Ishchemic Heart Dz

(IHD)

Damage to the heart as a result of partial or complete interuption of arterial blood flow the the myocardium (most often due to atherosclerotic narrowing of the corronary arteries).

May be silent or cause as angina, MI, or chronic IHD.

Episodic chest pain caused by inadequate oxygenation of the myocardium.

The most common form of angina.

Pain is precipitated by exertion and relievied by rest or vasodilators (ex: nitroglycerin).

Can be the result of narrowing of atherosclerotic coronary vessels.

Episodic chest pain caused by inadequate oxygenation of the myocardium.

Prolonged or reccurent pain at rest.

Often indicative of an impending MI

Episodic chest pain caused by inadequate oxygenation of the myocardium.

Intermittent chest pain at rest.

Caused by vasospasm of coronary vessels.

Myocardial Infarction (MI)

General charactaristics and types of MI

A form of IHD charactarizeed by myocardial coagulative necrosis caused by coronary artery occlusion and a series of progressive gross and microscpic changes, release of myocardial enzymes and involvement of neutrophils, macrophages and fibroblasts.

Transmural MI: myocardial necrosis that transverses the entire ventricular wall.

Subendothelial MI: necrosis is limited to the interior 1/3 of the ventricular wall.

Complications of MI:

Arrhythmia(most common cause of death fro MI in the first 6 hrs)

Myocardial/Pump Failure (can lead to CHF, shock)

Myocardial Rupture (risk at 4-7 d post-MI, catastrophic)

Ruptured Papillary Muscle

Mural Thrombosis (over the infarct, may lead to emboli)

Ventricular Aneurysm (greatest risk=3-6 mo post MI)

0-6 hours post-MI

Microscpic changes occuring at this time=vascular congestion at the perimeter of the lesion.

When do neutrophils first appear around a cardiac infarct (MI)?

When do they inflitrate the lesion?

Neutrophils appear around 12 hours at sites around the lesion, the infultrate ~12-24 hours post-MI.

12-24 hrs is also when there is a slight swelling and color change in the infarct along with a microscpic loss of striations and nuclei within the lesion.

By 24 hrs post-MI

Grossly the infarct is pale or reddish-brown with surrouding hyperemia.

Microscopically there is apparent coagulative necrosis with progressive neutrophilic infiltration.

Around day 3 post-MI, macrophages begin to replace neutrophils and phagocytosis begins.

This is also when the infarct becomes increasingly yellow.

4-7 days post-MI

In this time period the infarct becomes grossly yellow in appearence with a congested yellow border.

Fibroblasts also begin to infultrate at this time, forming new vessels into the lesion.

From 10 days post-MI onward

Red, vascularized CT gradually replaces the yellow necrotic tissue and the growth of fibrovascular tissue continues.

Progressive fibrosis continues from 5 weeks on which gives the infarct a pale appearence.

3-6 months post-MI

The infarct is now a well-developed grey-white scar made of mature fibrous tissue.

Weakly + 6 hrs post-MI

Strongly + 12-16 hrs post-MI

Peaks 24 hrs post-MI and persists for 2 days.

Is negative at 3 days post-MI.

Weakly + 6 hours post-MI

Peaks 24 hours post-MI

Persists up to 7 days post-MI

Weakly + 12-16 hours post-MI

More + 24 hours post-MI

Peaks 2 days post-MI

Negative by 3 days

Not detectible until it peaks at 3 days post-MI

Persists up to 7 days post-MI

Bacterial (or sometimes fungal) in origin [S. aureus most commonly].

Endocarditis is an infection of the endocardium with prominent involvement of the valvular surface (similar to but not to be confused with Rhumatic Fever).

Charactarized by large, friable (potential to embolize), vegetations on the valves consisting of fibrin, bacteria, and inflammatory cells. Can be complicated by ulceration, valve cusp performation, chord tendinae rupture or embolism.

Caused by less virulent organisms (most often Strep viridans). Has a tendency to occur in pt with congenital heart or preexisting valvular dz.

Micro side-note: Typically caused by Strep viridans.

Occurs in SLE pt Charactarized by small vegitations on the surfaces of valve leaflets (typically of the mitral)

These rarely embolize but are useful in dx SLE at times as it is one of the most common cardiac manifestations of SLE.

No

Even porsthetic valves are subject to physical deterioration, can be a site of thrombus formation or endocarditis.

Valves, both endogenous and prosthetic, can cause mechanical stress on RBC resulting in hemolytic anemia and schistocyte formation.

The most frequent valvular lesion*

Often in young women, can also be a feature of Marfan's.

Charactarized by myxoid degernation of the ground substance of the valve, the posterior valve leaflet stretches genreating a parachute deformity (floppy valve). Valve then slips into the atrium druing systole.

Late Systolic murmmur with a midsystolic click*

Typically benign, can be associated w/ arrhythmias, can cause mitral insufficency, and can predispose to endocarditis.

Tricuspid.

Rarely involved in rhumatic fever, though can be inovovled in endocarditis Carcinoid syndrome.

Frequently involved (w/mitral) in rhumatic heart dz and infective endocarditis.

Stenosis: often presents as calcific aortic stenosis with calcification being caused by age-related change (degenerative calcific arotic stenosis), congenital bicuspid valve, or a valve affected by RHD (often causes valve leaflet fusion).

Insufficency: Can be caused by a non-dissecting aortic aneurysm as the result of cystic medial necrosis, RHD (ususally w mitral valve dz), or Syphilitic/Leutic aortitis (w dialation of the aortic valve ring).

What congenital defect is associated with Turner's Syndrome?

With Marfan's Syndrome?

With Down Syndrome?

Turner's Syndrome is associated with coarctation of the aorta.

Marfan's syndrome pt are predisposed to aortic dissection and, to a lesser extent, to mitral valve prolapse.

Down syndrome pt (as well as some other trisomies) often have endocardial cushion defects, atrial and ventricular septal defects and valve deformities.

A constillation of fetal defects that can appear in infants whose mother had rubella during her first trimester.

Includes congenital cardiac defects, microcephaly w/ mental retardation, deafness, cataracts and growth retardation.

When there is a failure to sever the fetal connection between the pulmonary and aortic vessels (which allows the fetal blood to bypass the lungs).

Has been associated with living in high altitudes.

Can be closed after birth either pharmacologically (administration of Indomethacin, an NSAID which inhbits production of the prostaglandins keeping the ductus patent) or surgically.

If not closed, can lead to pulmonary HTN, R vascular hypertrophy, reversal of blood flow and late cyanosis.

Atrial Septal Defects

(ASD)

Can take several forms:

patent foramen ovale (usually insignificant), septum primium (lower part of the septum, can also have valve defects), septum secundum (defect in fossa ovalis), sinus venosus (upper septum near entrance of SVC) or Lutembacher syndrome (ASD+ mintral stenosis, often of rhumatic origin).

Clinical presentation often not until adulthood. Pt present with pulmonary HTN, reversal of flow leading to cyanosis, possible paradoxical embolism (venous).

Can be accompanied by a systolic ejection murmur.

Ventricular Septal Defects

(VSD)

Vary in size.

Small may close spontaneously while larger defects may lead to pulmonary HTN and eventual right sided heart failure. Reversal of flow with late cyanosis may also occur.

Can be accompanied by a pan/holosystolic murmur.

1) stenosis (pulmoanry infundibular or valvular)

2) VSD

3) Overriding aorta

4) Right ventricular hypertrophy.

Can cluster in families.

Cyanosis from birth, R to L shunting.

Pt often squat to lessen the effects of this shunting.

Narrowing of the aorta, ususally distal to the origin of the subclavian arteries.

Pt will have extensive development of collateral circulation with dialtion of the intercostal arteries (notching of ribs seen on XR).

Pt have HTN ltd to the upper extremities.

Associated notibly with Turner's Syndrome.

Aorta arises from the R ventricle and pulmonary artery from the L.

Incompatible with life unless there is a compensitory anomaly such as a patent ductus arteriosus which allows adequate oxygenation of tissues.

The most common form of cardiomyopathy (non-inflammatory dz of the herat muscle). Unknown etiology but has been linked to alcholism, thiamine deficiency (Beriberi heart) or prior myocarditis.

Charactarized by 4 chamber hypertorphy and dilation and by R and L sided complex heart failure.

Non-inflammatory dz of the heart muscle that is caused by infiltrative processes within the myocardium which result in stiffening of the heart muscle, impairing its pumping function.

Classic example of restrictive cardiomyopathy is in cases of Cardiac Amyloidosis (may result in bilateral heart failure).

May be inherited (AD)

Non-inflammatory dz of the heart muscle charactarized grossly by hypertrophy of all the walls of the 4 heart chambers, particularily of the ventricular septum (known as asymmetrical septal hypertrophy).

Microscopically, hypertrophic cardiomyopathy is charactarized by disoriented, tangeled and hypertophied myocardial fibers.

May result in LV outflow obstruction which may lead to syncope or even sudden death (as in unexpected deaths of young athletes).

Inflammation of the heart muscle.

Often prevents as biventricular heart failure in relatively young persons.

Most often is viral in origin (w Coxsakievirus being the most common cause).

May be a component of Chegas Dz (in S America, caused by the protozoan T. cruzi)

Charactarized by diffuse myocardial degeneration and decrosis with inflammatory infiltrate.

Acute

Serous (associted with viral infections, RF, SLE. Clear or straw-colored exudate, few inflammatory cells).

Fibrinous/Serofibrinous (may be caused by uremia, MI, ARF. Fibrin-rich exudate).

Purulent/Suppurative (Almost always bacterial in origin, cloudy, purulent exudate).

Hemorragic (from tumor invasion of the pericardium or TB, bloody inflammatory exudate).

Chronic

aka Constrictive Pericarditis: Usually caused by TB or pyogenic staphylococcal infection. Charactarized by thickening and scarring of the pericardium (fibrosis, calcificiation), loss of elasticity and symptoms mimicing R heart failure.

Rhabdomyoma (benign tumor of striated muscle, typically in young children).

Is not the most common cardiac tumor (that is a Myxoma of the LA, a tumor of the primitive CT most common in adults).

Causes: IHD (MI), HTN, Valvular Dz (aortic and mitral), myocardial dz (cardiomyopathies, myocarditis).

Clinical Manifestations: Dyspnea and orthopnea (due to pulmonary congestion/edema)* Pleural effusion w hydrothorax can result.

↓ renal perfusion causing actvation fo the Renin-AT system (leading to salt and water retention).

Causes: L-sided HF (most commonly)*

L-sided lesions such as mitral stenosis.

Pulmonary HTN (often due to chronic lung dz, cor pulmonale).

R-sided valve failures, cardiomyopathy, myocarditis.

Clinical Manifestations: Renal hypoxia leading to more fluid retention and edema than in L sided HF (often manifests first as pitting edema of the ankles) can lead to pleural effusion, hydrothorax (L or R) or ascites.

Organomegly, nutmeg liver.

Distention of the neck veins.

Causes: LV failure, chronic lung dz, mitral valve dz (?), congeinital heart dz w L to R shunt.

Cor Pulmonale

Heart issues that are caused by lung issues.

RV Hypertrophy and/or dilation secondary to lung dz or primary to dz of the pulonary vasculature (as in pulmonary HTN).

Frequently caused by emphysema.

Acute Cor is charactarized by dilation of the RV while chronic conditions lead to hypertrophy of the RV.

A general term for vascular dz charactarized by sclerosis (rigidity) and often by thickening of the blood vessels.

Three Types:

Mockenberg Arteriosclerosis (median calcific sclerosis), Arteriolosclerosis (hyline and hyperplastic)

and Atherosclerosis.

aka Medial Calcific Sclerosis

Involves the media of medium muscular arteries (most often the radial and ulnar) and typically in people 50+ y/o.

Charactarized by ring-like caclifications in the media of arteries that does not obstruct flow (intima is not involved). Results in calcific, pipe-like arteries.

Individuals with Mockenberg may also have atherosclerosis but they are unrelated in cause/course.

Hyaline thickening or proliferative changes in small arteries and arterioles.

Especially the renal vessels.

Typically associated with HTN or DM.

Two Types:

Hyaline Arteriolosclerosis: Charactarized by hyaline thickening of arteriolar walls.

Called benign nephrosclerosis in the kidneys (associated w/ HTN).

Hyperplastic Arterolosclerosis: Charactarized by concentric, onion skin thickening of arteriolar walls.

May be accompanied by necrotizing arterilitis (deposition of fivrinoid material in teh walls of the arterioles and the resulting vasuclar inflammation and necrosis).

In kidneys is called Malignant Nephrosclerosis and is associated w/ malignant HTN.

Charatarized by atheromas (fibrous plaques) in the intima.

Frequently in the proximal coronary arteries, branches of the carotid, circle of Willis, large vessels of the lower extremities, renal and mesenteric arteries.

May be complicated by Ulceration, hemorrage, calcification, thrombus formation at the site of the plaque (obstruction of the vessel), aneurysm formation, embolization of the overlying thrombus or plaque itself.

Often leads to IHD/MI, the most common cause of death in the US.

Also to stroke, ischemic bowel dz, renal ischemia, etc...

Plaques that form on the walls of vessels and are charactaristic of atherosclerosis.

Have a central core of cholesterol/cholesterol esters as well as foam cells, calcium, and necrotic debris.

Core is covered by a subendothelial fibrous cap made of smooth muscle cells, more foam cells, fibrin, and ECM proteins.

Can develop from a Fatty Streak, a lesion charactarized by focal accumulations of lipid-laden foam cells as well as lipid-laden smooth muscle cells in the subendothelum (intima) of vessels.

Appear in children and commonly in the aorta. Do not ness become atheromas but can.

Age,

Male Sex,

Hypercholestrolemia (high LDL:HDL ratio [should be 4:1], high absolute LDL, low HDL),

HTN,

Diabetes, and

Cigarette smoking.

Possibly obesity, inactivity, hyperuricemia, and using oral contraceptives.

A dz of the aorta associated with tertiary syphillis.

Begins as inflammation of the aortic adventitia (namely the vasa vasorum) which leads to hyperplasia of the vasa vasorum which restricts blood flow to the aortic vessel itself. Results in ischemia of the outer 2/3 of the aortic wall. Aortic fibers become patchy and necrotic with the necrosis of sm. muscle cells.

Charactarized by the presence of Plasma Cells*

These events weaken the aortic wall leaving it highly succeptible to aneurysm: Syphilitic/Luetic Aneurysm of the Ascending Aorta.

Abnormal dilation of either arteries or veins which can errode into adjacent structures, dissect (separate the layers of the wall resulting in a psudoaneurysm) or rupture.

* Be sure to understand the differences between an aneurysm, psudoaneurysm, dissection and rupture*

Most dissecting aneurysms are seen in pt with poorly controlled HTN***

An aneurysm arising in a large artery, as a result of weakening of the wall in severe atherosclerosis.

Occur (typically) in the descending/abdominal aorta and are saccular in shape*

A loss of elastic and muscle fibers in the media of the ascending aorta with accumulation of mucopolysaccharide and sometimes the formation of cyst-like spaces bw the fibers.

Pt with cystic medial necrosis are highly predisposed to developing aneurysms of the aortic root/ascending aorta.

This condition may be inherited.

Is commonly seen in Marfan's pt.

Small, saccular lesions seen in the smaller arteries of the brain, particularily in the Circle of Willis and at points of arterial bifurcation.

Unrelated to atherosclerosis.

The most frequent cause of subarachnoid hemorrages*

aka Syphillitc aneurysm

In the ascending aorta as a result of meidal necrosis of the aorta secondary to tertiary syphillis.

May widen the aorta to the point where it widens the aortic ring leading to aortic insufficiency and an early diastolic murmur.

aka dissecting hematoma

A longitudinal intraluminal tear within the wall of a blood vessel which allows blood to move between the layers of the vessel wall creating a hematoma or psudoaneurysm.

Typically occur in the wall of the ascending aorta forming a second arterial lumen within the media.

Aortic dissections cause tearing chest pain that is often mistaken for an MI, however, cardiac enzymes are normal.

Typically associated with HTN and/or cystic medial necrosis. Has no relationship to atherosclerosis.

Very often results in aortic rupture causing hemopericardium an dfatal cardiac tamponade.

Benign vascular malformations.

Small vessels are dilated and surrounded by fine, radiating channels. Typically occurs in superficial vessels of the skin an mucous membranes.

Assoc with hyperestrinism (seen in chronic liver dz and in pregnancy).

aka Osler-Weber-Rendu Syndrome

Autosomal Dominant (AD)

Characterized by locaized dilation and convolution of the venules and capillaries of the skin and mucous membranes.

Often complicated by epistaxis (nose bleeds) and GI bleeding.

Sometimes called just an 'angioma'

A tumor/malformation of a larger vessel which is composed of channels filled with blood.

Is the most common tumor of infancy.

Responsible for "port-wine stain" birthmarks.

Capillary Hemangiomas consisit of a tangle of tightly packed capillary-like channels in the skin, liver, lips, kidneys etc...

Cavernous Hemangiomas consist of large cavernous vascular spaces in teh skin, mucosal surface,s and internal organs (pancreas, liver, spleen, brain).

Can occur as a component of vonHippel-Lindau Dz (AD, marked by hemagioblastomas, adenomas and a predisposition for the development of renal cell carcinomas).

A rare tumor of the glomus bodies (temp sensory structures mostly in the finger tips and toes).

Benign but painful, typically subungal (below the nails)

A cavernous lymphangioma (lymphatic malformation).

Occur typically in the nec and axilla.

Malignant vascular tumors are rare.

Hemangioendotheliomas (bw an angiosarcoma and hemangioma),

Hemangiopericytoma (arises from pericytes),

Hemangiosarcoma/Angiosarcoma a malignant tumor of the endothelial cells lining blood vessels. Can occur in the skin, musculoskeletal system, breast or liver. Associated with exposure to arsenic and PVC*

Karposi Sarcoma (KS)

A malignant vascular tumor.

Several forms:

Classic KS: affects older men of Ashkenazi Jewish or Mediterranian descent.

Endemic/African KS: affects young African men and children, accounts fro 10% of all cancers in Africa.

Epidemic KS: is a component of aids and is in part related to infection with KS herpesvirus (HH8). Can be a feature of other immunosuppresive states.

Vasculitis Syndrome

Charatarized by necrotizing immune complex inflammation of small and medium-sized arteries.

Results in destruction of the arterial media and internal elastic lamella which results in the formation of aneurismal nodules.

Manifests clinically with fever, weight loss, malaise, abdominal pain, myalgia and HTN.

ANCA negative*

Can be assoc with Hep B viral infection.

Typical sites of PAN:

- Kidneys (immune complex vasculitis in the arterioles and glomeruli leads to renal failure and HTN, the cause of most PAN-related deaths).

- Coronary arteries (resulting in CAD)

- Musculoskeletal system (myalgia, arthralgia)

- GI tract (abdominal discomfort)

- CNS, PNS, Eye, Skin

aka Allergic Granulomatous Angiitis

Necrotizing vasculitis (related to PAN).

Charactarized by prominant involvement of the Pulmonary vasculature, marked peripheral eosinophilia and a clinical presentation similar to asthma*

aka Hypersensitivity Vasculitis (so-called because exogenous antigens may precipitate this disorder)

A group of immune complex-mediated vasculitides charactarized by acute infammation of small vessels.

These multiple lesions tend to be of the same age (a factor distinguishing this disorder from PAN).

Clinical Manifestation: palpable purpura when the skin is involved, but any site can potentially be involved. Also presents as distinctive clinical syndromes (incl Henoch-Schonlein purpura and serum sickness).

A clinical syndrome, one way that leukoclastic vasculitis can present.

Most common in young children.

Can be poststreptococcal or be assoc with an antecedent URI.

Charactarized by hemorragic urticaria of the extensor surfaces of the arms, legs and buttocks.

Fever

Arthralgia

GI and renal invovlemnt possible.

A possible clinical presentation of Leukoclastic Vasculitis

Systemic deposition of Ag-Ab complexes (particularily in the heart, joints and kindeys).

Unknown etiology.

Charactarized by necrotizing, granulomtous vasculitis of the small and medium sized vessels of the respiratory tract (and sometimes kidneys and other organs).

Fibrinoid necrosis of the small arteries and veins occurs: Early infultration of neutrophils followed by macrophages then fibroblasts. Formation of granulomas with giant cells is prominant.

Clinical presentation is dominated by Respiratory Tract signs/symptoms. Issues of the paranasal sinuses, lungs, and necrotizing glomerulonephritis are often present.

C-ANCA Positive*

Systemic vasculitis in medium to large sized arteries charactarized by granuloma formation and neutrophil/eosinophil/macrophage infultration and elevated ESR*

2 Types:

Temporal Arteritis

Takaysu/Pulseless Arteritis

The most frequently occuring form of giant cell arteritis, often in the elderly.

Typically affects branches of the carotid artery (often the temporal artery, hence name).

Clincal Manifestations

Malaise, fatigue, jaw weakness, loss of pulse and nodules along the involved artery,

polmyalgia rhumatica

(muscle and periarticular pain + am stiffness).

Elevated ESR*

aka 'Pulseless Disease' or Aortic Arch Syndrome

The less frequently occuring form of giant cell arteritis.

Charactarized by inflammation and stenosis of large arteries (the aortic arch is frequently involved).

Clinical Manifestation = Absent pulses in the carotid, radial or ulnar arteries.

Nonspeficic findings (fever, night sweats, myalgia, skin nodules, arthritis etc...)

Elevated ESR*

aka Mucocutaneous Lymph Node Syndrome

An acute, self-limited necrotizing vasculitis of small/medium vessels occuring in infants and young children.

Clinical Manifestation= Strawbery Tounge* (hemorragic edema of the conjunctivae, lips and oral mucosa), Cervical lymphadenopathy, and fever.

Most serious complication= Coronary artery vasculitis leading to aneurysm of the coronary artery

aka Thromboangiitis obliterans

Acute inflammation of the small/medium arteries of the lower extremities with involvement of adjacent veins and nerves* resulting in painful ischemic dz.

A disease of SMOKERS.

Rare granulomatous vasculitis charactarized by infiltration by atypical lymphocytoid and plasmacytoid cells.

This condition can progress from an inflammatory one to a lymphoproliferative neoplasm (most often a T-cell non-Hodgkin lymphoma).

Both manifest by recurrent vasospasm of small arteries/arterioles resulting in pallor/cyanosis of the fingers and toes, often precipitated by cold temps.

Raynaud Disease is a condition onto itself, commonly occuring in young, otherwise healthy women.

Raynaud Phenomenon is clinically similar to the dz but is always secondary to an underlying disorder, most commonly SLE or Scleroderma.

90-95% of all cases of HTN are Essential HTN

Causes: Unknown etiology (that's why it's essential!)

Risk Factors: Fm Hx of HTN, African descent, high dietary sodium intake, stress, obesity, cigarette smoking etc...

Results: Can lead to retinal changes, LV hypertrophy,, cardiac failure and benign nephrosclerosis.

Predisposes to ischemic heart dz/MI and/or stroke.

Only accounts for ~5% of cases of HTN

Causes:

- Renal Dz (most common, disorders of the parenchyma, renal artery stenosis)-triggers Renin-AT system.

- Diabetes (complicated by diabetic glomerulosclerosis)- triggers Renin-AT system.

- Endocrine disorders

     * Conn Syndrome (excess aldosterone)

     * Acromegaly

     * Cushings (excess cortisol)

     * Pheo (excess Epi/NE)

     * Hyperthyrodism

- Coarctation of the aorta (upper body HTN only, development of intercostal collateral circulation)

- Drugs: Amphetamines and Steroids

- Toxemia of pregnancy

- Toxic substances (Lead, Cadmimum)

Consequences are essentially the same as essential HTN with whatever additional consequences the causative dz has.

Can be a complication of either essential or secondary HTN. Occurs in less than 5% of pt w HTN and most often in young, AA males.

Accelerated clinical course involves a marked ↑ in diastolic bp, retinal hemorrages, papilledema, LV hypetrophy and LV failure.

Causes Malignant Nephrosclerosis:rupturing of arterioles/glomerular capillaries results in petechial hemorrages on the kidney surface "flea-bitten kidney" and congestion results in swelling of the kidney. Hyperplastic arteriolosclerosis affects both the glomeruli and the arterioles leading to renal failure.

Typically results in early death from CHF, stroke or renal failure.

Plays an vital role in the development of HTN secondary to renal disease.

JG cells respond to ↓ vascular tone by secreting Renin which converts angiotensinogen to AT-I which is further converted to AT-II (by ACE).

AT-II acts as a vasoconstrictor and an activator of aldosterone (both of which act to raise bp).

Vasoconstriction increases vascular resistance and aldosterone increases blood volume by promoting Na+/H2O retention.

Caused by: Aortic/Pulmonic Stenosis or ASD

Best Heard: Aortic/Pulmonic areas

Style: Crecendo-Decrecendo

Caused by: Mitral/Tricuspid Regurgitation or VSD

Best Heard: Apex, 4th intercostal space, midclavicuar (mitral), L 3-4th intercostal space (tricuspid and VSD)

Style: Pansystolic...

Caused by: Mitral Valve Prolapse

Best Heard: Apex (4-5th intercostal space, midclavicular)

Radiates to the axilla.

Style:No shape but begins half way through systole.

Caused by: Aortic or Pulmonic Regurgitation

Best Heard: R 2nd intercostal space (Aortic) or L 2nd intercostal space (pulmonic)

Style:Decrecendo, out by mid diastole.

Caused by: Mitral Stenosis

Best Heard: Apex (4-5th intercostal space, midclavicular)

Style:small silence post-S2 then decrecendo out with a slight crecendo just prior to S1.