What is an electrical cardioversion?

·         Brief procedure where an electrical shock is delivered to the heart to convert an abnormal heart rhythm back to a normal rhythm (Sinus Rhythm).

·         “Non-emergency": to treat atrial fibrillation or atrial flutter, benign heart rhythm disturbances originating in the upper chambers (atria) of the heart.

·         Emergency situations: to correct a rapid abnormal rhythm associated with faintness, low blood pressure, chest pain, difficulty breathing, or loss of consciousness.

Why do I need a cardioversion?

·         In atrial fibrillation, however, the atria fibrillate (or "quiver") due to chaotic electrical signals that circulate throughout both atria. This typically results in a fast and irregular heartbeat.

·         While some patients have no symptoms, others may experience shortness of breath, lightheadedness and fatigue.

·         Depending on your specific medical history and symptoms, your physician may recommend a cardioversion to return your heart to a normal rhythm.

What are the different types of cardioversion?

·         "Chemical" or "electrical".

o   Chemical cardioversion

§  Use of antiarrhythmia medications to restore the heart's normal rhythm.

§  Mode of action: Modifying the heart's electrical properties to reduce the frequency of abnormal heart rhythms and to help restore a normal rhythm.

§  May start your antiarrhythmia medication as an outpatient, or may choose to give you an intravenous (IV) or oral antiarrhythmia medication while heart rhythm is monitored.

o   Electrical cardioversion

§  a.k.a "direct-current" or DC cardioversion)

§  M.O.A: A synchronized (perfectly timed) electrical shock is delivered through the chest wall to the heart through special electrodes or paddles that are applied to the skin of the chest and back

§   The goal is to disrupt the abnormal electrical circuit(s) in the heart and to restore a normal heart beat.

§   The shock causes all the heart cells to contract simultaneously, thereby interrupting and terminating the abnormal electrical rhythm (typically fibrillation of the atria) without damaging the heart.

§  This split second interruption of the abnormal beat allows the heart's electrical system to regain control and restore a normal heartbeat.

§  Special cardioversion pads are placed on your chest and back (or alternatively, both pads can be placed on the front of the chest). The pads are connected to an external defibrillator by a cable.

§  Patient under anesthesia/sedated – not conscious during the procedure

Prognosis:

·         A normal heart rhythm can be restored more than 90% of the time, although abnormal rhythms may recur in about half the patients within 1 year.

·         The success of electrical cardioversion often depends on the duration of atrial fibrillation and the underlying cause (heart disease).

·         Cardioversion is not appropriate for every patient with atrial fibrillation.

Are there any other things I should know before my cardioversion?

·         Because the upper chambers of the heart are fibrillating (quivering) and do not squeeze uniformly in patients with atrial fibrillation, there is a potential risk that blood clots may form.

·         The process of restoring a normal rhythm could potentially dislodge a blood clot from the heart resulting in a heart attack or a stroke.

·         Thinning the blood prior to cardioversion can prevent most blood clots.

·         Prior to performing a cardioversion, risk of blood clot formation  is determined (and thus, your risk of stroke or heart attack) and an anticoagulant medicine is given.

·         Blood must be adequately thinned for at least 3-4 weeks prior to the cardioversion to reduce the risk of stroke.

·         Because it takes many hours for blood clots to form, cardioversion can be safely performed without blood thinning medication in patients who have had their heart rhythm problem for less than 48 hours.

·          Transesophageal echocardiogram or TEE may be used to allow the atria to be visualized and thus scan for potential blood clots.

·         Typically, anticoagulation is continued after the cardioversion for an additional 4 weeks to 6 months, even if the cardioversion is successful.

Digoxin

Digoxin

It is also known as digitalis and is extracted from the plant Digitalis lanata which is found in Eastern Europe.
Other names: Lanoxin, Digitek, and Lanoxicaps. It is also available as a 0.05 mg/mL oral solution and 0.25 mg/mL or 0.5 mg/mL injectable solution.

Its main cardiac effects are
• Negatively chronotropic - i.e. slowing the heart rate by decreasing conduction of electrical impulses through the AV node, making it a commonly used antiarrhythmic agent in controlling the heart rate during atrial fibrillation or atrial flutter.
• Positively inotropic - i.e. increasing the force of heart contraction via inhibition of the Na+/K+ ATPase pump

ATPase controls movement of calcium, sodium and potassium into heart muscle. Calcium controls the force of contraction. Inhibiting ATPase increases calcium in heart muscle and therefore increases the force of heart contractions.
Digoxin is usually given by mouth, but can also be given by IV injection in urgent situations (the IV injection should be slow, heart rhythm should be monitored). The half life is about 36 hours; digoxin is given once daily, usually in 125 μg or 250 μg dosing. Following drug administration, a 6- to 8-hour tissue distribution phase is observed.

This half life is only present for those with normal renal function, as this drug is metabolized through the kidneys.
Digoxin blood levels are used for adjusting doses in order to avoid toxicity. The usual starting dose is 0.0625-0.25 mg daily depending on age and kidney function. The dose may be increased every two weeks to achieve the desired response.

Side Effects:
Common side effects include nausea, vomiting, headache, dizziness, skin rash, and mental changes. Many digoxin side effects are dose dependent and happen when blood levels are over the narrow therapeutic range. Visual disturbances (blurred vision or yellow/green halos around objects), fast/slow/irregular heartbeat and overdosage may occur if patient is dehydrated.

Treatment of Atrial fibrillation
Goal of the treatment:
• To prevent formation of blood clots that might lead to blockage of other vessels.
• To control the rate of contraction so that ventricles have enough time to fill up.
• To restore the sinus rhythm so that the atria and ventricles work together in coordination.
• Preventive measures

Blood clot prevention
Drugs such as warfarin, heparin and aspirin are prescribed to reduce the risk of blood clot.
Warfarin and heparin are anticoagulants that act via the coagulation cascade.
Warfarin interrupts the coagulation pathway by causing an antagonising the effect of Vitamin K. The activity of clotting factors II, VII, IX,X are dependent on vitamin K.


Heparin inhibits the pathway by enhancing the effect of antithrombin. Antithrombin inactives the enzyme thrombin, that is responsible for the conversion of fibrinogen into fibrin.


Low-dose, long-term aspirin use irreversibly blocks the formation of thromboxane A2 in platelets.
Thromboxane A2 has the effect of increasing the number of platelets and also causing platelets to coagulate.
This anticoagulant property makes aspirin useful for reducing the incidence of heart attacks.


Rate control
Doctors prescribe medicines to slow down the rate at which the ventricles are beating so that the ventricles have time to fill up completely.
Beta blockers (for example, metoprolol and atenolol), calcium channel blockers (diltiazem and verapamil) are the drugs used.



Beta-blockers bind to beta-adrenoceptors located in cardiac nodal tissue, the conducting system, and contracting myocytes. The heart has both β1 and β2 adrenoceptors, although the predominant receptor type in number and function is β1. These receptors primarily bind norepinephrine that is released from sympathetic adrenergic nerves. Additionally, they bind norepinephrine and epinephrine that circulate in the blood. Beta-blockers prevent the normal ligand (norepinephrine or epinephrine) from binding to the beta-adrenoceptor by competing for the binding site.
Beta-blockers cause decreases in heart rate, contractility, conduction velocity, and relaxation rate.

Calcium channel blockers work by blocking voltage-gated calcium channels in cardiac muscle and blood vessels. This decreases intracellular calcium leading to a reduction in muscle contraction. In the heart, a decrease in calcium available for each beat results in a decrease in cardiac contractility.
Cardiac contractility is defined as the ability of cardiac muscles to contract to at a given fiber length.
Calcium channel blockers also tend to decrease the blood pressure and the sympathetic nerve will adjust for this drop in BP by causing increase in heart rate.

Therefore calcium channel blockers are often taken with a beta blocker to avoid the reflexive action.

Rhythm control
The longer you have AF, the less likely it is that an abnormal heart rhythm can be restored to a normal heart rhythm. This is especially true for people who have had AF for 6 months or more.
Medicines used to control the heart rhythm include amiodarone, sotalol, flecainide, propafenone, dofetilide, and ibutilide.
Most of the drugs that control rhythm act on the conduction velocity of electric impulses(Sodium-channel blockers) or the duration of the refractory periods of the muscles(Potassium-channel blockers).
Sodium-channel blockers decrease the conduction velocity by making only a few channels available for passage of ions. In reducing the conduction velocity, the time between atrial and ventricular contractions is increased. This type of drug is used to treat tachyarrhythmias.





Procedures
Cardioversion
Transient delivery of electrical current causes a momentary depolarization of most cardiac cells allowing the sinus node to resume normal pacemaker activity. In the presence of reentrant-induced arrhythmia electrical cardioversion interrupts the self-perpetuating circuit and restores a sinus rhythm.
http://www.youtube.com/watch?v=Ud0m7IrEQf0
To perform synchronized electrical cardioversion two electrode pads are used, each comprising a metallic plate which is faced with a saline based conductive gel.
The pads are placed on the chest of the patient, or one is placed on the chest and one on the back. These are connected by cables to a machine which has the combined functions of an ECG display screen and the electrical function of a defibrillator.
A synchronizing function (either manually operated or automatic) allows the cardioverter to deliver a reversion shock, by way of the pads, of a selected amount of electric current over a predefined number of milliseconds at the optimal moment in the cardiac cycle which corresponds to the R wave of the QRS complex on the ECG. Timing the shock to the R wave prevents the delivery of the shock during the vulnerable period (or relative refractory period) of the cardiac cycle, which could induce ventricular fibrillation. If the patient is conscious, various drugs are often used to help sedate the patient and make the procedure more tolerable.
http://www.youtube.com/watch?v=1rcg6Ce7p18&feature=related

Catheter ablation may be used to restore a normal heart rhythm when medicines or electrical cardioversion don't work. During this procedure, a wire is inserted through a vein in the leg or arm and threaded to the heart.

Radio wave energy is sent through the wire to destroy abnormal tissue that may be disrupting the normal flow of electrical signals.

Sometimes catheter ablation is used to destroy the atrioventricular (AV) node. The AV node is where the heart's electrical signals pass from the atria to the ventricles. This procedure requires your doctor to surgically implant a device called a pacemaker to maintain a normal heart rhythm.



Maze surgery
Another procedure to restore a normal heart rhythm is called "maze" surgery. During this procedure, the surgeon makes small cuts or burns in the atria that prevent the spread of disorganized electrical signals.
This procedure requires open-heart surgery, so it's usually done when a person requires heart surgery for other reasons, such as for valve disease


Prognosis
• the risk of stroke for lone atrial fibrillation was 4 times higher
• female sex in patients with AF without rheumatic heart disease is associated with a higher risk of stroke
• underlying heart disease increases the risk of stroke in non-rheumatic atrial fibrillation
• up to 20% of patients with atrial fibrillation and a stroke will have a second stroke within one year
• in a follow-up of the Framingham study, atrial fibrillation was independently associated with a 50-90% increase in the risk of death.
Reference
www.emedicine.com
www.nhlbi.nih.gov
http://www.cvpharmacology.com/

AF occurs when the SA is overwelmed by disorganized electrical impulses from the atria and pulmonary veins. One of the main factors that causes AF is the dialtion of the heart atrium. This is because, once dilation occurs, several enzymes and hormones are secreted to remodel the myo cardium in such a way that it is able to withstand the pressure. This happens over time. As the remodelling occurs, the heart muscle losses its elasticity and its efficiency. In order to overcome this, the heart forces more blood into its compartments to make up for its loss and once again, the atrium to dilate and the whole process happens all over again.

From here, there are two different ways in which AF could happen. The first one is when the heart undergoes fibrosis again and again until the SA node undergoes fibrosis as well. Or the electical conduction of the heart could be disrupted by muscle allignment due to fibrosis (myocaridal dissaray) which causes AF.


Table 1. Etiologies of Atrial Fibrillation

1. Atrial pressure elevation (leading to dilatation)
Valvular disease: mitral/tricuspid regurgitation or stenosis, mitral valve prolapse
Hypertrophic cardiomyopathy (HCM)
Pulmonary hypertension (COPD with cor pulmonale)
Pulmonary embolism
Intracardiac thrombi or tumor

2. Inflammatory and infiltrative process
Pericarditis/myocarditis
Age induced atrial fibrosis

3. Infectious process
Any infections and fever

4. Endocrine disorders
Hyperthroidism

5. Atrial ischemia
Myocardial infarction

6. Drugs
Alcohol (holiday heart)
Caffeine

7. Idiopathic
Lone afib if less than 60 years old

8. Familial


Risk Factors.

basically, the things that predisposes you to have Atrial Fibrillation are diseases or conditions that eventually leads to the fibrosis of the heart tissues, increased intra-cardial pressure, hypertension, especially in the pulmonary vessels, etc.

here are some of the risk factors which increases your chances of having AF

• coronary heart disease
• heart failure
• Rheumatic heart disease
• Structural heart defects, such as mitral valve disorders
• pericarditis (a condition in which the membrane, or sac, around your heart is inflamed)
• congenital heart defects
• Sick sinus syndrome (a condition in which the heart's electrical signals don't fire properly and the heart rate slows down; sometimes the heart will switch back and forth between a slow rate and a fast rate)

Sorry so late

Atrial Fibrillation
-most common type of arrhythmia (problem with rate or rhythm of the heartbeat)
Definition: AF occurs when rapid, disorganized electrical signals cause the atria to fibrillate. The term "fibrillate" means to contract very fast and irregularly.
In AF, blood pools in the atria and isn't pumped completely into the ventricles. As a result, the heart's upper and lower chambers don't work together as they should.
Often, people who have AF may not feel symptoms. However, even when not noticed, AF can increase the risk of stroke.(Clots can form in the pools of blood in the atria) In some people, AF can cause chest pain or heart failure, particularly when the heart rhythm is very rapid.
AF may occur rarely or every now and then, or it may become a persistent or permanent heart rhythm lasting for years. In such cases, treatment is aimed at controlling symptoms and preventing complications.
-National Heart Lung and Blood Institute
Incidence and prevalence
Incidence: Number of new cases within a specified time period
Prevalence: Total number of cases in the population at a given time (In this case number of people managing AF at a particular time)
In the US, approx 2million people are diagnosed with AF
-1 in 136/0.74%
Prevalence of AF rises almost exponentially with age:
• The prevalence of AF among persons younger than 55 years is 0.1%.
• The prevalence of AF among persons 60 years or older is 3.8%.
• The prevalence of AF among persons 80 years or older is 10%.
AF more common in whites than blacks
AF more common among men than women
Framingham data suggest that patients with atrial fibrillation have a 1.5-2 fold increase in mortality rate when compared with the general population.
People with AF have higher risk of stroke(up to 7 times general population)
-eMedicine

Investigation for Atrial Fibrillation

Laboratory Studies

• CBC- Complete Blood Count (looking for anemia, infection)
• Electrolytes and BUN/creatinine levels (looking for electrolyte disturbances or renal failure)
• Cardiac enzymes - CK and/or troponin level (to investigate myocardial infarction as a primary or secondary event)
• May include a D-dimer if the patient has risk factors to merit a pulmonary embolism workup
• Thyroid function studies (looking for thyrotoxicosis)
• Digoxin level may be obtained when appropriate (to look for subtherapeutic levels and/or toxicity). It is generally considered safe to administer digoxin to a patient with atrial fibrillation on digoxin for rate control without waiting for a level to return from the laboratory when the patient presents with atrial fibrillation with rapid ventricular response (RVR).
• Toxicology testing or ethanol level – Acute intoxication

Imaging Studies

• Chest radiographic findings are usually normal. Look for radiographic evidence of CHF as well as signs of lung or vascular pathology (pulmonary embolism, pneumonia).
• If patients have a positive D-dimer result, they may require chest CT angiography to rule out pulmonary embolus.
• Echocardiography may be used to evaluate for valvular heart disease, left and right atrial size, left ventricular (LV) size and function, left ventricular hypertrophy (LVH), and pericardial disease.
• Transthoracic echocardiogram (TTE)
• Evaluate for valvular heart disease
• Evaluate atrial and ventricular chamber and wall dimensions
• Estimate ventricular function and evaluate for ventricular thrombi
• Estimate pulmonary systolic pressure (pulmonary hypertension)
• Evaluate for pericardial disease
• Transesophageal echocardiogram (TEE)
• Evaluate for left atrial (LA) thrombus (particularly in the LA appendage)
• Computed tomography (CT) or magnetic resonance imaging (MRI): If atrial fibrillation ablation is planned, then 3-dimensional imaging technologies (CT scan or MRI) are often helpful to evaluate atrial anatomy. Imaging data can be processed to create anatomic maps of the left atrium and pulmonary veins.

Other Tests

• Six-minute walk test or exercise test
• Six-minute walk or exercise testing can help assess the adequacy of rate control.
• Exercise testing can exclude ischemia prior to treatment of patients with Class Ic drugs and can be used to reproduce exercise-induced atrial fibrillation.
• Holter monitoring or event recording: Helpful to establish diagnosis and evaluate rate control.

Jugular Venous Pressure (JVP) Pulsations

Jugular Venous Pressure ( JVP ) Pulsations

· Jugular Venous Pressure tells us about the right atrial and right ventricular function. Besides that, we can derive information such as mean venous pressure, venous pulse contour and the presence and type of cardiac dysarythmias.

· Technique :

o Positioning of the patient – lying down at 45 degrees to the horizontal with his or head on pillows and in good lighting condition ( directed tangentially at approximately 45 degrees across the right side of the neck towards the midline ).

§ The internal jugular vein is deep to the sternocleidomastoid while the external jugular vein lies lateral to it. Usually, the right internal and external jugular veins give consistent readings. However, left sided veins are less accurate because they cross from the left side of the chest before entering the right atrium. Pulsations that occur in the right sided veins reflect movements of the top of a column of blood that extends directly into the right atrium. It may be used as a manometer and enables us to observe pressure changes in the right atrium.

o The sternal angle which is taken as the zero point from which it is used to measure the vertical height of the column of blood in the jugular vein in centimeters should be noted when the patient is lying at 45 degrees.

o Usually the patient's chin must be extended to enhance this observation. But care should be exercised so that the sternocleidomastoid muscle is not excessively tensed, thus compressing the external and internal jugular veins and obliterating their pulsations. It is crucial that the examiner be certain to distinguish between venous and arterial pulsations, and that the top of the venous column is recognized. The former is accomplished by seeking the three crests in the venous pulse and comparing them to the carotid arterial pulse. Apparently, it is easiest to observe the pulsations in the right side of the neck while timing the carotid pulse in the left side of the patient's neck using the right third finger. If still uncertain as to whether or not you are observing the venous pulse, you could try to obliterate the venous pulse by placing your right thumb or index finger across the base of the patient's right neck. By compressing this area with a force of approximately 10 to 20 mm Hg, the venous pulse can be obliterated.

o The jugular venous pulse can be distinguished from the arterial pulse because :

§ It is visible but not palpable

§ It has a complex wave form, usually seen to flicker twice with each cardiac cycle ( if the patient is in sinus rhythm)

§ It moves on with respiration – JVP usually decreases on inspiration

§ It is at first obliterated and then filled from above when light pressure is applied at the base of the neck.

o The JVP must be accessed in height and character.

o The next step is to determine the height of the mean jugular venous pressure, measured in centimeters of water, above the midpoint of the right atrium.. To determine the mean jugular venous pressure, the examiner should observe the nadir of the venous column on inspiration and then the crest of this column on expiration. Next, the midpoint of the excursion of the venous pulse during normal respiratory cycles is estimated visually. Exaggerated breathing or breath holding distorts the normal mean venous pressure and should be avoided. A horizontal line is drawn from this estimated point to intersect a vertical line, which is erected perpendicular to the ground through the sternal angle of Louis. The distance between the sternal angle and this intercept is measure. The sum of this distance—plus the obligatory 5-cm fixed relationship to the midpoint of the right atrium—represents the mean jugular venous pressure.

§ When the JVP is more than 3 cm above the zero point, the right heart filling pressure is raised ( a normal reading is less than 8 cm of water : 5 cm+3 cm = 8 cm). This is a sign of right ventricular failure, volume overload or some types of pericardial disease.

· The assessment of character.

· There are two positive waves in the normal JVP. The first is called an ‘a’ wave and coincides with the right atrial systole. It is due with atrial contraction. The second impulse is called a ‘v’ wave and is due to atrial filling, in the period where the tricuspid valve remains closed during the ventricular systole.

Between the ‘a’ and ‘v’ waves there is a trough caused by atrial relaxation. This is called the x descent. It is interrupted by the c point, which is due to transmitted carotid pulsation and coincides with tricuspid valve closure. It is not usually visible. Following the v wave, the tricuspid valve opens and rapid ventricular filling occurs; this results in the ‘y’ descent.

· Any condition in which the right ventricular filling is limited can cause the elevation of venous pressure in which is more marked in inspiration when venous return to the heart increases. The rise in JVP on inspiration is called the Kussmaul’s sign. Sign is best elicited with the patient sitting up at 90 degrees and patient breathing quietly.

· Abdominojugular reflux test is a way of testing for left ventricular failure or reduced right ventricular compliance. Pressure exerted over the liver or middle of the abdomen for 10 seconds will increase venous return to the right atrium, The JVP usually rises following this manouevere.

Wave form	Causes
Dominant ‘a’ wave	Tricuspid stenosis ( also causes a slow y descent), Pulmonary stenosis, Pulmonary hypertension
Cannon ‘a’ waves	Complete heart block, Paroxymal nodal tachycardia with retrograde atrial conduction, Ventricular tachycardia with retrograde atrial conduction or atrioventricular dissociation
Dominant ‘v’ wave	Tricuspid regurgitation
X descent	Absent : Atrial Fibrillation Exaggerated : Acute cardiac tamponade, constrictive pericarditis
Y descent	Sharp : Severe tricuspid regurgitation, constrictive pericarditis Slow : Tricuspid stenosis, right atrial myxoma

Anatomy of heart

Anatomy of heart

Location: middle mediastinum

Anatomic position: left ventricle and small portion of right ventricle (separated by posterior interventricular groove) rests on the diaphragmatic surface

flow of the blood:

Four chambers: left and right atria & ventricles

Right atrium:

1. Receives blood from superior & inferior venae cavae and coronary sinus

2. Blood passes into right ventricle through right atrioventricular orifice.

3. Sulcus terminalis cordis separate the atrium externally

4. Interior of right atrium is divide by crista terminalis

5. Anterior to the crista is “atrium proper”, its wall is covered by musculi pectinati

6. Interatrial septum separate left/right atrium

a. Depression called fossa ovalis (oval fossa) with prominent margin (limbus fossa ovalis)

Right ventricle:

1. Conus arterious (infundibulum) is the outflow tract to pulmonary trunk

a. Has smooth walls

b. Derives from the embryonic bulbus cordis

2. Trabeculae carneae (papillary muscles)

a. Irregular structure muscle at inflow portion of the wall

b. One side attach to the ventricular surface, the other attach to the chordae tendineae

c. Three types of papillary muscle: anterior, posterior and septal papillary muscle

d. Septomarginal trabecula: carries right bundle of the atrioventricular bundle to the anterior wall of the right ventricle.

Left atrium:

1. embryologically derived from two structure

a. posterior half

i. receives the four pulmonary veins

ii. smooth walls

iii. derives from proximal parts of the pulmonary veins

b. anterior half

i. contains musculi petinati

ii. derives from embryonic primitive atrium

2. valve of foramen ovale

a. opposite the floor of fossa ovalis

b. prevents blood from passing from left to right atrium

c. may not be fused

Left ventricle:

1. blood enters through left atrioventricular orifice

2. thickesr layer of myocardium

3. aortic vestibule (outflow tract) has smooth walls and derived from embryonic bulbus cordis

4. trabeculae carneae are fine and delicate

a. anterior/ posterior papillary muscles

interventricular septum

1. muscular part: thick, major part

2. membranous part: thin, upper part of the septum

Tricuspid valve:

1. right atrioventricular valve

2. fibrous ring surrounds the atrioventricular orifice

3. named: anterior, septal posterior cusps

a. attach to chordae tendineae which helps prevent seperation of the cusps

Pulmonary valve:

1. three semilunar cusps

2. middle, thickened portion (nodule) and thin lateral (lunule)

3. named: left, right and anterior

4. form pocket-like sinus

5. blood fills pulmonary sinuses and force it to close after ventricular contraction

Mitral valve:

1. left atrioventricular valve aka bicuspid valve (anterior/ posterior)

2. secured by fibrous ring

3. similar to tricuspid valves

Aortic valve:

1. semilunar cusps

2. pocket-like sinuses + two opening for left/right coronary arteries

3. named: right, posterior (aka noncoronary), left

4. similar to pulmonary valve

a. but blood is forced into coronary arteries when it fills the aortic sinuses.

Cardiac skeleton:

1. fibrous rings

2. annulus fibrosus:

a. right/left fibrous trigone: thickened area of connective tissue between fibrous rings

b. maintain the opening

c. separates the atrial and ventricular musculature

Coronary vasculature

1. coronary arteries

a. supply the muscle and other tissue of the heart

b. circle in the coronary sulcus

c. empty into coronary sulcus (btwn left ventricle and atrium) then to right atrium

d. right coronary artery branch:

i. sinu-atrial node branch

ii. right marginal branch

iii. posterior interventricular branch

e. left coronary artery branch

i. anterior interventricular branch

ii. circumflex branch

iii. left marginal branch

2. cardiac veins

a. coronary sinus receives blood from great, middle, small, posterior cardiac veins

Cardiac conduction system

1. sinu-atrial node

a. pacemaker

b. superior end of the crista terminalis

2. atrioventricular node

a. near the opening of coronary sinus

3. atrioventricular bundle

a. direct continuation of atrioventricular node

4. the Purkinje fibre

Pericardium

1. fibroserous sac surrounding the heart

2. fibrous pericardium

a. tough connective tissue outer layer

3. serous pericardium

a. thin

b. parietal and visceral layer