-
Layers of the heart (deepest to superficial)
- Endocardium (covers heart wall)
- myocardium (middle layer, consists of cardiac muscle)
- epicardium (visceral layer of serous pericardium)
- pericardial cavity (paricardial fluid-prevents friction and heat)
- Parietal Pericardium
- Fibrous Pericardium (fibro-serous membrane, covers heart-made of collagen=high tensile strength/NO compliance)
-
Sequence starting with LT atrium
- 1.Aortic Semilunar valve
- 2.Coronary artery
- 3.Systemic Capillary bed
- 4.Coronary vein
- 5.Coronary sinus
- 6.Tricuspid valve
- 7.Pulmonary trunk
- 8.Pulmonary vein
-
Function of Papillary muscles
- -prevent eversion of bicuspid valve
- -contract during ventricular systole
-
Sequence of Depolarization
- -SA node depolarizes
- -depolarization of atrial myocytes (AP spreads through gap junctions in intercalated disks)
- -AV node depolarizes
- -signal is slowed down/delayed
- -signal reaches bundle of His
- -two bundle branches (right/left)
- -signal reaches APEX of ventricles
- -Purkinje fibers (originate from the bundle branches--spread superiorly and laterally; also spreads into the ventricular muscle.
-
Order of Systemic circulation (include structures)
OXYGENATED BLOOD: LT atrium-->AV valve-->LT ventricle-->aortic SL valve-->aorta-->elastic arteries-->muscular arteries-->arterioles-->capillaries (bed)-->
O2 blood out the aorta,--> elastic arteries-->muscular arteries--> to arterioles, to capillaries for exchange, back to heart via Vena Cava
-
structures for PULMONARY circulation
DEOXYGENATED: RT ATRIUM-->RT VENTRICLE --> pulmonary trunk-->pulmonary arteries-->lungs-->arterioles-->pulmonary capillaries-->OXYGENATED venules-->pulmonary veins-->left Atrium
-
What do veins have that arteries do not?
- -valves
- -compliance, stretch
-
ventricles vs. atria-- do what with blood?
- VENTRICLES: blood AWAY from heart
- ATRIA: RECEIVES blood
-
Pulmonary Valves
- tricuspid (right AV)-- supported by papillary musc/choridae tendon
- pulmonary SL
- SA node
-
Systemic Valves:
- Bicuspid (Left AV) --- supported by papillary musc/choridae tendon
- Aortic SL
-
Explain ventricular systole (pre-and systole)
BLOOD FLOW: vena cava OR pulmonary veins-->atrium-->AV valve-->Ventricle
-->AV/SL valves CLOSE (leading to isovolumetric)-->ventricular filling-->ventricular pressure EXCEEDS aortic or pulmonary trunk-->SL valves open-->ventricular ejection
-
Ventricular Diastole:
BEGINS: when ventricle relaxes after ejection, blood flowing back to ventricle causes SL to close. BOTH VALVES CLOSED
-
How does ventricular filling occur? (atrial systole)
atrial pressure GREATER than ventricular pressure, AV VALVES OPEN-->ventricular filling
-
When does Atrial contraction occur?
end of ventricular systole
-
Epicardium
visceral pericardium, squamous epithelium, areolar CT, fat
-
Myocardium
- cardiac muscle attached to fibrous skeleton of heart
- "wringing" contraction
- made of collagen and elastin
-
endothelium
- areolar CT and squamous endothelium
- anchored by thing CT layer
-
Explain coronary (heart) circulatory system
- -Coronary artery delivers O2 blood to cardiac muscle (branching off aorta)
- -capillary within cardiac muscle, blood drains into coronary veins
- -coronary vein--empty into coronary sinus
- -blood returned to RIGHT atrium
-
RT atrium receives blood from.....
- inferior vena cava-systemic circ.
- superior vena cava-systemic circ.
- coronary sinus
-
What is another word for the "bundle of his"
AV bundle
-
compare/contrast angina with MI
angina: ischemia (cut off blood flow), vasospasm, short-lived, no cell death
MI: blockage of O2 to cardiac muscle, cell death
-
what is another word for "discharge rate" in the pacemaker
sinus rhythem
-
equation for Stroke volume
EDV-ESV
-
Ejection fraction equation and normal range
(EDV-ESV)/EDV
>55%
-
MAP equation
Diastolic + 1/3 pulse pressure
-
Cardiac reserve equation
CO(max) - CO (rest)
-
EDV determined by:
- length of ventricular DIASTOLE
- venous return (inc. EDV)
-
ESV determined by:
- Mean Arterial Pressure
- contractility (harder contraction, dec. ESV)
-
Factors affecting stroke volume-PRELOAD:
- DEGREE OF STRETCH
- increased EDV (main INTRINSIC factor)
-
Frank-Starling Law of heart
- any factor that increases volume or speed of venous return, thus increasing EDV --> increase stretch and force of contraction to pump out "extra blood"INTRINSIC (ESV&EDV)
- due to length tension curve...
- the more the heart is filled with blood, the more blood will be pumped out.
-
Factors affecting stroke volume: Contractility
- EXTRINSIC: ANS/hormones
- -sympathetic stimulation
- -EPI from adrenal medulla (increase Ca2+)
- -increase force of contraction and rate-->more blood ejection
- (Independent to EDV/muscle stretch)
- -lower ESV, higher stroke volume
-
diameter calculation
radius(to the 4th power) THEN divide 1/R4
-
Factors affecting stroke volume: Afterload
- INTRINSIC:
- ventricular pressure must exceed arterial pressure
-
Mean arterial/aortic pressure
92!
-
Stroke volume with hypertension has what affect?
afterload increases, affecting ESV and lowering stroke volume
heart must increase force of contraction-->DAMAGE longterm
-
Blood flow equation
Flow=change of pressure/radius
-
Which node is more negative? SA or AV?
- AV....
- SA pushes AV to threshold
-
P-Wave
Depolarization of atria (following by Atrial contraction)
-
QRS complex
depolarization of ventricles (followed by ventricular contraction
-
T Wave:
Repolarization of ventricles
-
P-R complex
atria contract and begin to relax
-
Q-T
appx length of time it takes for ventricles to contract (depolarization) and relax (repolarization)
-
Ectopic pacemaker
Pacemaker in the wrong place
-
Sympathetic NS is controlled by:
- Medulla/cardioacceleratory
- inc rate and inc force
-
Paraympathetic NS is controlled by:
- Medulla/cardioinhibitory by G-protein inhibiting adenyl cyclase, decrease in cAMP, decrease activity of HCN acting on channels
- (vagus nerve)
-
parasympathetic affects...
heart rate ONLY
-
sympathetic affects...
heart rate AND ventricular muscle strength of contraction (stroke volume)
-
baroreceptors control....
blood pressure regulation
-
BP regulation
- increased MAP/BP-->
- increased strength of wall-->
- stimulate baroreceptors -->
- inhibit sympathetic
- increase parasympathetic .....
-
chemoreceptors control...
pH and O2 level
|
|