CARDIO ANAPHY

 Cone shaped
 Tilted to the left
 Mediastinum
 LAYERS:
 Pericardium- covered with sac, can be inflamed, can compress the heart
 Pericardial space- with fluid, no friction
 Epicardium
 Myocardium – muscular, heart attack
 Endocardium- inner, continuous to the valves of the heart
o Rheumatic heart disease- GABHS
o Valvular Damage
 CHAMBERS
o Right Atrium
o Right Ventricle
o Left Atrium
o Left Ventricle
o AV VALVES – endocardium is damaged, LUB
 Can damage the valves
 Blood goes back and forth
 Congestive heart failure
 Tricuspid -right sided heart failure
 Bicuspid- left sided heart failure, mitral
o Semilunar VALVES, DUB
 Goes out in the aorta- aortic valve
 Pulmonic valve
o LUB DUB IS NORMAL
o Extra heart sound- abnormal
 Coronary Arteries
o On top of the heart
o If there is obstruction, can remove and touch the vessels
o RCA and LCA
o Supplies blood to the heart
o Oxygenated blood
o Left circumflex
o Rca- r marginal, posterior interventricular
o Can become obstructed
o Blood Clot and Fat
o Atheroclerosis – Fat, anticholesterol drugs
o Blood Clot- Thrombus, anti coagulant
 CORONARY CICULATION
o Blood goes to the heart greatest at relaxed, reduced during contraction (systole)
o Rapid contraction interfere with blood supply
 o Increase hr = increased heart attack
o No aerobic exercise, small frequent feedings (metabloism increases hr)
o Incrased hr= increased demand for oxygen
o Heart attack- engage in sex, exert effort, increase hr,
o SNS – increased hr
o A1- increased bp
o B1- increased heart rate
o Anastomoses- rca and lca
 Obstruction in any artery Develops other blood vessels
 Collateral circulation
 Alternative source of blood
 So no lost of blood supply
 Exercise develops collateral circulation
o RCA- supplies the r side, inferior part of left ventricle
 SA NODE (pacemaker of the heart, 60-100), AV NODE – contained by right
atrium
 SA Node is damaged- come form the av node (40-60 hr)
 Not enough circulation, dizziness
 Hr is too slow= faster
 Hr is too fast= slower
 BLOCKAGE
 Conducation disturbances
o LCA – anterior walls of the ventricles, anterior spetum, bundle branches (goes to the
right and left side) goes to the prukinje fibers (in the ventricle, if damages av and sa, 20 -
40)
o Dizziness and Light headedness
o L circumflex- left atrium, lateral and posterior walls of AV
o Heart rate slow- impaired tissue perfusion, no blood supply
 Place a pace maker, more heart rate
o LCA is damaged
 Left v- to systemic circiulation
 Right v- to pulmonary
 Impair the pumping ability
 Most common that gets obstructed
 CARDIAC CYCLE
o Alternating sequence
o Atrium needs to pump for ALL THE blood to go down
o If systolic blood plresseure is high= heart is always contarcting
o Diastole
 PULSE
o Indicates theheart rate
o Ventricular systole- expands the artery
o Blood volume = determines the pressure
o When it contracts it pushes the blood
 o Apical pulse- PMI (point of maximal impulse)
 If patient has cardiomegaly, difference in the location of PMI
o Pulse deficit- difference in apical and radial
 Thready – weak pulse, volume low
 Bounding – feel without touch, vlomue high
 Apical Pulse
 Rate of the heart measured at the site
 If giving a cardiac drug- must be apical pulse
 CARDIAC OUTPUT
o Blood ejected Left ventricle/ per min
o 5-6L per minutes
o Stroke volume times HR
o If in shock- decreased CO
o Stroke volume- the blood ejected per heart beat
o Heart is trenched—the force of contraction- the more it pumps- the more force
o VOLUME EQUALS PRESSURE
o AFFECTS CO
 Pre load- venous return
 Rgoes back to the heart, right side, SVC, IVC
 Determines cardiac output
 If konti ang bumalik, mkonti ang lalabas
 Afterload- resistanct to left ventricular resistance (peripheral resistance)
 Must be low, so that the resistance is low
 Heart rate
 Is too high- increased contraction, no oxygen
 Is too low- impaired circulation, no blood
 VASCULAR SYSTEM
o Arteries- oxygenated blood
 Tunica intima- inner, endoloithial
 Tunica media – middle, smooth muscle, cause constriction and dilation
 Tunica adventitia – outer
o Arterioles- deoxygenated blood
o Capillaries
 AUTOREGULATION
o Self regulate
o If my blood suplly is impaired- it will compensate
 It will regulate itself
o Localized vasodilation – not much blood
o Vasoconstriction- if loosing blood
o REFLEX ADJUSTMENT
o Acidosis, hypoxia, release of histamine, hypercapnia
 Vasodilattion
o NORE, EPI, ANGIOTENSISN
 Vasoconstrict
  APHA 1
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