Download 16 Heart A

Myocardium
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Inflamed outer layer of the heart.
Pericarditis can be caused by damage to the blood
vessels (from infection, wound, autoimmune
disease, etc)--blood leaks into pericardial cavity
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Pericarditis can lead to pericardial friction rub,
adhesions, additional excess fluid in the pericardial
cavity, or improper heart beat (cardiac tamponade).
It does NOT cause myocardial infarction.
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CARDIAC TAMPONADE
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Endocarditis
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Pulmonary Semilunar Valves
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Deoxy blood  sup/inf vena cava  R atrium 
tricuspid valve  R ventricle  pulmonary
semilunar valve  pulmonary artery  lungs 
pulmonary veins  Left atrium  mitral
(bicuspid) valve  Left ventricle  aortic
semilunar valve  aorta  rest of body.
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The pulmonary circulation
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The Semilunar valves
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Vibrations that result from blood hitting the semilunar
valves after they slam shut.
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SYSTOLE
-Ventricles contract
-Atria relax
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DIASTOLE:
-Ventricles relax
-Atria contract
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Start of Systole (ventricles start to contract):
Closing of the large valves (tricuspid and mitral)
End of Systole (ventricles are relaxing):
Semilunar valves are closed (aortic and
pulmonary)
Note: Systole means that the ventricles are
contracting.
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Mitral valve prolapse
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1. First the Sinoatrial (SA) node starts an action
potential which causes the atria to depolarize.
2. This depolarization will then reach the AV node at the
bottom portion of the right atrium and there is a delay
here because these cells are so small in diameter.
3. Another delay in the transmission of the
depolarization at the bundle of His (AV bundle)
because these special heart cells travel through the
atrioventricular septum which is non-conductive
fibrous connective tissue.
4. Next, the depolarizing event travels through the left
and right bundle branches, found in the
interventricular septum, to finally arrive at the
Purkinje fibers in the ventricular myocardium.
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ARRHYTHMIA
Treatment is medicines or a pacemaker.
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Too fast: tachycardia
Too slow: bradycardia
VENTRICULAR FIBRILLATION
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Angina
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ISCHEMIA: Lack of blood/ oxygen
Myocardial infarction
No, death takes about 2 hours in 50% of the cases.
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t-PA (dissolves blood clots)
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Beta-blockers (slows heart rate)
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Aspirin (prevents blood clots)
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Nitroglycerine (dilates coronary arteries)
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Arteriosclerosis is hardening of the arteries,
caused by a build-up of calcium deposits in the
artery wall; artery cannot expand with blood surges.
Tends to be hereditary.

Atherosclerosis is caused by a build-up of fat in the
arteries, from eating fatty foods -narrowing of
artery -- Spasm shut or blood clot.
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Both cause High Blood Pressure
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A thrombis is a blood clot.
An embolism is a piece of blood or fat clot that has
broken off and travels in the bloodstream.
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If the embolism lodges in the coronary arteries -
myocardial infarct (Heart attack).
If the embolism lodges in an artery in the brain --
stroke
If the embolism lodges in the lungs- pulmonary
embolism
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An ANGIOGRAM
An ANGIOPLASTY
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CORONARY BYPASS.
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saphenous vein
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Aneurysm
Stroke
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Atherosclerosis- Fatty deposits
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Angina pectoris- chest pain
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Myocardial infarction- blocked coronary artery
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Silent ischemia- lack of blood flow that happens to
not cause any pain or other symptoms; leads to
unexpected heart attack.
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Congestive Heart failure:
 Progressive weakening of the heart
 Blood backs up into lungs (may clog up blood)
 Cannot meet the body’s demands for oxygenated
blood.
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Hypertrophic cardiomyopathy is a congenital
condition where the walls of the left ventricle are so
thick that the lumen is too small to hold much blood.
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at the start of the fourth week
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FOSSA OVALIS.
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