Term
| Name the three layers of the walls in order from the lumen outward. |
|
Definition
| Tunica intima, media, and adventitia |
|
|
Term
| What does the tunica intima do? HINT: in relation to the blood and hormones |
|
Definition
| It can help cleave angiotensin I to angiotensin II and it has enzymes that inactivate thrombin, serotonin, and NE |
|
|
Term
| Which is typically the thickest of the three tunicas? |
|
Definition
|
|
Term
| What is the tunica adventitia composed of? |
|
Definition
| Fibroblasts, Type I collagen and longitudinal elastic fibers |
|
|
Term
| What are the effects of parasympathetic and sympathetic nerves on the blood vessels? |
|
Definition
| sympathetics cause constriction, Para-->dilation. |
|
|
Term
| What are some distinguishing characteristics of elastic (conducting) arteries? |
|
Definition
| These include the aorta and big branches. They have elastic laminae, and endothelial von Willebrand factor (coagulant). Extra crdt: adventitia is thin. |
|
|
Term
| What distinguishes muscular (distributing) arteries from you average artery? |
|
Definition
| intima has internal elastic lamina, media has external lamina. Media has mostly muscle cells. |
|
|
Term
| Name 3 ways we can regulate our arterial blood pressure. |
|
Definition
3 or more of the following vasoconstriction, vasodilation, renin from kidneys, ACE increasing angiotensin II, Angiotenin II causing vasoconstriction, vasopressin release after hemmorrhage |
|
|
Term
| What are the different types of capillaries and where are these? |
|
Definition
Continuous-in muscles, nerves, CT Fenestrated-Organs used in digestion (pancreas, intestines) Sinusoid- (immune) bone marrow, liver, spleen... Sinusoid has no diaphragm |
|
|
Term
| What is the difference between pressure diuresis and pressure natriuresis? |
|
Definition
| Both are reactions to increase BP. Diuresis is when you increase water loss, natriuresis is when you increase sodium loss. |
|
|
Term
| What is the effect on cardiac output of increasing GFR (Glomerular Filtration Rate)? |
|
Definition
| You decrease the Q (cardiac output) because you have decreased blood volume and therefore the venous return. |
|
|
Term
| Daily sodium and fluid intake along with renal function are the two major determinants of what? |
|
Definition
| Arterial pressure. If they are equal to one another then you are balanced. If you have higher fluid and salt intake you will have higher MAP. |
|
|
Term
| What is the relation between MAP (mean Arterial pressure), Q (Cardiac Output), and TRP (Total Peripheral resistance)? |
|
Definition
|
|
Term
| Does our body control MAP long term with changing Q or TPR? |
|
Definition
| Q, TRP is changed to make short term effects and it is controlled by reflexes. |
|
|
Term
| What is the effect of drinking high Na containing fluids? |
|
Definition
| The pituitary will release more ADH, this will increase the reabsorption of water in the kidneys which will begin to dilute the high Na concentration in the blood. |
|
|
Term
| If you have kidney failure and then drink lots of salt, what will be the effect on MAP? |
|
Definition
|
|
Term
| Would increasing or decreasing the filtering of capillaries cause an increase in tissue edema? |
|
Definition
| Increasing. What you want to decrease is the absorption of capillaries. Absorption will drain the tissue. |
|
|
Term
|
Definition
| The accumulation of fluid in the cells or interstitium (between cells) |
|
|
Term
| You have invented a sodium/ potassium pump inhibitor and inject someones arm. Would you list edema as a side effect? |
|
Definition
| Yes. Edema occurs with decreased effectiveness of the pump |
|
|
Term
| Why would cardiovascular shock cause systemic edema? |
|
Definition
| Because the Na/K pump is inhibited with when there is decreased blood supply. |
|
|
Term
| Increasing the capillary fluid pressure would have what effect on net fluid movement between capillaries and tissue? |
|
Definition
| The fluid movement would be outward. There would be increased filtration and decreased absorption. |
|
|
Term
| What is the normal Lymph flow rate in ml/hr? |
|
Definition
|
|
Term
| T/F Oncotic pressure is determined by the lymph flow rate and capillary fluid pressure. |
|
Definition
| False. Plasma Oncotic pressure is determined by capillary permeability and lymph flow rate. |
|
|
Term
| What makes the lymph flow? |
|
Definition
| Two ways. Actively through smooth muscle contractions and passively through exercise of muslces and arterial pulastions |
|
|
Term
| How does Net Filtration pressure relate to the colloid osmotic pressures and physical pressures of the interstitium and capillaries. |
|
Definition
| NFP=(press of capillary - press of interstitium)+(osmo of interstitum - osmo of capillary) |
|
|
Term
| Why is edema in the pulp bad? |
|
Definition
| Because the increased interstitial fluid pressure will cause blood vessels to collapse and dental ischemia to ensue. |
|
|
Term
Which of these four factors, which, when increased, will cause edema? 1. capillary fluid pressure 2. Capillary permeability 3. Plasma oncotic pressure 4. Lymph flow rate |
|
Definition
1. capillary pressure 2. Capillary permeability The other two will lessen edema |
|
|
Term
| Why doesn't systemic hypertension usually cause systemic edema? |
|
Definition
| Because the major resistance causing high pressures occurs in the arterioles, which are upstream the capillaries, which will not have an increased pressure. |
|
|
Term
| How come pulmonary hypertension causes edema then? |
|
Definition
| Because the high arterial pressure in his case does not drop en route to the pulmonary capillaries as it did systemically. |
|
|
Term
| What three protections do we have against edema? |
|
Definition
1. under lower than atmostpheric pressures, there is low compliance (less free fluid) 2. Lymph can flow 10-50x normal rate 3. protein washout |
|
|
Term
| Which areas of the body can liquid get to where there aren't cells, but still lymphatics? |
|
Definition
| Around the lung (pleural), heart (pericardium), abdomen (peritoneum) and joints (synovium) |
|
|
Term
|
Definition
| When you have celular edema or there is coagulation going on. |
|
|
Term
| Which factors can increase capillary permeability? |
|
Definition
| Inflammation, scurvy, ischemia, and trauma. These will cause coagulation |
|
|
Term
| What can cause pumonary edema? |
|
Definition
| Left heart failure (more capillary pressure because it won't drain into the left heart as much), pulmonary capillary injury, hypoalbuminemia (decreased osmotic pressure in capillaries), or obstructed pulmonary lyphatics |
|
|
Term
Order the following during a clotting event: platelet plug forms, fibrous organization, vascular spasm, blood clot forms then retracts. |
|
Definition
1. Vascular spasm 2. Platelet plug forms 3. blood clot forms and then retracts 4. fibrous organization |
|
|
Term
| What causes vascular spasm? |
|
Definition
| muscle spasm, local reflex, and local promotors (endothelin from endothelium and thromboxane A2 from platelets) |
|
|
Term
2 statement T/F about platelets: 1. Surface glycoproteins activate coagulation steps 2. Surface phospholipid repulses normal endothelium, but binds to injured endothelium |
|
Definition
Both False. 1. Surface glycoproteins repulses normal endothelium, but binds to injured endothelium 2. Surface phospholipid activates coagulation |
|
|
Term
What factors promote the following: 1. Platelet adhesion to collagen 2. shape change and degranulation 3. Aggregation |
|
Definition
1. adhesion: von Willebrand 2. shape change: Thromboxane A2 and ATP 3. aggregation: Thromboxane A2 |
|
|
Term
| What are the key players in extrinsic prothrombin activator? |
|
Definition
| Tissue trauma leads to Factor III acting with VIIa to cause X to turn into Xa, leading to prothrombin activator which will convert prothrombin to thrombin. |
|
|
Term
| What are the key players in intrinsic prothrombin activator? |
|
Definition
| Blood in contact with collagen causes platelet phospholipids to convert X to Xa, leading to prothrombin activator which converts prothrombin to thrombin |
|
|
Term
| Which is faster extrinsic or intrinsic coagulation pathways? |
|
Definition
| the Extrinsic (non-platelet mediated) is fastest |
|
|
Term
|
Definition
| It turns fibrinogen into fibrin monomers, which will polymerize given Ca++ into fibers and then form cross-links with thrombin activated fibrin-stabilizing factor |
|
|
Term
| You simultaneously inject someone with a concoction of heparin and Compound Y, which releases gross amounts of interstitial fibrin stores into the blood stream. How will this affect coagulation. |
|
Definition
| The heparin will catalyze formation of more antithrombin III removes thrombin while the excess fibrin will tie up thrombin leading to extreme low levels of thrombin and low coagulation. |
|
|
Term
| A patient has a severe blood clot in his legs during a routine dental procedure. You have two wires, red and blue which do you cut? After cutting the wire, should you inject the person with t-PA, Streptokinase, or urokinase? |
|
Definition
| It doesn't matter which wire you cut. Injecting the person with either of these three compounds will bust the clot. t-PA catalyzes plasmin formation and the other two are clot destroying durgs. |
|
|
Term
| What do the intercalated disks of the Heart do? |
|
Definition
| They provide an electrical connection between the cells, allow ions and molecules to travel between cells, stabilize the 3D structure, and allow for optimal contractile efficiency |
|
|
Term
| You transported in time to the aztec era and see a heart being pulled from a human sacrifice. Is it beating? |
|
Definition
| It would be beating. The heart contracts automatically from pacemaker cells. Sorry for the vivid, gory image. |
|
|
Term
| What are the differences in terms of muscle contractile time and twitch between skeletal and cardiac muscle? |
|
Definition
| Cardiac contractions last 10x longer and have NO wave summation NOR tetanic contractions. |
|
|
Term
| Where is the delay in the heart? |
|
Definition
| The delay is at the AV node. After this delay, the potential is shot down the interventricular septum and through the purkinje system, which has the greatest contractile velocity. |
|
|
Term
| How many periods are there in diastole? Systole? |
|
Definition
| Diastole has 4 periods (not 3 like it says in the slides. Sheruli clarified this in lecture). Systole has 3 periods. |
|
|
Term
| List the 0-4 phases of cardiac action potential. |
|
Definition
0: depolarized by Na influx 1: outward flux of K and Cl 2: Ca influx (plateau) 3: Repolarization by K efflux 4: Resting membrane potential |
|
|
Term
| What is the difference in the phases of cardiac action potential between (1) Fast and (2) slow response cells |
|
Definition
|
|
Term
2 statement T/F P wave is caused by atrial depolarization. T wave is cause by repolarization of the ventricles. |
|
Definition
| Both True. The QRS however, is the depolarization of the ventricles. |
|
|
Term
| Name the section of the heart (atria or ventricle) and the polarization (de- or re-) that is normally not represented in EKGs and is a sign of a pathology. |
|
Definition
| Atrial repolarization is normally a sign of pathology and isn't normally visualizable on the ECG. |
|
|
Term
| You finally open up your stethoscope in your locker. What will you hear, opening or closing of valves? Which valve closes first? |
|
Definition
| Closing (think of slamming doors). The mitral (AKA A-V) valve closes first followed by the aortic (AKA semilunar) valve. |
|
|
Term
| What is the preload and what is a normal value for a preload. |
|
Definition
| Preload represents the Left Ventricle end diastolic volume (LVEDV) and usually hovers around 120 mL. |
|
|
Term
Order these stages starting at Atrial Contraction: Atrial contraction, reduced ejection, rapid filling, Isovolumic contraction, rapid ejection, reduced filling, isovolumetric relaxation. |
|
Definition
| atrial contraction, isovolumic contraction, rapid ejection, reduced ejection, isovolumetric relaxation, rapid filling, reduced filling (diastalsis) |
|
|
Term
| Your patient injects you with your own epinephrine containing lidocaine and hits a blood vessel. Your blood rate skyrockets. How will your ratio of systolic period to diastolic period be affected? |
|
Definition
| You will have relatively longer periods of systole than diastole compared to when you were at rest. |
|
|
Term
| How would you calculate ejection fraction? |
|
Definition
| It is equal to [Stroke volume (EDV-ESV)] / EDV |
|
|
Term
| KCl is used in lethal injection. What effect does it have on the heart? |
|
Definition
| decreases heart rate and contraction. |
|
|
Term
| What is calcium's effect on the heart? |
|
Definition
| It can cause increased contraction, not rate! |
|
|
Term
| 2 statement T/F. 1 the Sinus node has an intrinsic rate of 60-100 bpm. 2 the internodal paths have an intrinsic rate of 40-60 bpm. |
|
Definition
| 1 True, 2 False. The internodal paths do not have an intrinsic rate. The intrinsic rate of 40-60 belongs to the AV node. Also, the internodal paths have a quick velocity. |
|
|
Term
| 2 statement T/F. 1 The AV Node has an intrinsic rate of 40-60 bpm. 2 The purkinje fibers have an intrinsic rate of 15-40 bpm. |
|
Definition
|
|
Term
| What are the slowest fibers in the heart, internodal path, common bundle, bundle branches, transitional fibers, or purkinje fibers? |
|
Definition
| The transitional fibers of the AV node are the slowest. |
|
|
Term
| An electrician gets shocked by a power surge and his SA node stops. What will happen in respect to his cardiac pace? |
|
Definition
| When the SA node fails, the AV node of Purkinje fibers take over (they are latent pacemakers) and the beating will slow. This is called VENTRICULAR ESCAPE |
|
|
Term
| What do funny channels (If) do? FYI: the f in If is supposed to be subscript. What happens if you give someone a drug that blocks these channels? |
|
Definition
| If channels let sodium in slowly during repolarization. A blocker of If would cause a slower heart rate. |
|
|
Term
| What causes the AV delay? |
|
Definition
| The slow speed conduction (0.3m/sec) of the AV node compared to purkinje (~2.5m/sec) |
|
|
Term
| What happens to the membrane potential of pacemaker cells when Ach is added? |
|
Definition
| You hyperpolarize the membrane potential by K+ leak causing a delay in polarization and a slower heart rate. |
|
|
Term
| What does nor-epi do to myocardial cells and their the membrane potential? |
|
Definition
| It causes them to increase permeability to Na and Ca which will depolarize the cell causing an increased strength and rate of contraction. |
|
|
Term
| What is Stokes Adams syndrome? |
|
Definition
| syncope caused by the SA node currents don't propagating into the ventricles. Slowed cerebral perfusion. |
|
|
Term
| How long is the PR interval? What is a prolonged PR interval suggestive of? |
|
Definition
| .16 seconds. If it gets longer than 0.2 sec, you may be witnessing an AV block |
|
|
Term
| What if you have a widened QRS block? |
|
Definition
| Think bundle branch block. |
|
|
Term
| 2 statement T/F. 1 ST segment is useful in diagnosing myocardial infarction. Q-T interval is the full ventricular contractile element. |
|
Definition
|
|
Term
What of the following cardiac elements can you not understand with an ECG? 1. Cardiac hypertrophy 2. Coronary Lipofuscinoses 3. Heart Rate 4. Voltage |
|
Definition
| 2. Coronary Lipofuscinoses. I made this up |
|
|
Term
2 statement T/F. If you slow the complex the size of the P, QRS, and T waves will change. 2. If you change the path of excitation the intervals and duration will change |
|
Definition
| Both False. These need to be flip flopped. However, you may see some of each occur, but these would be the major changes. |
|
|
Term
|
Definition
| This is an example of altered automaticity. Note that there is an irregular T and P wave. |
|
|
Term
| What are the three degrees of blocks in the heart conduction? |
|
Definition
1st degree block= slow AV conduction 2nd degree= occasional complete AV block 3rd degree= complete AV block |
|
|
Term
| What are some of the notable issues with premature atrial complex? |
|
Definition
| P wave happens soon as does the QRS. there is a pause between that ones T wave and the next P wave. caffeine, smoking, and alcohol contribute |
|
|
Term
| What happens during a premature ventricular complex (PVC)? |
|
Definition
| You will have a wide QRS with a pause afterwords, lack of P wave. |
|
|
Term
| You notice an inverted P wave with a short P-R space. What could it be? |
|
Definition
| It is a high-site Premature Nodal Complex. mid sites have no P wave, low sites have a retrograde P wave. |
|
|
Term
| Why does reentry circuit cause tachycardia? |
|
Definition
| A current will travel a path that is usually inhibitory due to absolute refractory periods, but isn't, and this current will propagate through the node or atrium again and re-stimulate it. This occurs quickly and can lead to tachycardia. |
|
|
Term
| FILL IN: Cardiac output is almost entirely a function of ________ _______. |
|
Definition
|
|
Term
| What does distensibility mean? Are arteries or veins more distensible? |
|
Definition
| Ability of a vessel to stretch (calculated as increase in volume/ (original volume x pressure increase)). Veins are more distensible |
|
|
Term
|
Definition
| Compliance is the cange in volume/ change in pressure. |
|
|
Term
| 2 statement TF. 1 Arterioles provide the bulk of resistance that control BP. 2 capillaries are responsible for blood volume storage and redistribution. |
|
Definition
| 1 True. 2 False. capillaries are involved in passive exchange. The description listed is referring to veins. |
|
|
Term
| What do sympathetics act more on, veins or arteries? |
|
Definition
| veins. this causes a greater effect than sympathetic changes in arteries in terms of volume. sympathetic stimulation causes less blood in veins, while sympathetic inhibition does the opposite. |
|
|
Term
| What causes the sharp incisura near systole? |
|
Definition
| The aortic blood falling until the aortic valve closes. |
|
|
Term
2 statement T/F. 1 Prehypertension is from 130-140 systole. 2 It is easier to measure systole than diastole |
|
Definition
1 False. Prehypertension is from 120-140 2 True |
|
|
Term
| What does mean arterial pressure mean mathmatically? |
|
Definition
| It is the diastolic plus a third the value of systolic minus diastolic. |
|
|
Term
| If you increase the stroke volume while simultaneously decreasing arterial compliance, what is the effect on pulse pressure? |
|
Definition
| Increasing stroke volume will increase the pulse pressure. Decreasing the arterial compliance will also increase the pulse pressure. |
|
|
Term
| What happens to BP and pulse pressure if you have arteriosclerosis? How about Aortic stenosis? |
|
Definition
| Both will go up due to reduced compliance. Aortic stenosis will reduce stroke volume causing reduction in pulse pressure. |
|
|
Term
| You have more compliance in the aorta than in small arteries. What affect does this have on the pulse transmission speed? |
|
Definition
| The pulse will travel quickest in areas of low compliance, therefore, it travels quicker in the small arteries than in the aorta. |
|
|
Term
| Which will cause dampening (less pulsation), arteries becoming harder (less compliance) or vasocontraction (increased resistance)? |
|
Definition
| vasocontraction (increased resistance) will cause increased dampening. |
|
|
Term
Which of the below will NOT cause increased venous return? 1. giving someone an IV (BP upper) 2. Giving them a venous constriction drug 3. Increasing renal filtration 4. injecting them with an arterial vasodilator |
|
Definition
| 3. Increasing renal filtration |
|
|
Term
| What is a normal RAP (right arterial Pressure) AKA central venous pressure? |
|
Definition
|
|
Term
| What is the cause of the hypertension experienced in alcoholics? |
|
Definition
| Increased abdominal pressure affecting the venous system |
|
|
Term
| Are expanded/ distended veins and liver congestion caused by RAP elevation or reduction? |
|
Definition
| Elevated Right Atrial Pressure. Lower RAP causes dehydration and collapse of veins (increasing resistance). |
|
|
Term
| What changes occur to the venous system upon standing? |
|
Definition
| gravity causes vascular volume and pressure to increase in lower extremities, decrease in thorax. RAP decreases. Less Cardiac Output and arterial blood pressure will also result. |
|
|
Term
| How does the venous system react to standing? |
|
Definition
| The baroreceptors are activated and will cause vasoconstriction to occur. Also the venous valves allow unidirectional flow to prevent pressure extremes in the lower body |
|
|
Term
2 statement T/F. 1 vericose vanes are a result of venous insuficiency. 2 Veins hold 64% of total blood. |
|
Definition
|
|
Term
| You have lipid material A in a capillary. Will it diffuse quicker to the interstitial fluid through the pores or through the cell membrane? |
|
Definition
|
|
Term
| Which is more readily RETAINED in capillaries, glucose or albumin? |
|
Definition
| Albumin. Albumin has a relative permeability of .001 and has is much larger in terms of molecular size than glucose. |
|
|
Term
| What is the difference between net diffusion and filtration in terms of microcirculation? |
|
Definition
| Net diffusion rates define the movement rate of a particular substance depending on a concentration gradient. Filtration occurs due to hydrostatic AND osmotic pressure differences causing outward flow. |
|
|
Term
| What are the forces that cause plasma to move out of the arteries (1) and into the veins (2)? |
|
Definition
1. 13 mm Hg 2. 7 mm Hg Also, 9/10 of fluid lost in the arteries is recovered in the veins. |
|
|
Term
| If you lower the Interstitial fluid pressure, what will be some effects? |
|
Definition
| better tissue mobility, blood flow, and nutrition. This negative pressure is caused by lymph flow |
|
|
Term
Which one of the following forces causes fluid to go into the capillaries? 1. positive capillary fluid pressure 2. positive plasma oncotic pressure 3. negative interstitial fluid pressure 4. positive interstitial oncotic pressure |
|
Definition
| 2. positive plasma oncotic pressure |
|
|
Term
Fill in the values: 1. ____ Liters of lymph circulate per day. 2. Net fluid loss/hr from capillaries is _________ ml/hr. |
|
Definition
| 2-3 L of lymph circulation/day and 120 mL/hr of capillary fluid loss |
|
|
Term
| Will increasing IF pressure will cause higher lymph flow rates? |
|
Definition
|
|
Term
| IMPORTANT: How can you calculate cardiac output? |
|
Definition
| Multiply the heart rate times the Stroke Volume. Average CO is 5-8L/minute |
|
|
Term
Which of the five is NOT a DIRECT contributor to cardiac output? 1. afterload 2. myocardial contractility 3. Heart rate 4. Right Atrial Pressure 5. Preload |
|
Definition
|
|
Term
| Which law would causes preload to increase contractility (force) and stroke volume? |
|
Definition
| The Frank-Starling law. Increased sarcomere length causes increased force generation. |
|
|
Term
| What valve action marks the end of the stage where left ventricular volume increases without change in LV pressure? |
|
Definition
| The mitral valve closing. This stage is ventricular filling. |
|
|
Term
| What is happening to the ventricle in terms of pressure and volume before the aortic valve closes? |
|
Definition
| The LV volume has been decreasing. After the aortic valve closes the LV pressure will also decrease. |
|
|
Term
| What is the effect of heart rate on cardiac output? |
|
Definition
| As heart rate increases, stroke volume decreases. So, the cardiac output will increase up to about 150 bpm, but once you get past 200 bpm, stroke volume is so low that increasing bpm decreases CO. |
|
|
Term
Which will cause an increase in contractility: 1 increased end systolic volume or 2 cessation of inotropic drug usage |
|
Definition
| 1 Increased end systolic volume. This causes increased contractility. Inotropic agents increase contractility, so cessation of these drugs will lower contractility |
|
|
Term
| What will happen if RAP or LAP is too high or too low? |
|
Definition
| If it is too high or low we could get systemic edema |
|
|
Term
| What causes metabolic and hypoxemic hyperemias? |
|
Definition
| Both are local blood flow controls. Metabolic hyperemia is for when tissues need more blood because they are metabolizing faster. Hypoxemic hyperemia is when you need more blood in an area because they didn't have much oxygen before. |
|
|
Term
Which is a vasodilator: CO2, endothelin, or nitric oxide |
|
Definition
| Both CO2 and Nitric oxide are vasodilators, except that CO2 works on cerebral vessels. Nitric Oxide is a potent vasoconstrictor. |
|
|
Term
| What are the constrictors and dilators regulators of the blood? |
|
Definition
|
|
Term
| Name three of the four reasons for syncope? |
|
Definition
Here are the four: Orthostatic hypotension vasovagal response to fear carotid sinus syndrome cardiac or cerebrovascular disease |
|
|
Term
Which of the following receives NO sympathetic innervation?
arteries, arterioles, capillaries, venules, veins |
|
Definition
|
|
Term
| Describe vasomotor nerve activity. |
|
Definition
| It comes from the brain's vasomotor center down the spinal cord and provides a continuous signal that can be dropped by blockage or enhanced with nor-epi. |
|
|
Term
| Which causes people in painful situations to pass out? |
|
Definition
| Vasovagal syncope. Parasymp tone increases and drops heart rate and BP. Simultaneously sympathetics drop causing vasodilation and BP drop. The sympathetic inhibition DOESN'T affect heart rate. |
|
|
Term
| Under which pressures is your baroreceptor response most sensitive? Where does the signal go? |
|
Definition
| at 100 mm Hg. This signal goes to the tractus solitaris and inhibits vasoconstrictors while exciting parasympathetics. This causes decreased Heart rate and BP. |
|
|
Term
| When pressure is low and the baroreceptor recognizes it and sends a signal to the nucleus tractus solitarius, how does the NTS respond? |
|
Definition
| It will cause decreased vagal nerve input (parasymp) and increased sympathetics. Also, it can act to cause ADH or vasopressin release which will increase retention of plasma and fluids. |
|
|
Term
| T/F: Total peripheral resistance (TPR) is a function of arteriole constriction. |
|
Definition
|
|
Term
What won't you secrete under hypotensive conditions? Renin ADH ACTH Epinephrine |
|
Definition
| ACTH is not secreted. Renin causes increased angiotensin II and aldosterone. ADH causes less fluid loss, and epinephrine increases sympathetics to heart. |
|
|
Term
| What causes orthostatic hypotension? |
|
Definition
| You mechanism for increasing BP during standing have failed. Usually your baroreceptors will cause increased sympathetic outflow with less parasymp. This leads to light headedness, weakness, and fatigue. |
|
|
Term
| What are the effects of the volume receptor reflex (if there is too much volume)? |
|
Definition
| Causes increased heart rate and diuresis (ups diuresis by vasodilation of kidney, ADH, ANP) |
|
|
Term
| Describe the CNS ischemic response. |
|
Definition
| When BP goes under 60, it stimulates symp vasoconstrictors to increase mean arterial pressure (MAP) |
|
|
Term
| What happens to contractility and stroke volume when you sit from laying or stand from sitting? Heart rate? |
|
Definition
| Your contractility goes up and your stroke volume goes down while heart rate increases. |
|
|
Term
| Define Glomerular filtration rate. |
|
Definition
| filtration of arteries into collecting tubules. The glomeruli are units composed of collecting ducts and vasculature. The glomerulus has its own hydrostatic pressure and osmotic pressure that are affected by the nervous system |
|
|
Term
| What is the difference between diuresis and natriuresis? |
|
Definition
| diuresis is increase in water loss. Natiuresis is increase in sodium loss. |
|
|
Term
| What is the bainbridge response? |
|
Definition
| volume receptors cause an increased heart rate due to direct stretch of the SA node. The bainbridge reflex is when the atrial receptors signal via the vagus to vasomotor center, which will increase heart rate by symp and parasymp paths |
|
|
Term
2 statement T/F 1 increasing sympathetic stimulation causes hypereffective cardiac output 2 MI and hypertensives have hypoeffective cardiac outputs |
|
Definition
|
|
Term
| What happens to total peripheral resistance during excercise? |
|
Definition
| It decreases because the skeletal muscle demand more oxygen from the blood. Also, BP and CO usually rise. |
|
|
Term
| What happens if you increase intrapleural pressure to -2mm Hg? |
|
Definition
| You will need higher atrial pressures to maintain the previous cardiac output. |
|
|
Term
Which will drive venous return (the others oppose it): Right Atrial pressure, Systemic filling pressure, or resistance to venous return? |
|
Definition
| Systemic filling pressure (increased by vasoconstriction). RAP goes up during tamponade (pleural pressure increase). Resistance to venous return caused by venodilation and hypovolemia (less blood volume) |
|
|
Term
| What is the capacity of the circulatory system without distension and stretch? |
|
Definition
| 4000 ml. This means that there is still 0 mm Hg at this point. Every mL after this will cause and increase in filling pressure. |
|
|
Term
| What is the term applied to this idea: In a circulatory system, how hard to I need to squeeze the right atrium in order to stop blood from filling it? HINT: In other words, the pressure of blood rushing into the right atrium. |
|
Definition
| Termed the Systemic Filling Pressure |
|
|
Term
| If there is a big gap between the Right atrial pressure and the systemic filling rate (higher SFR), what happens to venous return? |
|
Definition
| It is significantly great. |
|
|
Term
2 statement T/F 1 if you decrease blood volume, SFP goes down 2 If you decrease sympathetics, SFP goes up |
|
Definition
| 1 True, 2 False. Sympathetics cause you to have greater systemic filling, in this way, the Cardiac output will be higher. |
|
|
Term
Which would affect resistance of venous return more, A. constricting the arterioles and small arteries to give more blood to venous system, or B constricting veins |
|
Definition
| Constricting veins. Remember, the arteries don't hold near as much blood as the veins do. |
|
|
Term
Fill in the values: Normal cardiac output ____L/min normal right atrial pressure _____mmHg mean systemic filling pressure ______mmHg |
|
Definition
|
|
Term
| How can edema be caused by increased SFP? |
|
Definition
| You will have more venous return, higher CO, increased capillary pressure, so increased filtration from capillaries to tissue |
|
|
Term
What will NOT happen if you cut sympathetics to the heart? 1 SFP will fall to ~4 mmHg 2 CO decreases to 60% 3 RAP decreases to 80 mmHg |
|
Definition
| 3 RAP decreases to 80 mmHg. The right atrial pressure shouldn't change if you cut the sympathetics. |
|
|
Term
| What determines RAP then? |
|
Definition
| The balance of Cardiac Output (CO) and Venous return. If higher CO, then RAP decreases, vice versa |
|
|
Term
2 statement T/F 1 Systole is the period where coronary blood flow is greatest 2 Tachycardia puts greater demand on coronary arteries while, simultaneously, causing less blood to be effectively delivered. |
|
Definition
1 False. The correct period is diastole. 2 True |
|
|
Term
| How does cardiac demand for oxygen relate to the potential increase in coronary blood flow? |
|
Definition
| Demand can increase 6-9x the normal, whereas coronary arteries can only increase 3-4x their circulation, so the heart learns to be Über efficient. |
|
|
Term
| A patient comes in with Coronary Artery Disease (CAD), you can either give him adenosine, ATP, or epinephrine. Which do you give him? |
|
Definition
| You should give him either the adenosine or ATP. Epinephrine will not specifically affect the coronary arteries. |
|
|
Term
| Describe the direct effect on Coronary blood flow? |
|
Definition
| The direct effect is all about neurotransmitters. ACh and symp beta receptors will dilate coronary arteries, whereas alpha adrenergics will cause constriction |
|
|
Term
| Describe the indirect effect on coronary blood flow. |
|
Definition
| These are MORE IMPORTANT than direct effects. These effects are more systemic than local by increasing cardiac work and by stimulating metabolism. |
|
|
Term
| What is the hearts principle fuel? What happens when it runs out? |
|
Definition
| It uses mainly fatty acids. When it undergoes ischemia it has adenosine loss because it runs off of ATP which looses phosphates until adenosine, then adenosine is sent off to cause local vaso-dilation |
|
|
Term
| What is the main cause of Ischemic heart disease? |
|
Definition
| Atherosclerosis, a buildup of plaque that breaks epithelial barrier in coronary artery. Inflammation/ thrombosis to the LDL and LDL itself cause blockage or cause coronary spasm. |
|
|
Term
| You get off your 18 hr flight to the majestic South African safari. After walking around 15 minutes you get extreme chest and left arm pain. You are experiencing CAD, how did this happen? |
|
Definition
| While on board the plain, you had stasis of the blood in you legs, this formed a clot that, after moving around dislodged from your legs and unfortunately ended up obstructing your coronary artery. This is called embolus |
|
|
Term
| My new favorite word, infarction, is important with respect to the heart. How does this occur and what symptoms present with this? |
|
Definition
| AKA heart attack causes interrupted blood supply and cell death in an area of the heart. The symptoms of myocardial infarction include dyspnea (messed up breathing), sweating, light headedness, fatigue, and chest discomfort. |
|
|