heart julia Flashcards
CHF pt presentation, frank starling, and workup
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)
CHF: systolic dysfunction vs diastolic dysfunction
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
Left sided Heart Failure
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
Right sided Heart Failure
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
Cardiac Hypertrophy: Pathophysiology
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
Congenital Heart Disease: def and left to right shunt
- 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
List right to left shunts, Tetralogy of Fallot
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
Ischemic Heart Disease
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)
atherosclerotic plaque: stable vs unstable
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
Angina pectoris def and types
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
Myocardial infarction definition
= 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)
sequence leading to most MIs
Atheromatous Plaque Disruption by endothelial injury, mechanical forces
- collagen + necrotic plaques erupt and platelets adhere -> induce vasospasm + coagulation cascade -> thrombus -> complete coronary occlusion
Changes over time in an evolving MI and complications associated with time
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
Diagnosing MI
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
Hypertensive heart disease
usually causes ventricular hypertrophy, CHF may develop, myocardial dysfunction, or sudden death.
Cardiac valves – stenosis versus regurgitation
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)
Aortic Stenosis
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
Aortic Regurgitation
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
Mitral stenosis
Primarily caused by chronic rheumatic heart disease
Mitral regurgitation and MVP
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
Acute rheumatic heart disease: overview and histology
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
acute rheumatic heart disease: jones criteria/clinical presentation
major and minor criteria
may include fever, migratory polyarthritis, myocarditis, subcutaneous nodules, erythema marginatum rash, Sydenham chorea movement disorder.
Chronic rheumatic heart disease
= 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
Heart tumors
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
Pericarditis (the following types describe the pericardial fluid)
Serous – Rheumatic fever, lupus, uremia, etc.
Fibrinous – Dressler syndrome, uremia, radiation
Purulent – acute bacterial
Hemorrhagic – Malignancy, Tuberculosis
Caseous – Tuberculosis
Chronic - adhesive, constrictive
Myocarditis
inflammation of myocardium
- infiltrating lymphocytes in myocardium
Causes:
- Coxsackie A and B and other enteroviruses (MCC)*
- others: CMV, HIV, Trypanosoma cruzii, toxoplasmosis, Lyme disease
Cardiomyopathies: Dilated, Hypertrophic, Restrictive
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
Infectious endocarditis : cause and prognosis
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.
Types of Vegetations
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
