Amaurosis fugax

Sudden blindness due to embolization to the retina.  Can see Hollenhorst spots on fundoscope

Cystic Medial Necrosis

(4 causes)

Degeneration of the media layer of the vascular wall.  Predisposes to aneurysm formation

Seen in:

1. Normal degeneration with age

2. Pregnancy

3. Bicuspid aortic valve

4. Marfan Syndrome

Difference between true and

pseudo-aneurysm

A true aneurysm is an outpouching of a blood vessel that includes all three layers of the vessel wall.  Can be serpentine (ectasia), balloon like (saccular), or sausage shaped (fusiform). 

A pseudoaneurysm forms via a hole in the vessel wall which clots.  A fibrous tissue grows over the clot and when the clot is lysed, the hollowed area fills with blood, but is not lined by the walls of the vessel

Risk Factors for

Abdominal Aneurysm

(and thoracic)

Atherosclerosis (due to weakening of wall), genetic predisposition, inflammation (especially in vasculitides including Takayasu's Arteritis), and infection.  

Thoracic aneurysm risk is also greatly increased by increased pressure from blood being ejected from the heart, especially in volume overloaded states like aortic regurgitation (of secondary to bicuspid valve)

Popliteal Artery Aneurysm

Risks

A popliteal artery aneurysm will very very rarely rupture, but will commonly form thromboses, which can embolize down the leg and result in necrosis/gangrene

Etiology and Pathology of

Aortic Dissection

Tear in the wall of the aortic arch, with formation of a false lumen.  If there is a true rupture, death occurs immediately.  If the tear occurs proximal to the great vessels the blood is contained within only a thin layer of adventitia (Proximal/Early rupture dissection) and has a poor prognosis. 

A less severe case is if the dissection takes place distal to the great vessels (distal/slow enlargement dissection) with the blood usually well contained because of the relatively decreased pressure there

MRI and CT are best for visualization of the two lumens, though echo could be used as well

Predisposing Factors for

Non-Bacterial Thrombotic Endocarditis

Turbulent flow (secondary to valvular abnormality, increased pressure gradient), mechanical damage (R heart commonly from IVDU, L heart commonly from catheter), ventricular septal defect (NBTE at point on wall where jet strikes), malignancy, TB, collagen vascular disease

Bacteria must be able to be transported to the site and be able to adhere, Gram positives tend to be best

Differences Types of

Native Valve Endocarditis

Community acquired NVE - Symptoms of endocarditis within 48 hrs in hospital, without extensive contact with health care system

Health care associated NVE - Symptoms of endocarditis within 48 hrs in hospital, and has had extensive out of hospital contact with health care system

Nosocomial acquired NVE - Patient develops symptoms of NVE >48 hrs after entering hospital

Spectrum of Bacteria in

Prosthetic Valve Endocarditis

Early PVE - Early PVE requires that the bacteria be present with insertion of the valve and is defined as developing endocarditis within 60 days of surgery.  Bacteria involved are atypical and include skin organisms (eg S. aureus), fungi, enterococci, and others

Late PVE - Very similar to NVE, with symptoms developing >60 days post-operatively and organisms similar to those seen in NVE

Important Pathogens in

Infective Endocarditis

Strep viridans

Enterococci

S. aureus

Coagulase Negative Staph

HACEK

Fungi (almost exclusively in Early PVE)

S bovis (use colonic lesions as portal of entry)

4 Groups that should take

Antibiotics prophylactically before dental surgery

(for endocarditis)

1. Those with prosthetic valves

2. Those who have had endocarditis before

3. Those with pre-existing valvular pathology

4. Transplant Patients

Should get it not only in (bleeding) dental surgery but also in skin surgery (to avoid S. aureus).  Most therapy targets Strep viridans

Duke Criteria of Diagnosing

Infective Endocarditis

(2 Major + 5 Minor)

1. Cultured bacteremia with appropriate organism

2. Visualization of lesion with Echo

1. Fever

2. Predisposing heart disease

3. Vascular Phenomena (emboli, peripheral stigmata)

4. Immunological phenomena (glomerulonephritis, encephalopathy)

5. Positive blood culture not meeting criteria of appropriate organism

Immunological and Vascular Sequelae

of Infective Endocarditis

Emboli are common manifestations due to breaking of pieces from the lesion.  Emboli can be bland (no infected material) which can cause stroke, claudication etc; or can be infected (contain infective material) which can not only cause occlusion, but can also cause abscesses (must be drained)

The most common immunological manifestions are IC deposition in the glomerulus (glomerulonephritis) or the brain (encephalopathies) resulting in behavioral changes

5 Peripheral Stigmata of

Infective Endocarditis

1. Janeway lesions - Purpuric plaques on palms and soles

2. Osler's Nodes - Tender papules on the pads of the fingers (come and go)

3. Roth Spots - Light spots in fovea

4. Subconjunctival petechiae - Red spots in white of eye

5. Splinter hemorrhages - Seen in nails and on tips of fingers

Treatment of Endocarditis

It is essention to treat infectious endocarditic aggressively with a cidal antibiotic for an extended period in order to ensure elimination of the organism.  Valve replacement can be done if the damage is extensive. 

Abscesses in the heart and other parts of the body (where infected emboli have been showered) must also be drained

Causes of Pericarditis

Infectious MCRUNTD

Infectious causes (most commonly viral, but also TB), post MI, Collagen vascular disease, post Radiation, Uremia, Neoplasia, Traumatic, Drug-induced

5 Types of Pericarditis

(differences/causes)

Differentiated by content of fluid present

1. Serous - Relatively few cells, small cells

2. Serofibrinous - Most common form, many etiologies, rough appearance with scarring

3. Hemorrhagic - Containing blood, typically TB or neoplasia

4. Caseous - Containing a caseous focus, only in TB

5. Purulent - Containing pus, in any infective pericarditis

Characteristic Clinical Presentation

of Pericarditis and Test Findings

Commonly have low grade fever and sharp chest pain that is slightly relieved by leaning forward.  A pericardial friction rub is heard in both systole and diastole, though it may be absent if there is significant effusion.  Dyspnea is also common, but due to pain with inspiration because of pericardial irritation

The ECG has a characteristic concave-up ST elevation (distinguishable from STEMI) and echo may show effusion if present.  Other diagnostic tests include testing for potential causes

Etiologies of Pericardial Effusion

1. Any type of pericarditis

2. Block of lymph drainage

3. Cirrhosis - secondary to decreased albumin

4. CHF

5. Aortic dissection with rupture into pericardium

6. Malignancy

Clinical Presentation of Pericardial

Effusion and Tamponade

Effusion will typically be asympomatic unless it is accompnanied by tamponade.  Chest pain, dyspnea, dysphagia (due to pressing on espophagus), hoarseness and hiccups possible.  Heart sounds will be muffled, and pericardial rub typically not heard. 

There will commonly be a pulsus paradoxus (due to greatly exagerrated decrease in ventricular filling potential during inspiration because of effusion pressure)

Distinguishing Constrictive Pericarditis

from Restrictive Cardiomyopathy

CP - Results from fusion of the two layers of pericardium, and will typically have calcifications and a thick pericardium.  Also, LV and RV pressures will typically be equal

RC - Congenital stiff myocardium that manifests as a diastolic defect.  Does not have thickened pericardium or calcifications and LV pressure typically greater than RV.

Clinical Presentation of

Constrictive Pericarditis

Patients will typically present with pulmonary edema as well as peripheral edema secondary to decreased filling of the ventricles.  In order to distinguish from other disease, look for Kussmaul's sign:  JV will distend with inspiration (should go away due to increased flow into RA, but it has nowhere to go).

There is typically a pericardial knock following S2 and there is no pulsus paradoxus because there isn't enough blood in the right heart to displace the septum

Volume overload will lead to _____ hypertrophy

Pressure overload will lead to _____ hypertrophy

Eccentric - Increase in myofibers in series with existing ones resulting in increased volume of the cavity.  Occurs in LV in response to aortic regurgitation, mitral regurgitation, and states with high circulating volume

Concentric - Increase in myofibers in parallel with existing ones resulting in increased ventricular thickness, and better contractility.  Occurs in response to aortic stenosis most commonly. 

Collagen in Ventricular

Remodeling

Collagen Type I is a major component of the ECM in normal cardiac tissue and has excellent contractility and elasiticity

Ventricular remodeling leads to deposition of collagen type III which is significantly stiffer and results in increased filling pressures/contractile pressures.

Dystrophins and the Cardiac

Extracellular Matrix

Proteins that connect the working fibers of the myocardium to the extracellular matrix for force transmission.  Defective dystrophins result in defective force, and resulting heart failure.

Myocardial Fibrosis

Structure of Semilunar and

Atrioventricular Valves

Semilunar valves include the pulmonic and aortic valves which have three cusps.  The semilunar valves are entirely avascular. 

AV valves include the the mitral and tricuspid.  The anterior leaflets of each valve are the largest, and the lower 2/3 of the valves are avascular.  The posterolateral papillary muscle holding the mitral valve is especially susceptible to rupture secondary to MI

Normal Pressures in the

Cardiac Chambers

RA - 1-5mmHg

RV - 1-5mmHg, 15-30mmHg

LA - 5-15mmHg

LV - 5-15mmHg, 100-120mmHg

Acute, Chronic Compensated

and Chronic Decompensated Volume Overload

Acute volume overload typically results from papillary muscle rupture, with blood flowing backward and overloading the ventricles, which do not have time to compensate

Chronic compensated volume overload typically occurs with mitral prolapse or aortic regurgitation, with the ventricle responding with eccentric hypertrophy

Chronic decompensated volume overload occurs after ventricular remodeling can no longer compensate and systolic heart failure (with impaired forward flow results)

Clinical Presentation and Effects

of Mitral Regurgitation

Can cause acute or chronic volume overload depending on mechanism of regurgitation.  Systolic dysfunction due to acute overload or chronic decompensated overload (increased diastolic filling) can result with decreased forward flow. Commonly causes pulmonary edema and dyspnea.  This could back up to cause RHF

Physical exam will reveal a holosystolic murmur with resonance to the apex

Etiologies of Mitral Regurgitation

I CREPPD because of my mitral regurgitation

Congenital, Rheumatic heart disease, infective Endocarditis, Papillary muscle rupture, mitral valve Prolapse (common myxomatous degeneration of the valve), Dilatation

Treatment of Mitral Regurgitation

Treatment of volume overload is typically an initial first line treatment for a chronic compensated regurgitation and use of an ACE inhibitor can prevent further remodelling. 

Acute overload and chronic overload with depleted ejection fraction or distinct ventricular enlargement should be treated with valve replacement.  Mechanical valves tend to last longer but require anti-coagulation therapy (can't get pregnant) while bioprosthetics don't require use of anti-coagulants

Mitral Valve Prolapse

Extremely common myomatous degeneration of the mitral valve, being the most common cause of mitral regurgitation.  Leads to chronic compensated (eventually decompensated) volume overload.  Severe mitral prolapse seen in Marfan Syndrome

Easily diagnosed with echo and doppler

Etiologies and Clinical Manifestation

of Aortic Regurgitation

You will hear a DCRESCD murmurwith Aortic Regurg

Diet pills, Connective tissue disorders, Rheumatic heart disease, Endocarditis, Senile calcific degeneration, Congenital, Dilatation

Commonly hear hammer pulse with wide pulse pressure

Etiologies and Treatment of

Pulmonic Regurgitation

Almost exclusively caused by annular dilatation secondary to pulmonary hypertension. 

Generally does not require treatment, though diuretics can be used to relieve pulmonary edema

Etiology and Pathophysiology of

Aortic Stenosis

Pressure overload in the LV resulting in concentric hypertrophy, eventually leading to impaired diastolic filling.  Characteristic is a harsh, loud, diamond-shaped systolic ejection murmur

Etiologies include more turbulent flow across the valve or rheumatic heart disease. Diastolic heart pressure can develop.  Valvular replacement of the valve is almost always necessary.  Cracking the stenotic valve is not suggested because pieces can come off and cause embolism

Etiology, Pathophysiology and Treatment

of Mitral Stenosis

Most commonly caused by rheumatic heart disease and is the most commonly involved valve.  There is generally atrial dilatation and resulting pulmonary edema that can back up to the right heart.  Dyspnea/chest pain are common manifestations. 

Typically, an opening snap is heard after S2 with a low pitched rumbling. 

 Opening with percutaneous valvuloplasty is the treatment of choice

Risk Factors for Dilated

Cardiomyopathies

You're at risk if you see a CHIC FISH AD

Collagen vascular disease, Hypothyroidism, Infection (coxsackivirus), Chemotherapy, Familial, Idiopathic, Sarcoidosis, Hypocalcemia/phosphatemia, Alcohol abuse, Dystrophy

Risk Factors for Hypertrophied

Cardiomyopathies

A common valvulopathy associated with

hypertrophic cardiomyophathies is ______

Mitral regurgitation due to thickening of the ventricular septum putting the anterior leaflet in close contact with the septum.  This draws the septum toward it during systole which not only allows flow back into the LA, but also blocks outflow from the LV

Risk Factors for Restrictive

Cardiomyopathy

Having this makes you want to MASH FIGS

Metastases, Amyloidosis, Sarcoidosis, Hemochromatosis, Fibrosis, Idiopathic, Glycogen storage disorder, Scleroderma

Effects of Angiotensin II

(and mechanisms)

VORSCRAP

Vasoconstriction, Oxidative stress, Retention of sodium and water, increased Sympathetic activity, Cell growth, Remodeling of the ventricles and vasculature, Activation of platelets, Proteinuria

Renin is released in response to low perfusion of the kidneys.  This converts angiotensinogen to angiotensin I.  ACE then converts this to AngII which acts on Angiotensin 1 receptors to mediate above

[image]If curve 1 represents the normal P-V curve, curves 2 and three are representative of hearts with increasing ________

This is commonly a result of ______

Preload

Commonly a result of increased circulating volume, or pathologically to valve insufficiency resulting in increased filling

[image]If curve 1 represents a normally functioning heart, curves 2 and 3 represent progressively increasing ____

This can be commonly caused by ____ and will typically lead to _______

Afterload

Commonly caused by hypertension, aortic stenosis

Results in pressure overload with concentric ventricular hypertrophy and diastolic dysfunction heart failure

[image]If curve 1 represents normal heart, curve two represents a heart with increased _______

This typically occurs due to _____

Contractility

Typically occurs due to sympathetic stimulation and other positive inotropes