·       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:

·       Causes: PIRATES --> P-pulmonary disease, P-pericarditis, I-ischemia, R-rheumatic heart disease, A-anemia, A-atrial myxoma, T-thyrotoxicosis, E-ethanol, S-sepsis.

·       EKG: Wavy baseline without discernible P waves.  Irregular, irregular rhythm.

·       Treatment:  Same as A-flutter.  Anti-coagulation more important because greater chance of embolism

v  P _______________, _______________, _______________, _______________, ______________

v  I _______________, _______________, _______________, _______________, ______________

v  R _______________, _______________, _______________, _______________, _____________

v  A _______________, _______________, _______________, _______________, _____________

v  T _______________, _______________, _______________, _______________, ______________

v  E _______________, _______________, _______________, _______________, ______________

v  S _______________, _______________, _______________, _______________, ______________

ECG of atrial fibrillation (top) and normal sinus rhythm (bottom). The purple arrow indicates a P wave, which is lost in atrial fibrillation.

By J. Heuser - Own work, CC BY-SA 3.0,

Leads V4 and V5 of an electrocardiogram showing atrial fibrillation with somewhat irregular intervals between heart beats, no P waves, and a heart rate of about 150 BPM.

A 12-lead ECG showing atrial fibrillation at approximately 150 beats per minute.

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

Non-modifiable risk factors (top left box) and modifiable risk factors (bottom left box) for atrial fibrillation. The main outcomes of atrial fibrillation are in the right box. BMI=Body Mass Index.

How a stroke can occur during atrial fibrillation.

By National Heart Lung and Blood Institute (NIH) - National Heart Lung and Blood Institute (NIH), Public Domain,

MAT (multifocal atrial tachycardia):

·       EKG: Must have three different consecutive P-wave morphologies on a given lead (examine lead II).   Irregularly irregular rhythm

·       Usually associated with end-stage COPD and hypoxia

·       Treatment:  Underlying problem.  Rate control with (BCD --> B-beta-blocker, C-calcium channel blocker, D-digoxin)

Multifocal atrial tachycardia

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

o  Supraventricular tachycardia ( SVT):  SPAM --> S-sinus tachycardia, P-PSVT (paroxysmal SVT), A-atrial flutter, A-atrial fibrillation, M-MAT (multifocal atrial tachycardia)

Ø  S _______________, _______________, _______________, _______________, ______________

Ø  P _______________, _______________, _______________, _______________, ________________

Ø  A _______________, _______________, _______________, _______________, _______________

Ø  M _______________, _______________, _______________, _______________, _______________

o   Ventricular tachycardia (VT):  fast rhythm that originates in one of the ventricles of the heart. This is a potentially life-threatening arrhythmia because it may lead to ventricular fibrillation and sudden death.  Types VT --> V-ventricular tachycardia (VT), V-ventricular fibrillation (VF), Torsades

Ø  VT:  can be monomorphic or polymorphic (Torsades de Pointes)

Monomorphic VT:  

·      EKC:  ≥ 3 premature ventricular contractions (PVCs).  Broad & bizarre QRS complexes (> 0.12 sec) in a regular rapid rhythm

·       Associated with coronary artery disease & myocardial infarction

Treatment:  Anti-arrhythmics (ALP --> A-amiodarone, L-lidocaine, P-procainamide).  Treat as VF is hemodynamically unstable.

Normal sinus top, ventricular tachycardia bottom

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

A run of ventricular tachycardia as seen on a rhythm strip

12 lead electrocardiogram showing a run of monomorphic ventricular tachycardia (VT)

By Image created by Karthik Sheka, M.D., CC BY-SA 2.5,

Ø  Ventricular fibrillation (VF):

Causes:  Coronary artery disease, myocardial infarction

EKG: erratic tracing

Treatment: Immediate electrical cardioversion and ACLS protocol

Ventricular fibrillation

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

Fine ventricular fibrillation as seen on a rhythm strip

Ventricular fibrillation as seen in lead II

By Glenlarson - Own work, Public Domain,

Micrograph showing myofibre break-up with squared nuclei, a morphologic correlate of ventricular fibrillation. H&E stain.

Ø  Torsades de Pointes (also known as polymorphic ventricular tachycardia):

Potential causes:  Associated with PHAT --> Phenothiazine, HypoK+/Ca++/Mg++, Hereditary long TQ syndrome, Heart failure, Anti-arrhythmics (class Ia+III), Acidosis, TCA (tricyclic anti-depressant)

·       Treatment:  Magnesium

12-lead ECG of Torsades de Pointes (TdP) in a 56-year-old white female with low blood potassium (2.4 mmol/L) and low blood magnesium (1.6 mg/dL.)

Lead II ECG showing a TdP patient being shocked by an implantable cardioverter-defibrillator back to their baseline cardiac rhythm.

o   VT:    Types ventricular tachycardia (VT)  --> V-VT, V-VF, T-Torsades

Ø  V _______________, _______________, _______________, _______________, ________________

Ø  T _______________, _______________, _______________, _______________, ________________

Quick summary of therapy for Tachyarrythmias:

Synchronized shock for:  1) 50 J for arrhythmias with regular rhythm (atrial flutter, AVVNRT) 2) 100 J for atrial fibrillation and VT with pulse
Unsynchronized shock 200J (defibrillation) for pulseless VT and VF
Therapies that cause AV node block ABCDV --> A-adenosine, B-beta blockers, C-calcium channel blocker, D-digoxin, V-vagal maneuver:  treat SVT (remember SPAM?)
Adenosine: use for regular narrow complex tachycardia that use re-entry through the AV node (AVNRT).  It has no effect on sinus or atrial tachycardia
Lidocaine:  choice treatment for VT.  Side effect: confusion and seizure
MgSO4: for treatment of Torsades
Procainamide: for treatment of WPW syndrome
Another way to categorize tachyarrhythmias.  J SAW MAT VT (J saw Matt’s VT- Imagine J is the doctor Matt is the patient):

·      Regular narrow complex tachycardia:  J SAW --> J-junctional tachycardia (AV node), Sinus tachycardia, Atrial tachycardia, AVNRT, Atrial flutter, WPW syndrome

Ø  J _______________, _______________, _______________, _______________, _______________

Ø  S _______________, _______________, _______________, _______________, _______________

Ø  A _______________, _______________, _______________, _______________, _______________

Ø  W _______________, _______________, _______________, _______________, _______________

·      Irregular narrow complex tachycardia: MAT --> M-MAT, Atrial fibrillation, Atrial flutter with variable block

Ø  M _______________, _______________, _______________, _______________, _______________

Ø  A _______________, _______________, _______________, _______________, _______________

·      Wide complex tachycardia: VT --> V-VT, VF, Torsades

Ø  V _______________, _______________, _______________, _______________, ________________

Ø  T _______________, _______________, _______________, _______________, ________________

Cardiomyopathy: Non-inflammatory intrinsic disease of the myocardium.  Not associated with hypertension, congenital heart disease, valvular disease, coronary artery disease.   Diagnostic test: CXR, EKG, echocardiogram, biopsy

·      Major types of cardiomyopathy:  Hard Dick Requires Sex = HDRS --> H-HCM (hypertrophic cardiomyopathy), D-dilated cardiomyopathy (DCM), R-restrictive cardiomyopathy, S-stress-induced cardiomyopathy

o   HYPERTROPHIC CARDIOMYOPATHY (aka IHSS-Idiopathic Hypertrophic Subaortic Stenosis):  Autosomal dominant inheritant in 50% of patient and is the most common cause of sudden athlete death.  Mutations in one of a number of genes that encode for one of the sarcomere proteins.  45% of these mutations occur in the β myosin heavy chain gene, 35% involve the cardiac myosin binding protein C gene.  Asymetric, all 4 chambers & IVS (interventricular septum) hypertrophy.  Histology:  disoriented/tangled myocardial fibers;

Ø  Evaluation:  Exertional syncope, dyspnea, palpitations, chest pain, arrhymia.  LV hypertrophy (thickened wall) --> diastolic dysfunction --> S4.  Thickened interventricular septum --> left ventricular outflow obstruction --> SEM (systolic ejection murmur).  Obstruction made worse by ↑ myocardial contractility or ↓ LV filling (e.g. exercise, dehydration, Valsalva maneuvers, vasodilators) --> SEM ↑ with Valsalva maneuver or rising from squatting to standing (the only other murmur that behaves in a similar manner is the one due to MVP-mitral valve prolapse).  CXR: boot-shaped heart. EKG: LVH (S in V2 + R in V5 > 35 mm) & varying ST segment changes (elevations and depressions).  Echo: diagnostic and shows thickened LV wall and dynamic outflow obstruction

Ø  Treatment:  Beta-blockers are the initial treatment in symptomatic individual.  Calcium channel blocker (e.g. verapamil) is an alternative. Surgical septal myectomy is the gold standard for relief of symptoms for patients who do not experience relief of symptoms from medications.  The use of a pacemaker has also been advocated  In cases that are refractory to all other forms of treatment, cardiac transplantation is an option.

llustration of asymmetric septal hypertrophy in HCM

Intravenous pressure tracings demonstrating the Brockenbrough–Braunwald–Morrow sign
AO = Descending aorta; LV = Left ventricle; ECG = Electrocardiogram.
After the third QRS complex, the ventricle has more time to fill. Since there is more time to fill, the left ventricle will have more volume at the end of diastole (increased preload). Due to the Frank–Starling law of the heart, the contraction of the left ventricle (and pressure generated by the left ventricle) will be greater on the subsequent beat (beat #4 in this picture). Because of the dynamic nature of the outflow obstruction in HCM, the obstruction increases more than the left ventricular pressure increase. This causes a fall in the aortic pressure as the left ventricular pressure rises (seen as the yellow shaded area in the picture).

By Karthik Sheka, M.D. - Own work, CC BY-SA 3.0,

o   DILATED cardiomyopathy (DCM) (most common --> comprising of 90% of all cardiomyopathy, > 600 g, mean age of presentation 20-50 year-old): the heart becomes weakened and enlarged--> cannot pump blood efficiently. No cause is apparent in many cases.

Ø  Causes:  ABCD --> A-alcohol, A-AIDS/HIV, A-AZT, B-beriberi, B-balloon x-ray, C-coxsackie B, C0-chaga’s, C-cocaine, D-doxorubicin, peripartum, hemochromatosis; 4 chambers dilated (vacuoles in myocytes) --> both L&R CHF.

v  A ______________, _______________, _______________, _______________, ______________

v  B ______________, _______________, _______________, _______________, ______________

v  C ______________, _______________, _______________, _______________, ______________

v  D ______________, _______________, _______________, _______________, ______________

Ø  Evaluation: Left ventricular enlargement --> systolic dysfunction --> congestive heart failure (CHF), S3, tricuspid and mitral regurgitation.  CXR: enlarged, balloon-like heart and pulmonary congestion.  ECG.  Echo: LV dilatation with normal or thinned walls & ↓ EF.

Ø  Treatment: Treat congestive heart failure (DABS --> D-diuretics, D-digoxin, A-ACE-inhibitor, B-beta-blocker, S-spironolactone).  Consider anticoagulation.  Artificial pacemakers used in patients with intraventricular conduction delay.  ICD (implantable cardioverter-defibrillators) for those at risk of arrhythmia. In patients with advanced disease who are refractory to medical therapy, cardiac transplantation may be considered

Illustration of a Normal Heart vs. Heart with Dilated Cardiomyopathy

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,

Dilated cardiomyopathy on CXR

Dilated cardiomyopathy on CT

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

Serial 12-lead ECGs from a 49-year-old black man with cardiomyopathy. (TOP): Sinus tachycardia (rate about 101/min) with LBBB accompanied by RAD (here about 108°). Frequent multifocal PVCs (both singly and in pairs) and left atrial enlargement. (BOTTOM): Same patient about 5 months later status-post orthotopic heart transplant.

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

Mouse heart slice showing dilated cardiomyopathy

o   RESTRICTIVE cardiomyopathy: restricts the heart from stretching --> impair diastolic filling

Ø  Causes:  1) Infiltrative disease (sarcoid, amyloid, hemochromatosis) 2) Fibrosis (secondary to radiation, adriamycin…).

Ø  Evaluation:  LHF & RHF.  Biopsy is diagnostic

Ø  Treatment:  underlying disease and heart failure symptoms (DAbS--> D-diuretics, D-digoxin, A-ACE-inhibitors, B-beta blockers, S-spironolactone; Na+ restriction)

High magnification micrograph of senile cardiac amyloidosis, a cause of restrictive cardiomyopathy. Congo red stain. Autopsy specimen. The micrograph shows amyloid (extracellular washed-out red material) and abundant lipofuscin (yellow granular material).

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

o   Stress-induced cardiomyopathy (aka Takotsubo cardiomyopathy or transient apical ballooning): non-ischemic cardiomyopathy in which there is a sudden temporary weakening of the myocardium.

Ø  Evaluation:  Most commonly seen in post-menopausal women with a history of recent severe emotional or physical stress (possible that the cardiomyopathy is due to stress-induced catecholamine release) --> sudden onset of congestive heart failure (CHF) or chest pain.  EKG:  changes suggestive of an anterior wall heart attack.  Coronary angiography:  no significant blockages that would cause the left ventricular dysfunction.  Echo:  bulging out of the left ventricular apex with a hypercontractile base of the left ventricle

Ø  Treatment:  Supportive (in individuals with hypotension, support with inotropic agents or an intra-aortic balloon pump have been used).  Provided that the individual survives their initial presentation, the left ventricular function improves within 2 months.

Schematic representation of takotsubo cardiomyopathy (A) compared to a normal heart (B)

By J. Heuser JHeuser - Own work, CC BY-SA 3.0,

ECG showing sinus tachycardia and non-specific ST and T wave changes from a person with confirmed takotsubo cardiomyopathy

(A) Echocardiogram showing dilatation of the left ventricle in the acute phase (B) Resolution of left ventricular function on repeat echocardiogram six days later

By Tara C Gangadhar, Elisabeth Von der Lohe, Stephen G Sawada and Paul R Helft - Takotsubo cardiomyopathy in a patient with esophageal cancer: a case report., CC BY 2.0,

Left ventriculography during systole showing apical ballooning akinesis with basal hyperkinesis in a characteristic takotsubo ventricle

Left ventriculogram during systole displaying the characteristic apical ballooning with apical motionlessness in a patient with takotsubo cardiomyopathy

·      CARDIOMYOPATHY:  Hard Dick Requires Sex = HDRS --> H-HCM (hypertrophic cardiomyopathy), DCM, Restrictive cardiomyopathy, Stress-induced cardiomyopathy

o   H _______________, _______________, _______________, _______________, _______________

o   D _______________, _______________, _______________, _______________, _______________

o   R _______________, _______________, _______________, _______________, _______________

o   S _______________, _______________, _______________, _______________, _______________

CHF (congestive heart failure):  condition that can result from any structural or functional cardiac disorder that impairs the ability of the heart to fill with or pump a sufficient amount of blood throughout the body.

·      Causes:

o   Most commonly due to CHF --> C-coronary artery disease (CAD) (50-75% of cases), H-Hypertension (HTN), F-failure of valves

Ø  C _______________, _______________, _______________, _______________, _______________

Ø  H _______________, _______________, _______________, _______________, _______________

Ø  F _______________, _______________, _______________, _______________, _______________

o   Recurrent CHF:  FAILURE --> F-Forgot meds, A-arrythmia, A-anemia, I-ischemia, Infarct, Infection, Lifestyle (most common cause, e.g. high Na+ intake/sedentary), Upregulation (↑ CO e.g. hyperthyroidism, pregnancy), Renal failure (fluid overload), Embolus (pulmonary)

Ø  F _______________, _______________, _______________, _______________, _______________

Ø  A _______________, _______________, _______________, _______________, _______________

Ø  I _______________, _______________, _______________, _______________, _______________

Ø  L _______________, _______________, _______________, _______________, _______________

Ø  U _______________, _______________, _______________, _______________, _______________

Ø  R _______________, _______________, _______________, _______________, _______________

Ø  E_______________, _______________, _______________, _______________, _______________

·      Classification: MD HIT VIC TAR (MD hits Victor – use you imagination)

o   Systolic dysfunction (↓ cardiac contractility --> EF <50% --> ↑ ESV [end systolic volume], ↓ CO):  most common category of CHF.  Causes: MD HIT --> Myocardial infarction (MI), D-dilated cardiomyopathy (DCM), H-hyperstension (HTN), I-ischemia & I-infiltrative heart disease (amyloid, sarcoid), Toxin (doxorubicin, EtOH)

Ø  M _______________, _______________, _______________, _______________, _______________

Ø  D _______________, _______________, _______________, _______________, _______________

Ø  H _______________, _______________, _______________, _______________, _______________

Ø  I _______________, _______________, _______________, _______________, _______________

Ø  T _______________, _______________, _______________, _______________, _______________

o   Distolic dysfunction (ventricles cannot relaxes --> ↓ ventricular filling, ↓ CO; ventricular contraction is relatively normal).  Causes: VIC --> V-valvular heart disease, I-infection, C-constrictive pericarditis

Ø  V _______________, _______________, _______________, _______________, _______________

Ø  I _______________, _______________, _______________, _______________, _______________

Ø  C _______________, _______________, _______________, _______________, _______________

o   Extracardia: TAR --> T-thyroid disease, A-anemia, R-renal failure.

Ø  T _______________, _______________, _______________, _______________, _______________

Ø  A _______________, _______________, _______________, _______________, _______________

Ø  R _______________, _______________, _______________, _______________, _______________

The major signs and symptoms of heart failure

By National Heart, Lung, and Blood Institute, National Institutes of Health; originally uploaded by Wouterstomp at en.wikipedia. -; transferred from en.wikipedia to Commons by Stevenfruitsmaak using CommonsHelper., Public Domain,

·      Evaluation:

o   ↓ CO --> activate

Ø  Rennin-angiotensin-aldosterone system --> Fluid & salt retention --> LVEDP (LV end diastolic pressure) =  ↑ preload --> heart must work harder

Ø  Sympathetic signal --> vasoconstriction --> ↑ afterload --> heart must work harder

·       These 2 mechanisms initially allow the heart to compensate.  However, eventually the heart compensatory capacity is exceeded --> blood back flow to the lungs.

o   Pulmonary congestion --> PND (paroxysmal nocturnal dyspnea), orthopnea, basilar rales, cough, JVD (jugular venous distention), hepatomegaly, hepatojugular reflux, pitting edema.

o   CBC, CMP, TSH, cardiac enzymes, EKG, CXR (cardiomegaly, cephalization of pulmonary vessels, pleural effusions), Echo (systolic dysfunction --> cardiomegaly & ↓ EF; diastolic dysfunction --> ventricular wall thicken without dilation & normal EF).

·      NYHA (New York Heart Association Clases):

o   I: No symptoms with normal activity

o   II: Comfortable at rest or mild exertion

o   III: Comfortable only at rest

o   IV: Symptoms at rest

A comparison of healthy heart with contracted muscle (left) and a weakened heart with over-stretched muscle (right).

A man with congestive heart failure and marked jugular venous distension. External jugular vein marked by an arrow.

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

Severe peripheral (pitting) edema.

Chest radiograph of a lung with distinct Kerley B lines, as well as an enlarged heart (as shown by an increased cardiothoracic ratio, cephalization of pulmonary veins, and minor pleural effusion as seen for example in the right horizontal fissure. Yet, there is no obvious lung edema. Overall, this indicates intermediate severity (stage II) heart failure.

By Mikael Häggström - Own work, CC0,

Congestive heart failure x-ray.

Kerley b lines.

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

Congestive heart failure with small bilateral effusions.

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

Ultrasound showing severe systolic heart failure.

Kerley B lines in acute cardiac decompensation. The short, horizontal lines can be found everywhere in the right lung.

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

·      Treatment

o   Systolic dysfunction:  DABS --> D-dietary restriction (↓Na+ & H2O), D-diuretics (for systolic dysfunction & pulmonary congestion), D-digoxin (for systolic dysfunction [only] uncontrolled with diuretics + ACEI), A-ACE inhibitor (associated  with 10-15% ↑ in creatinine after initiation of therapy but creatinine should ↓ after diuretic dosae is reduced; if creatinine ↑ > 30% --> could be signs of renal insufficiency), B-beta blocker (added after diuretic + ACEI has been on board & after 2-4 week of stability in patient’s condition; target HR 50-60 bpm), S-spironolactone (NYHA class III & IV already on DAB)

Ø  D _______________, _______________, _______________, _______________, _______________

Ø  A _______________, _______________, _______________, _______________, _______________

Ø  b _______________, _______________, _______________, _______________, _______________

Ø  S _______________, _______________, _______________, _______________, _______________

o   Diastolic dysfunction:  goal is to ↓ LVEDP by inducing ventricular relaxation --> ↑ ventricular filling.  B-beta blocker (↓ HR --> ↑ ventricular filling time.  Calcium channel blocker (actively relaxs the myocardium)

CAD (coronary artery disease):

·      Clinical manifestation: CAD --> C-CHF, A-angina (stable & unstable), A-arrhythmias, A-attack-heart, D-dyspnea on exertion (DOE), D-death

o   C _______________, _______________, _______________, _______________, _______________

o   A _______________, _______________, _______________, _______________, _______________

o   D _______________, _______________, _______________, _______________, _______________

·      Risk factors for CAD:  CHAD --> C-cigarrettes smoking, H-hypertension (HTN) (>140/90), H-hypercholesterolemia, H-HDL ↓ (< 40), H-homocysteinemia, H-history of acute myocardial infarction (AMI) in a first degree relative (≤ 55 y/o for male & ≤ 65 for female), A-age (≥ 45 for males & ≥ 55 for female), D-diabetes mellitus (DM = CAD risk equivalent).

o   C _______________, _______________, _______________, _______________, _______________

o   H _______________, _______________, _______________, _______________, _______________

o   A _______________, _______________, _______________, _______________, _______________

o   D _______________, _______________, _______________, _______________, _______________

Illustration depicting atherosclerosis in a coronary artery.

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,

Micrograph of a coronary artery with the most common form of coronary artery disease (atherosclerosis) and marked luminal narrowing. Masson's trichrome.


o   Risk factors: E HONDA (a fat sumo wrestler from Street Fighter II) --> E-endocrine disease (hypothyroidism, Cushing’s disease), H-hypothyroidism, H-hepatic disease, H-hypercholesterolemia-familial, O-obese, O-OCP (oral contraceptive) use, N-nephrotic syndrome, D-diabetes melitus (DM), D-diuretic use (thiazide), A-alcoholism

Ø  E _______________, _______________, _______________, _______________, _______________

Ø  H _______________, _______________, _______________, _______________, _______________

Ø  O _______________, _______________, _______________, _______________, _______________

Ø  N _______________, _______________, _______________, _______________, _______________

Ø  D _______________, _______________, _______________, _______________, _______________

Ø  A _______________, _______________, _______________, _______________, _______________

o   Evaluation: Physical examination (copper-wire retina, bruits, ↓ pulses, xanthomas, xanthelasmas, S3, pulmonary edema, JVD), FLP (fasting lipid panel)

Xanthelasma palpebrarum, yellowish patches consisting of cholesterol deposits above the eyelids. These are more common in people with familial hypercholesterolemia.

By Bobtheowl2 at the English Wikipedia, CC BY-SA 3.0,

Two bags of fresh frozen plasma: The bag on the left was obtained from a donor with hyperlipidemia, while the other bag was obtained from a donor with normal serum lipid levels.

Coronary angiogram 

CC BY 3.0,

Treatment for coronary artery disease:

- Lifestyle changes (e.g. smoking cessation, diet, excercise)
- Medical treatment – drugs (e.g., cholesterol lowering medications, beta-blockers, nitroglycerin, calcium channel blockers, etc.);
- Coronary angioplasty and coronary stent;
- Coronary artery bypass grafting (CABG)

Drugs treatment of hypercholesterolemia:

·       Anti-lipid drugs: Hate Bad Fat N Cholesterol --> H-HMG-CoA reductase-I (STATIN), B-bile acid resin (C’s --> Colestipol/tyramine), F-fibrates (gemFibrozil, clo/beza/fenoFIBRATES), N-niacin, C-cholesterol-absorption blocker (Ezetimibe)

o   H _______________, _______________

o   B _______________, _______________

o   F _______________, _______________

o   N _______________, _______________

o   C _______________, _______________

ANGINA PECTORIS:  chest pain due to ischemia of the myocardium. 

·      Major types Stable, Unstable, Prinzmetals

o   Stable angina: Triad of 1) Substernal chest pain 2) Precipitated by exertion 3) Relief by resting or nitroglycerin

o   Unstable angina: see ACS (acute coronary syndrome)

o   Prinzmetal’s angina (aka variant angina or angina inversa):  caused by vasospasm of the coronary arteries rather than directly by atherosclerosis

·      Evaluation: Chest pain, diaphoresis, dyspnea, anxiety, N/V, light-headedness.  EKG, cardiac enzymes, stress test coronary catheter

·      TreatmentNeed to Block Cardiac Angina = NBCA --> N-nitrates (venous & coronary vasodilators), B-beta blocker (↓ myocardial work), C-calcium channel blocker, A-antiplatelets (ASA, clopidogrel), A-anti-coagulation (heparin)

o   N _______________, _______________, _______________, _______________, _______________

o   B _______________, _______________, _______________, _______________, _______________

o   C _______________, _______________, _______________, _______________, _______________

o   A _______________, _______________, _______________, _______________, _______________

Diagram of discomfort caused by coronary artery disease. Pressure, fullness, squeezing or pain in the center of the chest. Can also feel discomfort in the neck, jaw, shoulder, back or arm

Illustration depicting angina

ACS (acute coronary syndrome): 

·      Major types:

o   Unstable angina:  chest pain that is new onset or increasing or at rest

o   MI (myocardial infarction): most due to acute thrombus formation on a ruptured atherosclerotic plaque

Ø  NSTEMI (non-ST segment elevated MI)

Ø  STEMI (ST segment evlevated MI)

Ø  Transmural: endo, myo, & epicardium infarction --> ST elevation, Q-wave

Ø  Subendocardial: interior 1/3 of LV --> ST depression, no Q-wave

·      Evaluation:  Chest pain radiates to the left arm/neck/jaw, diaphoresis, dyspnea, anxiety, palpitations, N/V, light-headedness.  EKG, cardiac enzymes, stress test coronary catheter

Blockage of a coronary artery

By Unknown -, Public Domain,

Classification of acute coronary syndromes.

Blockage of a coronary artery

By Unknown -, Public Domain,

Areas where pain is experienced in myocardial infarction, showing common (dark red) and less common (light red) areas on the chest and back.

Range of myocardial infarction symptoms in women.

12 Lead ECG EKG showing ST Elevation (STEMI), Tachycardia, Anterior Fascicular Block, Anterior Infarct, Heart Attack. Color Key: ST Elevation in anterior leads=Orange, ST Depression in inferior leads=Blue

An acute STEMI involving the inferior and right ventricular wall. Reciprocal changes are seen in the anterior leads.

HTN (hypertension):

Diagnosis of HTN:

·      Elevation of BP on 2 consecutive visit at least 2 weeks apart

·      Exception:  BP >210/120

o   Primary (essential) HTN: 95% of total cases of HTN

Ø  Risk factors: Black Smoking Diabetic OG (original gangster) --> B-black race, S-smoking cigarettes, D-DM, O-old age, G-genetics

Ø  B _______________, _______________, _______________, _______________, _______________

Ø  S _______________, _______________, _______________, _______________, _______________

Ø  D _______________, _______________, _______________, _______________, _______________

Ø  O _______________, _______________, _______________, _______________, _______________

Ø  G _______________, _______________, _______________, _______________, _______________

o   Secondary HTN:  CHINKS --> C-cushing’s syndrome, C-conn’s syndrome, C-coartation of the aorta, C-contraceptive (OCP) use, H-hyperthyroidism, H-hyperparathyroidism, I-ICP (intracranial pressure) ↑, N-neuroblastoma & pheochromocytoma (both are tumors of the adrenal gland), K-kidney conditions (RAS-renal artery stenosis [fibromuscular dysplasia versus atherosclerosis]; diagnosis made with MRA & RVRR [renal vein renin ratio]; treat with angioplasty/open surgery or use ACEI with unilateral disease), S-sleep apnea.

Ø  C _______________, _______________, _______________, _______________, _______________

Ø  H _______________, _______________, _______________, _______________, _______________

Ø  I _______________, _______________, _______________, _______________, _______________

Ø  N _______________, _______________, _______________, _______________, _______________

Ø  K _______________, _______________, _______________, _______________, _______________

Ø  S _______________, _______________, _______________, _______________, _______________

o   Hypertensive urgencyBP >200/120.  Asymptomatic or mild symptoms (HA, chest pain, syncope).  Treatment: ↓ BP slowly with PO anti-hypertensive.

o   Hypertensive emergency: BP >200/120 with sign of end-organ damage (ARF-acute renal failure, altered mental status, ICH-intracranial hemorrhage, retinal damage, angina, MI, pulmonary edema).  Treatment: ↓ BP 25% in 1 hr with IV anti-hypertensive.

o   Malignant HTN: Renal failure (malignant nephosclerosis --> flea-bitten kidney) &/or encephalopathy (N/V, HA, ataxia, mental status changes, seizure) with papilledema

·      Evaluation: usually asymptomatic until complications develop.  Thorough PE including ophthalmologic (retinal changes [copper wires, AV nicking]), cardiovascular (S4, systolic click), abdominal exam (bruits), neurologic exam.  CBC, fasting blood glucose, CMP (K+,Cr,Ca++), FLP-fasting lipid panel, renal function test, uric acid level (HCTZ contraindication), EKG/CXR (detect CHF), TSH

By Mikael Häggström.When using this image in external works, it may be cited as:Häggström, Mikael (2014). &quot;Medical gallery of Mikael Häggström 2014&quot;. WikiJournal of Medicine 1 (2). DOI:10.15347/wjm/2014.008. ISSN 2002-4436. Public Domain.orBy Mikael Häggström, used with permission. - 

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

·      TreatmentShould initiate treatment with either diuretic (HCTZ) or Beta-Blocker. 

o   For pre-hypertension & stage I:  consider lifestyle therapy first (Na+ intake < 2.4 g/d, exercise) --> if still hypertensive after 3-6 months --> add 1 med

o   For stage II & III or diabetic patient with BP > 130/80: start 2 meds (thiazide & ACEI), lifestyle therapy

o   See anti-hypertensive drugs in pharmacology section.

·      Complication of HTN: SCAR (HTN will scar your blood vessels-you know it!) --> Stroke, CHF, CVA-cerebrovascular accident, Aortic dissection, RF, Retinopathy

o   S _______________, _______________, _______________, _______________, _______________

o   C _______________, _______________, _______________, _______________, _______________

o   A _______________, _______________, _______________, _______________, _______________

o   R _______________, _______________, _______________, _______________, _______________


The pericardium is a double-walled sac that contains the heart and the roots of the great vessels.  The 2 layers to this sac are the fibrous pericardium and the serous pericardium

·      PERICARDITIS: inflammation of the the pericardium. Pericarditis is further classified according to the composition of the inflammatory exudate: serous, purulent, fibrinous, and hemorrhagic types

o   Causes: DAMN TITS --> Drugs (e.g. isoniazid, cyclosporine), Dressler’s syndrome, ARF (uremia), MI, Neoplasm, Tuberculosis, Infection, Trauma, SLE

Ø  D _______________, _______________, _______________, _______________, _______________

Ø  A _______________, _______________, _______________, _______________, _______________

Ø  M _______________, _______________, _______________, _______________, _______________

Ø  N _______________, _______________, _______________, _______________, _______________

Ø  T _______________, _______________, _______________, _______________, _______________

Ø  I _______________, _______________, _______________, _______________, _______________

Ø  T _______________, _______________, _______________, _______________, _______________

Ø  S _______________, _______________, _______________, _______________, _______________

o   Evaluation: PERICARDITIS --> Phever, Positional Pleuritic chest pain (worsen in the supine position & improves with shallow breathing or leaning forward), PR depression & diffuse ST elevation on EKG, ESR ↑, Rub-friction, Inflammation of the pericardium, Cough, ↑ CRP, Anxiety, Dyspnea, Diffuse ST elevation, Thickening of the pericardium on echo supports the diagnosis, ST segment elevation on EKG.   CXR & ECHO (r/o MI/angina, tamponade, PTX-pneumothorax, EKG (low-voltage, diffuse ST segment elevation, PR segment depression)

Ø  P _______________, _______________, _______________, _______________, _______________

Ø  E _______________, _______________, _______________, _______________, _______________

Ø  R _______________, _______________, _______________, _______________, _______________

Ø  I _______________, _______________, _______________, _______________, _______________

Ø  C _______________, _______________, _______________, _______________, _______________

Ø  A _______________, _______________, _______________, _______________, _______________

Ø  R _______________, _______________, _______________, _______________, _______________

Ø  D _______________, _______________, _______________, _______________, _______________

Ø  I _______________, _______________, _______________, _______________, _______________

Ø  T _______________, _______________, _______________, _______________, _______________

Ø  I _______________, _______________, _______________, _______________, _______________

Ø  S _______________, _______________, _______________, _______________, _______________

Figure A shows the location of the heart and a normal heart and pericardium (the sac surrounding the heart). The inset image is an enlarged cross-section of the pericardium that shows its two layers of tissue and the fluid between the layers. Figure B shows the heart with pericarditis. The inset image is an enlarged cross-section that shows the inflamed and thickened layers of the pericardium.

By National Heart Lung and Blood Institute (NIH) - National Heart Lung and Blood Institute (NIH), Public Domain,

A pericardial effusion as seen on CXR in someone with pericarditis

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

Ultrasounds showing a pericardial effusion in someone with pericarditis

An ECG showing pericarditis

Diffuse ST elevation in a young male due to myocarditis / pericarditis

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

An ECG showing pericarditis. Note the ST elevation in multiple leads with slight reciprocal ST depression in aVR.

o   Treatment:  mild (viral or idiopathic pericarditis) can be followed or treated with non-steroidal anti-inflammatory drugs. Severe cases may require pericardiocentesis, antibiotics, steroids, colchicine, surgery

·      TAMPONADEfluid accumulates in the pericardium --> ↑ pericardial pressure puts significant pressure on the heart --> ↓ diastolic filling of the ventricles --> ↓ stroke volume --> ↓ CO.  The end result is ineffective pumping of blood, shock and often death

o   Risk factorspericarditis, malignancy, SLE, TB, trauma

o   EvaluationTAMPONADE --> Tachycardia, Tachypnea, Alternans & ↓ Amplitude on EKG, Must have JVD (which is an estimation of the CVP-central venous pressure), Pulsus Paradoxus (> 10 mmHg ↓ SBP during inspiration-also occur with asthma), hypOtension, Narrow pulse pressure, Distant heart sound, Diastolic pressure equalization in all 4 chambers of the heart, Echocardiography shows Enlarge heart.

Ø  T _______________, _______________, _______________, _______________, _______________

Ø  A _______________, _______________, _______________, _______________, _______________

Ø  M _______________, _______________, _______________, _______________, _______________

Ø  P _______________, _______________, _______________, _______________, _______________

Ø  O _______________, _______________, _______________, _______________, _______________

Ø  N _______________, _______________, _____________.__, _______________, _______________

Ø  A _______________, _______________, _______________, _______________, _______________

Ø  D _______________, _______________, _______________, _______________, _______________

Ø  E _______________, _______________, _______________, _______________, _______________

v Beck’s triad (hypotension, JVD, and a clear lung field) is consistent with both right RV INFARCTION  or TAMPONADE

A very large hemorrhagic pericardial effusion due to malignancy as seen on ultrasound which was causing tamponade. closed arrow: the heart, open arrow: the effusion

Add Text Here...

By Jmh649 - Own work, CC BY-SA 3.0,

o   Treatment:  IVF to expand volume and relieve hypotension.  Pericardiocentesis, pericardial window.

VALVULAR HEART DISEASEmost occur after 70 y/o except for MS, which likely to occur between 40-50’s.  Pre-antibiotic age, RHD (rheumatic heart disease) was the most commom cause.  Now the leading cause is normal wear & tear.

·      Types:  The valves in the right side of the heart are the TV (tricuspid valve) and the PV (pulmonic valve). The valves in the left side of the heart are the MV (mitral valve) and the AV (aortic valve).

o   Systolic murmur: MI AS TIPS (My ass tips!) --> MI (mitral insufficiency), AS (aortic stenosis), TI (tricuspid insufficiency), PS (pulmonic insufficiency).

o   Diastolic murmur:  The remaining valvular dysfunctions.  MS, AI, TS, PI.

o   MS & TS --> opening snap

o   AS & PS --> ejection click

This diagram shows the valves of the heart. The aortic and mitral valves are shown in the left heart, and the tricuspid and pulmonic valves are shown in the right heart.

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

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

Phonocardiograms from normal and abnormal heart sounds

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

ECG showing left ventricular hypertrophy, these findings may be present in aortic stenosis.

·      Evaluation: PE (ausculatation, JVP), CXR, EKG, ECHO

Aortic Stenosis (AS)Symptoms: SAD --> Syncope, Angina, DOE. Causes: RHD-rheumatic heart disease, bicuspid valve, calcification of AV. PE: Carotid pulse parvus et tardus.   Paradoxical splitting of S2.  Ejection click follows by a crescendo-decresendo murmur (SEM-systolic ejection murmur).  Murmur ↓ with Valsalva maneuver.  CXR: boot-shaped heart.  ECHO: Concentric LV hypertrophy, LA hypertrophy secondary to ↑ role of atrial contraction in diastolic filling --> ↓ EF. 
Ø  Associated syndrome: Heyde's syndrome, AS is associated with angiodysplasia of the colon. The stenosis causes a form of von Willebrand disease by breaking down its associated coagulation factor (factor VIII-associated antigen, also called von Willebrand factor), due to increased turbulence around the stenosed valve.

Illustration depicting aortic stenosis

By BruceBlaus - Own work, CC BY 3.0,

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&#039;s Public Health Image Library (PHIL), with identification number #848.

Simultaneous left ventricular and aortic pressure tracings to demonstrate a pressure gradient between the left ventricle and aorta, suggesting aortic stenosis. The left ventricle generates higher pressures than what is transmitted to the aorta. The pressure gradient, caused by aortic stenosis, is represented by the green shaded area. (AO = ascending aorta; LV = left ventricle; ECG = electrocardiogram.)

By derivative work: McSush (talk)Aortic_Stenosis_-_Hemodynamic_Pressure_Tracing.png: Original uploader was Ksheka at en.wikipedia - Aortic_Stenosis_-_Hemodynamic_Pressure_Tracing.png, CC BY-SA 3.0,

Aortic Insufficiency (AI): Symptoms: SAD → Syncope, Angina, DOE. Causes: idiopathic in over 80% of cases, RHD, collagen vascular disease (Marfan & Ehler-Danlos syndrome), syphilitic aortitis, aortic dissection, aging and hypertension. PE: Short diastolic blowing murmur. Soft S1 (because the elevated filling pressures close the MV in diastole rather than at the beginning of systole). ↑ pulse pressure (SBP – DBP) because regurgitant flow  DBP in the aorta. ECHO: provide 2-D views of the regurgitant jet, and measure the velocity & volume of the jet.

By BruceBlaus. When using this image in external sources it can be cited staff (2014). &quot;Medical gallery of Blausen Medical 2014&quot;. WikiJournal of Medicine 1 (2). 

Micrograph of myxomatous degeneration – a cause of aortic regurgitation.

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

o Mitral Stenosis (MS): Symptoms: HAD → Hemoptysis, Atrial fibrillation, DOE. Causes: RHD (#1), calcification of the mitral valve leaflets. PE: Opening snap → mid-diastolic rumbling murmur, sign of LHF & RHF. ECHO:  opening of the MV leaflets & blunted flow of blood in early diastole.

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

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

By, Public Domain,

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

By CDC/Dr. Edwin P. Ewing, Jr. - Public Health Image Library (PHIL) ID#: 847, Public Domain,

By Ksheka (talk) (Uploads) - Image is scanned in from measurements I made on one of my patients, with all distinguishing factors removed. Image edited by me to add color and descriptions. Ksheka 02:53, Aug 19, 2004 (UTC), CC BY-SA 3.0,

Intracardiac pressure measurements in an individual with severe mitral stenosis. Pressure tracings in the left atrium (LA) and the left ventricle (LV) in an individual with severe mitral stenosis. Blue areas represent the diastolic pressure gradient due to the stenotic valve.

Mitral Insufficiency (MI): Symptoms: HAD → Hemoptysis, Atria fibrillation, DOE. Causes: RHD, myxomatous degeneration of the mitral valve (50% of primary mitral insufficiency), myocardial infarction, MVP, Collagen vascular diseases (ie: SLE, Marfan's syndrome), drugs (e.g. fenfluramine). PE: Holocystolic murmur radiates to the axilla, sign of LHF & RHF. EKG: LAE, LVH, AF. ECHO: reveal a jet of blood flowing from the left ventricle into the left atrium during ventricular systole

Mitral regurgitation (schematic drawing)
During systole, contraction of the left ventricle causes abnormal backflow (arrow) into the left atrium.
1 Mitral valve
2 Left ventricle
3 Left atrium
4 Aorta

Transesophageal echocardiogram of mitral valve prolapse

By J. Heuser JHeuser - Own work, CC BY-SA 3.0,

·      TreatmentAlways Surgery for AS.  For remaining lesion, medications is first-line treatment (similar to CHF with DAbS + anticoagulaiton, IE prophylaxis) then consider surgery if symptoms not controlled.  Surgery: valve replacement, percutaneous balloon valvuloplasty.

Illustration of mitral valvuloplasty

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


·      Aortic aneurysmarterial dilatation.

o   Classification

Ø  1) Saccular: outpouching from an arterial wall

Ø  2) Fusiform: entier diameter of an artery grows

Ø  3) True: involves all layers of arterial wall (Intima, Media, Adventitia)

Ø  4) False: involve only adventitia

By en:National Institutes of Health -, Public Domain,

Figure A shows a normal aorta. Figure B shows a thoracic aortic aneurysm (which is located behind the heart). Figure C shows an abdominal aortic aneurysm located below the arteries that supply blood to the kidneys.

o   Thoracic aortic aneurysmThoracic aorta lies between the heart and the diaphragm.  It gives off the following branches on the left side of the body (in order): brachiocephalic artery, left commom carotid artery, left subclavian artery, bronchial artery, esophageal artery, and intercostals artery. 

Ø  Causes:  cystic medial necrosis, atherosclerosis, trauma, infection, aortic dissection (most commonly from HTN)

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

Ø  Evaluation: Most asymptomatic.  Rupture --> 1) Chest pain 2) Aneurysmal expansion compresses and erodes into trachea or bronchus --> cough &/or hemoptysis 3) Tamponade.  If aneurysm occurs close to the AV (aortic valve), it can dilate the aortic valve annulus --> aortic insufficiency.  CXR: widen thoracic aorta.  CT & ECHO: determine involvement of the AV & presence of tamponade.  Aortography: for planning operation. 

Thoracic aortic aneurysm with arrow marking the lateral border of the aorta.

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

A contrast enhanced CT demonstrating a large thoracic aneurysm of about 7 cm which has ruptured.

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

A stent graft placed in the thoracic aorta to treat a thoracic aortic aneurysm.

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

o   AAA (abdominal aortic aneurysm)Abdominal aorta lies between the diaphragm and the iliac vessels.  It gives off the following branches (in order): the celiac trunk, SMA (superior mesenteric), IMA (inferior mesenteric), renal artery, gonadal artery.  Most AAA begins distal to the renal arteries.

Ø  Causes:  95% due to atherosclerosis.  Other risk factors: trauma, infection, Marfan’s syndrome, syphilis

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

Abdominal aortic aneurysm location

Sagittal CT image of an AAA

The faint outline of the calcified wall of an AAA as seen on plain X-ray

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

By Glitzy queen00 at English Wikipedia - Transferred from en.wikipedia to Commons., Public Domain,

By Mikael Häggström, M.D.- Author info- Reusing images- Conflicts of interest:NoneMikael HäggströmConsent note: Written informed consent was obtained from the individual, including online publication. - Own work, CC0,

Aortic measurement on abdominal ultrasonography in the axial plane between the outer margins of the aortic wall.

An aortic aneurysm as seen on CT with a small area of remaining blood flow

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

Ø  Evaluation: Most asymptomatic.  Pain usually occurs with acute aneurysmal changes (enlarge, rupture).  Pain might locate in the abdomen, back, or flank and associated with diminished peripheral pulses.  US: assess size & presence of clot.  CT/MRI: gives precise location.  Aortogram:  help plan surgery

o   Treatment of thoracic aortic aneurysm and AAA:  Asymptomatic < 4 cm: may be managed with bea-Blocker and close monitoring.  > 5 cm:  25% risk of rupture in 5 years, should consider surgical repair.  Symptomatic or rupture:  emergency surgery

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Abdominal aortic endoprosthesis, CT scan, original aneurysm marked in blue

By Dr Haudebourg - Own work, Public Domain,

·      Aortic dissection:  intimal defect allows blood to penetrate the intima and enters the media layer. The high pressure rips the tissue of the media apart, allowing more blood to enter. This can propagate along the length of the aorta. The initial tear is usually within 100 mm of the aortic valve.  The aorta may rupture, leading to massive blood loss resulting in death.

Dissection of the descending part of the aorta (3), which starts from the left subclavian artery and extends to the abdominal aorta (4). The ascending aorta (1) and aortic arch (2) are not involved in this image.

By Fvasconcellos. Image:AoDissekt_scheme_StanfordB.png by JHeuser. - Adapted from Image:AoDissekt_scheme_StanfordB.png, made by JHeuser, based upon image:gray621.png and image:Fetal_circulation.png from Gray&#039;s Anatomy, CC BY-SA 3.0,

o   Causes: Most commonly due to HTN.  Also associated with trauma, Marfan’s syndrome, coartation of the aorta. 

o   Evaluation:  Sudden horrible tearing substernal chest pain radiating to the back, N/V, lightheadedness, hypotension, ↓ peripheral pulses.  If dissection into 1) Aortic root --> may compromise coronary blood supply  causing an MI 2) Mesenteric artery --> abdominal pain 3) Renal artery --> oliguria 4) Spinal blood supply --> neurologic deficit.  CXR: widened mediastinum). CT: show dessection or clot in the lumen.  Transesophageal US/MRI/Aortogram: to diagnose.

By Usmlepearls - {{own}}, CC BY-SA 4.0,

Diagnostic algorithm of aortic dissection

By J. Heuser JHeuser - own patient, CC BY-SA 3.0,

Aortic dissection on CXR: Note is made of a wide aortic knob.

Chest CT with descending (type B Stanford) aortic dissection (red circle)

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

By Dr. Lars Grenacher (, uploaded by J. Heuser JHeuser - scan courtesy of Dr. Lars Grenacher (, CC BY-SA 3.0,

MRI of an aortic dissection 1 Aorta descendens with dissection 2 Aorta isthmus

o   Treatment:  Ascending aorta dissection: require immediate surgery because risk of dissection into the aortic root.  Abdominal aortic dissection can be managed with nitroprusside & beta-blockers

·      Carotid Artery Disease:  Common Carotid Artery: right arises from the brachiocephalic artery, left from the aorta.  ICA (internal carotid artery) gives off opthalmic artery before continuing to the Circle of Willis.  Atherosclerotic occlusive disease of the carotid is a major cause of CVA (cerebrovascular accident).

Carotid Artery Disease.

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

o   Risk factors (same factors as for coronary artery disease):  CHAD --> Cigarrettes smoking, HTN (>140/90), Hypercholesterolemia, HDL ↓ (< 40), Atherosclerosis, DM.

Ø  C _______________, _______________, _______________, _______________, _______________

Ø  H _______________, _______________, _______________, _______________, _______________

Ø  A _______________, _______________, _______________, _______________, _______________

Ø  D _______________, _______________, _______________, _______________, _______________

o   Evaluation:  Symptoms result from plague rupture/ulceration/hemorrhage/thrombosis à occlude blood flow to the brain --> CVA (focal neurologic deficit, weakness, clumsiness, aphasia) or TIA (when symptoms resolve within 24 hrs).  PE:  amaurosis fugax (transient monocular blindness described as “a shade in front of the eye”) is characteristic due to opthalmic artery occlusion, carotid bruits, Hollenhorst plague on retina.  CAROTID DUPPLEX SCANNING, MRA

70 percent stenosis of the right internal carotid artery as seen by ultrasound. Arrow marks the lumen of the artery.

CT image of a 70 percent stenosis of the right internal carotid artery

o   Treatment (depends on degree of stenosis): Prevention of stroke with ASA.  Treat acute non-hemorrhagic stroke (as determined by CT) with heparin.  CEA (carotid endarterectomy) if >75% stenosis or ≥ 70% with symptoms or ≥ 50% with recurrent TIA or bilateral disease.

Section of carotid artery with plaque. Blood flows from the common carotid artery(bottom), and divides into the internal carotid artery (left) and external carotid artery (right). The atherosclerotic plaque is the dark mass on the left

By Ed Uthman, CC BY 2.0,

·      Mesenteric vascular disease (celiac trunk, SMA, IMA): 50% mortality