 100 and 240 beats per minute, SVT usually begins and ends suddenly. SVT occurs when an electrical impulse 're-enters' the atrial muscles. A disorder that a person may have at birth, SVT is commonly caused by a variation in the electrical system of the heart. SVT often begins in childhood or adolescence and can be triggered by exercise, alcohol, or caffeine. SVT is rarely dangerous, but can cause a drop in blood pressure, causing lightheadedness or near-fainting episodes, and, rarely, fainting episodes.��Atrial flutter. Differentiated from atrial fibrillation by its coordinated, regular pattern, atrial flutter is a coordinated rapid beating of the atria. Most who experience atrial flutter are 60 years and older and have some heart disorder, such as heart valve problems or a thickening of the heart muscle. Atrial flutter is classified into two types, according to the pathways responsible for it. Type I normally causes the heart rate to increase to and remain at 150 beats per minute. Rarely, the rate may reach 300 beats per minute; sometimes it decreases to 75 beats per minute. Type II increases the atrial rate faster, so the ventricular rate may be 160 to 170 beats per minute. As with atrial fibrillation, atrial flutter increases the risk of stroke.��Sick sinus syndrome (SSS). Common among older people, SSS is an improper firing of electrical impulses caused by disease or scarring in the sinus or Sinoatrial node (SA node). SSS normally causes the heart rate to slow, but sometimes it alternates between abnormally slow and fast. A progressive condition, with episodes increasing in frequency and duration, SSS can be caused by: Degeneration of the heart's electrical system; or Diseases of the atrial muscle. Sinus tachycardia. The sinus node emits abnormally fast electrical signals, which increases the heart rate to between 100 beats per minute to 140 beats per minute at rest, and 200 beats per minute during exercise. A normal response to exercise or stress, it can also be caused by: Adrenaline; Consumption of caffeine, nicotine, or alcohol; and Heart conditions. http://www.mccardio.com/handler.cfm?event=practice,template&cpid=3330
Possible causes of AF • MI – 90% of pt with MI experience arrhythmia • Idiopathic? • Drugs
– e.g. caffeine, nicotine, alcohol, pseudoephedrine
• lots of other reasons, too!
Presenter
Presentation Notes
Patient in Case Study developed AF……..but “why?” we don’t know. It progressed to VF……… she had a MI! should have been monitored earlier!
• Control ventricular rate during AF – Drugs – antiarrhythmics
• Prevention of blood clot formation. – Drugs – anticoagulants
Presenter
Presentation Notes
We will treat the drugs again in Lecture 4…….. Note the use of anti-coagulants because of formation of emboli……
Cardioversion vs defibrillation
• Cardioversion refers to elective procedure to restore normal SA node control…common in AF not responsive to drugs
• Defibrillation…….. Refers to emergent shock applied
• Both will stop all electrical activity
• Several YouTube videos available to see the procedure…..
Presenter
Presentation Notes
“Defibrillation is a nonsynchronized delivery of energy during any phase of the cardiac cycle, whereas cardioversion is the delivery of energy that is synchronized to the large R waves or QRS complex. The delivered shock in both defibrillation and cardioversion causes electric current to go from the negative to the positive electrode of the defibrillator, passing the heart on its way. It causes all the heart cells to contract simultaneously, thereby interrupting and terminating the abnormal electrical rhythm without damaging the heart, and thus allowing the sinus node to resume normal pacemaker activity.” http://emedicine.medscape.com/article/80564-overview
Nodal? AV node
• If the p wave is not always transmitted to the ventricles
• “blocked” at the AV node
• In third degree block: Ventricles have a separate pacemaker, 2 different rhythms going on…an atrial rhythm and a ventricular (slower) rhythm……
• Must implant a mechanical pacemaker
Presenter
Presentation Notes
Heart blocks are complicated…..!st degree blocks may not cause any problems, 2nd degree blocks cause dizziness, fainting………… 3rd degree “complete block” is emergency, as ventricular rate is insufficient to support circulation
Note the 2 wires to stimulate signal in atrium, then in ventricle…..mimics the normal spread of electrical signals……… many other types of pacemakers!
Location? Is it ventricular? • VT
Presenter
Presentation Notes
Ignore the atria! This starts in the ventricles. http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001239/ check this for details! This is driven by mis-behaving cells in the conducting system down stream from the Bundle of His…..it overrides whatever the SA or AV nodes are trying to do……… the problem here is inadequate filling, decreased CO, perhaps no effective pumping……maybe no peripheral pulse! So the symptoms and seriousness of this rhythm depend on how long it lasts. If it only lasts a few beats, then resolves, to come back irregularly, it may be OK. If it lasts longer than a few minutes, then syncope? Problems!
VF • Fibrillation is an uncontrolled twitching or
quivering of muscle fibers (fibrils).
• During ventricular fibrillation, blood is not pumped.
• Sudden cardiac death results.
• The most common cause of VF is MI.
• However, VF can occur whenever the heart does not get enough oxygen or if a person has other heart disorders…
Even beginning students should recognise this rhythm!
http://drugster.info/img/term/asystole-1392_2.gif
Asystole!
Presenter
Presentation Notes
No electrical activity ……….”flatline”……… no chances here! Can’t defibrillate as there is no fibrillation!
Cardiac myopathies
• Many types....... many causes
• Dilated… most common
• Hypertrophic
• Restrictive
Presenter
Presentation Notes
Dilated means the ventricles are large, but not strong.. Most common form “There are many causes of dilated cardiomyopathy. Some of these are: Alcohol (alcoholic cardiomyopathy) or cocaine abuse Atrial fibrillation, supraventricular tachycardia, or other heart rhythm problems in which the heart beats very fast for a long period of time (called Tachycardia-mediated cardiomyopathy)” http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001221/ Hypertrophic means the ventricles are thick but the chamber is small…usually inherited, so affects young people Restricted means the wall does not relax in diastole to allow filling: “stiff wall”
Restrictive not shown because heart usually looks OK…would need to see it moving, measure CO. One reason that less blood can be pumped out in Hypertrophic CM is that the enlarged septum blocks the aortic outlet! But note small chamber, so limited end diastolic volume. The dilated one is obvious…….just weakened contractions: chamber is so large that filling does not stretch the walls enough to get a rebound….Frank-Startling.
Causes & effects
• often secondary to MI
• 2/3 idiopathic
• valvular disorders
• DM
• renal failure
• Alcohol use
• nutritional deficiencies
• drug toxicity
• post- infection..viral..sudden
• Hyperthyroid
• genetic
• ↓ contractility
• ↓ stroke volume
• ↓ cardiac output • ..... failure
Presenter
Presentation Notes
Will progress to heart failure if not corrected………… Especially important to note is the damage done by alcohol & associated nutritional deficiencies. Report of a study showed differences in alcohol damage in men vs women. “They found men who were the heaviest drinkers were the most likely to have high blood pressure and stiffening of the arteries and heart muscle. Women who were the heaviest drinkers were most likely to have enlarged hearts. Mahmud said heavy drinking seemed to accelerate the effects of high blood pressure in men, and cause a direct toxic effect to heart tissue in women.” http://www.reuters.com/article/2008/05/14/us-heart-alcohol-idUSN1432515120080514
“Bicuspid aortic valve is the most common cause of aortic stenosis in patients under age 65. Normal aortic valves have three thin leaflets called cusps. About 2% of people are born with aortic valves that have only two cusps (bicuspid valves). Although bicuspid valves usually do not impede blood flow when the patients are young, they do not open as widely as normal valves with three cusps. Therefore, blood flow across the bicuspid valves is more turbulent, causing increased wear and tear on the valve leaflets. Over time, excessive wear and tear leads to calcification, scarring, and reduced mobility of the valve leaflets. About 10% of bicuspid valves become significantly narrowed, resulting in the symptoms and heart problems of aortic stenosis. The most common cause of aortic stenosis in patients 65 years of age and over is called "senile calcific aortic stenosis." With aging, protein collagen of the valve leaflets is destroyed, and calcium is deposited on the leaflets. Turbulence across the valve increases causing scarring, thickening, and stenosis of the valve once valve leaflet mobility is reduced by calcification. Why this aging process progresses to cause significant aortic stenosis in some patients but not in others is unknown. The progressive disease causing aortic calcification and stenosis has nothing to with healthy lifestyle choices, unlike the calcium that can deposit in the coronary artery to cause heart attack.” http://www.medicinenet.com/aortic_stenosis/page2.htm
Prolapse shown here is not causing regurgitation yet….loosening of chordae tendinae or papillary muscles…….If the prolapse is not severe, may be few if any symptoms. If regurgitation is severe, valve replacement may be necessary. Regurgitation cause extra work for left ventricle and may lead to other heart problems……..>Heart failure. Mitral valve prolapse is more common in women; about 6% of women, especially thin ones, may have a prolapsed valve. Such a valve may also be more prone to endocarditis……. Murmurs heard on auscultation for all valve problems….different murmurs can be diagnostic!
What has this got to do with heart disease? Scabies infestation common among children in third world countries, and in Aboriginal communities where overcrowding is prevalent. At least 50% of children in such communities have scabies before 2 years of age……..itchy, so scratch, open up to infection.
scabies
Bacterial Skin
infection
Rheumatic fever
Rheumatic Heart
Disease
Heart Valve
damage
Endo carditis Sore
throat
Presenter
Presentation Notes
This shows the link. Scabies and sore throat…portasl of entry for Streptococcus which leads to rheumatic fever, rheumatic heart disease and permanent scarring of valves. This makes a person susceptible years later to bacterial growth on the valves ….= endocarditis, largest single reason for valve failure and valve replacement.
Definitions
Rheumatic Fever: • is a complication following Group A Streptococcus infection (sore throat) • damages collagen fibrils & ground substance of connective tissue • affects mostly heart, joints, CNS, skin. • Outcomes include Rheumatic Heart Disease, Rheumatoid arthritis, and mental illness. (Franks, 2002; McCance & Huether, 2002).
Presenter
Presentation Notes
Facts can be left for students to read about later.
Streptococcus Infection • Reservoirs of infection
– Group A Streptococcus pyogenes – endogenous in oral cavity (5% of ATSI)
– Group A Streptococcus pyoderma – endogenous in skin (70% of ATSI)
These vegetations are made of bacteria hidden within fibrous material, hard to treat, high levels of IV antibiotics for weeks………… or just surgery! Throw this valve out and replace it.
Lots of different ways to replace valves…….mechanical valves are good but damage RBC, patient requires constant anticoagulation. Pig valves or human cadaver valves better but don’t last as long. Treated so no rejection….. Note bloodless field in lower picture…..means bypass machine is being used.
What is Heart Failure?
• Heart cannot circulate enough blood to supply organs with sufficient oxygen, nutrients to support cells
• Common end-point for many cardiac diseases
• Long-term, slow decline of Cardiac Output
• Compensatory mechanisms
• Eventual failure
Presenter
Presentation Notes
This is a whirlwind tour of Heart Failure, hitting some high-lights…..not comprehensive! Definition is failure of the heart…… simple! Progression and compensatory mechanisms not simple!
What Causes Heart Failure?
Any health condition that either damages the heart or makes it work too hard
Just to emphasise that many pathways lead to HF….many of the problems already discussed can lead to HF. So, some of these damage the muscle making it unable to pump (MI, cardiaomyopathies) others make it work too hard (valves, HTN) and eventually “wear it out”.
• What Causes Heart Failure?
Severe lung disease (COPD > cor pulmonale)
Diabetes (↑ CAD)
Severe anemia
Hyperthyroidism
Arrhythmias
Congenital heart defects
3/28/2012 36
Presenter
Presentation Notes
More.. Diabetes leads to Coronary artery disease. “Cardiovascular disease is the major cause of death in diabetes, accounting for some 50% of all diabetes fatalities, and much disability. On average, people with type 2 diabetes will die 5-10 years before people without diabetes and most of this excess mortality is due to cardiovascular disease.” http://www.idf.org/fact-sheets/diabetes-cvd OK…not all of this is HF, some is stroke, some is sudden MI …but still a major cause. Severe anemia makes the heart work harder to try to circulate enough oxygen….. Arrhythmias make the heart contract too often (sinus tachy) or prevent efficient ejection ……
Heart disease (any)
Hypertension Diabetes,
Hypercholesterolemia
Asymptomatic LV dysfunction
Systolic / Diastolic
Marked symptoms at rest despite max. therapy
Dyspnea, Fatigue Reduced exercise
tolerance
Stages in the Evolution of Heart Failure
A
B
C
D
AHA guidelines 2001
Presenter
Presentation Notes
Risk factors / contributory factors Many paths to HF…early stages are asymtomatic due to compensatory mechanisms Symptoms in later stages largely due to compensatory mechanism now counter-productive Later still these symptoms are disabling… leading to death
Left heart failure Ischemia,
Myocarditis, Valvular heart diseases
et cetera!
Forward failure Backward failure
↓ cardiac output
Tissue anoxia
↓ renal perfusion
Activation of RAAS
PULMONARY CONGESTION and OEDEMA
Na+, H2O retention
Residual blood in left ventricle
Left atrial pressure and volume
Pressure in pulmonary venous circulation
Pulmonary arterial hypertension
Right ventricular pressure
SYSTEMIC VENOUS CONGESTION and PERIPHERAL OEDEMA
Right heart failure
Presenter
Presentation Notes
There are many ways to classify heart failure (left vs right, systolic vs diastolic, backward vs forward, high output ….) Most problems are related to left ventricular failure……. Even if initial cause was COPD & right sided failure…. the failure to circulate blood will be due to left ventricular failure. So, follow steps around to explain the symptoms. RAAS retains fluids…..which at first increases Venous Return and stimulates myocardium contraction.. so increases C.O. but eventually overworks the heart & causes failure. RAAS also increases vasoconstriction to maintain BP & renal perfusion, but causes HTN which increases workload on left ventricle………..
Diastolic versus Systolic
Systolic– “can’t pump” Aortic valve Stenosis,
Insufficiency
HTN (↑ PR) Mitral valve
Regurgitation
Muscle Loss
Ischemia
Fibrosis
Infiltration
Diastolic- “can’t fill” Mitral valve Stenosis
Tamponade
Hypertrophy
Infiltration
Fibrosis (stiff wall)
3/28/2012 39
Presenter
Presentation Notes
Can’t fill..refers to restriction of end diastolic volume in left ventricle (mainly) so mitral valve stenosis will prevent filling in timely manner…& remember that tachycardia may also be a compensatory mechanism for reduced CO so even less time for filling. Other restrictions are stiff wall, inability to relax to fill, or “squeeze” by tamponade…but this would have to be subtle, chronic tamponade, not acute. Anything that pushes back on blood leaving left ventricle will impede forward blood flow… increased peripheral resistance anywhere in circulation…….. At aortic valve, or later in arteries by HTN. So, at first the heart just pushes harder! Can’t keep that up!
DIASTOLIC HEART FAILURE
“can’t fill”
SYSTOLIC HEART FAILURE
“can’t pump”
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Presenter
Presentation Notes
Either way CO is reduced. Note the difference in volume of chambers……. Either extreme is bad.
Activation of Sympathetic NS
Tachycardia
CONGESTIVE HEART FAILURE
Further stress on myocardium
Activation of Sym NS > Myocardial contractility
cardiac workload
Cell stretching
COMPENSATORY HYPERTROPHY and DILATATION
COMPENSATORY MECHANISMS
Lt. VENTRICULAR FAILURE
• Ischemia, Myocarditis, Valvular heart disease
Rt. VENTRICULAR FAILURE
• Pulmonary HTN, Valvular heart disease
Activation of RAAS mechanism
Na+ and water retention
Presenter
Presentation Notes
Doesn’t matter where the problem starts, it all triggers the same compensatory mechanisms. Reduced blood supply to kidneys activates RAAS fluid retention to increase venous return…..increases preload & stretch of ventricles increasing contraction…but increases myocardial oxygen demand, too. Sympathetic NS increases HR & contractility to increase CO… but more O2 demand. Hypertrophy means more muscle to contract, but also more oxygen demand. So, eventually all compensations are counterproductive.
The more common forms of heart failure cannot be cured, but can be treated/managed Lifestyle changes Medications Surgery Heart transplant
Treatment Options
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Presenter
Presentation Notes
We will follow up on medications in the 4th lecture. Students already know the lifestyle changes that are recommended……. Surgery like valve replacement has been mentioned……..heart transplant for younger patients certainly can prevent death! But because of complications of immunosuppressant drugs, I would hesitate to call this a “cure”.
