Review of Test 3 -HEART stuff
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| OVERVIEW: CIRCULATION | OVERVIEW: CIRUCLATION
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| ****KNOW EQUATION ON P. 201*** | **PRETTY LIKELY THAT IT WILL BE ON THE TEST****
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| Know how to manipulate it. Example: What would MOST influence resistance? | Radius of the tube to the fourth power
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| What is directly related to resistance? | Viscosity of the fluid and the length
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| What is indirectly related (and hence has the most ifnluence) on resistance/ | Radius of the tube to the fourth power
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| What are you suppoed to do to increase RBCs? | Live HIGH train LOW
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| HEART I | HEART I
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| Where does blood flow in order? | Inf and Sup Vena Cava-->Right atrium-->right ventricle-->Pulm ciculation-->Left atrium-->right atrium-->systemic ciculation (aerota)
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| What is the purpose of all the valves? | prevent the backflow of blood. We don't want deoxygenated blood in an oxygenated blood section....
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| What are the THREE main characteristics of cardiac muscle cells? | Straited (actin and myosin here), intercalated disks, gap junctions (conduct APs)
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| What do sympathetic fibers release? | Ach
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| Sympathetic fibers release? | NE and EPI
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| What is the sequence of excitation starting from the PACEMAKER (SA-NODE)? | SA Node (atria)-->AV node-->bundle of his-->perkinje fibers (both ventricles)
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| With an AP, the membrane permeability of what 3 elements changes? | K+, Na+, Ca+
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| At rest, what is amount of sodium and calcium in cell? | Low
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| What happens when the sodium allowance increases? | Depolarization
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| What does this force calcium channels to do? | Open and stay open for a while (b/c of a slow permeability for calcium to enter)
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| EKG | EKG
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| What is the P-wave? What does it look like? | Atrial depolarization
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| QRS wave: | Ventricular depolarization
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| T-wave: | Ventricular repolarization
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| What is needed for excitating coupling? Where is ti released form? | Ca+ released from SR
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| What is the major signal for calcium releases in the SR? | The PRESENCE of Calcium
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| What is this phenomena called? | Calcium induced calcium release
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| Where does the calcium bind? Is all the calcium bound to troponin (do we usually have full saturation)? | Binds to troponin, which isn't fuly saturdated
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| Can cardiac muscle udnergo tetnus? | Nope, not like skeletal muscles can
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| Why NOT? | There's a refractory period (where you can't excite and excitable membrane)
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| Systole: What contracts/relaxes? | Ventricular contraction
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| Diastole: What contracts/relaxes ? | Ventricular depolarization
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| Explain an isovolumetric/baloonic ventricular contraction: | When the AV valves close b/c pressure in the ventricles > atrial pressure. But, the blood doesn't MOVE out of the ventricles since there isn't enough pressure to get the pulmonary valves to open
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| What is an isovolumentric ventricular relaxation? | closing of the aerotic and pulmonary valves
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| Ventricular filling is in systole of diastole? | Diastole
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| Ventricular ejection is in systeole of diastole? | Systole (think it contracts = ejection)
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| End-diastolic volume? | Blood in ventricles before systole
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| End-systole? | Volume remaining after ejection
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| Stroke volume? | End Diastole - End systole (volume ejected)
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| What has greater pressure, the right heart or the left heart? | LEFT heart. Just think, it has to pump blood throughout our ENTIRE system
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| CO = | Heart Rate * Stroke Volume
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| Increase parasymp does what to HR? INcrease symp? Increase EPI? | Parasymp = Decrease HR Symp = Increase HR. EPI: Remeber that EPI is realed from Symp, so EPI also increases HR
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| What two primary things influnce stroke volume? | End diastolic volume and magnitude of SNS input to ventricles
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| What does starling's law of the heart state? | Increasing end-diastolic volume will produce a greater force of contraction
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| What does this result in? | Greater stroke volume
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| How can increased venous return increase CO? | Distending the ventricles and icnreasing stroke volume
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| An increase in afterload leads to? | Increase end systolic volume = DECREASE stroke volume
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| What is pre-load? | Cardiac filling during diastole
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| What impacts stroke volume??? | Pre-load, afterload, and contractility (force of contraction per SNS EPI)
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| VASCULAR SYSTEM | VASCULAR SYSTEM
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| What are low resistance conduits for easy blood flow? | Arteries
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| MAP = | DBP + 1/3 (SBP-DPB)
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| What does compliance equal? | Change in volume / change in pressure (how easily can a structure be stretched)
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| Which of the following is impacted by compliance? A. Pulse Pressure B. MAP C. None of the above. D. All of the above | Pulse pressure. NOT MAP!!
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| Arterioles have how much ressitance? What do they determine therefore? | Lots of Ressitance; determine MAP
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| Flow in an Organ is = | MAP/Resistance in an organ
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| ***This is key to understanding most pathophys stuff: HYPER means too little or too much? HYPO means too little or too muich? | HYPER = too MUCH. HYPO = TOO LITTLE
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| Thus, hyperemia =? | TOO MUCH blood flow
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| What causes vasodilation? | EDRF, NO, lots of stuff
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| What 4 main things cause vasoconstriction? | NE, EPI, Angiotensin II, and vasopressin
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| How fast does blood flow through capillaries? | Slowly, because remember that exchange of nutrients takes place here
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| Veins have what kind of resistance? Where is the majority of your blood located most of the time? | LOW RESISTANCE; most of the blood is HERE
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| REGULATION OF BLOOD PRESSURE | REGULATION OF BLOOD PRESSURE
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| What is MAP = ? | Cardiac Output * TPR
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| What is the function of arterial baroreceptors? | they buffer changes in arterial blood pressure
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| What do cardiopulmonary baroreceptors do? | They keep the brain informed of changes in Blood pressure
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| How do baroreceptors buffer the changes in BP? | They increase PS output and decrease SNS output
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| So what do they decrease? (rememer the MAP equation) | Decrease CO, TPR, and MAP. REMEMBER, baroreceptors DECREASE MAP because they respond to an INCREASE in BP
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| What happens if there is a DECREASE in BP? | Efferent stimulates SNS input, and inhibits PS input
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| How long does regulation by baroreceptors last? | SHORT TERM
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| So how do we control MAP in the lONG TERM??? | VOLUME
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| So, if we increase blood volume, what happens to blood pressure? | INCREASE Blood pressure (distention and all that)
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| In the upright position, increased venous pressure distends the veins, causing venous pooling and increased filtration out of the capillaries. How do we deal with this? | Skeletal muscle contraction
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