CH 8: Cardiac Pathology (mine)

Ischemic Heart Disease (IHD) is?

Ischemic Heart Disease (IHD) is?

Group of syndromes related to myocardial ischemia

Left sided heart failure presents as?

-Decreased Ejection Fraction

-Bibasilar crackles in lung/rales

• liquid accumulates in alveoli due to left heart pressure overload —> alveoli pop open during inhalation, causing rales

-S3 or S4

-exertional dyspnea, orthopnea, paroxysmal nocturnal dyspnea, or persistent coughing.

-ankle edema + abdominal fullness (ascites +hepatojugular reflex)

Describe Right-sided heart failure

-Atrial fibrillation

- JVD (don’t be confused w/JVP)—> Kussmaul breathing (PARADODIXAL INCREASE IN jvp WHEN INSPIRATION

-hepatojugular reflux

-Nutmeg liver & hepatomegaly

-Ankle edema & Ascites

Differentiate between S3 & S4

S3 = systolic failure, diastolic rumble due to excess blood volume in overload (normal in young ppl)

• Increased volumes of blood move from the LA —> compliant LV ventricle resulting in a characteristic low-pitched sound as blood fills the chamber.

• Systolic heart failure with decreased left ventricular contractility and increased end systolic volumes.
  

S4 = Diastolic failure,, systolic rumble bc of hypertrophic/thick heart

What causes S3 & S4

S3 = young, pregnant, CHF, mitral regurgitation, dilated cardiomyopathy

S4 = HCOM, Restrictive cardiomyopathy(will have Kussmaul)

What is the leading cause of death in the US?

IHD

IHD is usually due to?

Atherosclerosis of coronary arteries which decreases blood flow to the myocardium

Risk factors for IHD?

Increase in age bc it correlates with risks for atherosclerosis

Stable angina is?

Chest pain that arises with exertion or emotional stress

Stable angina is due to?

Atherosclerosis of coronary arteries with >70% stenosis.

The decreased blood flow is not able to meet the metabolic demands of the myocardium during exertion --> injury to myocardium causing chest pain

Damage to myocytes in stable angina?

Reversible injury (cellular swelling)

*No necrosis

Stable angina presents as?

Chest pain lasting <20mins that radiates to the left arm or jaw, diaphoresis, and SOB

What is diaphoresis?

Sweating, especially to an unusual degree as a symptom of disease or a side effect of a drug.

EKG on a patient with stable angina reveals?

ST segment depression due to subendocardial (between myo & endo) ischemia

What relieves stable angina?

• rest

• Nitroglycerin (vasodilates)

What is unstable angina?

Chest pain that occurs at REST

Unstable angina is usually due to?

Rupture of an atherosclerotic plaque with thrombosis and incomplete occlusion of a coronary artery

*So a baby bit of blood can flow through, just enough to keep myocardium alive

Keywords for stable vs unstable angina?

Stable = atherosclerosis caused stenosis (>70%)

Unstable = thrombosis due to ruptured plaque (incomplete occlusion)

Damage to myocytes in unstable angina?

Reversible injury to myocytes with no necrosis

EKG on patient with unstable angina shows?

ST segment depression due to subendocardial ischemia

What relieves unstable angina?

nitroglycerin

What does unstable angina carry a risk of?

Progression to myocardial infarction

Prinzmetal angina clinically presents as?

episodic chest pain unrelated to exertion

Prinzmetal angina is due to?

coronary artery vasospasm

Damage to myocytes in prinzmetal angina?

reversible injury with no necrosis

EKG on patient with prinzmetal angina shows?

ST segment elevation due to transmural ischemia

*not ST depression like unstable & stable

What relieves prinzmetal angina?

• Balloon Angioplasty, Stents, Coronary Bypass surgery

• nitroglycerin (decrease preload)

• calcium channel blockers (reduce vasospasm)

What drug should you NOT give in Prinzmental angina?

Beta blockers bc they can cause more spasm

*** So only give Beta blockers in Stable & Unstable angina (can combine with NTG)

What does transmural mean?

existing or occurring across the entire wall of an organ or blood vessel- like in prinzmental angina

Myocardial Infarction(MI) is?

Usually due to?

Other causes include?

Necrosis of cardiac myocytes

Rupture of atherosclerotic plaque with thrombosis and complete occlusion of a coronary artery.

What are some causes/risk factors for MI?

• coronary artery vasospasm(due to Prinzmetal angina or cocaine use),

• Emboli

• vasculitis(ie Kawasaki disease)

• Also unstable angina can lead to it (incomplete occlusion)

Clinical features of MI?

Severe crushing chest pain lasting >20mins that radiates to left arm or jaw, diaphoresis, and dyspnea (due to pulmonary congestion & pulmonary edema).

*Symptoms are not relieved with nitroglycerin

MI usually involves what portion of the heart?

Left ventricle; RV and both atria usually spared

Most commonly involved artery of MI? 2nd most common?

Left anterior descending artery

Right coronary artery

Occlusion of LAD leads to infarction of?

Occlusion of RCA leads to infarction of?

Occlusion of left circumflex artery leads to infarction of?

Anterior wall and anterior septum of LV.

Posterior wall, posterior septum, and papillary muscles of LV.

Lateral wall of LV

Initial phase of MI leads to?

Continued or severe ischemia leads to?

Subendocardial necrosis involving < less than 50% of the myocardial thickness (subendocardial infarction).

Since still subendocardial, still shows ST segment depression (not yet characteristic ST elevation)

Continued MI or severe ischemia

Transmural necrosis involving most of the myocardial wall(transmural infarction) = ST elevation

Laboratory findings in MI? What are the cardiac enzymes?

EKG - ST segment depression

Troponin I - Levels rise for 2-4hrs after MI, peak at 24hrs, and return to normal in 7-10 days. This is the most sensitive and specific marker, the gold standard for MI.

Creatine Kinase - MB (CK-MB) - rise 4-6 hrs after infarction, peak at 24 hrs, and return to normal by 72 hrs

What is CK-MB useful for?

Detecting reinfarction that occurs days after initial MI

Treatment for MI includes? Include what each treatment accomplishes.

Aspirin and/or heparin - limits thrombosis

Supplemental O2 - minimizes ischemia

Nitrates - vasodilates veins and coronary arteries

ß blockers - slows heart rate, decreases O2 demand and risk for arrhythmia

ACE inhibitor - decreases LV dilation (blocks vasoconstriction of peripheral arterioles & decrease blood volume

Fibrinolysis or Angioplasty - opens blocked vessel

What does Fibrinolysis & Angioplasty essentially do?

What are the 2 bad outcomes?

Once dissolving clot it reperfuses (brings in new blood to) the irreversibly damaged cells

Contraction band necrosis & Reperfusion Injury

What occurs when you reperfuse irreversibly damaged cells after MI?

Results in calcium influx —> hypercontraction of myocytes (contraction band necrosis)

The return of oxygen and inflammatory cells —> ROS generation further damaging myocytes (reperfusion injury)

What are the gross changes, microscopic changes, and associated complications at different time points after MI?

<4hrs: no gross/microscopic changes —> cardiogenic shock(massive infarct), congestive heart failure, and arrythmia.

4-24hrs: Dark color = Coagulative necrosis (removal of nucleus due to necrosis)—> arrhythmia

1-3days: yellow pallor; Inflammation so neutrophils —> Fibrinous pericarditis

4-7 days: yellow pallor; Macrophages to clean up dead stuff —>Rupture of:

• ventricular free wall (leads to cardiac tamponade)

• interventricular septum (leads to shunt)

• Papillary muscles (leads to mitral insufficiency)

  • Especially in Right coronary artery occlusion

1-3 weeks (starting to heal, softening): Red border emerges as granulation tissue enters from edge of infarct; granulation tissue with plump fibroblasts, type 1 collagen, and blood vessels —> then red —> gray

Months: White scar; Fibrosis —>

• Aneurysm, mural thrombus, or Dressler Syndrome

How to remember all these stages of MI?

Fibrinous Pericarditis (like in MI)presents with?

Chest pain with friction rub- only in trasmural ischemia

What is Dressler Syndrome? When can you get it?

Autoimmune pericarditis

Months after an MI

Sudden cardiac death is _____ and usually due to?

When and how does it occurs?

Unexpected death due to cardiac disease that is usually due to fatal ventricular arrhythmia

Occurs without symptoms or

Most common etiology for sudden cardiac death?

Less common causes?

Acute ischemia

mitral valve prolapse, cardiomyopathy, and cocaine abuse

Most patients who died as a result of sudden cardiac death had?

Preexisting atherosclerosis(90% of patients)

Chronic Ischemic Heart Disease is?

Poor myocardial function due to chronic ischemic change(with or without infarction) that progresses to congestive heart failute (CHF)

CHF is?

Pump failure, can be right or left sided

Causes of left sided CHF?

Think DR. HIM

• Dilated cardiomyopathy

• Restrictive cardiomyopathy

• HTN —> Hypertrophy

• Ischemia

• MI

What is dilated cardiomyopathy? What is restrictive cardiomyopathy

D: 4 chamber dilation that stretches the muscle —> can’t contract as well

R: can’t fill the heart properly —> so can’t pump it properly either

Clinical features of left sided CHF are due to?

Features include?

Pulmonary congestion & decreased forward perfusion

1. Pulmonary congestion= pulmonary edema w/ dyspnea, paroxysmal nocturnal dyspnea, orthopnea, and crackles (fluid)

   1. Heart failure cells (hemosiderin laden macrophages): small congested capillaries may burst leading to intra-alveolar hemorrhage

   2. Pleural effusions, pulmonary edema, pulmonary congestion

2. Decreased flow to kidneys leads to activation of RAS system (txt w/ ACE inhibitor)

*Secondary hypoperfusion —> renal + cerebral dysfunction

How does pulmonary congestion lead to paroxysmal nocturnal dyspnea?

Increased venous return while lying flat

What can exacerbate CHF?

Increased total peripheral resistance bc of Angiotensin II

Increase in Fluid retention- bc of release of aldosterone (due to Angiotensin II)

Treatment of CHF?

Mainstay is an ACE inhibitor

Right sided CHF is most commonly due to?

Other important causes include?

Left sided heart failure.

Left to right shunt and chronic lung disease (cor pulmonale = pulmonary HTN & right heart hypertrophy)

Clinical features of right sided CHF are due to?

Features include?

Congestion.

• JVD,

• painful hepatosplenomegaly with characteristic 'nutmeg' liver that may lead to cardiac cirrhosis, dependent pitting edema.

How does congestion in right sided CHF lead to pitting edema?

Increased hydrostatic pressure

Congenital heart defects arise during?

Seen in what % of births?

Most defects are?

Embryogenesis(usually weeks 3-8)

1% of live births

Sporadic

Congenital heart defects often result in?

Shunting between left(systemic) and right(pulmonary) circulations

Defects of left to right shunting at birth result in?

Can be relatively asymptomatic at birth but eventually shunts can reverse.

How do the L—> R shunts reverse?

Increased flow through pulmonary circulation—> Hypertrophy of pulmonary vessels and pulmonary HTN —> both leading to increased pulmonary resistance —> reverse shunt

What are the consequences of a L-R shunt reversal?

Late cyanosis(eisenmenger syndrome) with RV hypertrophy, polycythemia, and clubbing.

Defects with right to left shunting usually present as ______ after birth.

Cyanosis

What is Eisenmenger syndrome?

Late cyanosis, pulmonary hypertension, and erythrocytosis. Seen in LEFT to right shunt (not right to left)

Most common congenital heart defect?

Ventricular Septal Defect(VSD)

A VSD is?

Associated with?

Defect in septum that divides RV and LV

Fetal alcohol syndrome & Teratology of Fallot

A VSD results in?

Left to right shunt

Size of VSD defect determines?

Extent of shutting and age of presentation.

• Small defects are often asymptomatic and large defects can lead to eisenmenger syndrome

Treatment of VSD?

Surgical closure, small defects may close spontaneously

Atrial Septal Defect (ASD) is?

A defect in septum that divides the atria(ostium primum and ostium secundum types)

Most common type of ASD?

Ostium secundum(90% of cases)

Ostium primum ASD is associated with?

Down syndrome

ASD results in?

Important complication of ASD?

Left to right shunt with split S2 on auscultation.

Paradoxical emboli

What causes an S2 split?

Increased blood in Right heart delays closure of pulmonary valve

Patent Ductus Arteriosus(PDA) is?

Associated with?

Failure of ductus arteriosus to close at birth

congenital rubella

PDA results in?

left to right shunt between aorta and pulmonary artery bypassing lungs

Normal function of ductus arteriosus?

During development, shunts blood from pulmonary artery to aorta to bypass lungs

Symptoms of PDA?

Asymptomatic at birth with continuous 'machine like" murmur; may lead to Eisenmenger syndrome (late cyanosis), resulting in lower extremity cyanosis

Treatment of PDA?

Indomethacin= an NSAID that decreases PGE1 (prostaglandin E1 that keeps PDA) resulting in PDA closure.

Tetralogy of Fallot is?

A right to left shunt that leads to early cyanosis

What congenital heart defect causes Left to right shunts (that can lead to late cyanosis or Eisenmenger)?

• PDA

• ASD (but can also be R-L in tricuspid atresia)

• VSD (large, but can also be R-L in teratology of fallot)

• AVSD (atrioventricular septal defect)

• L—R shunt reversal due to increased pulmonary resistance

Tetralogy of Fallot is characterized by?

Think VORS

VSD

Overriding Aorta

RV hypertrophy

Stenosis of RV outflow tract

What determines that extent of shunting and cyanosis in Tetralogy of Fallot?

Degree of stenosis

What do patients learn to do with Tetralogy of Fallot that helps alleviate cyanotic spells? Why does this work?

Squatting.

Increases arterial resistance = decreases shunting and allows more blood to reach lungs

What do you find on X-Ray in tetralogy of fallot?

"boot shaped" heart

Transposition of the Great Vessels is characterized by?

Results in?

Pulmonary artery arising from LV and aorta arising from RV (the arteries are the opposite places!)

Hypertrophy of RV and atrophy of LV

Transposition of the Great Vessels is associated with?

Maternal diabetes

Transposition of the Great Vessels presents with?

Presents early with cyanosis, as pulmonary and systemic circuits do not mix (so txt will fix this)

Transposition of the Great Vessels treatment?

Creation of shunt, to allow blood to mix, after birth is necessary for survival. Surgical correction is required.

• PGE can be administered to maintain a PDA until definitive surgical repair is performed

Truncus Arteriosus is characterized by?

Single large vessel arising from both ventricles due to the truncus failing to divide.

Truncus Arteriosus presents with?

Early cyanosis. Deoxygenated blood from RV mixes with oxygenated blood from LV before pulmonary and systemic circuits separate

Tricuspid Atresia is?

Often associated with ______ which results in?

Presents with?

Tricuspid valve orifice fails to develop so the RV is hypoplastic

Associated w/ ASD —> resulting in R-L shunt (early cyanosis)

Coarctation of the Aorta is?

Narrowing of the aorta; adult and infantile forms

Infantile Form of Coarctation of the Aorta is associated with?

Where does the narrowing lie?

Presents as?

PDA and also Turner Syndrome (think PDA in front of kids is bad!)

Distal to aortic arch but proximal to PDA (after arch, before PDA)

Lower extremity cyanosis in infants, often at birth

Adult form of Coarctation of the Aorta is associated with?

Where does the narrowing lie?

Presents as?

What is seen on Xray? Why?

Associated w/ Bicuspid aortic valve

Distal to aortic arch (bc adults don’t have their PDA anymore)

What does Adult Coarctation of the aorta present as? What are the symptoms?

Symptoms: HTN in upper extremities and hypotension with weak pulses in lower extremities.

Notching of ribs due to engorged arteries ( collateral circulation developing across intercostal arteries)

What are the four valves of the heart and what do they do?

Bicuspid(mitral), tricuspid, pulmonary and aortic.