Cardiac Pathology Flashcards
(47 cards)
Pericarditis features
Pericardial friction rub which is relieved when leaning forwards
Pleuritic chest pain after recent infection
Diffuse concave ST elevation and PR depression on ECG
Pericarditis causes
Viral and idiopathic (most common – 90%)
Uraemia (seen in Chronic Kidney Disease)
Post MI (Dressler’s syndrome)
Granulomatous (TB)
Fibrous (a.k.a. restrictive) (arises from any of above)
Pericardial Effusion/Cardiac Tamponade/Haemopericardium causes
Chronic heart failure
Exudative fluids occur secondary to inflammatory, infectious, malignant, or autoimmune
Pericardial Effusion/Cardiac Tamponade/Haemopericardium presentation
Can lead to cardiac tamponade
Beck’s triad -
1. Muffled Heart Sounds
2. Raised JVP
3. Hypotension
Haemopericardium
Blood in the pericardial sac, which can arise following myocardial rupture from myocardial infarction or traumatic injury.
Atherosclerosis definition
Chronic inflammation in tunica intima (innermost layer) of large arteries characterized by intimal thickening and lipid accumulation.
Damage mainly from cigarette smoke and high blood pressure.
Atherosclerosis diseases
Stroke
Ischaemic heart disease
Peripheral arterial disease
Chronic mesenteric ischaemia
Atherosclerosis steps
Endothelial injury causes accumulation of LDL.
LDL enters intima and is trapped in sub-intimal space.
LDL is converted into modified and oxidized LDL causing inflammation.
Macrophages take up ox/modLDL via scavenger receptors and become foam cells.
Apoptosis of foam cells causes inflammation and cholesterol core of plaque.
Increase in adhesion molecules on endothelium due to inflammation results in more macrophages and T cells entering the plaque.
Vascular smooth muscle cells form the fibrous cap, segregating thrombogenic core from lumen.
Atherosclerotic plaque components
Cells - including SMC, macrophages and other leukocytes
Extracellular matrix proteins including collagen
Intracellular and extracellular lipid
Atherosclerosis site
Abdominal aorta affected more than thoracic aorta – can lead to an AAA which typically presents as an older man who is a long-term smoker who has presented with back pain and LOC.
More prominent around origins (ostia) of major branches - turbulent blood flow has low/oscillatory shear stress, which is atherogenic. High laminar flow is protective.
Increased cap thickness confers greater stability and lower rupture risk.
Atherosclerosis risk factors
Modifiable: Type 2 Diabetes Mellitus, Hypertension, Hypercholesterolaemia, Smoking
Non-modifiable: Gender (Males>Females), increasing age, Family History
Ischaemic heart disease definition
Group of conditions that occur when oxygen supply < demands of the myocardium due to narrowed coronary vessels. Includes stable/unstable angina.
Ischaemic heart disease features
Stable angina: ~70% vessel occlusion – pain on exertion
Unstable angina: ~>90% vessel occlusion – pain at rest also, and usually normal troponins which distinguishes it from NSTEMI. High likelihood of impending infarction.
Prinzmetal angina: Rare, due to coronary artery spasm rather than atherosclerosis.
Myocardial infarction pathogenesis
Coronary atherosclerosis
Plaque rupture
Superimposed platelet activation
Thrombosis and vasospasm
Occlusive intracoronary thrombus overlying disrupted plaque
This results in myocardial necrosis secondary to ischaemia. Severe ischaemia lasting >20-40mins results in irreversible injury and myocyte death.
Complications of MI
Death
Rupture of the ventricle
Edema (congestive cardiac failure)
Arrhythmia/Aneurysm
Dressler’s syndrome – pericarditis signs 4 weeks after MI
Evolution of MI - histological findings
Under 6 hours - normal by histology (CK-MB also normal)
6–24 hrs - loss of nuclei, homogenous cytoplasm, necrotic cell death
1-4 days - infiltration of polymorphs then macrophages (clear up debris)
5-10 days - removal of debris
1-2 weeks - granulation tissue, new blood vessels, myofibroblasts, collagen synthesis
Weeks to months - strengthening, decellularising scar tissue.
Heart failure principles
Preload: Initial stretch of cardiomyocytes before contraction due to ventricular filling → increase will
increase stroke volume.
Afterload: Pressure of vessels (aortic or pulmonary artery pressures) against which heart must contract to eject blood → increase in afterload will decrease stroke volume.
Common causes of heart failure
Cardiomyopathy (dilated)
Hypertension
Arrhythmias
Valve disease
Ischaemic heart disease
Myocarditis
Heart failure complications
Sudden Death (largely arrythmia)
Systemic emboli
Arrhythmias
Heart failure pathophysiology
Pulmonary oedema with superimposed infection
Haemosiderin-laden macrophages (heart failure cells)
Hepatic cirrhosis (nutmeg liver)
Heart failure cycle
Chronic preload -
Cardiac damage - decreased cardiac output - activation of RAS (renin-angiotensin system) - salt and water retention = compensatory mechanism to maintain perfusion. Decompensation - fluid overload.
Chronic after load -
Cardiac damage - decreased stroke volume - activation of sympathetic nervous system via baroreceptors (detect low BP) - maintains perfusion. Eventually - increased total peripheral resistance - increased afterload - LVH and increased EDV - dilatation and poor contractility
LV failure
Pooling of blood in pulmonary circulation due to L side of the heart pumping against high pressures - dyspnoea, orthopnoea (shortness of breath when lying flat), paroxysmal nocturnal dyspnoea (waking up short of breath at night), wheeze, fatigue, pulmonary oedema; eventually - decreased peripheral blood pressure and flow.
RV failure
Most common cause is secondary to LVF, but can be primarily caused by chronic severe pulmonary hypertension.
Minimal pulmonary congestion, but engorgement of systemic and portal venous systems - peripheral oedema, ascites, facial engorgement clinically. Congestion and stasis of venous blood
in the liver causes nutmeg liver.
Heart failure investigations
BNP/ NT-proBNP – elevated
CXR – pulmonary oedema (batwing appearance)
ECG, Echo
