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)
Coronary Atherosclerosis
Most common cause of CAD
Slow & progressive
Begins at very young age among developed countries
Can affect one or all three major epicardial coronary arteries
causes ACS and IHD
Stable Angina
Associated with fixed coronary obstruction
Heart’s blood supply transiently exceeded by myocardial oxygen demand
Relationship between workload/demand & ischemia is usually relatively predictable-is brief and fixed with medication
Typically provoked by exertion or stress
Delay of 5 – 10 minutes pre-relief (rest or nitrates)
Silent Myocardial Ischaemia
Absence of anginal pain, but causative factors same as angina
-common in people with diabetes as have screwed pain factors
Variant (Vasospastic/Prinzmetal) Angina
Spasm of coronary arteries
Causative factors not completely understood
May be associated with dysregulation of vasoactive substances (NO, calcium), endothelium dysfunction, or hyperactive sympathetic NS responses
Usually occurs during rest/with minimal exercise
Frequently occurs nocturnally
Arrhythmias may occur with severe pain
why CAD causes movement to smaller vessels
With gradual occlusion of larger vessels, smaller vessels increase in size to provide alternative channels for blood flow
Consequently, CAD is asymptomatic until far advanced, as collateral channels develop at same time as atherosclerotic changes occur
heart failure
-heart cannot pump sufficiently to meet body’s needs
- A result of functional or structural disorders of heart that reduce pumping ability
-causes low cardiac output & pulmonary or systemic congestion
-either Left- or right-sided failure
-Systolic dysfunction (inability for the heart to contract)
Diastolic dysfunction (inability for the heart to relax)
Initial event causing heart failure may be one-sided, but eventually involves both sides
right sided heart failure
- blood backlogs into right atrium & peripheral circulation
-Due to ineffective right ventricular contractility
-Deoxygenated blood from systemic circulation cannot be moved into pulmonary circulation and left side of heart
-Causes decreased left ventricular c/o, Congestion of blood in systemic venous system, increased right ventricular, atrial systemic venous pressures
-Peripheral oedema develops
Accumulates according to gravity
causes-CAD, Hypertension, dilated cardiomyopathy, & valvular heart disease
left sided heart failure
-left ventricle working ineffectively so cardiac output decreases, and blood backlogs into left atrium & lungs
-Movement of blood from low-pressure pulmonary circulation into high-pressure arterial systemic circulation impaired
-Causes decreased cardiac output to systemic circulation
-Blood accumulates in left ventricle, atrium & pulmonary circulation, causing increased venous pressure
-Intravascular fluid shifts into interstitium of lung causing pulmonary oedema
-LV dysfunction commonly caused by hypertension and MI
Heart failure & pulmonary congestion can occur rapidly in acute MI
common cause of right-sided hf
Most common cause of right ventricular failure is left failure
Sustained pulmonary hypertension also causes right ventricular dysfunction & failure
Jugular veins are large veins that drain blood from the head & return it to the heart.
When they bulge, it indicates systemic venous pressure: when the heart in unable to pump blood back out, venous pressure increases & they ‘pop’ out of neck
Pedal oedema occurs with increasing hydrostatic pressure
