Physio Midterm 2 PDF

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Summary

Trace the flow of blood through the cardiac chambers, systemic circulation and pulmonary circulation and describe the principle properties of the different branches of the circulation Right atrium Tricuspid valve Right ventricle Pulmonary semilunar valve Pulmonary arteries Lungs Pulmonary veins Left...

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! ! ! ! ! ! • Trace the flow of blood through the cardiac chambers, systemic circulation and pulmonary circulation and describe the principle properties of the different branches of the circulation!

• List the advantages to a circulation connected in parallel rather than in series! A. Total resistance is less than resistance of any one resistor! a. Cardiac output = pressure gradient/total resistance, so lower resistance = higher CO! A. Blood composition is uniform at the entry to each organ system ! B. Blood pressure is maintained and similar at the entry to each organ system! C. Independent control of blood flow to each system! ! • Calculate the resistance to blood flow in series and parallel circulations! A. In series, resistance = sum of the individual resistor ! B. In parallel, 1/total resistance = sum of 1/each resistance! ! • Describe the various cell types in the heart and their functional importance! A. Pacemaker cells! a. In sinoatrial and atrioventricular nodes! b. Initiate heartbeat and control heart rate! c. Spontaneously generate action potential! B. Conducting myocytes! a. In the bundle of his and bundle branches, purkinje fibers, and tracts within atria! b. Conduction system that delivers the APs generated in pacemaker cells to the contracting myocytes in a coordinated way! C. Contracting myocytes! a. In the atria and ventricles! b. Contract forcefully to generate pumping of blood ! c. 99% of cardiac cells! • Graphically represent the action potential for the various cardiac cell types and describe the ionic currents contributing to the voltage changes.!

‣ Rapid depolarization (upstroke) —> more positive/less negative! • Sodium influx down both its electric and chemical gradient (more chemical though)! ‣ Brief partial depolarization —> more negative! • Potassium efflux down its chemical and electrical gradient! ‣ Plateau —> no change! • Calcium influx (calcium elec points out of cell but chem gradient points into cell and is stronger) and potassium efflux (both gradients point out of cell) balance out! ‣ Repolarization —> more negative! • Potassium chemical gradient points out of the cell and electrical points inwards, but chemical is stronger in this case and potassium leaves the cell! ‣ Resting membrane potential —> no change! • Potassium elec and chem gradients are now balanced! ‣ Spontaneous decrease in outward K+ current and increase in inward Na+ current! ‣ Spontaneous increase in inward Ca++ current due to opening of primary T channels! ‣ Triggered opening of voltage-gated Ca++ channels (primarily L channels)! ‣ Triggered increase in K+ current (repolarization) and closing of L channels! ! • Describe the significance of the “plateau phase” in the AP of cardiac myocytes!

• Differentiate mechanisms of excitation-contraction coupling in cardiac and skeletal muscle and the describe the implications of these differences to force modulation in the heart.!

‣ Ca++ release is graded! ‣ Implications: this graded Ca++ induced Ca++ release prolongs the period of depolarization in the cardiac myocyte while the muscle contracts, resulting in the plateau phase! ‣ Tetany cannot occur, force modulation is only based on the amount of Ca++ released (strength of contraction) or frequency of contraction!

change in voltage, change conformation, and transmit the change to RyRs which function as calcium channels)! ‣ Ca++ release is all or none!

‣ Implications: all or none leads to sudden depolarization followed by a latent period and then contraction, which allows for tetany if another AP is generated before [Ca++] returns to normal (fused or infused)! ! • Identify the heart cells with the fastest rate of depolarization and explain why these cells become the “pacemakers” of the heart.!

has a stronger electrochemical gradient into the cell!

causes very fast rise in Ca++!

! • Explain how changes in: threshold potential, resting membrane potential, and rate of depolarization of the pacemaker cells affect the heart rate.! A. Threshold potential: raising threshold potential decreases AP frequency! B. Resting membrane potential: decreasing resting potential decreases AP frequency! C. Rate of depolarization: decreasing rate of spontaneous depolarization decreases AP frequency! ! • Trace the spread of excitation through the heart and describe how the arrival of excitation at different regions of the heart maps to the wave forms of the EKG.!

! • Describe the significance of phospholamban on calcium homeostasis in cardiac muscle.!

• List the phases of the cardiac cycle and describe the relationships between: ventricular pressure, aortic pressure, atrial pressure, ventricular volume, and the electrocardiogram associated with each

phase.!

• Pvent > Patrial! • Pvent < Paortic! • Ventricles are at full volume and increasing pressure (contracting)! • Semilunar and AV valves are closed! ‣ Ventricular ejection: ! • Pvent > P atrial! • Pvent > Paortic! • Ventricles are decreasing volume (ejecting) and at full pressure! • Semilunar valves open!

P vent > Patrial! Pvent < Paortic! AV valves are closed! Atria are filling up, increasing pressure! ‣ Passive ventricular filling: ! • Pvent < Patrial! • Pvent < Paortic! • AV valves open, semilunar closed, ventricles fill slowly! ‣ Atrial contraction (P): ! • Pvent < Patrial! • Pvent < Paortic! • AV valves are open, semilunar closed! • Ventricles fill up quickly as atria contract! • • • •

! • Identify the timing of the first and second heart sounds within the Wiggers diagram and the source of these sounds.!

‣ Sound comes from mitral valve closing!

‣ Sound is Aortic valve closing! ! • Represent the cardiac cycle graphically by the pressurevolume relationship and define the terms: stroke volume, end systolic volume, and end diastolic volume.!

ejected from the heart)!

! • Write the equation relating Cardiac Output, Heart Rate, and Stroke Volume!

• Describe the effects of parasympathetic and sympathetic innervation on heart rate and the cellular mechanisms underlying these effects!

‣ ACh is released from vagus nerve to SA and AV nodes! ‣ ACh causes hyperpolarization of pacemaker cells, decreases rate of rise, and elevates the threshold potential! ‣ Heart rate is decreased ‣ Quick on/off response, shorter duration of the effect!

to the thoracic spinal ! ‣ Sympathetic fiber connects thoracic spinal cord to a sympathetic chain ganglion, and then another fiber carries the signal to the SA and AV nodes! ‣ Epinephrine/Norepinephrine causes increased rate of rise and lowers the threshold potential! ‣ Epi/Norep binds to beta 1 receptors, which results in a GPCR signaling cascade of multiple phosphorylations in the cell and causing these effects:! • DHPRs (L-calcium channels): opening of voltage-gated Ca++ channels! • RyRs (SR calcium release): faster calcium release! • phospholamban (turned OFF by phosphorylation): relieves SERCA inhibition which increases rate of relaxation! • Troponin I (decrease Ca++ affinity): more sensitive, contract easier! ‣ Heart rate is increased! ‣ Extra interneurons result in slower on/off response but longer duration of the effect! ! • Discuss the significance of the cardiac myocyte calcium transient on contractility!

! • Describe mechanisms by which phosphorylation alters contractility and discuss the significance of phospholamban on the calcium transient and rates of relaxation!

‣ Ca++ transient returns to normal faster after an AP, able to have higher frequency APs! ! • Diagram and describe the cellular mechanisms by which cardiac glycosides increase the force of cardiac muscle contraction.!

! • Draw a graph showing the relationship between [Ca++] (pCa) and force production in cardiac muscle and show how calcium sensitizing drugs and acidosis effect this relationship. !

production at higher pCa values!

! • Explain the differences between modulation of force by calcium concentration and calcium sensitivity and the importance of this difference to the Frank/Starling Law of the heart. !

• Explain the principles underlying the Frank/Starling Law of the Heart and the connection between the cardiac length/tension relationship.!

before contracting!

relationship)!

increases! ! • Draw a graph showing the effect of sympathetic stimulation on the Frank/Starling Law of the heart!

sensitivity! ! • Draw a graph showing the effect of heart failure on the Frank/Starling Law of the heart!

! • Use Pouiselle’s Law to calculate the resistance to blood flow with changes in vessel radius!

(Q = delta P/R), so just change the resistance! !

• Explain how blood doping by artificially increasing red blood cell content of the blood can force the heart to generate more force. !

• Compare and contrast mechanisms of active and reactive hyperemia!

interstitial fluid —> arterioles dilate —> blood flow to active organ increases!

• Describe the mechanism by which nitric oxide regulates vascular resistance in smooth muscle cells!

‣ This causes the smooth muscle to relax and vasodilation to occur!

! • Define pressure autoregulation and describe its significance!

• Describe the effects of sympathetic stimulation on arterial diameter and resistance and describe the cellular mechanisms.!

‣ Arterial diameter decreases, resistance increases! ! • Explain how adrenergic stimulation produces vasodilation in coronary and skeletal muscle blood vessels, but constriction throughout most of the rest of the vascular beds.!

‣ Binds to alpha receptor in the vascular smooth muscle cells! ‣ Look at Gaq signaling cascade... stimulates crossbridge formation —> vasoconstriction! • Slight affinity for alpha receptors, so can cause some vasoconstriction ! ‣ Greater affinity for beta 2 receptor, which are at high density in the smooth muscle cells of the arterioles supplying coronary arterioles and skeletal muscle arterioles than other tissues ! ‣ Similar effect to NO stimulation because they both activate the same receptor! • Vasodilation in blood vessels with lots of beta receptors! ! • Diagram the Renin-Angiotensin-Aldosterone-System and explain its significance to the regulation of vascular resistance! ! 1. Decreased BP results in decreased blood flow to the kidney via renal artery! 2. Stimulates juxtaglomerular cells to secrete renin! 3. The liver produces angiotensinogen, which is converted to Angiotensin I by renin! 4. Endothelial cells in the lungs contain angiotensin converting enzyme (ACE)! 5. ACE converts angiotensin I to angiotensin II! 6. Ang II triggers release of aldosterone from adrenal cortex! 7. Increases Na+ retention in the kidneys; water follows salt so blood volume is increased! 8. Angiotensin II stimulates the posterior pituitary gland to release ADH (vasopressin) —> Vasopressin causes vasoconstriction, Ang II also directly causes vasoconstriction! 9. After vasoconstriction and water retention, BP is returned to normal and the cycle stops! ! • Graphically demonstrate changes in blood vessel compliance and write equations for blood vessel compliance and elastance.!

‣ Arteries have high elastance!

‣ Veins have high compliance! ! • Provide a graphical representation of the cardiac function curve and explain how it is related to the Frank/Starling Law of the heart. !

!

• Describe the effects of: blood volume, the respiratory pump, skeletal muscle pump, sympathetic vasoconstriction, and cardiac suction on central venous pressure!

‣ Inhalation reduces intrathoracic pressure, right atrial pressure, jugular vein pressure! ‣ Greater pressure gradient between extrathoracic and intrathoracic veins causes blood to flow into the chest cavity (where the heart is...)! ‣ Venous return to the heart via superior vena cava increases in rate!

‣ Contracting muscle pumps blood through the veins, increasing the venous pressure! ‣ Valves ensure one-way flow back to the heart!

‣ CVP is not directly affected but venous return increases! ! • Explain how increases in central venous pressure can cause increases in cardiac output!

• Compare and contrast the concepts of “blood flow rate” and “velocity of blood flow”!

‣ Because organs are connected in parallel, this remains constant throughout circulation!

‣ Increase in total cross sectional area results in decreased flow velocity! ‣ Having many small vessels increases overall area as opposed to few large ones! ‣ Slow speed through capillaries gives more time for exchange of nutrients and waste! ! • List different types of capillaries and contrast their structure and function!

!

• Compare and contrast driving forces for diffusion and bulk flow across a capillary wall!

‣ Depends on concentration gradient or partial pressure! ‣ Equation: J = -P(A)(Ci – Co) —> rate = -permeability coefficient x area x conc. gradient!

‣ Used infrequently, does not account for most of flow across capillary wall!

‣ Either go through fenestrations or intercellular clefts! ‣ Filtration: net fluid movement goes out of the capillaries into tissue! ‣ Reabsorption: net fluid movement goes into the capillaries from tissue! ‣ Starling’s bulk flow equation: Pnet = k [ (Pc - Pi) - sigma (πc - πi) ]! • K = filtration coefficient!

• Describe the anatomy and primary functions of the lymphatic circulation! ‣ Entry of untrafiltrate into lymphatic circulation is dependent on the pressure gradients between blood vessels and interstitial fluid! • Fluid pressure on outside of lymphatic vessels pushes endothelial cells’ free edge inward so fluid can enter! ‣ Rhythmic smooth muscle contraction and skeletal muscle contractions drive fluid movement through the lymphatic circulation, NOT cardiac pump! ‣ Smallest lymph vessels are blind-ended vessels, pick up a portion of ultrafiltrate! ‣ Terminal lymphatic capillaries converge on the collecting lymphatic! ‣ The terminal capillaries have pores that allow the interstitial fluid to enter! ‣ Channel valves throughout lymphatic circulation prevent back flow ! ‣ Defense against disease! ‣ Transport of absorbed fat! ‣ Return of filtered protein! ! • Describe the relationship between mean arterial pressure, central venous pressure, total peripheral resistance and cardiac output!

• Biggest drop is across the arterioles! ‣ Pulsatile nature of pressure during systole and diastole is eliminated by arteriolar resistance! ‣ MAP is the driving force for blood flow and must be maintained for good tissue perfusion! blood flow (R = delta P/Q), so if blood flow is constant than high R results in high P!

‣ Increase in CVP results in higher EDV, SV, and finally CO!

• Calculate mean arterial pressure using values for systolic + diastolic pressure!

• Identify the locations of the major baroreceptors in the circulatory system and describe how changes in blood pressure causes homeostatic responses to return blood pressure to normal!

‣ Afferent nerves synapse onto the cardiovascular medullary center (brain stem)! ‣ Fire afferent neurons more frequently when MAP/PP increases (depressor response)! ‣ When BP decreases, baroreceptors fire less frequent APs (press or response)! • Parasympathetic drive to the heart decreases, raising the heart rate! • Increased sympathetic drive to the heart raises contractility and heart rate! • Increased sympathetic drive to arteries and veins increases venous return and TPR! • Triggered release of epinephrine from adrenal medulla has similar effects to sympathetic innervation to the heart and most vasculature! ! • Outline the roles of the sympathetic and parasympathetic nervous systems within the baroreceptor regulation of blood pressure.!

‣ Decreases HR, which decreases CO, which lowers BP!

‣ Increase in HR, which increases CO and increases BP! ‣ Increase in contractility, which increases SV, which increases CO which raises BP!

increases CO and raises BP! !

• Describe the responses to a loss in blood volume, including mechanisms mediated by the baroreceptor reflex and hormonal systems.!

‣ Vasopressin causes vasoconstriction! ‣ Ang II triggers aldosterone release from adrenal cortex into kidneys! ‣ Increases Na+ retention in the kidneys; water follows salt so blood volume is increased ! ‣ Ang II also directly causes vasoconstriction!

‣ Stimulates red blood cell production! ‣ Need to replenish blood osmolarity after increasing its volume via RAAS!

‣ Would not be released if blood volume is too low! ! ! ! ! • Differentiate between structures in the Conducting and Respiratory Zones of the respiratory system and explain why the conducting zone is known as the Anatomic Dead Space.!

‣ Air is warmed and humidified! ‣ Smell is detected in nasal cavity, which detects danger! ‣ Lined with mucociliatory escalator, which carries pathogens and foreign particles toward the pharynx to be stalled or coughed out! ‣ Cilia beat to move the mucus in the sole layer, paralyzed by cigarette smoke! ‣ Mucous is secreted by the goblet cells, others secrete antimicrobiano peptides, reactive oxygen/nitrogen species, or cytokine signals! ‣ Conducting zone: consists of trachea, primary and smaller bronchi! • Acts as an atomic dead space because no gas exchange occurs but air is stored there! ‣ Respiratory zone: respiratory bronchioles and 500 million alveoli! • Gas exchange occurs here! ! • Calculate the partial pressures of gases in inspired air and alveolar air! ! " " N2" " O2" " CO2"" H2O"" Partial pressure sum (total pressure)! ! P atm" 600 " " 160" " 0" " 0" " 760 mm Hg! P alv""573" " 100" " 40" " 47" " 760 mm Hg! ! • Explain why intrapleural pressure is a "negative" pressure and describe the significance of a negative intrapleural pressure to changes in alveolar volume and alveolar pressure.!

cohesion of water! ‣ Elastic nature of lungs creates a collapsing force! ‣ Chest wall creates expanding force! ‣ Balance between expanding and collapsing force keeps the lungs open! ‣ Pleura are caught between two opposing forces, creating a negative pressure within intrapleural fluid! • 4 mmHg below pressure within lungs and atmospheric (which are both at 760)! ‣ Intrapleural pressure differential becomes more negative with respect to external air! ‣ Transmural pressure difference (across lung wall) increases to 8! ‣ Change in pressure creates a force that expands alveoli! • Boyle’s law: P1V1 = P2V2, expand alveolar volume to decrease pressure! • Want the alveolar pressure to match the pleural pressure! • Now, the pressure within the lungs is less than atmospheric pressure...! • Air flows into the alveoli to make up pressure change (inspiration)!

chest and causing inspiration! • Aided by external intercostal muscles! • Sternocleidomastoid muscles make minor contribution (during exercise) by increasing the height of the chest cavity! ‣ Exhalation is the passive decrease in expanding force (relax diaphragm)! • Internal intercostal and abdominal muscles increase force of expiration during exercise ! ! • Describe the effects of the following on airway resistance: Oxygen, Carbon Dioxide, Sympathetic Stimulation, Parasympathetic Stimulation, Epinephrine, and Histamine!

‣ G alpha q (GPCR) complex causes a signaling cascade that leads to smooth muscle contraction, causing bronchoconstriction

‣ Smooth muscle relaxes and causes bronchodilation!

• Draw a graph showing both an increase and decrease in lung compliance and explain why a decrease in lung compliance primarily makes inspiration more difficult.!

trans pulmonary pressure (alveolar pressure - pleural pressure) ! ‣ Compliance is inversely proportional to elasticity, so decreased compliance means the elastic collapsing force of the lung...