week 2 heart Flashcards
pericarditis
Inflammation of the pericardium, typically from bacterial infection, friction caused when inflamed pericardial layers rub together. Can be fibrous or effusive- prulent (pus) or hemorrhagic.
acute-superficial myocardium and adjacent pleura- can be fix itself may form scar tissue
chronic- fibrous calcified scar develops between visceral and parietal pericardium can no longer fully fill/expand
Pericardial Effusion
-Accumulation of fluid in pericardial cavity, usually from inflammatory/infectious process
-If severe can cause cardiac tamponade.
Pericardial cavity has little reserve volume (normal volume: ~50ml)
-Increased pressure impedes venous return to heart
Cardiac output and blood pressure decreased
Cardiac Tamponade
Compression of heart secondary to fluid/blood/pus accumulation in pericardial sac
Rapid rise in pressure compresses heart
Obstructs ventricular filling
Limits cardiac output and sv, increases intracardiac pressure- life threatening.
Severity depends on amount of fluid present and speed of accumulation
50 – 100ml can cause tamponade if accumulates rapidly
2000ml if slow accumulation with adaptation
With each contraction, more fluid accumulates, further limiting ventricular filling
becks triad-cardiac tamponade
A constellation of findings indicative of cardiac tamponade:
Muffled heart sounds (due to fluid accumulation)
Jugular vein distension (JVD) (due to
Hypotension
Normally accompanied by a history of thoracic trauma, either penetrating or blunt
Cardiogenic shock
Aortic Aneurysm
Involves any part of aorta; multiple aneurysms may be present
Common cause: atherosclerosis or vessel media degeneration
Thoracic aortic aneurysms account for <10%
Abdominal aneurysms commonly occur below the renal artery bifurcation (90%)
aortic dissection
Acute, life-threatening condition
Haemorrhage into vessel wall and tearing down vessel wall, forming blood-filled channel
Occurs without evidence of vessel dilation
Most involve tearing of ascending aorta
coronary artery disease
CAD- change in blood vessels such as loss of elasticity, narrowing of the lumen and vessel walls becoming thick and less compliant.
-due to fatty plaques accumulating in the coronary vessels. Atherosclerosis ( fatty build up on walls causing Turbulent and decreased blood flow)
-Results in less oxygen & nutrients to heart- myocardial ischaemia
-As atherosclerosis progresses, vessels cannot dilate causing
“double whammy” – limited space and no dilation
When oxygen demand increases, localised myocardial ischaemia occurs
concequences of CAD
- 10secs decreased myocardial function, but reversable
- several minutes-heart muscles forced into anerobic mechanism- lactic acid build up
- prolonged-tissue injury death
- also may cause May cause myocardial ischaemia, angina, MI, cardiac arrhythmias, conduction defects, heart failure & sudden cardiac death
causes of CAD
Major risk factors include smoking, hypertension, hypercholesterolemia, diabetes, advancing age, abdominal obesity, & physical inactivity
Patients with diabetes & metabolic syndrome experience much higher risk of CAD & significant morbidity
Stable vs Unstable Plaque
-Fixed/stable plaque: fixed obstruction of coronary blood flow; myocardial ischaemia occurs when increased metabolic need
Common cause of stable angina
-Unstable/vulnerable plaque: can rupture, causing platelet adhesion & thrombus formation
Cause of myocardial ischaemia, acute MI, stroke &SCD
Precipitated by abrupt plaque changes, followed by thrombosis
Acute Coronary Syndrome (ACS)
includes MI, UA and NSTEMI and STEMI
Unstable Angina (UA)
Formation of a thrombus that does not cause a complete occlusion or myocardial damage
Rapid onset, irrespective of activity
Lasts longer than ~20 minutes
Unrelieved/little effect with nitrates or with little affect
Characteristic, with at least one of the following:
-Occurs at rest/minimal exertion; >20 minutes duration
-Severe & of new onset (within last 4 – 6 weeks)
-Occurs with crescendo pattern (distinctly more severe, prolonged, or frequently than previously)
MI
- death of a portion of heart muscle from prolonged deprivation of oxygenated arterial blood.
- also if hearts oxygen demand exceeds its supply over an extended time.
- is most often associated with atherosclerotic heart disease.
- precipitating event is commonly the formation of a thrombus within a coronary artery that is already diseased from arthrosclerosis.
- location and size of the infarction depend on the vessel involved and the site of the obstruction.
- Most involve the Left ventricle.
- An MI may involve changes on the ECG (STEMI) or not (NSTEMI),
- can also be determined by blood tests performed in hospital, which examine whether troponin has been released by the dying muscle. An initial blood test is completed, followed by another 1-4 hours later (as it takes this long for a release to be seen in the bloods).
NSTEMI & STEMI
differ in extent of myocardial damage
STEMI may result in fatal arrhythmias, heart failure & cardiogenic shock, pericarditis, thromboemboli, rupture of cardiac structures, & ventricular aneurysm
acute myocardial infarction
Death of portion of heart muscle from prolonged deprivation of oxygenated arterial blood (>30-45 minutes)
