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PHYST3
Review of Test 3 -HEART stuff
| Question | Answer |
|---|---|
| OVERVIEW: CIRCULATION | OVERVIEW: CIRUCLATION |
| ****KNOW EQUATION ON P. 201*** | **PRETTY LIKELY THAT IT WILL BE ON THE TEST**** |
| Know how to manipulate it. Example: What would MOST influence resistance? | Radius of the tube to the fourth power |
| What is directly related to resistance? | Viscosity of the fluid and the length |
| What is indirectly related (and hence has the most ifnluence) on resistance/ | Radius of the tube to the fourth power |
| What are you suppoed to do to increase RBCs? | Live HIGH train LOW |
| HEART I | HEART I |
| Where does blood flow in order? | Inf and Sup Vena Cava-->Right atrium-->right ventricle-->Pulm ciculation-->Left atrium-->right atrium-->systemic ciculation (aerota) |
| What is the purpose of all the valves? | prevent the backflow of blood. We don't want deoxygenated blood in an oxygenated blood section.... |
| What are the THREE main characteristics of cardiac muscle cells? | Straited (actin and myosin here), intercalated disks, gap junctions (conduct APs) |
| What do sympathetic fibers release? | Ach |
| Sympathetic fibers release? | NE and EPI |
| What is the sequence of excitation starting from the PACEMAKER (SA-NODE)? | SA Node (atria)-->AV node-->bundle of his-->perkinje fibers (both ventricles) |
| With an AP, the membrane permeability of what 3 elements changes? | K+, Na+, Ca+ |
| At rest, what is amount of sodium and calcium in cell? | Low |
| What happens when the sodium allowance increases? | Depolarization |
| 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) |
| EKG | EKG |
| What is the P-wave? What does it look like? | Atrial depolarization |
| QRS wave: | Ventricular depolarization |
| T-wave: | Ventricular repolarization |
| What is needed for excitating coupling? Where is ti released form? | Ca+ released from SR |
| What is the major signal for calcium releases in the SR? | The PRESENCE of Calcium |
| What is this phenomena called? | Calcium induced calcium release |
| 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 |
| Can cardiac muscle udnergo tetnus? | Nope, not like skeletal muscles can |
| Why NOT? | There's a refractory period (where you can't excite and excitable membrane) |
| Systole: What contracts/relaxes? | Ventricular contraction |
| Diastole: What contracts/relaxes ? | Ventricular depolarization |
| 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 |
| What is an isovolumentric ventricular relaxation? | closing of the aerotic and pulmonary valves |
| Ventricular filling is in systole of diastole? | Diastole |
| Ventricular ejection is in systeole of diastole? | Systole (think it contracts = ejection) |
| End-diastolic volume? | Blood in ventricles before systole |
| End-systole? | Volume remaining after ejection |
| Stroke volume? | End Diastole - End systole (volume ejected) |
| What has greater pressure, the right heart or the left heart? | LEFT heart. Just think, it has to pump blood throughout our ENTIRE system |
| CO = | Heart Rate * Stroke Volume |
| 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 |
| What two primary things influnce stroke volume? | End diastolic volume and magnitude of SNS input to ventricles |
| What does starling's law of the heart state? | Increasing end-diastolic volume will produce a greater force of contraction |
| What does this result in? | Greater stroke volume |
| How can increased venous return increase CO? | Distending the ventricles and icnreasing stroke volume |
| An increase in afterload leads to? | Increase end systolic volume = DECREASE stroke volume |
| What is pre-load? | Cardiac filling during diastole |
| What impacts stroke volume??? | Pre-load, afterload, and contractility (force of contraction per SNS EPI) |
| VASCULAR SYSTEM | VASCULAR SYSTEM |
| What are low resistance conduits for easy blood flow? | Arteries |
| MAP = | DBP + 1/3 (SBP-DPB) |
| What does compliance equal? | Change in volume / change in pressure (how easily can a structure be stretched) |
| 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!! |
| Arterioles have how much ressitance? What do they determine therefore? | Lots of Ressitance; determine MAP |
| Flow in an Organ is = | MAP/Resistance in an organ |
| ***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 |
| Thus, hyperemia =? | TOO MUCH blood flow |
| What causes vasodilation? | EDRF, NO, lots of stuff |
| What 4 main things cause vasoconstriction? | NE, EPI, Angiotensin II, and vasopressin |
| How fast does blood flow through capillaries? | Slowly, because remember that exchange of nutrients takes place here |
| 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 |
| REGULATION OF BLOOD PRESSURE | REGULATION OF BLOOD PRESSURE |
| What is MAP = ? | Cardiac Output * TPR |
| What is the function of arterial baroreceptors? | they buffer changes in arterial blood pressure |
| What do cardiopulmonary baroreceptors do? | They keep the brain informed of changes in Blood pressure |
| How do baroreceptors buffer the changes in BP? | They increase PS output and decrease SNS output |
| 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 |
| What happens if there is a DECREASE in BP? | Efferent stimulates SNS input, and inhibits PS input |
| How long does regulation by baroreceptors last? | SHORT TERM |
| So how do we control MAP in the lONG TERM??? | VOLUME |
| So, if we increase blood volume, what happens to blood pressure? | INCREASE Blood pressure (distention and all that) |
| 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 |
Created by:
talkglitter2486