Cardio Pathology

Cardiac By The Dark Horse

Cardiac Tumors

Cardiac Tumors •

Rare

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Usually benign and pedunculated

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Three types:  – 

Cardiac myxomas

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Rhabdomyomas

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Metastatic tumors

Right atrial

With stalk

Cardiac Myxomas •

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The most common primary adult tumor (35-50%) Most arise from the left atrium (90%) Complications:  – 

“Ball-valve” effect may obstruct the mitral valve orifice in over half half of patients patients with with myxomas myxomas of the left atrium •

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Blocks diastolic filling of the ventricle, stimulating mitral valve valve stenos stenosis is -> may cause cause syncop syncopal al episodes episodes

One third of these patients die of embolization of  embolization of the tumor to the brain

Dx: transe transesopha sophageal geal ultrasoun ultrasound d

Stellate Stellate cells and and fibroblas fibroblasts ts

Amorphous extracellular matrix

Histology of Cardiac Myxomas •

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Loose Loose myxoid yxoid matrix matrix Abundan Abundantt prot proteog eogly lycan canss with with ste stella llate te cells cells within the matrix

Grossly

Striated Striated muscle (“Spider”) (“Spider” ) cells

Rhabdomyomas •

Most common primary cardiac tumor in infan infants ts and children  – 

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Forms Forms hamartomas hamartomas in the myocar myocardium dium Almost all are multiple  – 

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Involve Involve both the left and right ventricles, and the atria in 1/3 of cases Projects into the cardiac chamber in ½ of cases

Grossly:  – 

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Major association with tuberous sclerosis

Pale gray masses, up to several centimeters

Histologically:  – 

Derived from striated muscle cells with abundant glycogen

Metastatic Metastatic Breast Cancer

Metastatic Melanoma to the Heart

Metastatic Tumors to the Heart •

Metastasis is more common than primary tumors  – 

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The pericardium is the most common site for metastasis  – 

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Derived from cancers of the lungs, breast, GI tract, lymphomas, leukemias, malignant melanomas

Leads Leads to pericarditi pericarditiss and effusio effusions ns

Metastatic cancers of the myocardium ma result in manifestations of restrictive cardiomyopathy

Heart Emboli

Types of Emboli •

Thromboemboli  – 

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Liquid Emboli  – 

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Fat emboli Amniotic fluid emboli

Gas Emboli  – 

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Fragments of thrombi Most common Infected thrombi give rise to septic emboli

Air emboli Decompression Decompression sickness

Solid Particle Emboli  – 

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Cholesterol crystals from atherosclerotic plaques Tumor cells Bone marrow emboli Bullets

Classification of Emboli •

Venous emboli  – 

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Originate in the heart, aorta, and major arteries Cause infar infarction ction

Paradoxical Emboli  – 

Sources of Venous Emboli

Typically lodge in pulmonary artery and branches -> pulmonary embolism

Arterial emboli  – 

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Originate in veins

Venous emboli that reach the arterial circulation through an atrial septal defect

Pulmonary Embolism •

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Pulmonary Saddle Embolus

Most important complication of venous of  venous emboli Saddle emboli @ entry of main pulmonary artery  – 

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Wedge-shaped pulmonary infarct

Often lethal

Smaller emboli lodge in minor branches and cause wedge-shaped infarcts

Arterial Emboli •

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Most originate from endocardium, valvular thrombi, ulcerated atherosclerotic plaques Tend to lodge lo dge in mediumsized and smaller arteries Lodge in: Brain (middle cerebral artery) Spleen Kidneys Intestines  – 

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Sources of Arterial Emboli

Fat Embolism •

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Following fractures of long bones -> platelets adhere to fat globules -> thrombocytopenia Fat Embolism Syndrome appears 1-3 days after injury  – 

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Respiratory symptoms: ARDS Neurologic symptoms: mental changes

Amniotic Fluid Embolism •

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Entry of amniotic fluid into the maternal circulation Usually occurs @ the end of  labor Histology: fet fetal al squamous cells within pulmonary vasculature vasculature Clinical presentation: presentation:  – 

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Fetal Epithelial Squames

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Sudden severe dyspnea Cyanosis Hypotensive shock Seizures and coma Pulmonary edema DIC

Bone Marrow Embolism •

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Usually after cardiac resuscitation No symptoms

Decompression Decompression Sickness •

Form of gas embolism

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Seen in scuba divers divers

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Nitrogen gas released from solution during rapid ascent -> obstructing blood flow

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Commonly known as the “bends”

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Temporary muscle, joint pain

Caisson Disease •

Chronic decompression sickness where vascular obstruction causes avascular necrosis of bone, bone, primarily affecting head of the femur, tibia, and humerus

Hyperemia •

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Accumulation of blood in the peripheral circulation Active hyperemia: dilatation of the arterioles mediated by neural signals Passive congestive: increased venous back pressure Consequence of CHF Associated with pulmonary edema with L heart failure failure RBC’s taken up by alveolar macrophages = hemosiderin-laden macrophages (heart failur failure e cells) Associated with passive liver congestion (Nutmeg liver) with R heart failure  – 

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Hemosiderin-Laden Macrophages

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Hemorrhage •

Cardiac  – 

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Trauma, aortic aneurysm dilation, dissection

Arterial  – 

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Often fatal

Aortic  – 

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Resulting from a stab wound, or a softened heart muscle from a MI can result in ventricular rupture -> pericardial tamponade

Penetrating wounds, fractured bones Usually fatal

Venous  – 

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Usually traumatic; blood flows out of the body -> hypovolemia May fill body cavities and form hematomas

Petechiae, purpura, and ecchymosis •

Petechiae  – 

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Purpura  – 

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Small hemorrhages into skin, mucosa < 1mm in diameter Measure 1mm to 1cm

Ecchymoses  – 

Larger blotchy areas under the skin due to trauma

Fate of the Thrombi •

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Small thrombi are lysed or dissolved Larger thrombi stimulate inflammatory inflammatory cells -> granulation tissue deposition (organization organization); ); inflammatory cells of granulation tissue dissolve the thrombus & replaced with collagen Occlusive thrombi may be recanalized If thrombus cannot be organized or dissolved, may embolize

Thrombus Classification By Location •

Intramural  – 

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Attached to the arterial wall; typically cover ulcerated atheromas

Venous  – 

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May embolize

Arterial  – 

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Attached to mural endocardium; commonly found overlying a MI

Usually found in dilated veins Long-standing are organized by granulation tissue

Microvascular  – 

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Found in arterioles, capillaries, and venules Typical of Disseminated Intravascular Coagulation

Thrombus Classification Pathologically •

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Red Thrombi  – 

RBC’s and fibrin

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Thrombi in small vessels

Layered Thrombi  – 

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Lines of Zahn

Lines of Zahn: alternating white (fibrin) and red (RBC) lines Thrombi in larger arteries, veins, mural thrombi

Infarction •

Classified as red or white

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White infarcts  – 

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Red infarct of the intestine

Typical or arterial occlusion in solid organs (heart, kidneys) Paler than surrounding tissue; often rimmed by a thin red zone with extravasated blood

Red infarcts  – 

Typical of venous of venous obstruction involving intestines, or testes

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Also typical of organs with a dual blood supply, supply, i.e. liver l iver,, lungs

Septic infarcts  – 

Infarcts caused by infected thrombi, emboli

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Show signs of inflammation; may transform into an abscess

Shock •

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State of hypoperfusion of hypoperfusion of tissues -> hypoxia -> multiple organ failure Hypoxia -> shift from aerobic to anaerobic metabolism -> lactic acidosis Three mechanisms:  – 

Cardiogenic shock •

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Hypovolemic shock •

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Loss of circulatory volume, due to hemorrhage or water loss

Septic shock •

Pathogenesis of Septic Shock

Pump failure of the heart, often secondary to a MI

Most often due to endotoxin(LPS)-producing gram negative bacteria such as E.coli

3 Stages of Shock •

Nonprogressive  – 

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Progressive  – 

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Characterized Characterized by tissue hypoperfusion, and development of metabolic imbalances (acidosis) Metabolic acidosis -> dilates arterioles -> worsens CO -> stagnation of blood in pulmonary circulation -> favors ARDS (shock lungs) Urinary output falls due to constriction of the renal cortical vessels marking transition between reversible and irreversible stage

Irreversible  – 

Survival is not possible

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Multiple organ failure is usually present

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DIC is common

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Compilations of Shock

Initial phase when reflex compensatory mechanisms maintain perfusion of vital organs

Patients have marked hypotension, respiratory distress, acidosis, and anuria

ARDS with hyaline membranes •

In shock, alveolar capillaries in the lungs may necrotize and slough off to be covered and lined by fibrin (hyaline (hyaline membranes)) membranes

Waterhouse Friderichsen syndrome •

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Commonly associated associated with meningococcal (Neisseria) septic shock Bilateral hemorrhagic infarction of the adrenals

Bacterial Endocarditis

Infective Infective Endocarditis Endocarditis •

Infective endocarditis: Micro-organism infection of inside of heart.  –   –   –   – 

Can infect Aorta, Blood vessels, prosthetic prosthetic heart valves. Fungi, Rickettsia, Rickettsia, and Chalydimdia Chalydimdia are other rare rare causes. Divided into acute and subacute. Causes •

Usually pt is predisposed due to:  –   –   –   – 

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Artificial Valves Valves Congenital Defects Degenerative Calcified valvular stenosis Bicuspid Aortic Valves Valves Myxomatous Mitral Valve Valve (mitral valve valve prolapse)

Infective Infective Endocarditis Endocarditis vs Rheumatic Heart disease vegetations. vegetations.  –   – 

Rheumatic Heart disease has sterile thrombi. Infective Infective Endocarditis vegetations vegetations are composed of thrombi and bacteria.

Acute Acute Bacte Bacterial rial Endocar Endocarditi ditiss due to to S. Aur Aureu eus. s. Des Destruc tructi tion on of of Aorti Aorticc Val Valv ve.

Gram Negative Bacterial Endocarditis

Acute and Chronic Infective Endocarditis •

Acute Bacterial Endocarditis  – 

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High destruction of previously normal valve. Staph Staph Aureus Aureus or Gram Gram Negati Negative. ve. May perforate valve. Necrotic Necrotic Valvu Valvular lar Lesions Lesions

Subacute Subacute Bacteria Bacteriall Endocardidi Endocardiditis tis  – 

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Slower, less virulent disease St. Viridans Infection is previously abnormal heart valves Less destructive and show evidence of healing.

Subacut Subacute e Bacte Bacterial rial endoca endocard rditi itiss

Fischione: Infective Endocarditis Acute, Staph Aureus •

Infective Infective Endocarditis Endocarditis •

Infective endocarditis: Micro-organism infection of inside of heart.  –   –   –   – 

Can infect Aorta, Blood vessels, prosthetic prosthetic heart valves. Fungi, Rickettsia, Rickettsia, and Chalydimdia Chalydimdia are other rare rare causes. Divided into acute and subacute. Causes •

Usually pt is predisposed due to:  –   –   –   – 

 – 

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Artificial Valves Valves Congenital Defects Degenerative Calcified valvular stenosis Bicuspid Aortic Valves Valves Myxomatous Mitral Valve Valve (mitral valve valve prolapse)

Infective Infective Endocarditis Endocarditis vs Rheumatic Heart disease vegetations. vegetations.  –   – 

Rheumatic Heart disease has sterile thrombi. Infective Infective Endocarditis vegetations vegetations are composed of thrombi and bacteria.

Acute Acute Bacte Bacterial rial Endocar Endocarditi ditiss due to to S. Aur Aureu eus. s. Des Destruc tructi tion on of of Aorti Aorticc Val Valv ve.

Acute and Chronic Infective Endocarditis •

Acute Bacterial Endocarditis  – 

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High destruction of previously normal valve. Staph Staph Aureus Aureus or Gram Gram Negati Negative. ve. May perforate valve. Necrotic Necrotic Valvu Valvular lar Lesions Lesions

Subacute Subacute Bacteria Bacteriall Endocardidi Endocardiditis tis  – 

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Slower, less virulent disease St. Viridans Infection is previously abnormal heart valves Less destructive and show evidence of healing.

Subacut Subacute e Bacte Bacterial rial endoca endocard rditi itiss

Staph on prosthetic tricuspid (top) Infected Infected Artifical Mitral Mitral Ball Valve (bot.

Mitral Valve Prolapse

Pathogenesis of Endocarditis •

Risk Factors  – 

Seeding of the blood with microbes due to infection infection in the body… Pneumonia, UTI, Dental/Surgical procedure causing a bacterima.

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Neutropenia

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Immunodeficiency

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Diabetes

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EtO tOH H abu abuse

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Drug abuse (IV)

Subacu Subacute te endoc endocar ardi ditis tis St. Viridans

Pathology of Infective endocarditis •

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Prosthetic Valve Prosthetic Valve endocarditis endocarditis -> Staph Epidermis Vegetations  –   – 

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Large, bulky Contain fibrin, thrombin, inflammatory cells and bacteria. Most commonly on Mitral #1, and Aortic #2 of non IV drug abusers. May cause septic emboli following detachment. Fungal vegetations tend to be larger than bacterial vegetations. Septic Emboli most feared complication.

Candi Candidal dal Endo Endoccardi arditi tiss

Note: Fungi produce some of the largest vegetations seen in endocarditis

Clinical features of Endocarditis •

Fever is present in all pts.

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Murmur is common due du e to vegetations. vegetations.

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Acute. BE -> quick onset, chills, night sweats and weakness. Subacute. BE ->low grade fever, fatigue and flu like symptoms.

Diagnosing Endocarditis Endocarditis •

Positive blood culture required for conformation conformation can be obtained in 90% of cases.

Gram Negative Bacterial Endocarditis

Infective Vegetation Vegetation (3) With Fibrin, Necrosis and Acute Inflammation (2)

Infective Infective Vegeta Vegetation tion with Pink Fibrin Fibrin and Blue Staining Coccal Organisms

Signs/Symptoms of Bacterial Endocarditis “FROM JANE”: Fever Roth’s oth’s Spots Spots Osler’s nodes Murmur (New) Janew anewa ay lesi lesion onss Anemia Nail-bed hemorrhage Emboli •

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Janew Janewa ay lesio lesions ns are seen in people with acute bacterial endocarditis. They appear as flat, painless painless , red to bluish-r bluish-red ed spots spots on the palms palms and soles.

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Roth spots: a round white retina spot surrounded by hemorrhage in bacterial endocarditis, and in other retinal hemorrhagic conditions.

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Osler's nodes: These are small (the size of  split peas), tender, transient nodules in the pads of fingers and toes and the palms and soles. They are a highly diagnostic sign of  bacterial infection infection of the heart (subacute ( subacute bacterial endocarditis endocarditis). ). Named for the Canadian-born physician Sir William Osler (1849-1919).

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Splinter hemorrhage in patients with heart murmur and unexplained fever can herald endocarditis.

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(verrucous) ous) endocar endocarditis ditis is the most Libman-Sacks (verruc characteristic cardiac manifestation of the autoimmune disease systemic systemic lupus erythematosus. Seen as mulberrylike cluster clusterss of verrucae verrucae on the ventricul ventricular ar surface of the posterior mitral leaflet. The lesions typically consist of accumulations of immune complexes and mononuclear cells. Vegetations develop on both sides of valve (Mitral valve stenosis ), but do not embolize. Seen in Lupus

SLE causes LSE

Rheumatic Heart Disease

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Rheumatic heart disease is a complication of  rheumatic fever in which the heart valves are damaged. damaged. Rheumatic Rheumatic feve feverr is an inflamma inflammatory tory disease that begins with a strep throat. throat. It can affect connective tissue throughout the body, especially in the heart, joints, brain and skin. Rheumatic fever develop following following pharyngitis with group A beta-hemolytic Streptococcus. Streptococcus. Acute rheumatic fever fever and rheumatic heart disease are thought to result from an autoimmune response (Immune mediated not direct effect of bacteria)

Rheumatic heart disease Signs/Symptoms •

Valves effected: Mitral> Aortic>>T Ao rtic>>Tricuspid ricuspid (High pressure valves affected most)

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Aschof Aschofff bodies bodies (Gr (Granu anulom loma a with with giant giant cell cells) s)

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Anitschkow’ Anitschkow’ss cells (Activated (Activated histiocytes) histiocytes)

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Migratory Polyarthritis

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Erythem Erythema a Margin Marginatu atum m

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Sydenham chorea

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Fish Fishmo mout uth h Sten Stenos osis is-- Fusi Fusion on of the the valv valvul ular ar cusp cuspss

Extr Extracar acardiac diac Finding Findingss in RHD •

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Mnmonic: CANCER Carditis Arthritis Nodules odules – most most common common in childre children, n, overlies overlies extensor tendons. Chorea ERythema ythema Margin Marginatu atum: m: macopa macopapul pular ar rash appearing mostly on trunk and proximal extremties.

Diagnostic findings in RHD •

RHD Lab Findings  –   –   – 

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RF Symptoms after strep throat infection Pos. Titers of serum antibodies to Group A strep. ↑ESR, ↑WBC, C-Reactive Protein

Diagnosis  – 

Jones Criteria (2 major; or 1 major + 2 minor fufilled) •

Major Criteria  –   –   –   –   – 

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Pancarditis Polyarthritis Sydenh Sydenhams ams Chorea Chorea SubCute SubCuteneou neouss Nodules Nodules Erythema Erythema Margina Marginatum tum

Minor Criteria  –   –   –   – 

Hx of RF Fever Arthagias EKG + for heart damage

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Erythem Erythema a margina marginatum tum: A condition which is characterized characterized by reddened areas of the skin which are disk shaped with elevated edges.

Acute Rheumatic Fever and Rheumatic Heart Disease •

Acute Rheumatic Fever  – 

Systemic immunologically mediated disease related to Streptococcal infection.

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Occurs 2 weeks after strep throat infection.

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Immune Reaction •

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Immune rxn damages connective connective tissue tissue of the heart. Anti-strep antigen -> Antis Antistr treol eolysi ysin n O (ASLO or ASO) develop in all pts.

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Not all pts with ASO titers develop ARF.

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Principally disease of children. Can occur in adults.

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Asch Aschof offf body body:: A granuloma granulomatou touss inflammat inflammation ion characteristic of acute rheumatic carditis, consist consisting ing of fibrinoid fibrinoid changes changes in connecti connective ve tissue and lymphocytes.

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Anit Anitsch schk kow cell: cell: large mononuclear cells with an undulating, ribbon-like ribbon-like formation of  'caterpillar cells cel ls' are nuclear chromatin. These 'caterpillar found in myocardium and thought to be macrophages.

Valve Changes in RHD •

Insuffiency  – 

Mitral Valve Insufficiency •

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Aortic Insufficiency •

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Blood reflux across mitral valve. Blood reflux back from aorta to LV -> left ventricular hypertrophy and dilation.

Stenosis  – 

Mitral Stenosis •

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Stagnation of blood in left atrium -> RHF

Aortic Stenosis •

Impedes blood flow from LV into Aorta -> LV hypertrophy -> Cor Cor Pulm Pulmon onae ae -> RHF RHF

Myocardial Infarction

Clinical Signs of MI •

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Crushing Crushing preco precordi rdial al chest chest pain Constricting suffocating pain Substernal Substernal pain that may may radiate radiate to to the left left arm, neck, jaw Loss of consciousness/fainting Nausea/vomiting Fatigue/weakness Tachycardia, anxiety, restlessness Pale, cool, moist skin Pain prolonged, not relieved by nitro

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Diagnosis of MI •

ECG changes in acute MI:  –   –   – 

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Increased lactic acid production -> metabolic acidosis  – 

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Potassium released into the ECF, affecting membrane potentials of functioning myocardial cells

Eleva Elevate ted d Creat Creatine ine Kinase Kinase and CK-MB  – 

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Ischemic myocardial cells revert to anaerobic metabolism

Hyperkale Hyperkalemia mia -> arrythmias arrythmias  – 

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Prolonged Q wave Elevated ST segment Inverted T wave

Absence of change in first 2 days excludes MI

Elevate Elevated d troponins troponins in the serum  –   – 

Remain elevated for 7-10 days Gold standard for for diagnosis of acute MI because more specific for myocardial myocardial tissue •

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Not pathognomonic pathognomonic

Lactate dehydrogenase dehydrogenase (LDH) flip  – 

Normally LDH2 is higher than LDH1 •

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In acute MI, LDH1 is released, causing the “flip”

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Too many Big Macs may cause? Acute

Progressive Coronary Artery Disease: Atherosclerosis Atherosclerosis of the coronaries -> myocardial ischemia May be chronic progressive ischemia from atherosclerosis atherosclerosis May be acute coronary thombosis due to a sudden occlusion Results in a MI in an anatomically defined area

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Distribution of MI’s: Anterior wall infarct Occlusion of  the Left Anterior Descending (LAD) Artery – over 50% Lateral wall infarct Occlusion of  the Left Circumflex Artery – 3040% Infarct of the right ventricle and posterior wall of  the left ventricle Occlusion of  the Right Coronary Artery (RCA) – (RCA) – 10-20%

Calcified plaque

Pathology of CAD: Coronaries -> atherosclerosis atherosclerosis -> narrowing of the lumen due to fibrotic plaques and atheromas Plaques may be covered with fibrinous fibrinous clots in an acute acute occlusion occlusion Granulation tissue of the plaque and thrombi in older lesions may reestablish blood flow via recanalization Wall contains calcium and cholesterol deposits 1/ 28/ 09

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Myocardial Infarction: Rapid, sudden occlusion of  a coronary artery •

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Causes: Thrombosis of a coronary artery (80-90%) Ulceration of an embolized atherosclerotic plaque Prolonged vasospasm •

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Sudden cardiac death in ~25% Among survivors of the onset: inadequate perfusion -> multisy multisyst stemic emic major organ failure Cerebral ischemia most dangerous Kidney damage most often

Types of MI’s

Subendocardial

Transmural Transmural: •

Most common

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All 3 layers of the heart involved

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Subendocar Subendocardial dial or Intramur Intramural: al: Infarction Infarction usually concentric around the subendocardial layer of the left ventricle Q waves are absent •

Free wall of the left ventricle and/or interve interventri ntricular cular septum septum usually usually involved

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New Q-waves develop 1/ 28/ 09

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Wavy, Wavy, eosinophilic myocytes with contraction bands

Subacute Subacute Myocardial Myocardial InfarctInfarctGranulation Tissue and Macrophages (over 1 week)

Histology of MI: Microscopic changes precede macroscopic changes •

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During 0-24 hours During 1-3 days Myocardial cell death Eosinophili Eosin ophilicc myo myocytes cytes devoid of nuclei and striations Coagulative Coagul ative necr necrosis osis Contraction bands Predomination of PMN’s that lyse dead myocar myocardial dial cells Days 3-4 Macrophage infiltration End of first week Granulation tissue invading the infarct Macrophages phagocytize necrotic debris Chronic MI Necrotic myocardium myocardium replaced by white fibrous scarring •

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Pink Coagulative Coagulative Necrosis Necrosis and PMN’s (3-4 (3-4 Days Old)

Old, Remote Infarct with White, Myocardial Fibrous Scarring •

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Acute with soft yellow and hemorrhagic hemorrhagic tissue Subacute with deposition deposition of granulation granulation tissue tissue

Gross Pathology of MI: First 1-2 days Cannot be definitively identified May be pallor pallor of infarcted infarcted myocardium myocardium 3-5 days Infarct becomes yellow Hemorrhagic rim Soft infarcted infarcted myocardium myocardium from hydrolytic hydrolytic enzymes released from neutrophils 1-2 weeks Granulation tissue imparting a gray-pink gray-pink,, mottled appearance Chronic infarct White-tan fibrosis •

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Complications of MI

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Myocardial Rupture

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Left Ventricular Aneurysm

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Mural Thrombus

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Myocardial Myocardial Rupture Myocardial Rupture: Softened necrotic myocardium ruptures Blood fills the pericardial sac (hemopericardium (hemopericardium)) -> cardiac tamponade (compression (compression of  the heart) • •

Hemopericardium Hemopericardium due to Rupture Causing Cardiac Tamponade

Ventricular rupture with necrosis

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Left Ventricular Ventricular Aneurysm Aneurysm •

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MI’s MI’s of the left ventricle -> granulation and fibrous tissue replacement -> bulge under pressure -> ventricular aneurysm Fibrous tissue does not contract -> heart dilated and contracts irregularly

Ventricular Aneurysm W/ Mural Thrombus Ventricular Aneurysm With Infarcted Myocardial Wall 1/ 28/ 09

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Mural Thrombus •

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Endocard Endocardium ium damaged/d damaged/disru isrupte pted d Blood coagulates in contact with the necrotic endocardium/exposed myocardium -> thrombus attached to the wall Complications:  –   – 

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Impede blood flow Weakens ventricular ventric ular contractions May detach giving rise to emboli -> cerebral Infarcts

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4 Stages of MI-Microscopic Findings 24 Hours: Myocardial cell death with wavy, eosino eosinophi philic lic myocyt myocytes( es(Pink Pink), ), coagulative necrosis (Myocyt (Myocytes es have have no nucleus), nucleus), and and contraction bands. The nuclei are either faint or dead.

Acute MI With Wavy, Eosinophilic Myocytes with Contraction Bands

4 Stages of MI-Microscopic Findings •

Days 1-3: 1-3: The appearance of PMN’s which will predominate for the next three days.

Pink (eosino (eosinophili philic) c) Coagulat Coagulative ive Necrosis Necrosis and PMN’s

Note: PMN’s Have segmented Nuclei, they are granulomas (Innate immunity)

4 Stages of MI-Microscopic Findings •

Days 3-7: 3-7: The The infa infarct rcted ed area area become becomess infiltrated with macrophages, which persist in the lesion for about a week that phagocytize and remove necrotic debris and myocytes.

Subacute Myocardial Myocardial Infar Infarctct- Granulation Granulation Tissue and Macrophages (over 1 week)

4 Stages of MI-Microscopic Findings •

Days 7-28 : Toward the end of the first week, the infarct is invaded with granulation tissue composed of small blood vessels (angiogenesis), myofibroblasts and fibroblasts deposi depositin ting g colla collagen genous ous matri matrix. x. Macrophages replace the PMN’s and phagocytiz phagocytized ed the necrotic necrotic debris. debris. (these (these are are subacu subacute te findin findings gs in an MI) MI)

Subacute Myocardial Infarct with Collagen and Angiogenesis (Granulation Tissue)

4 Stages of MI-Microscopic Findings •

Months: Ultimately, the necrotic myocardium Months: is replaced by white fibrous scarring between islands of myocytes.

Old, Remote Infarct with White, Myocardial Fibrous Scarring

4 Stages of MI-Gross Findings The infarc infarcted ted area cannot cannot be definitiv definitively ely identified identified during the first 1-2 days. There may be some some pallor pallor of the infar infarcted cted area. area. 1-7 days : After the occlusion, the infarct infarct becomes yellow.

Acute Myocardial Infarct-Soft Yellow Yellow and Hemorrhagic Tissue

4 Stages of MI-Gross Findings •

7-28 days :After the occlusion, the infarct becomes pallor and is surrounded by a hemorrhagic rim, and the infarcted infarcted myocardium myocardium is soft as a result of action of  hydrolytic enzymes released from the neutrophils.

Acute Myocardial InfarctionGranulation Tissue (Pallor surrounded by Red rim)

•

White-tan fibrosis predominates Months: White-tan Months: within an older or chronic infarct. infarct.

Old Myocardial Infarct

Pericarditis

Pericarditis •

•

Inflammation of the visceral or parietal pericardial layers Most often associated with myocarditis, tuberculosis

Causes of Pericarditis: Bacteria, viruses, fungi (rarely) Severe autoimmune diseases (SLE) Rheumatic Heart Disease Chronic renal failure -> metabolic waste products in the blood (uremia) Trauma, radiation injury, and open-heart surgery •

•

•

•

•

1/ 28/ 09

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Pathology Pa thology of Pericarditis Exudation of fluid into the pericardial sac  – 

Clear yellow yellow with serous serous pericarditis (viral infections) infections)

 – 

Purulent with bacterial ba cterial infections

 – 

Serofibrin Serofibrinous ous exudat exudate e associat associated ed with more seve severe re damage damage (Rheumatic fever)

Bacterial (Suppurative)

1/ 28/ 09

Serous

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Fibrin Fibrinous ous Perica ericard rditi itiss •

Does not resolve as easily as a serous exudate

•

Fibrin bridges the space between the two layers of the pericardial sac  – 

•

•

When separated separated the epicardium epicardium and pericardium resemble bread and butter taken apart

Macrophages invade invade exudate exudate -> stimulate stimulate fibroblasts -> further fibrous adhesion = adhesive pericarditis pericarditis Blood vessels invade invade exudate exudate ->

organization = blood vessels fill space occupied by fibrin and obliterate it •

Fibrous scarring may prevent expansion in diastole = constrictive

pericarditis

1/ 28/ 09

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Pericarditis 3 types: Serous Fibrinous Hemorrhagic ECG findings: Diffuse ST Elevation Pulsus Pulsus Parad Paradox oxus us: an exaggeration of the normal variation in the pulse during the inspirato inspiratory ry phase of respiration, respiration, in which which the pulse becomes weaker as one inhales and stronger as one exhales. It is a sign that is indicative of several conditions including cardiac tamponade, pericarditis. Pericardial pain Friction Rub Distant Heart Sounds

Serous Pericarditis •

Serous Pericarditis etiologies:

•

SLE (Lupus)

•

Rheumatoid Arthritis

•

Infection

•

Uremia

(Serous) Rheumatoid Pericarditis

Fibri Fibrino nous us Peric ericar ardi diti tiss •

•

•

Fibrinous Fibrinous Perica Pericardi rditis tis etiologies: Uremia MI ( Dressler’s syndrome) - The syndrome consists of a persistent low-grade fever, chest pain (usually pleuritic in nature), nature), a pericardial pericardial friction rub, and /or a pericardial effusion. The symptoms tend to occur after a few weeks or even months after infarction and tend to subside in a few days. An elevated ESR is an objective laborat l aboratory ory finding.

•

Rheumatic fever

Fibrinous (Bread & Butter) Butter) Pericard Pericarditis itis

Hemorrhagic Pericarditis Hemorrhagic Pericarditis etiologies: TB Malignancy (Melanoma)

Pericarditis •

•

•

Viral Infections: The fluid is clear yellow in serous pericarditis. Bacterial Infections Infections: Purulent exudate is a hallmark of bacterial ba cterial infections infections and is caused by pus-forming bacteria, such as Staph or Strept. Constrictive Pericarditis: The fibrous scarring of the pericardial pericardial sac may completely encase the heart and prevent prevent its expansion in diastole.

Serous (Viral) Pericarditis

Bacterial (Purulent) Pericarditis

Constrictive Pericarditis

Myocarditis

Myocarditis Clinical Presentation: Mild fever Shortness of breath Malaise Signs of heart failure if severe and chronic • • • •

 –   –   – 

•

Tachycardia Peripheral cyanosis Pulmonary edema

Males > females

Diagnosis & Treatment: Treatment: Diagnosis: •

 – 

•

Treatment:  – 

1/ 28/ 09

Endomy Endomyocar ocardial dial biopsy biopsy Supportive measures P h l

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Myocarditis •

Acute inflammation of the myocardium myocardium  – 

Most often due to viral infections •

 – 

Also can be caused by parasite pa rasitess •

 – 

Coxsackie B virus Toxoplasmosis

Can be due to a secondary disorder •

Rheumatic fever  – 

Toxoplasm oxoplasma a Myocard Myocarditis itis cyst

Aschof Aschofff bodies bodies:: granuloma granulomass in the myocardi myocardium um

 – 

Bacteria are a rare cause •

 – 

Epimyocardial Epimyocardial microabscesses microabscesses

Other causes:

1/ 28/ 09

•

Radiation

•

Hypersensitivity

•

Sarcoidosis P h l

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Myocardial Aschoff Bodies in Rheumatic Heart Disease

Viral Myocarditis •

•

•

Viruses damage organelles > cell death Myocardium invaded by Tlymphocytes -> secrete interleukins, TNF -> destroy virus-infected myocardial cells Pathology:  – 

Viral (interstitial) myocarditis

Tiger Effect •

• • •

1/ 28/ 09

Pale, congested areas with mild hypertrophy hypertrophy Biventricular dilatation Generalized hypokinesis Flabby, dilated heart

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Tiger Effect from Acute Viral Myocarditis

Acute Viral Myocarditis •

Histology:  – 

 – 

1/ 28/ 09

Patchy, diffuse infiltrate of T-cells and macrophages surrounding individual myocytes Focal Focal or patchy patchy acute myocyte myocyte necrosis necrosis

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Vasculitides

Vasculitis •

•

Inflammation/necrosi s of blood vessels Pathogenesis thought Pathogenesis to involve immune mechanisms:: mechanisms  – 

 – 

 – 

2/ 17/ 200 9

LG4.5 & LG4.7 Pathology

Deposition of  Immune complexes Direct attack on vessels by antibodies Cell-mediated immunity 12 9

Pathogenesi Pa thogenesiss of Vasculitis asculitis May be associated with a viral infection Small vessel vasculitides vasculitides  – 

C-ANCA’ss seen in Wegener’s C-ANCA’ Wegener ’s

 – 

i.e. Wegener granul granuloma omatosi tosiss and Polya Polyarte rteritis ritis Nodosa Nodosa associated with ANCA (anti-neutrophil cytoplas cytoplasmic mic antibod antibodies) ies) •

Common patterns are:  – 

 – 

P-ANCA’’s seen in Polyarteritis P-ANCA Polyarteritis Nodosa 2/ 17/ 200 9

LG4.5 & LG4.7 Pathology

perinuclear immunoflou immunoflouresn resnce ce (PANCA)) ANCA cytoplasmic immunoflou immunoflouresce rescence nce (CANCA)) ANCA 13 0

Polyart olyarteri eritis tis Nodosa Nodosa •

Acute systemic necrotizing necrotizing vasculitis vasculitis that affects affects medium and smaller-sized muscular arteries

•

Associated with Hepatitis B

•

Primarily in whites

•

Men > women

•

noid necro necrosis sis Patchy lesions with area of fibri of  fibrinoid

•

Obliteration of the tunica media and intima

•

Acute inflammatory response surrounds area of  necrosis

•

Heals with fibrosis that obstructs the lumen

•

Associated with P-ANCA

•

Clinical Presentation:  – 

 – 

 – 

•

Destruction of arterial wall with fibrinoi fibrinoid d necrosis necrosis

Fever, Fever, weight weig ht loss Kidney, heart, skeletal muscle, skin, mesentery involvement Fatal without treatment

Treatment:  – 

Corticosteroids, cyclophosphamide

2/ 17/ 200 9

LG4.5 & LG4.7 Pathology

13 1

Complica Complications tions of Poly Polyarte arteritis ritis Nodosa Nodosa •

•

•

Healing Healing Polyar Polyarter teritis itis Nodosa Nodosa with transmural transmural fibrosis & inflammation inflammation 2/ 17/ 200 9

Thrombosis of smaller arteries with infarcts in involved organs Formation of small aneurysms in larger arteries -> may cause hemorrhage Healing with fibrosis of  the media leaving gaps in the elastic laminae

LG4.5 & LG4.7 Pathology

13 2

Temporal (Giant (Giant Cell) Arteritis • •

• • •

Most common form of vasculitis Focal chronic granulomatous inflammation of the temporal arterities Average age of onset: 70 Women > men Etiology:  – 

•

Gross pathology:  – 

•

 – 

 –   – 

2/ 17/ 200 9

Throbbing, pain over temporal artery with swelling, tenderness, redness Associated with Polymyalgia Polymyalgia Rheumatica Rheumatica:: generalized generalized muscular aching, stiffness in the shoulders or hips Visual symptoms Malaise, fever, weight loss

Diagnosis:  – 

•

Cord-like, nodular thickening of vessel; lumen reduced

Clinical presentation:  – 

•

Obscure, perhaps genetic, or immunological due to presence of  activated CD4+ T-cells

Temporal artery biopsy

Treatment:

LG4.5 & LG4.7 Pathology

Corticosteroids

13 3

Microscopic Pathology of Temporal Arteritis •

•

•

•

2/ 17/ 200 9

Granuloma Granulomatous tous inflammati inflammation on of the media and intima Presence of Giant Cells Foci of necrosis in the elastic lamina with fragmentation fragmentation Thrombosis may obliterate the lumen

LG4.5 & LG4.7 Pathology

13 4

3 year old presents w/ a high fever for the past week. Physical exam reveals:

Rash

Mucocut Mucocutaneo aneous us lesions lesions

Peeling of the fingertips 2/ 17/ 200 9

Desquamation of the sole of foot LG4.5 & LG4.7 Pathology

13 5

Kawasaki Disease •

•

•

AKA muc mucocut ocutaneou aneouss lymph lymph node syndrome Acute necrotizing vasculitis of infancy of infancy and early childhood Symptoms:  –   – 

Coronary artery with with aneurysmal formations formations

 –   – 

•

•

In 70%: affects coronary arteries -> *coronary artery aneurysms* Possible association with Parvovirus B19

Large coronary artery aneurysmLG4.5 & LG4.7 Pathology

2/ 17/ 200 9

High fever, rash Conjunctival, oral lesions Lymphadenitis Desquamation of the fingertips, fingertips, soles and palms

13 6

Taka akayasu yasu Arteriti Arteritiss Inflammatory disease of large of  large arteries, arteries, especially the aortic arch and its major branches Primarily affects young women < 30 Clinical Findings: Dizziness, visual disturbances As disease progresses -> Cardiac symptoms, symptoms, claudication claudication of the arms/legs arms/legs Asymmetrical BP Pulse in one extremity may be absent Majority eventually manifest CHF and visual defects Gross pathology: Aorta thicke thickened; ned; intima exhibits focal, focal, raised plaques Branches of aorta exhibit “Pulseless less Diseas Disease” e” stenosis/occlusion = “Pulse when subclavians affe affected cted Thoracic/abdominal aorta commonly show aneurysms Treatment: Aortic angiogram: narrowing of great vessels Steroids for early disease Surgery 2/ 17/ 200 9 LG4.5 & LG4.7 Pathology 13 7 •

• •

 –   – 

 – 

 –   – 

•

 – 

 – 

 – 

•

 –   – 

Microscopic Microscopic Findings Findings of Taka Takayasu yasu Arteritis Panart anarter erit itis is with with granulomatous inflammation  – 

Infiltrates of neuts, lymphs, and giant cells

Inflammatory destruction of media 2/ 17/ 200 9

LG4.5 & LG4.7 Pathology

13 8

Wegener Granulomatosis •

•

•

Necrotizing Necrotizing granulomatous granulomatous inflammation inflammation of the lung

•

Systemic necrotizing vasc vasculi ulitis tis with with granulomatous lesions in the upper respiratory tract, and the kidneys Men > women usually in 5th-6th decades 90% exhibit C-ANCA in the blood Microscopic pathology:  –   – 

2/ 17/ 200 9

LG4.5 & LG4.7 Pathology

Parench Parenchymal ymal necrosis necrosis Acute inflammation, granulomatous inflammation and fibrinoid necrosis leading to medial thickening, intimal proliferation, and narrowing of the lumen 13 9

Clinical Presentation of Wegener granulomatosis •

Respiratory tract symptoms: pneumonia, sinusitis  – 

•

Necrotizing segmental glomerulonephritis

•

2/ 17/ 200 9

Rash

Hematuria Hematuria and prot proteinu einuria ria  – 

•

Most prominent pulmonary feature: persistent bilateral pneumonia with nodular infiltrates that undergo cavitation Most prominent kidney features: focal necrotizing glomerulon glome rulonephr ephritis itis whic which h progresses to crescentic glomerulon glome rulonephr ephritis itis (ra (rapidl pidly y progressive progressi ve glomeruloneph glomerulonephritis) ritis)

Rashes, muscular pains, joint involvement, neurologic symptoms Treatment: Cyclophosphamide

 –  LG4.5 & LG4.7 Pathology

14 0

Churg-Strauss Syndrome •

•

•

Granulomatous foci around blood vessels

•

AKA allergic granul granuloma omatos tosis is and angiitis Systemic vasc vascul ulit itis is in young people with asthma Both C-ANCA and PANCA are demonstrated in 2/3 of patients Microscopic findings:  – 

2/ 17/ 200 9

LG4.5 & LG4.7 Pathology

Granulomas with intense eosinophilic infiltrate -> fibrinoid necrosis & thombosis

14 1

Thromb Thromboang oangiit iitis is oblit obliterans erans • •

•

•

Thrombosis with *microabscesses* (specific)

•

AKA Buerger Buerger disease disease Occlusive, inflammatory disease of medium/small arteries in distal arms/legs in middle-aged heavy smokers Cessation of smoking can be followed by remission Etiology: tobacco byproducts elicit antibodies -> inflammation inflammation Microscopic pathology:  – 

•

Complications:  – 

 – 

 – 

2/ 17/ 200 9

LG4.5 & LG4.7 Pathology

Acute inflammation of mediumsized and small arteries with PMN infiltrates Thrombosis and obliteration of  the lumen Microabscesses Microab scesses with neutrop neutrophils hils and giant cells Gangrene of the extremities

14 2

Clinical Clinical Findings Findings of Thromboangi Thromboangiitis itis obliter obliterans ans

•

•

Claudication Painful ulceration ulceration of  the digits

Necrosis of finger tips

2/ 17/ 200 9

LG4.5 & LG4.7 Pathology

14 3

Varicose Veins •

Etiology:  –   – 

• •

Stasis Dermatitis •

Predisposed to clotting More likely to occur with family histories of connective tissue disease, in professions requiring long hours of standing, and during pregnancy Complications:

Clotting, thrombosis -> may embolize Leakage of blood into tissues -> brownish discoloration, “stasis dermatitis” (small pinpoint hemorrhages from ruptured capillaries) Ischemia -> skin may necrotize necrotize and stasis ulcers may form LG4.5 & LG4.7 Pathology 14 4  – 

 – 

 – 

2/ 17/ 200 9

Incompetence of venous valves Pooling of blood, i.e. from back pressure from a failing heart -> veins remain dilated/tortuous dilated/tortuous

Cardiomyopathies

Cardiomyopathies •

Cardiomyopathy: heart disease resulting form abnormality in myocardium.

Dilated Cardiomyopathy Cardiomyopathy •

Progressive Progressive chamber dilation and systolic dysfunction.  –   – 

 – 

Results in EF < 25% Most common type of  Cardiomyopathy . Causes: •

• • •

•

Toxic (Alcoho (Alcohol, l, Adriamycin, Cytoxin, Cocaine, Cobalt) Viral Myocarditis Pregnancy High Catecholamines (pheochromocytoma pheochromocytoma)) Primary (genetic) -> mostly AD but can be AR and sex linked recessive.

Dilated Cardiomyopathy Cardiomyopathy  – 

Gross and Microscopic Findings: •

•

•

•

•

•

Thin Wall partially replaced by fibrous tissue. Heart Size 2-3x normal. Impaired Contractility Eventual CHF Normal Coronary Arteries Muscle cells are hypertrophied w/ enlarged nuclei and interstitial fibrosis

Hypertrophic Cardiomyopathy •

Gross Findings  – 

 –   – 

•

Asymmetrical thickening of  ventricular septum. Banana-Shaped Septum Endocardia Endocardiall thickening thickening with mural plaque formation of  outflow tract.

Histology  – 

 – 

Extensive Myocyte Hypertrophy w/ “Myocyt “Myocyte e Dissarra Dissarray” y” Primary cause unknown typically affects young males. Geneti Geneticc- AD. AD.

Restrictive Cardiomyopathy Cardiomyopathy •

Decrease in ventricular compliance  – 

 – 

 – 

•

Gross and Microscopic Findings  – 

 – 

•

Impaired ventricular filling during diastole normal systole function. Heart cannot expand to receive inflowing blood. Idiopathic or associated with abnormal infiltrate. IE; Amyloid Sarcodosis, metastatic tumor, radiation fibrosis. Slightly enlarged ventricles, firm mycocardium Patchy or diffuse interstitial fibrosis.

Diagnosis  – 

 – 

Slightly enlarged ventricles, firm mycocardium Patchy or diffuse interstitial fibrosis.

Congo Stain for Amyloid; Yellow-Green birefringent birefringent under polarized polarized light

Congenital Heart Defects (CHD)

Congenital Heart Defects (CHD) •

Heart is formed by 10 th week.  – 

 – 

CHD form before this time. Rubella Virus infection in mother best known cause of  CHD. • • •

 – 

Ventricular Septal Defect Defect Paten Pa tentt Ductus Arteriosu Arteriosuss Tetralogy etralogy of Fallot

Chromosomal Abnormalities • • • •

Down syndrome 21 (VSD, ASD) Edward 18 Pat atau au 13 Turner XO XO -> coarctation coarctation of the aorta

Tetralogy etralogy of Fallot •

Early R -> L Shunt *Cyanosis*  –   – 

 –   – 

10% of CHD Heart is enlarged and boot-shaped due to RVH. Most common form of cyanotic CHD. 4 Features Mmnonic: PROV •

Pulmonary Artery Stenosis  – 

• • •

•

Right Ventricular Hypertrophy Overriding Aorta (overrides the VSD) Ventricular Ventricular Septal Defect

Infant Clinical Presentation  –   – 

•

If mild then ToF ToF shunt is left to right.

Cyanosis after birth (blue babies) RHF is rare due to pulmonary stenosis

Treatment and Prognosis  –   – 

Without surgery dismal outlook Open Heart Surgery total correction possible. <10% mortality

Transposition of the Great Vessels •

Aorta arises from right ventricle; Pulmonary artery arises from left ventricle.  –   –   – 

•

Children of diabetic moms Cyanosis at Birth 4% of CHD

Death without a shunt  –   – 

 – 

VSD allows life. -> stable shunt Patent Pat ent Foramen Foramen Ovale or PDA -> unstable shunt; needs surgery before closure. “corrected transposition ” surgery entails switching of great vessels as well as coronary arteries.

Ventricu entricular lar Sept Septal al Defect Defect L > R Shunt •

Most common congenital heart defect  – 

 – 

 – 

 – 

•

Incomplete closure of ventricular septum. Usually size of aortic valve orifice. 90% below pulmonary valve in membranous septum. 10% lie within muscular septum. 50% of small muscular VSDS close spontaneously.

Clinical Presentation  – 

 – 

RVH and Pulmonary Hypertension Overtime shunt reversal; Cyanosis, Clubbing, Polycythemia, and death

Pat aten entt Duct Ductus us Arteri Arteriosu osuss •

Cause:  – 

•

Low O2 tension cause relaxing effect on the ductus maintain its patency. patency. RSD -> prolonged patency of ductus.

Presentation  – 

 –   –   – 

 – 

10% associated with VSD and Coarctation Coarctation of the Aorta Machine Like Murmur No Cyanosis initially Eventual pulmonary HTN and RVH with reversal of flow. Ductus empties into aorta distal distal to origin of left subclavian. Cyanosis of L.E

and toes but not fingers. •

Treatment  –   – 

Closed early as possible. Indocin Indocin suppresses suppresses PgE synthesis. synthesis. -> closes patent ductus

Atri trial Sep Septal Def Defects cts L>R • • • • • •

Most common CHD that is asymptomatic until adulthood. excessive e flow through through pulmonic pulmonic valve. Murmor Murmor Prese Present nt due to excessiv More common in males Eventual reversal of flow with RVH Treatment: Surgical Closure Secund Secundum um Type: ype:  –   –   – 

•

90% of all ASD Defect in area of foramen ovale Fenestrated or deficient septum.

“Endocardial dial Cushion Cushion Defect”: Defect”: Prim Primum um Type ype “Endocar  –   –   – 

10% of all ASD Adjacent to AV valves Foramen Foramen ovale ovale is closed closed

Secu Secunu num m Type ype ASD ASD

Coarct Coarctat ation ion of the Aorta Aorta •

Infantile Form:  – 

 – 

•

coarctation coarctation proximal proximal to a PDA. symptomatic in early children.

Adult Form:  – 

 – 

 – 

 –   – 

 –   – 

discrete discrete infolding infolding of the aorta distal distal to a ligamentum ligamentum arteriosus. asymptomatic until well into adult life . Presents with hypertension in U.E, weak pulses and low BP in L.E. Claudication Enlarged Enlarged intercost intercostal al and internal internal thoracic arteries. arteries. Notching of the ribs on X-ray Significant Significant coarctation coarctation -> LVH LVH and Murmors Murmors Tx: Surgery Surgery excellent results

Rib Notching

Heart Formation (1) •

Heart formation begins at 4 th week.  – 

 – 

 – 

Mesoderm -> pericardial cavity and heart forming region. HFR remodels into a heart tube with 3 layers at the midline. Five Dilations become apparent. •

•

•

•

•

Truncus runcus Arteriosu Arteriosuss -> ascending ascending aorta aorta and pulmonary pulmonary trunk. trunk. Bulbus Bulbus Cordis Cordis -> smooth parts parts of LV LV and RV (outflow (outflow tract) tract) Primitive Ventricle Ventricle -> trabeculated trabeculated parts of LV LV and RV Primitive Atrium -> trabculated trabculated LA and RA. Sinus Venosus Venosus -> Coronary Sinus, Sinus, smooth part part RA

Heart Formation (2) •

Partit Pa rtitoning oning of Primitive Primitive Atrium Atrium  – 

 – 

 – 

 – 

 – 

 – 

1. Foram Foramen en primum primum narrows narrows as septum septum primum grows grows toward toward endocar endocardial dial cushion. cushion. 2.Perforation 2.Perforation in septum primum form foramen foramen secundum. 3. Foramen Foramen secundum maintains right to to left shunt as septum septum secundum secundum begins begins to grow. grow. 4.septum 4.septum secundum secundum contains contains permanent permanent opening opening (Foramen Ovale). 5.Foram 5.Foramen en secundum secundum enlarges enlarges and upper part of septum priumum priumum degenera degenerates. tes. 6. Remaining Remaining portion portion of septum primum forms forms valve valve of  foramen ovale.

Fetal Circulation •

Fetal lungs, kidneys, liver, digestive tract need very little O2.  – 

 – 

 – 

 – 

Oxygenated Oxygenated blood enter into umbilical vein and ascends ascend s to the the fetal liver. liver. Small portion of blood passes portal sinuses Most blood bypasses liver by entering Ductus Venosus which connects with IVC. Blood in IVC is not well oxygenated. •

•

UE -> good O2 conc. LE -> 50% sat

Fetal Changes After Birth •

•

Lungs, GI, Liver become functional. Pulmonary Resistance drops -> pulm. Blood flow increases

•

LA > RA pressure pressure for foramen amen ovale ovale closes. closes.

•

Duct Ductus us Arte Arteri rios osus us -> Lig Ligamen amentu tum m Arte Arteri rios osum um

•

Duct Ductus us Venos enosus us -> Lig Ligam amen entu tum m Venos enosum um

•

Umbilical Arteries -> Medial Umblical Ligaments Ligaments -> Ligament Ligamentum um Teres eres (remains (remains pat patent ent for some time).

Umbilical Vein Connecting Ductus Venosus

Congestive Heart Failure Failure Failur e of the heart as a pump

•

Characterized by forward failure, backward failure, or both

•

Compensatory Mechanisms to Prevent CHF (but eventually become a burden) •

Increased sympathetic stimulation  –   – 

•

Fluid retention  – 

 – 

•

↓CO activates the ReninAngiotensin-Aldosterone System -> ↑VR -> ↑preload -> ↑contractility Leads to edema as failure failure progresses

Cardiac muscle hypertrophy  – 

 – 

Left ventricular hypertrophy as a compensatory mechanism

Norepi ↑HR, contractility Leads to myocardial myocardial ischemia, angina in severe CHF

Volume overload (↑preload) (↑preload) causes dilation and hypertrophy Usually will have a combination of both dilation and hypertrophy

Left Heart Failure •

Etiology:  –   –   –   – 

•

Ischemic heart disease HTN Aortic and mitral valve disease Non-ischemic myocardial disease

Pathology:  – 

 – 

LVH with dilation -> secondary enlargement of the left atrium atrium -> atrial fibrillation -> blood blood stasis -> thromboemboli thromboemboli Lungs due to backward failure: • •

Lung Hemosiderin-laden macrophages  – 

Kidneys due to forward failure: •

 – 

↓CO -> activation of the RAS -> fluid retention -> pulmonary edema

Brain due to forward failure: •

•

Pulmonary congestion and edema **Hemosiderin-laden **Hemosiderin-lad en macrophages (“heartfailure cells”)** : macrophages phagocytize RBC’s in alveolar sacs

Hypoxia -> hypoxic encephalopathy -> stupor, stupor, loss of consciousness, restlessness, coma

Clinical:  –   –   –   –   – 

Dyspnea Orthopnea Cough Fatigue Limb weakness

Right Heart Failure •

Etiology:  – 

 – 

•

Pathology:  – 

Centrilobular passive congestion of  the liver (Nutmeg liver)

Most common cause is left heart failure If isolate isolated: d: cor cor pulmonale pulmonale

 – 

 –   – 

 – 

Backward failure -> congestion of the venous system Hepatomegaly: chronic passive congestion of the liver (“Nutmeg liver”) Splenomegaly Ascites Ascites (fluid (fluid within within the abdomen) Peripheral edema • •

 – 

Pitting ankle (petal) edema

 – 

Ankle Sacrum

JVD Pleural effusions