·       Cardiogenesis begins on day 18 and completes by day 63 --> first functional organ

·       Mesodermal-derived angiogenic clusters coalesce within the cardiogenic region --> forming a pair of endocardial tube.

·       Initial cardiogenic area is craniolateral to the oral membrane but cranial flexion and lateral folding carries endocardial tubes into the thoracic area.  The endocardial tubes fuse to form the primitive heart tube, which develops into the endocardium.

·       Mesoderm around the primitive heart tube develops into the myocardium (secretes cardiac jelly) and epicardium (forms the visceral pericardium).

·       The primitive heart tubes forms 5 dilatations

Development of the human heart during the first eight weeks (top), and the formation of the heart chambers (bottom). In this figure, the blue and red colors represent blood inflow and outflow (not venous and arterial blood). Initially, all venous blood flows from the tail/atria to the ventricles/head, a very different pattern from that of an adult.

By OpenStax College - Anatomy & Physiology, Connexions Web site., Jun 19, 2013., CC BY 3.0,

Primitive heart tube 5 dilatations:

1.     SV (sinus venosus):

a.     Left horn --> Coronary sinus

b.     Right horn --> Smooth part of right atrium

2.     PA (primitive atria) --> Trabeculated left & right atrium

3.     PV (primitive ventricle) --> Trabeculated parts of left & right ventricles

4.     BC (bulbus cordis) --> Smoth part of the right (conus arteriosus) & left (aortic vestibule) ventricle.

5.     TA (truncus arteriosus) --> Aorta and Pulmonoary trunk

Cardiac looping: PA moves cranially & dorsally to BC and bends right & ventrally.  PV bends left & dorsal to BC (if bends right --> dextrocardia).

Atrial septation:

o   The septum primum forms from the top down --> grows toward the AV septum

o   Note the ostium primum (hole), which never completely closes on its own. Later, cells from the interventricular septum grow up into the septum to close the hole.

o   The ostium secundum forms. Cells in an area near the cranial end of the septum primum undergo apoptosis, causing this hole to form. Note that the ostium primum and secundum both form in the septum primum

o Septum secundum starts forming on cranial end of atrium to the right of the septum primum, and grows downward and posteriorly. It grows over the septum primum but the two don’t fuse until after birth

o This leaves a hole – the foramen ovale, which allows for right to left blood flow. After birth, because of increased pressure in the left atrium, the foramen ovale should close within a few months.

The developing heart at day 30. The septum primum (top, middle) develops downwards to separate the initially joined primitive atrium into left and right atria.

By Henry Vandyke Carter - Henry Gray (1918) Anatomy of the Human Body (See "Book" section below) Gray's Anatomy, Plate 465, Public Domain,


Arterial supply to the heart (red), with other areas labelled (blue).

By Coronary.pdf: Patrick J. Lynch, medical illustratorderivative work: Fred the Oyster (talk)adaption and further labeling: Mikael Häggström - Coronary.pdf, CC BY-SA 3.0,

·       Coronary circulation begin at sinus of Valsalva where the RCA & LCA (right & left coronary artery) arise. 

·       LCA -->

o   LAD (left anterior descending artery): Supplies the LV (left ventricle), Apex, IVS (interventricular septum)

o   LCX (left circumflex): Travels in a groove between LA & LV and gives marginal branches to LV

§  Gives PDA (posterior descending artery) in 10% of the population

·       RCA: Gives PDA in 90% of the population

The heart, showing valves, arteries and veins. The white arrows show the normal direction of blood flow.

With the atria and major vessels removed, all four valves are clearly visible.

By OpenStax College - Anatomy & Physiology, Connexions Web site., Jun 19, 2013., CC BY 3.0,

Layers of the heart wall, including visceral and parietal pericardium.

By OpenStax College - Anatomy & Physiology, Connexions Web site., Jun 19, 2013., CC BY 3.0,

Cardiac and Vascular Function Curves:

·       Cardiac Function Curve : Frank-Starling curve for the ventricle showing the relationship of CO (cardiac output) as a function of EDV (end diastolic volume) = VR (venous return) 

·       Venous Return Curve :  This is the relationship between blood flow in the vascular system (VR) and RAP (right atrial pressure)

·       Mean Systemic Pressure (MSP):  This is the point where the venous return curve intersects the X axis. The mean systemic pressure reflects the right atrial pressure when there is ‘no flow’ in the system.  At this point the pressure is equal throughout the circulatory system. 

·       Equilibrium:  This is the steady-state where the two curves intersect; it reflects the point where CO =VR.

Cardiac function curve In diagrams illustrating the Frank–Starling law of the heart, the y-axis often describes the stroke volume, stroke work, or cardiac output. The x-axis often describes end-diastolic volume, right atrial pressure, or pulmonary capillary wedge pressure. The three curves illustrate that shifts along the same line indicate a change in preload, while shifts from one line to another indicate a change in afterload or contractility. A blood volume increase would cause a shift along the line to the right, which increases left ventricular end diastolic volume (x axis), and therefore also increases stroke volume (y axis).

o   Mean Systemic Pressure Changes:  MSP is affected by blood volume as well as venous compliance.  Changes in the mean systemic pressure will shift the VR curve left or right. 

§  ↑ MSP (↑ blood volume or ↓ venous compliance) --> shift VR curve right --> ↑ VR  & CO

§  ↓ MSP : opposite as above

o   Inotropic Changes : Inotropic changes will alter the slope of the cardiac curve up or down

§  Positive ionotropes (digitalis, epinephrine): shifts cardiac curve up --> ↑ CO & ↓ RAP

§  Negative ionotropes (b-blocker): opposite as above

o   Total Peripheral Resistance Changes : TPR is determined by the resistance of the arterioles.  Changes in TPR will change the slope of both the cardiac function curve and the venous return curve.

§  ↓ TPR will cause blood to be retained on the arterial side of circulation --> ↑ aortic pressure against which the heart must pump à shift both cardiac curve and VR curve downward.   ↓ both CO & VR; however the right atrial pressure remains the same because of the simultaneous change. 

§  ↓ TPR: opposite as above

·      Left Ventricular Pressure-Volume Curve

Steps in the cardiac cycle:

·       1 --> 2 (isovolumetric contraction):   MV closes when LV > LA pressure (at point 1).  LV is filled with blood from LA.  All valves are closed.

·       2 --> 3 (ventricular ejection): AV opens when LV > aortic pressure (at point 2) --> blood is ejected into the aorta.  Volume ejected = SV.

·       3 --> 4 (isovol umetric relaxation):  AV closes when LV < aortic pressure (at point 3).  All valves are closed.

·       4 --> 1 (ventricular filling): MV opens when LV < LA pressure --> LV being filled with blood from the LA again. 

Idealized pressure-volume diagram featuring cardiac cycle components






·       S1: MV & TV closes

·       S2: AV  & PV closes

·       S3: Occurs at end of rapid ventricular filling; indicates LV overload;  associated with DCM (dilated cardiomyopathy), PDA (patent ductus arteriosus)….

·       S4: Atrial kick; indicates  with a hypertrophic LV; associated with HCM (hypertrophic cardiomyopathy)

JVP (jugular venous pulse): JVD associated with RHF (right heart failure):

·       a wave – atrial contraction

·       c wave – RV contraction (TV bulges into RA)

·       v wave - ↑ atrial pressure due to filling against a closed TV

Cardiac output as shown on an ECG.

Major Factors Influencing Cardiac Output - Cardiac output is influenced by heart rate and stroke volume, both of which are also variable.

Summary of Major Factors Influencing Cardiac Output - The primary factors influencing HR include autonomic innervation plus endocrine control. Not shown are environmental factors, such as electrolytes, metabolic products, and temperature. The primary factors controlling SV include preload, contractility, and afterload. Other factors such as electrolytes may be classified as either positive or negative inotropic agents.

By OpenStax College - Anatomy & Physiology, Connexions Web site., Jun 19, 2013., CC BY 3.0,


·      0:  Ventricular depolarization due to the opening of  voltage-gated Na+ channel

·       1:  Early repolarization due to inactivation of Na+ channels and opening of voltage-gated fast K+ channels

·       2:  The plateau.  ↑ Ca++ conductance & ↓ K+ conductance

·       3: Rapid repolarization due to massive K+ departure from the cell as a result of opening of slow K+ channels and closure of Ca++ channel

4:  Resting potential is dominated by K+

The action potential of a ventricular myocyte

By Action_potential2.svg: *Action_potential.png: User:Quasarderivative work: Mnokel (talk)derivative work: Silvia3 (talk) - Action_potential2.svg, CC BY-SA 3.0,


·      P wave (<0.12s): atrial depolarization (repolarization is buried in QRS)

·      PR segment (0.12-0.20s): conduction delay in AV node

·      QRS complex (<0.12s): ventricular depolarization

·      QT interval (<0.45s): ventricular contraction

·      T wave: ventricular repolarization

·      ST segment: isoelectric, ventricles depolarized

ECG of a heart in normal sinus rhythm

By Created by Agateller (Anthony Atkielski), converted to svg by atom. - SinusRhythmLabels.png, Public Domain,

Proper placement of the limb electrodes. The limb electrodes can be far down on the limbs or close to the hips/shoulders as long as they are placed symmetrically.

Placement of the precordial electrodes.

By Mikael Häggström - Own work, CC0,

Spatial orientation of EKG leads.

By Npatchett - Own work, CC BY-SA 4.0,

Congenital defects:

o   22q11 (Di George syndrome) --> Truncus arteriosus, Tetralogy of Fallot

o   Down syndrome --> atrial septal defect (ASD), ventricular septal defect (VSD)

o   Rubella --> Septal defect, patent ductus arteriosis (PDA); congenital rubella syndrome (CRS): CRS --> C-cardiovascular defect, C-cephalic-small, C-cataracts, R-retard-mental/growth, S-sound-impair (deaf).

o   Turner’s syndrome --> Coarctation of aorta

o   Diebetic mom --> Transposition of the great vessel

DiGeorge syndrome (thymic hypoplasia):

90% due to 22q11 deletion, which occurs sporadically and may be associated with Accutane usage during pregnancy
Malformation of 3rd and 4th pharyngeal pouches that normally form the aortic arch, part of the face, thymus, and parathyroid
Presentation: CATCH-22: C-cardiac defect (anomalies of the great vessels), A-abnormal facies, T-thymic hypoplasia, C-cleft palate, H-hypoCa2+
T-cells are absent --> vulnerable to viral, fungal, protozoal and intracellular bacterial infections

A patient with DiGeorge syndrome, showing characteristic facial appearance, with tubular nose and carp-shaped mouth

By Prof Victor Grech -, CC BY-SA 3.0,

Truncus arteriosus:  An arterial trunk that originates from both ventricles of the heart present during embryonic development.   It is later divides into the aorta and the pulmonary trunk.  Failure of the truncus arteriosus to close results in persistent truncus arteriosus (often just referred to as truncus arteriosus). Other pathologies of the truncus arteriosus include transposition of the great vessels and tetralogy of Fallot.

Illustration of truncus arteriosus in a fully formed heart

Tetralogy of Fallot (TOF): 

EPIDEMIOLOGY:   Risk factors include a maternal gestation alcohol use, maternal diabetes, advanced maternal age (> 40), rubella during pregnancy,  Down syndrome.

PATHOPHYSIOLOGY Classically there are four defects:  PROV --> P-pulmonary stenosis (narrowing of the exit from the right ventricle), R-right ventricular hypertrophy (thickening of the right ventricular muscle), O-overriding aorta (allows blood from both ventricles to enter the aorta), V-ventricular septal defect (hole between the two ventricles). 

A diagram showing a healthy heart and one suffering from the tetralogy of Fallot, which constitutes four different malformations.

By Mariana Ruiz LadyofHats - the image i made myself using adobe ilustrator using this images as source: [1], [2] ,[3], [4] , [5],[6] .and a diagram found on the book "Pädiatrie" from Karl Heinz Niessen., Public Domain,

Right to Left shunt (early cyanosis): child squat to ↑ ventricular return & lessen right to left shunt; 3T’s -->

o   Tetralogy of Fallot: PROVe --> P-pulmonary stenosis, R-right ventricular hypertrophy, O-overiding aorta, V-ventricular septal defect; x-ray boot-shaped heart,  cyanotic spells; Anterosuperiorly displaced infundibular septum

o   Transpositon of great vessels: Right venticle (aneriorly located) bloood flows out to aorta, while left ventricle (posteriorly located) flows out into the pulmonary trunk.  Separate systemic & pulmonary circulation are created.  CANNOT LIVE unless have shunt to mix blood (VSD, PDA, PFO) --> without surgery correction will die within 1st month.  Cause: failure of aorticpulmonary septum to spiral.

o   Truncus ateriosus:

o   Eisenmenger’s syndrome: Uncorrected VSD, ASD, PDA -> reverse shunt due to ↑ pulmonary resistance --> late cyanosis (Polycythemia & Cyanosis)

Left to Right shunt (late cyanosis): Ventricle --> Atrium --> Pulmonary artery 

o   Ventricular septal defect (VSD): Varying sizes with small ones may spontaneous close.  Large ones may lead to pulmonary hypertension --> right ventricular hyperplasia --> reverse flow & late cyanosis. 

o   Atrial septal defect (ASD) (may cause paradoxic emboli): manifest in Adult; pulmonary hypertension --> reverse flow --> cyanosis

§  Septum primum: lower septum; if large --> deform atrioventricular valves

§  Septum secundum: defect fossa ovalis

§  Sinous venosus: upper septum near superior vena cava entrance

§  Patent foramen ovale (PFO): usually insignificant

§  Lutembacher syndrome: Atrial septal defect with mitral stenosis (often of rheumatic origin)

o   Patent ductus arteriosus (PDA): fetal shunt right to left; neonate left to right shunt --> right ventricular hypertrophy (RVH);  Patent for a machine (continuous machine-like murmur).  IndomethaCin Closes PDA, PGE keeps oPen (required in Transposition).

o   Coarctation of Aorta (M>F 3:1, PE check femoral pulse):

      §  INfantile: IN close to heart; aortic stenosis proximal to ductus arteriosus (preductal)

     §  ADult: Distal/postductal; NOTCH ribs, HTN upper, weak pulses in lower extremities.

Transposition of the great vesselsIn transposition of the great arteries, the aorta is connected to the right ventricle, and the pulmonary artery is connected to the left ventricle — the opposite of a normal heart's anatomy.  Two separate circuits are formed — one that circulates oxygen-poor (blue) blood from the body back to the body, and another that recirculates oxygen-rich (red) blood from the lungs back to the lungs.

Transposition of the great vessels

By Centers for Disease Control and Prevention - Centers for Disease Control and Prevention, CC0,

Ventricular septal defect (VSD):  Defect in the ventricular septum, the wall dividing the left and right ventricles of the heart. The extent of the opening may vary from pin size to complete absence of the ventricular septum, creating one common ventricle. The ventricular septum consists of an inferior muscular and superior membranous portion and is extensively innervated with conducting cardiomyocytes.  The membranous portion, which is close to the atrioventricular node, comprising over 80% of cases.

PRESENTATION: Pansystolic (Holosystolic) murmur along lower left sternal border (depending upon the size of the defect) +/- palpable thrill (palpable turbulence of blood flow). 

X-ray showing characteristic finding in case of Transposition of the great vessels which is called egg on side sign

By Madhero88 - Own work, CC BY-SA 3.0,

Echocardiogram in transposition of the great arteries. This subcostal view shows the left ventricle giving rise to a vessel that bifurcates, which is thus identified as the pulmonary artery. Abbreviations: RA=right atrium, RV=right ventricle, LV=left ventricle, PT=pulmonary trunk, LPA and RPA=left and right pulmonary artery.

A CXR (Chest X-Ray) of a child with tetralogy of Fallot.

By James Heilman, MD - Own work, CC BY-SA 3.0,

Illustration showing various forms of ventricular septal defects.
1. Conoventricular, malaligned
2. Perimembranous
3. Inlet
4. Muscular

By Centers for Disease Control and Prevention - Centers for Disease Control and Prevention, Public Domain,

Echocardiographic image of a moderate ventricular septal defect in the mid-muscular part of the septum. The trace in the lower left shows the flow during one complete cardiac cycle and the red mark the time in the cardiac cycle that the image was captured. Colours are used to represent the velocity of the blood. Flow is from the left ventricle (right on image) to the right ventricle (left on image). The size and position is typical for a VSD in the newborn period.

A nitinol device for closing muscular VSDs, 4 mm diameter in the centre. It is shown mounted on the catheter into which it will be withdrawn during insertion.

By No machine-readable author provided. Ekko assumed (based on copyright claims). - No machine-readable source provided. Own work assumed (based on copyright claims)., Public Domain,

Atrial septal defect (ASD): Blood flows between the atria of the heart. Some flow is a normal condition both pre-birth and immediately post-birth via the foramen ovale, however when this does not naturally close after birth it is referred to as a patent (open) foramen ovale (PFO), causing oxygen-rich blood to flow directly from the left side of the heart to mix with the oxygen-poor blood in the right side of the heart. This can lead to hypoxemia and paradoxical emboli causing cryptogenic strokes.

llustration of an atrial septal defect.

Ultrasound picture of the heart, seen in a subcostal view: The apex is towards the right, the atria are to the left. ASD secundum seen as a discontinuation of the white band of the atrial septum. The enlarged right atrium is below. The enlarged pulmonary veins are seen entering the left atrium above.

Public Domain,

Abnormal chest X-ray as seen in a patient of atrial septal defect.

Septum primum defect:  Failure of the septum primum to fuse with the endocardial cushion can lead to an ostium primum atrial septal defect, causing a shunt to occur from the left atrium to the right atrium.  This is the second most common type of atrial septal defect and is commonly seen in Down's syndrome.

The developing human heart, at day 30. The septum primum (top middle) grows down to separate the primitive atrium into the left and right atrium of the human heart.

Septum secundum defect:  The septum secundum, semilunar in shape, grows downward from the upper wall of the atrium immediately to the right of the septum primum and ostium secundum.  Shortly after birth it fuses with the septum primum, and consequently the foramen ovale is closed, but sometimes the fusion is incomplete and the upper part of the foramen remains patent causing an atrial septal defect.

Interior of dorsal half of heart of human embryo of about thirty-five days. (Septum secundum visible at center top.)

Patent ductus arteriosus: The ductus arteriosus is a fetal blood vessel that closes soon after birth. Patent ductus arteriosus (PDA) results when the ductus arteriosus fails to close after birth and allows a portion of oxygenated blood from the left heart to flow back to the lungs by flowing from the aorta (which has higher pressure) to the pulmonary artery.  Early symptoms are uncommon, but in the first year of life include increased work of breathing and poor weight gain. An uncorrected PDA may lead to congestive heart failure with increasing age.  Ifan some congenital heart defects (such as in transposition of the great vessels) a PDA may need to remain open, as it is the only way that oxygenated blood can mix with deoxygenated blood. In these cases, prostaglandins are used to keep the DA open and NSAIDs should not be administered, until surgical correction of the heart defect is completed.

Summary: Fetal shunt R→L; neonate L→R → RVH; Patent for a machine (continuous machine-like murmur). IndomethaCin Close PDA, PGE keeps oPen (req’d in Transposition).

Diagram of a cross-section through a heart with PDA

Illustration of Patent Ductus Arteriosus

By BruceBlaus. When using this image in external sources it can be cited staff (2014). "Medical gallery of Blausen Medical 2014". WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.010. ISSN 2002-4436. - Own work, CC BY 3.0,

Congenital defects:

I. Acyanotic:

o   Left to right shunt --> ↑ pulmonary blood flow: atrial septal defect (ASD), ventricular septal defect (VSD), patent ductus arteriosis (PDA)

o   Obstructive defect:  Coarctation of aorta

II. Cyanotic: T's T-tetralogy of Fallot (TOF), T-transposition of great arteries (TGA), T-truncus arteriosus (TA), T-total anomalous pulmonary venous return (TAPVR)

Fetal circulation:  The degree of oxygenation of blood in various vessels differs from that in the postnatal state as the consequences of exygenation being provided by the placenta rather than the lungs and the presence of three major vascular shunts:

1) Ductus venosus

2) Foramen ovale

3) Ductus arteriosus

The fetal circulatory system includes three shunts to divert blood from undeveloped and partially functioning organs, as well as blood supply to and from the placenta.

Coarctation of the aorta (also called aortic narrowing):  Congenital condition whereby the aorta is narrow, usually in the area where the ductus arteriosus (ligamentum arteriosum after regression) inserts.  Since the aorta is narrowed, the left ventricle has to work harder.  If the narrowing is severe enough, it results in hypoxia to the lower half of the body. 

Illustration depicting Coarctation of the Aorta.

By BruceBlaus. When using this image in external sources it can be cited staff (2014). "Medical gallery of Blausen Medical 2014". WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.010. ISSN 2002-4436. - Own work, CC BY 3.0,

Total anomalous pulmonary venous return/connection (TAPVR):  A rare cyanotic congenital heart defect in which all four pulmonary veins are malpositioned and make anomalous connections to the systemic venous circulation (pulmonary veins enters right atrium, superior vena cava or coronary sinus, instead of going to the left atrium). A patent foramen ovale, patent ductus arteriosus or an atrial septal defect must be present, or else the condition is fatal due to a lack of systemic blood flow.

§  INfantile: IN close to heart; aortic stenosis proximal to ductus arteriosus (preductal)

§  ADult: Distal/postductal; NOTCH ribs, HTN upper, wk pulse lower extremities.

Ilustration of totaly anomalyous pulmonary venous return

•       Aortic stenosis: Narrowing of the exit of the left ventricle of the heart due to calcific aortic stenosis (senile degeneration by highly repetitive valvular mechanisms lead to thickening and in some individuals massive calcification) or congenital abnormal bicuspid valve.  Rarely may occur secondary to rheumatic heart disease (<10%), but never syphilis.  May cause angina, syncope and moderate left ventricular hypertrophy.  Tend to be advanced age (except for bicuspid valves).

In the center an aortic valve with severe stenosis due to rheumatic heart disease. The valve is surrounded by the aorta. The pulmonary trunk is at the lower right. The right coronary artery, cut lengthwise, is at the lower left. The left main coronary artery, also cut lengthwise, is on the right.

By CDC/Dr. Edwin P. Ewing, Jr. - This media comes from the Centers for Disease Control and Prevention's Public Health Image Library (PHIL), with identification number #848.Note: Not all PHIL images are public domain; be sure to check copyright status and credit authors and content providers., Public Domain,

Aortic regurgitation: Leaking of the aortic valve of the heart that causes blood to flow in the reverse direction during ventricular diastole, from the aorta into the left ventricle.  May be due to degenerative aortic dilation (due to hypertension & aging with myxomatous degeneration, syphilitic aortitis, osteogenesis imperfecta, aortic dissection, Behçet's disease, reactive arthritis) or collagen disorders (Marfan’s, Ehler-Danlos, etc), infectious endocarditis (causes acute aortic regurgitation), rheumatic heart disease (rare and usually cause stenosis also), an syphilis (rare today).  May leads to massive left ventricular hypertrophy and congestive heart failure. 

Aortic valve regurgitation vs aortic valve stenosis

By BruceBlaus - Own work, CC BY 3.0,

Micrograph of myxomatous degeneration – a cause of aortic insufficiency.

Mitral stenosis:  Narrowing of the orifice of the mitral valve of the heart almost always due to chronic rheumatic endocarditis.  Rarely it may be a congenital abnormality.  A reduction in cardiac output, associated with acceleration of heart rate frequently leads to congestive heart failure, while pooling of blood in the left atrium lead to pulmonary edema, atrial dilatation causing atrial fibrillation and mural thrombosis. 

Illustration of mitral stenosis, with close-up on mitral valve

By Blausen Medical Communications, Inc. - Donated via OTRS, see ticket for details, CC BY 3.0,

Rheumatic heart disease at autopsy with characteristic findings (thickened mitral valve, thickened chordae tendineae, hypertrophied left ventricular myocardium).,_gross_pathology_20G0013_lores.jpg

Mitral stenosis with marked thickening of the leaflets and left atrial hypertrophy. Superior view. Autopsy preparation.

By, Public Domain,

Mitral regurgitation: Disorder of the heart in which the mitral valve does not close properly when the heart pumps out blood causing abnormal leakage of blood back from the left ventricle, through the mitral valve, into the left atrium, when the left ventricle contracts.  MR is the most common form of valvular heart disease.  It can be caused by mitral valve prolapse (#1), papillary muscle dysfunction (from myocardial infarction), rheumatic heart disease (due to post inflammatory scaring and usually accompanied by mitral stenosis also) and infective endocarditis (#1 cause of acute mitral regurgitation).    

Illustration comparing nonstenotic mitral valve insufficiency to mitral valve stenosis.


Bradyarrhythmias:  HR (heart rate) < 60 bpm.  Causes by problem with either 1) Impulse formation or 2) Impulse conduction.

·       Causes:

o   Systemic causes: HI --> H-hypopoxia, Hypothermia, Hypoparathyroidism, ↑ ICP (intracranial pressure)

§  H _______________, _______________, _______________, _______________, _______________

§  I _______________, _______________, _______________, _______________, _______________

o   Cardiac disease:  LIARS --> L-lenegre-Lev’s syndrome, IHD (ischemic heart disease), Amyloidosis of the heart, RHD (rhematic heart disease), Sarcoidosis of the heart.

§  Lenegre-Lev’s syndrome (acquired complete heart block due to idiopathic fibrosis and calcification of the electrical conduction system of the heart. Lev's disease is most commonly seen in the elderly, and is often described as senile degeneration of the conduction system.  Also associated with the general calcification of the cardiac skeleton including the aortic & mitral valve).

§  IHD (ischemic heart disease): 

§  Amyloidosis of the heart: 

§  RHD (rhematic heart disease):

§  Sarcoidosis of the heart:

§  L _______________, _______________, _______________, _______________, _______________

§  I _______________, _______________, _______________, _______________, _______________

§  A _______________, _______________, _______________, _______________, _______________

§  R _______________, _______________, _______________, _______________, _______________

§  S _______________, _______________, _______________, _______________, _______________

o   Drugs causing bradyarrhythmia: BCD --> B-beta-blocker, C-calcium channel blocker, D-digoxin

§  b _______________, _______________, _______________, _______________, _______________

§  C _______________, _______________, _______________, _______________, _______________

§  D _______________, _______________, _______________, _______________, _______________

·       Evaluations:  Hypotenstion (SBP < 90), light-headed, syncope, CHF, angina.  EKG (should be first diagnostic test)

·       Types of bradyarrhythmias:  SLow Ass Rate = SLAR --> S-sick-sinus syndrome, S-sinuse bradycardia, L-LBBB (left bundle branch block), A-AV (atrioventricular) block, R-RBBB (right bundle branch block).

o   Sick-sinus syndrome: more common in elderly adults, where the cause is often a non-specific, scar-like degeneration of the cardiac conduction system.  It can result in many abnormal heart rhythms (arrhythmias), including sinus arrest, sinus node exit block.

Schematic representation of a normal ECG

ECG of a heart in normal sinus rhythm

By Created by Agateller (Anthony Atkielski), converted to svg by atom. - SinusRhythmLabels.png, Public Domain,

Electrocardiogram grid
ECGs are normally printed on a grid. The horizontal axis represents time and the vertical axis represents voltage. The standard values on this grid are shown in the adjacent image:

A small box is 1 mm × 1 mm and represents 0.1 mV × 0.04 seconds.
A large box is 5 mm × 5 mm and represents 0.5 mV × 0.20 seconds.
The "large" box is represented by a heavier line weight than the small boxes.

By User:Markus Kuhn modified trace by User:Stannered of original PowerPoint JPEG by User:MoodyGroove - This file was derived from: ECG Paper.jpg, Public Domain,

Phonocardiograms from normal and abnormal heart sounds

By <a href="//" title="User:Madhero88">Madhero88</a> - <span class="int-own-work" lang="en">Own work</span><span class="mw-headline" id="Reference">Reference</span><a rel="nofollow" class="external text" href="">netter image</a>, <a href="" title="Creative Commons Attribution-Share Alike 3.0">CC BY-SA 3.0</a>, <a href="">Link</a>

Electrocardiogram from a man with bradycardia-tachycardia syndrome following mitral valvuloplasty, resection of the left atrial appendage and maze procedure. The ECG shows AV-junctional rhythm resulting in bradycardia at around 46 beats per minutes. The second beat is most likely an atrial extrasystole, given the atypical P wave (negative in I, positive in aVR).

By Steven Fruitsmaak - Own work, CC BY-SA 3.0,

This ECG from the same patient shows atrial fibrillation at around 126 beats per minute.

Sinus bradycardia:  

·       Potential causes: ↑ vagal tone, intrinsic disease of the sinoatrial (SA) node, effect of drugs (BCD --> B-beta-blocker, C-Calcium channel blocker (CCB), Digoxin or quinidine, and sleep.  It could also be a normal finding in a healthy, well-conditioned person

·       EKG: Normal except for HR < 60

  §  Treatment:  If asymptomatic --> no treatment.  If symptomatic --> Atropine 0.5 mg, pacemaker

Sinus bradycardia seen in lead II with a heart rate of about 50.

By Sinusbradylead2.JPG: James Heilman, MDderivative work: Mysid (using Perl and Inkscape) - This file was derived from: Sinusbradylead2.JPG:, CC BY-SA 3.0,

o   LBBB (left bundle branch block):  QRS > 0.12s

·       Potential causes:  Hypertension, acute myocardial infarction,  coronary artery disease, cardiomyopathy, primary disease of the cardiac electrical conduction system

·       EKG: wide QRS complexes (>0.12s) with abnormal morphology in leads V1 (rS with deep S wave) and V6 (wide tall notched R wave without Q wave).

·       Treatment: If asymptomatic --> no treatment.  If symptomatic --> ventricular pacemaker is definitive therapy


·      P wave (<0.12s): atrial depolarization (repolarization is buried in QRS)

·      PR segment (0.12-0.20s): conduction delay in AV node

·      QRS complex (<0.12s): ventricular depolarization

·      QT interval (<0.45s): ventricular contraction

·      T wave: ventricular repolarization

·      ST segment: isoelectric, ventricles depolarized

ECG characteristics of a typical LBBB showing wide QRS complexes with abnormal morphology in leads V1 and V6.

By A. Rad at the English language Wikipedia, CC BY-SA 3.0,

Electrocardiogram showing left bundle branch block and irregular rhythm due to supraventricular extrasystoles.

A left bundle branch block.

By James Heilman, MD - Own work, CC BY-SA 3.0,

o   Atrioventricular (AV) block:  disease of the electrical conduction system of the heart. It refers to a conduction block between the atria and ventricles.

§ First degree

·       Potential causes:  ↑ vagal tone.  Can occur in normal individual.

·       EKG: PR interval > 0.2s

·       Treatment:  None necessary

An ECG showing a first degree AV block of greater than 300 ms

By James Heilman, MD - Own work, CC BY-SA 4.0,

§  Second degree:

Ø  Morbitz Type I (Wenkebach)

o   Potential causes:  usually due to nodal disease, ↑ vagal tone, drugs (BCD --> B- beta-blocker, C-calcium channel blocker (CCB), D-digoxin)

EKG:  progressive prolongation of the PR interval on consecutive beats followed by a blocked P wave ('dropped' QRS complex).  PR then resets and the cycle repeats.

Treatment:  almost always a benign condition for which no specific treatment is needed.  Stop the offending drug.

§  Second degree:

Ø  Morbitz Type II (Wenkebach)

o   Potential causes:  almost always a disease of the distal conduction system (His-Purkinje System), Post-myocardial infarction

EKG: intermittently nonconducted P waves not preceded by PR prolongation.  May progress to complete heart block à Stokes-Adams attack, cardiac arrest, or Sudden Cardiac Death.

Treatment:   pacemaker

Second-degree atrioventricular block

Sinus rhythm with acute inferior infarction complicated by Type I A-V block manifest in the form of 5:4 Wenckebach periods; R-P/P-R reciprocity.

By <a href="//" title="User:Jer5150">Jer5150</a> - <span class="int-own-work" lang="en">Own work</span>, <a href="" title="Creative Commons Attribution-Share Alike 3.0">CC BY-SA 3.0</a>, <a href="">Link</a>

Sinus rhythm (rate = 100/min) with 3:2 and 2:1 Type II A-V block; RBBB.

Third degree:

o   Potential causes: impulse generated in the atria does not propagate to the ventricles --> AV dissociation

o   EKG:  no apparent relationship between P waves and QRS complexes

o   Treatment: pacemaker

12-lead ECG showing complete heart block

By James Heilman, MD - Own work, CC BY-SA 3.0,

Leads I and II demonstrating complete AV block. Note that the P waves are not related to the QRS complexes (PP interval and QRS interval both constant), demonstrating that the atria are electrically disconnected from the ventricles. The QRS complexes represent an escape rhythm arising from the ventricle.

Atrial tachycardia with complete A-V block and resulting junctional escape

By Jer5150 - Own work, CC BY-SA 3.0,

o   RBBB (right bundle branch block).

·       Potential causes: COPD, valvular disease, CAD, or after repair of VSD.  Can occur in normal individual.

·       EKG: wide QRS complexes (>0.12s) with a terminal R wave in lead V1 (rSR’) and slurred wide S wave in lead V6

·       Treatment: None necessary

Normal electrical conduction system of the heart (Schematic). All myocardial segments are excited almost simultaneously (purple staining).
1 Sinoatrial node
2 Atrioventricular node

By J. Heuser - self made, based upon Image:Heart anterior view coronal section.jpg by Patrick J. Lynch (Patrick J. Lynch; illustrator; C. Carl Jaffe; MD; cardiologist Yale University Center for Advanced Instructional Media ), CC BY 2.5,

Conduction in RBBB (Schematic): With a blockage in the right bundle branch (red), the left ventricle is excited in time (purple), while the excitation of the right ventricle takes a detour via the left bundle branch (blue arrows).

The characteristic wave patterns of a typical right bundle branch block as seen in an ECG. Only the precordial lead V1 and V6 are shown. Wide QRS complexes are present and there's T wave inversion in lead V1 which is normal in this condition. Note the typical wide and deep s wave in V6. The small q wave in V6 may not always be present. Below each QRS complex is its designation (rSR and qRs) according to nomenclature.

By A. Rad - I drew this image in Xara X¹ using my own knowledge and several sources for checking whether I drew the image correctly., CC BY-SA 3.0,

RBBB with associated first degree AV block.

RBBB with associated tachycardia.

By James Heilman, MD - Own work, CC BY-SA 3.0,


·       Overall treatment strategy for bradyarrhythmias:  1) treat underlying causes:  stop meds… 2) meds: atropine 0.5 mg if symptoms of congestive heart failure (CHF --> CHF, Hypotension, Faint/syncope) 3) pacemaker

Bradyarrhythmias:  SLow Ass Rate = SLAR --> S-sick-sinus syndrome, Sinuse bradycardia, LBBB (left bundle branch block), AV block, RBBB (right bundle branch block)

§  S _______________, _______________, _______________, _______________, _______________

§  L _______________, _______________, _______________, _______________, _______________

§  A _______________, _______________, _______________, _______________, _______________

§  R _______________, _______________, _______________, _______________, _______________

Tachyarrhythmias:  HR > 100 bpm.  Classification by rate:  a) 150-250 bpm: paroxysmal tachycardia b) 250-350: flutter c) 350-450: fibrillation

Causes by either

·       1) ↑ intrinsic pacer automaticity or

·       2) re-entry pathway (most common cause):  requires 2 paths with different conduction speeds and recovery periods.  The impulse is blocked in one arm of the loop, descends the other arm, and then returns up the loop in a tretrograde fashion.

·       Evaluation:  Asymptomatic or present with dizzy, diaphoresis, palpitation, chest pain, syncope, hypotension (indicate hemodynamic stability).  EKG should be first diagnostic test.

·       Types:  SVT (supraventricular tachycardia) & VT (ventricular tachycardia)

ECG showing sinus tachycardia with a rate of about 100 beats per minute

By Madhero88 - Own work, CC BY-SA 3.0,

o   Supraventricular tachycardia (SVT):  narrow QRS rapid rhythm of the heart in which the origin of the electrical signal is either the atria or the AV node.  Subdivided into SPAM --> S-sinus tachycardia, P-PSVT (paroxysmal SVT), A-atrial flutter, A-atrial fibrillation, M-MAT (multifocal atrial tachycardia)

§  Sinus tachycardia: normal physiologic response to fear, pain, exercise

EKG:  normal sinus rhythm (normal P waves before every QRS complex) except for its fast rate

Treatment:  none necessary

ECG readout of an individual with sinus tachycardia. Here the heart rate is around 150.

By User:MoodyGroove -, CC BY-SA 3.0,

A 12 lead ECG showing sinus tachycardia.

§  PSVT (paroxysmal SVT):  sudden rapid pacing from a very irritable focus located above the ventrical.  Types: PAT (paroxysmal atrial tachycardia), PJT (paroxysmal junctional tachycardia).

Ø  PAT (paroxysmal atrial tachycardia):  impulses originate from an irritable automaticity focus in the atrium.  EKG:  HR > 100 bpm.  P wave with unusual axis before each normal QRS.   Usually idiopathic, but can also be seen in rheumatic heart disease, COPD, mitral valve prolapse & digitalis toxicity (especially PAT with 2:1 AV block)

·       P-wave may or may not be visible, depending on the rate

·       If present, P-waves are usually regular and inverted in lead II, and may be seen before, during, or after the QRS complex

Treatment:  Vagal maneuvers (carotid massage/Valsalva) or adenosine (slows AV node for diagnosis).  Cardioversion if hemodynamically unstable.  Transcatheter ablation of one of the two pathways

PJT (paryxysmal junctional tachycardia): impulses originate from an irritable automaticity focus in the AV junction (node). Types:   AV nodal reentrant tachycardia (AVNRT) and Atrioventricular reentrant tachycardia (AVRT).  

 v   AV nodal reentrant tachycardia (AVNRT)

·       Dual conduction pathways within the AV node allow electrical impulses to recycle within the AV nodal region

·       EKG: P-waves may not be visible or may occur before, during or after the QRS complexes

·       Most commonly appear in the late teens or early twenties

·       Treatment: same as for PAT.

An example of an ECG tracing typical of uncommon AV nodal reentrant tachycardia. Highlighted in yellow is the P wave that falls after the QRS complex.

By <a href="//" title="User:Ceccomaster">Ceccomaster</a> - <span class="int-own-work" lang="en">Own work</span>, <a href="" title="Creative Commons Attribution 3.0">CC BY 3.0</a>, <a href="">Link</a>

Atrioventricular reentrant tachycardia (AVRT):  Involves an “accessory pathway”.    Usually utilizes the AV node as the anterograde & the accessory pathway as the retrograde limbs.  Examples include the pre-excitation syndromes: WPW syndrome (Wolff–Parkinson–White).

·       PR interval is shortened (< 0.12 sec)

·       QRS is widened with a “slurred upstroke” (AKA the delta-wave)

·       delta-waves are due to the accessory conduction pathway (bundle of Kent) from the atria to the ventricles, that bypasses the AV node

·       Treatment:  Procainamide

Conduction pathway in atrioventricular reentrant tachycardia, a form of supraventricular tachycardia

By Jackpickard1985 - Own work, CC BY-SA 3.0,

12 lead electrocardiogram of an individual with Wolff–Parkinson–White syndrome exhibiting 'slurred upstrokes' or 'delta waves' before the QRS complexes

§  Atrial flutter:  Circular movement of electrical activity around atrium at rate of 300 times/min

·       Associated with coronary artery disease, congestive heart failure, COPD, valvular disease, pericarditis

·       Carotid sinus massage may exaggerate the degree of AV-block & consequently slow down the QRS rate, to assist with the diagnosis

·       EKG: regular rhythm.  “Sawtooth” appearance of P waves.

·       Treatment:  1)  Anticoagulation with warfarin 2) Rate control with AV nodal agent  (bCD --> B-beta-blocker, C-calcium channel blocker, D-digoxin) 3) Cardioversion only if new onset (<36 hrs), it TEE shows no clot in the LA, or after 6 weeks of warfarin treatment.  Electrical (50 J synchronized shock) or pharmacological (Class IA or III anti-arrhythmic drug).

Atrial flutter with varying A-V conduction (5:1 and 4:1)

By Atrial_flutter34.JPG: James Heilman, MDderivative work: Mysid (using Perl and Inkscape) - This file was derived from: Atrial flutter34.JPG:, CC BY-SA 3.0,

Type I atrial flutter, counterclockwise rotation with 3:1 and 4:1 AV nodal block.

Atrial flutter with a two to one block. Note the P waves hiding in the T waves in leads V1 and V2

By James Heilman, MD - Own work, CC BY-SA 4.0,

Atrial fibrillation: