Cardiovascular pathology 2 Flashcards
HEART FAILURE (RIGHT AND LEFT)
Inability of the heart to pump enough blood needed to meet the metabolic demands of the tissue.
Occurs insidiously or suddenly.
Cumulative effects of chronic workload (Hypertension and valve diseases) – Insidious
Acute haemodynamic stress (fluid overload and large myocardial infarction) – sudden.
Aetiology: increased cardiac work, increased all stress and cell stretch enhanced contractility.
LEFT SIDED heart failure
Low cardiac output and hypoperfusion of tissues or Pulmonary congestion and oedema.
Pulmonary congestion Symptoms: dyspnea, orthopnea (difficulty breathing lying down), paroxysmal nocturnal dyspnea, blood tinged sputum, cyanosis and elevated pulmonary wedge pressure.
Low cardiac output: Reduced kidney perfusion: pre-renal azotemia / renin-angiotensin-aldosterone activation salt and fluid retention (expansion of interstitial and intravascular fluid volume)
Advanced cardiac failure can lead to cerebral hypoxia – irritability, restlessness, stupor and coma
RIGHT SIDED heart failure
Aetiology: left heart failure and cor pulmonale.
Symptoms: Engorgement of systemic and portal systems.
Liver and spleen (portal congestion) passibe congestion (nutmeg liver)m Congestive splenomegaly, ascites, congestion and oedema of peripheral and dependent parts of body wall.
Pleura/pericardium (systemic nevous congestion): pleural and pericardial effusions, transudates. Oedema of peripheral and dependent parts of body.
Cardiac changes of heart failure: cardiomegaly, chamber dilatation, hypertrophy of myocardial fibres, boxcar nuclei.
VALVULAR HEART DISEASE
Opening problems: stenosis. Failure of valve to open completely impeding forward flow. Leads to pressure overload of heart. Almost always due to chronic abnormality.
Closing problems: regurgitation or incompetence/insufficiency.
70% of all VHD = Aortic stenosis: calcification of a deformed valve, Mitral stenosis: rheumatic heart disease
Rheumatic heart disease
Follows a group A strep infection a few weeks later. Decreased in MEDC.
Pancarditis: 1) endocarditis, 2) myocarditis 3) pericarditis.
Acute: inflammation, aschoff bodies, anitschkow cells, pancarditis, vegetations on chordae tendinae at leaflet junction.
Chronic: Thickened valvles, commissural fusion, thick, short chordae tendinae.
Clinical features: evidence of preceding strep infection, +2 major manifestations or 1 major + 2 minor. Major = migratory arthritis/pericarditis. Appears many years after initial episode of rheumatic fever. Depends on which cardiac valve involved. Cardiac murmurs, cardiac hypertriphy
Calcific aortic stenosis
most common valuvular abnormality.2% prevelance. Consequence of age related wear and tear. Bicuspid valve undergoes
Acquired Aortic stenosis
2X gradient pressure, LVH (but no hypertension), ischemial Cardiac decompensation, angina, CHF, 50% die in 5 years if angina present, 50% die in 2 years if CHF present.
Acquired Regurgitations
Aortic: Rheumatic, infectious, aortic dilatations (syphilis, rheumatic arthritis, marfan).
Mitral: MVP- infectious, fen-phen, papillary muscles, chordae tendinae, calcification of mitral ring (annulus).
Mitral Valve Prolapse: myxomatous degeneration of the mitral valve, associated with connective tissue disorders. “Floppy valve”, F>M and easily seen on echocardiogram.
Clinical features: Usually asymptomatic, Mid-systolic “click”, Holosystolic murmur if regurg. present
Occasional chest pain, dyspnea. 97% NO untoward effects. 3% Infective endocarditis, mitral insufficiency, arrhythmias, sudden death.
Mitral annular calcification:
Calcification of the mitral “skeleton”. Usually NO dysfunction. Regurgitation usually, but Stenosis possible, F»M +60yrs. Increased risk of infective endocarditis
CONGENITAL HEART DISEASE: due to faulty embryogenesis (week 3-8). 1% all births.
Sporadic genetic abnormalities. Region of chromosome 22 important in heart development: 22q11.2 deletion conotruncus. Also downs syndrome.
Environmental factors: rubella, gestational diabetes and teratogens
L–>R shunts
“D’s” in their names, NO cyanosis, Pulmonary hypertension
SIGNIFICANT pulmonary hypertension is IRREVERSIBLE. ASD, VSD, AVSD, Patent Ductus arteriosus.
R–> L shunts
T’s” in their names, CYANOSIS (i.e., “blue” babies).
Tetralogy of fallot, transposition of great arteries, truncus arteriosus, total anomalous pulmonary venous connection, tricuspid atresia.
Obstructions
aorta or pulmonary artery. VENOUS EMBOLI become SYSTEMIC “paradoxical”
ASD- Atrial septal defect: L–> R shunt
NOT patent foramen ovale, usually asymptomatic until adulthood. Secundum (90% defective fossa oxalis). Primum (next to AV valves, mitral cleft. SINUS VENOSUS (5% next to SVC with anomalous primary veins draining to superior vena cava OR RA.
VSD- Ventricular septal defect: L–> R shunt
. Most common CHD defect. Only 30% are isolated. Often with TETRALOGY of FALLOT. 90% involve the membranous septum. If muscular septum is involved, can have multiple holes (“swiss-cheese”septum). SMALL ones often close spontaneously. Large progress to pulmonary hypertension.
