heart julia

Question 1

CHF pt presentation, frank starling, and workup

Answer 1

Presents - tachypnea, dyspnea, edema, cardiomegaly

Frank-Starling mechanism
- inc filling volume –> dilate heart + inc actin-myosin cross bridges –> enhance stroke volume and contractility
- ex: dilated cardiomyopathy, ischemic heart ds

Measure by BNP: indicates ventricular strain
- released by ventricular cardiomyocytes in response to increased wall stress from high filling pressures)

Echo to measure EF and eval valves/walls/clots

tx: salt restriction, diuretics, ACEi, correct underlying cause (valve)

Question 2

CHF: systolic dysfunction vs diastolic dysfunction

Answer 2

Systolic dysfunction = dec ejection fraction; can’t pump blood

Diastolic dysfunction = expanded and stiff chamber, can’t fill well
- normal ejection fracture
- ex: hypertrophic cardiomyopathy, restrictive

Question 3

Left sided Heart Failure

Answer 3

PASSIVE congestion of blood

Presents w/…
- Dyspnea on exertion and at rest
- Orthopnea – redistribution of peripheral edema fluid when lying down to sleep
- Paroxysmal nocturnal dyspnea
- Blood-tinged sputum
- Cyanosis

Complications in organs
- Pulmonary edema: HF cells in lung (hemosderin laden macrophages)
- Fine rales @ lung bases
- Blood back-up into lungs –> lung macrophages eat up the blood

Dec EF -> dec renal perfusion –> activate RAAS –> Na and fluid retention (leading to edema)
- If severe renal hypoperfusion: Pre-renal azotemia (excess nitrogen waste in blood ~~> renal failure)

brain: Irritability and confusion from reduced perfusion

Question 4

Right sided Heart Failure

Answer 4

MCC = left sided heart failure, aka cor pulmonale

Presents w/…
- Fatigue
- Dependent edema
- JVD
- abdominal fullness or discomfort
- Hepatomegaly, ascites
- Pleural and pericardial effusions

Complications in organs - congestion of hepatic and portal vessels –>
Nutmeg liver (patchy congested and necrosed liver) -> hepatomegaly + liver ds AND Congestive splenomegaly

Question 5

Cardiac Hypertrophy: Pathophysiology

Answer 5

Cardiac hypertrophy: increase in the size of cardiomyocytes, which is driven by sustained increases in mechanical work due to:
- Hypertension, Valvular Disease, or Myocardial Infarction
- increases pressure or volume overload = increase cardiac work and wall stress

outcome: hypertrophy or dilation

Question 6

Congenital Heart Disease: def and left to right shunt

Answer 6

• faulty embryogenesis at 3 – 8 weeks of gestation

Left to right shunts: all have D’s in them; can lead to pulmonary HTN, no cyanosis
- ASD
- VSD: MC
- PDA: Patent Ductus Arteriosus; harsh, machinery-like murmur

ASD (Atrial Septal Defect)

VSD (Ventricular Septal Defect) = most common congenital heart defect, associated with Tetralogy of Fallot (30% isolated)
- if large, needs to be surgically corrected, can lead to pulmonary hypertension
- Small ones can close on its own

PDA (Patent Ductus Arteriosus)
- has harsh, machinery-like murmur

Question 7

List right to left shunts, Tetralogy of Fallot

Answer 7

Right to left shunt (all have T’s in them)
- Tetralogy of Fallot *
- transposition of the great arteries *
- persistent truncus arteriosus
- tricuspid atresia
- total anomalous pulmonary venous connection
-> CYANOSIS, HYPOXEMIA, venous emboli become systemic

Tetralogy of Fallot: 4 heart abnormalities
- Obstruction to RV outflow (pulmonic stenosis)
- RV Hypertrophy: needs to be surgically corrected –> “boot-shaped” heart
- VSD
- Overriding Aorta = aorta on top of VSD, not LV –> aorta sends blood from LV AND RV

Transposition of great arteries: Complete switching of the aorta and pulmonary artery –> need shunt for survival + arterial surgical switching
- right ventricle bigger than left ventricle
- fatal in a few months without surgery

Question 8

Ischemic Heart Disease

Answer 8

Ischemic Heart Disease – 90% related to atherosclerosis (plaque)
- Acute atherosclerotic plaque changes include rupture, erosion, hemorrhage

Acute Coronary Syndromes
- Unstable angina
- Acute MI
- Sudden cardiac death (SCD)

Question 9

atherosclerotic plaque: stable vs unstable

Answer 9

Acute atherosclerotic plaque changes include rupture, erosion, hemorrhage
- Happens ONLY when there’s an endothelial injury
- Plaques DON’T have to be severely stenotic to cause acute changes
- Plaques DON’T have to be severely stenotic to cause MI, but it MUST be severely stenotic to cause angina (more chronic changes)

Stable: low macrophages

unstable:
- high macrophage count

Question 10

Angina pectoris def and types

Answer 10

Angina pectoris = chest pain, sudden recurrent lasting up to 15 minutes
- No infarct, but reduced perfusion
- Plaques DON’T have to be severely stenotic to cause MI, but it MUST be severely stenotic to cause angina (more chronic changes)

Types
- Stable angina = chest pain with exertion, relieved by rest or nitroglycerin
- Unstable angina (aka pre-infarct angina) = chest pain at rest, progressive chest pain -> disruption of atherosclerotic plaque + partial thrombus not occluding the coronary artery
- Prinzmetal angina = vasospasm, relieved by nitro

Question 11

Myocardial infarction definition

Answer 11

= necrosis (death) of myocardial tissue
- COAGULATIVE NECROSIS: no nucleus, ghost cell outline

MC = coronary thrombosis superimposed on ruptured plaque –> complete occlusion of affected coronary artery (Aka Coronary artery occlusion)

Most MIs are transmural (full thickness of myocardial wall)
Others are subendocardial (inner 1/3 wall)

Question 12

sequence leading to most MIs

Answer 12

Atheromatous Plaque Disruption by endothelial injury, mechanical forces
- collagen + necrotic plaques erupt and platelets adhere -> induce vasospasm + coagulation cascade -> thrombus -> complete coronary occlusion

Question 12

Changes over time in an evolving MI and complications associated with time

Answer 12

First few hours to 1 day: Wavy fibers/edema followed by coagulative necrosis
- arrhythmias

1-3 days: Neutrophils infiltrate to remove necrotic myocytes and are dominant along with coagulative necrosis (no nucleus + ghost cell outline)
- pericarditis

3 – 7 days: Macrophages dominate
- myocardium softest here: risk of myocardial rupture = CARDIAC TAMPONADE, papillary muscle rupture

7-10 days:
- granulation tissue: macrophages, FIBROBLASTS (which lay down collagen), and angiogenesis
- beginning of scar formation

Weeks to months: Collagen Deposition and Fibrosis
- More and more collagen is laid down by fibroblasts and area becomes acellular
- by 2 months after the MI: scar tissue (fibrosis)
- heart muscle = permanent tissue and cannot regenerate, and therefore heals by scarring/fibrosis
- risk: ventricular aneurysm, Dressler’s Syndrome (2 Weeks to 2 Months, autoimmune pericarditis)

other risk: Congestive Heart Failure (CHF)
- Occurs when >40% of the left ventricular (LV) wall is infarcted

Question 13

Diagnosing MI

Answer 13

chest pain, shortness of breath, diaphoresis, EKG changes, elevation of cardiac enzymes like CK-MB and Troponin

Troponin stays elevated for a longer period of time

Question 14

Hypertensive heart disease

Answer 14

usually causes ventricular hypertrophy, CHF may develop, myocardial dysfunction, or sudden death.

Question 15

Cardiac valves – stenosis versus regurgitation

Answer 15

Stenosis: narrowing of the valve, creating pressure overload.
- Examples: Aortic stenosis (calcification), Mitral stenosis (rheumatic disease).

Regurgitation: Refers to leaky valves, causing volume overload.
- Examples: Mitral regurgitation (MVP), Aortic regurgitation (aortic dilation)

Question 16

Aortic Stenosis

Answer 16

Caused by calcification of deformed valves -> aortic stenosis -> usually results in left ventricular hypertrophy
- Some people are born with a congenital bicuspid aortic valve and calcification will occur earlier

Tx = sx valve replacement

Question 17

Aortic Regurgitation

Answer 17

Occurs when the aortic valve fails to close properly, allowing blood to flow back into the left ventricle during diastole

associated with conditions causing aortic dilation:
- Syphilis
- Rheumatoid arthritis
- Marfan syndrome

Results in left ventricular dilation and hypertrophy due to increased volume load

Question 18

Mitral stenosis

Answer 18

Primarily caused by chronic rheumatic heart disease

Question 19

Mitral regurgitation and MVP

Answer 19

Most Common Cause: Mitral Valve Prolapse (MVP): = myxomatous degeneration of mitral valve resulting in a “floppy” valve)
- 3% pop, F>M
- Ballooned leaflets, long and thin tendinous cords, dilated annulus
- associated with marfan syndrome

Clinical presentation:
- often asymptomatic
- MR: mid-systolic click, followed by a late systolic murmur
- 3 % of cases of MR –> infectious endocarditis, mitral insufficiency, arrhythmias, or even sudden death can occur

Question 19

Acute rheumatic heart disease: overview and histology

Answer 19

Occurs a few weeks after a Group A streptococcal (GAS) infection
- pancarditis (inflammation of all three layers of heart – endocardium, myocardium, and epicardium)

Histology:
- Aschoff bodies
- Anitschkow cells (“caterpillar cells”): Activated macrophages with characteristic wavy nuclei
- Valve vegetations: Form at the valve leaflet junctions, commonly affecting the MITRAL valve

Question 20

acute rheumatic heart disease: jones criteria/clinical presentation

Answer 20

major and minor criteria
may include fever, migratory polyarthritis, myocarditis, subcutaneous nodules, erythema marginatum rash, Sydenham chorea movement disorder.

Question 21

Chronic rheumatic heart disease

Answer 21

= deformed fibrotic valvular dx (mitral valve) -> MITRAL STENOSIS
most commonly affects mitral valve causing thickening and fusion as well as thick, short chordae tendinae

Histological features: Calcified and fibrous valvular commissures –> “fish mouth” stenosis

Question 22

Heart tumors

Answer 22

90% benign, metastasis is rare

Myxomas = rare, MC primary benign heart tumors in adults
- Usually @ left atrium
- if large enough, will affect blood flow

Rhabdomyoma = MC primary benign skeletal mm heart tumor in children
- assoc. with tuberous sclerosis

Question 23

Pericarditis (the following types describe the pericardial fluid)

Answer 23

Serous – Rheumatic fever, lupus, uremia, etc.

Fibrinous – Dressler syndrome, uremia, radiation

Purulent – acute bacterial

Hemorrhagic – Malignancy, Tuberculosis

Caseous – Tuberculosis

Chronic - adhesive, constrictive

Question 24

Myocarditis

Answer 24

inflammation of myocardium
- infiltrating lymphocytes in myocardium

Causes:
- Coxsackie A and B and other enteroviruses (MCC)*
- others: CMV, HIV, Trypanosoma cruzii, toxoplasmosis, Lyme disease

Question 25

Cardiomyopathies: Dilated, Hypertrophic, Restrictive

Answer 25

Dilated (DCM):
- systolic dysfunction, ejection fraction eventually less than 40%
- Many causes including idiopathic, alcohol, peripartum, genetic, myocarditis (especially viral (Coxsackie)), Adriamycin

Hypertrophic:
- dec chamber V –> dec SV –> dec diastolic filling dysfunction
- Many cases are GENETIC: MC gene = Beta-myosin heavy chain
- Sudden death in young athletes

Restrictive (RCM)
- myocardial wall is rigid (NOT thick or dilated)
- Diastolic dysfunction
- Cause - myocardial wall infiltrated with various things such as fibrosis, amyloidosis, or could be idiopathic

Question 26

Infectious endocarditis : cause and prognosis

Answer 26

usually bacterial = Strep viridans
if IV drug user: Staph aureus
Other organisms include enterococci and HACEK (normal oral flora) including Haemophilis influenzae, Actinobacillus, Cardiobacterium, Eikenella, and Kingella

Acute infective endocarditis has a 50% mortality rate, whereas subacute infective endocarditis has a low mortality rate.

Question 27

Types of Vegetations

Answer 27

Rheumatoid – small at chordae tendinae junction

Infectious – large, greater than 5 mm

Non-bacterial thrombotic endocarditis (aka marantic endocarditis) – small, less than 5 mm ; Sterile thrombi - nondestructive, no inflam

Libman-Saks endocarditis (in Lupus) – vegetations on both sides of valves