High Yield Pt4 PDF

  Stiffening of the mitral valve increases the resistance the left atrium faces as it attempts to fill the left ventricle with blood. Once the LAP is less than the mitral valve resistance, diastole will stop. Increased mitral resistance will prematurely halt ventricular filling.  Crossing a reg...

  Stiffening of the mitral valve increases the resistance the left atrium faces as it attempts to fill the left ventricle with blood. Once the LAP is less than the mitral valve resistance, diastole will stop. Increased mitral resistance will prematurely halt ventricular filling.  Crossing a region of high resistance causes a large pressure drop, so a large LAP-LVP gradient will be seen on Wiggers Diagram. Since there is more resistance during diastole, a reduced EDV will be seen on PV loop. Contractility remains constant, ESV also reduces Mitral Regurgitation: systolic murmur  A leaky mitral valve will cause backflow of blood from the left ventricle into the left atria during ventricular contraction. This is a reduction of effective stroke volume because the blood is going in the wrong direction.  Ventricular contraction pushes blood into the atria, this progressively increases LAP throughout the ventricular contraction (seen on Wiggers) this will increase the preload for the next beat and will be seen on the PV loop by increased EDV. On the PV loop there will also be volume loss during isovolumic contraction and relaxation 28: Cardiac-Vascular Interactions (Mayrovitz)  Cardiac-vascular function graphs  The heart’s contractility and the venous return are major determinants of cardiac output. Vascular properties like TPR, and vessel compliance mediate venous return. If you increase the arteriole resistance, there will be less venous return, increasing resistance will lower the CVP.  These graphs are a Vascular function curve, and a cardiac function curve laid on top of one another, their intersection is called the operating point  As CVP increases, cardiac output increases. This will be seen on the vascular function line.  CVP increases when there is lower TPR, when arteries are more compliant, vasodilated  As cardiac contractility increases, cardiac output increases. This will be seen on the cardiac function curve. 29: Arterial Pressures (Mayrovitz)       Vascular Function Line: preload  The X intercept is the mean circulatory pressure, it is the pressure in the veins when there is no flow. There is larger Pmc when there is more volume(blood transfusion) or less compliant veins  The slope of the vascular function curve is dependent on TPR. Constricted arteries will cause a large pressure drop as blood makes its way to veins, seen as a reduced slope on the vascular function line. Vasodilation will create a steeper slope on the line.  The flat portion of the line shows when the veins collapse in the system. Cardiac Function Curve: inotropy  Increasing contractility allows the myocardium to increase cardiac output at lower CVP, compared to the normal system.  Decreasing contractility will decrease CO even at higher CVP.  Pulse Pressures  The aorta is a tube constantly filled with blood, and the left ventricle is a pump that ejects a stroke volume into that fluid filled tube.  This SV enters the filled tube, transmural pressure increases inducing a transient wall expansion, smooth muscle and elastin of the aorta will contract against the SV propelling it forward.  Remember Pulse pressure=P(systolic)-P(diastolic)  MAP is the average aortic blood pressure, dependent on CO, TPR, compliance, and blood volume, MAP=Pd+1/3PP Change in pulse pressure  Pulse pressure increases if there is:  increased rate of left ventricular ejection  increased stroke volume  decreased aortic compliance Auscultating BP  1. Inflate the cuff to a pressure that completely compresses the artery, at this point there is no flow in the artery  2. Slowly release the cuff pressure, listen for the first Korotkoff sound, the first rush of blood through the narrowed artery will have high velocity and we will hear that high velocity surge bounding against the vessel wall, this is Systolic BP  3. Continue to hear the accelerated blood flow through the narrow artery as the cuff deflates (A1V1=A2V2)  4. When the cuff pressure is no longer greater than vessel pressure, there will be no acceleration surge, and we will stop hearing the Korotkoff sounds, this is diastolic BP  Automatic BP machines take their measurement based on oscillations in the cuff, systolic will be the start of cuff oscillations, diastolic will be the end of cuff oscillations HTN classification  If given numbers fitting in two different categories, stage the patient in the worse category HTN causes: Primary or secondary  Primary HTN is due to increased TPR, it is a vessel problem  Structural wall changes like loss of elastin  Vasoconstriction  Secondary HTN is from organ dysfunction that as a result, effects blood volume, and increases TPR  Renal artery stenosis(decrease flow to kidney will activate RAAS)  Conn’s syndrome(primary hyperaldosteronism)  Pheochromocytoma(excess catecholamines)  Chronic renal disease  Gestational HTN(preeclampsia)  Hyper/hypothyroidism 30: Arterial Pulse Propagation and Reflection (Mayrovitz)     Transmission of Pulses  Pulse wave speed is inverse to Compliance  Siffer vessels (arteries) have higher pulse wave speed  Pulse reflections mostly happen at arterial branch point  We are hitting many different walls at many different directions  Pulse is the sum of forward and backward waves  Transmission  As volume is ejected, it distends the aorta and progresses from 1 to 2 to 3 along the vessel  Think about it like you are pushing a bowling ball down the vessel  The wave moves faster than the RBCs  This idea works like the billiard ball concept, the ball on the end goes flying off but the group as a whole hardly moves Pressure Gradient and Pulsatile Flow  The pressure upstream minus the pressure downstream divided by the space between the measurements is the pressure gradient  Pulsatile flow is dependent on the pressure gradient  Pressure gradient is determined by wave speed  As the wave moves down the vessel it attenuates (gets smaller in amplitude) and disperses (gets longer in duration or spreads out over time)  Reflected waves will return to the start before the initial pulsatile flow is done  Reflected waves  Reflected pressure (P) waves ADD ----> P = Pf + Pb  Reflected flow (Q) waves SUBTRACT -----> Q = Qf + -Qb  There is less reflected energy if the vessel is branched because branched vessels have less resistance.  Therefore vessels with greater resistance have greater reflection Pulse Pressure Variations  Pressure pulses increase and smooth as you move more peripheral  High frequency filtering  If you remove low frequencies then instead of many smaller waves you get one bigger wave  Greater transmission speed  Arteries have little compliance and therefore do not expand rapidly increasing speed  Wave reflections  Pulse wave velocity increases in peripheral arteries due to small compliance  Ankle Brachial Index (ABI)  Take blood pressure in the arm and in the leg and divide them  Ankle/brachial = ABI  Tells you how much if any blockage there is in a peripheral vessel Forming normal waves  Pressure Wave  Pm = measured pressure wave (forward + backward)  Pf = the forward wave or the wave if there was no reflection  Pb = the backward wave or the reflected wave  Flow Wave  Qm = measure flow wave (forward + backward)  Qf = forward flow wave without any reflections  Qb = backward flow wave or reflected wave  Central Pressure Augmentation  As we age our arteries lose even more compliance and that increases wave speed resulting in an earlier reflected wave return  This results in higher systolic blood pressure and lower diastolic blood pressure  Leading to a high risk of stroke, LVH and MI  The blood vessels that provide blood flow to heart muscles do so during diastole ---> if diastolic pressure decreases too much the heart muscle does not get proper blood flow 31: Cardiovascular Physiology Applications  Watch lecture. 32: Microcirculation (Benmerzouga)   Microcirculation: Smallest unit of cardio system that works by providing nutrients and removing waste in the capillaries  Interface between organs and the circulation Includes: Arterioles, capillaries and venules  Arterioles control blood flow to each tissue       Venules influence hydrostatic pressure by altering tone via SNS Capillaries are highly permeable and can be continuous, fenestrated or discontinuous Capillary Exchange  Happens via diffusion, filtration and osmosis  Determined by hydrostatic and osmotic pressure ----> substances leave at one end and enter at the other end  Blood flows directly through membrane  More capillaries = more perfusion  Parallel arrangement -----> slow flow and allows for redirection of flow based on changes in capillary diameter Capillaries  More capillaries in more metabolically active tissues like the heart  Changes in capillary flow  Vasomotion = contractile behavior of smooth muscle (rhythmic)  Transmural Pressure = vessel contraction and relaxation due to SNS input  Made up of Endothelium  Contains substance that result in contraction or relaxation (ex: endothelin is a potent vasoconstrictor)  Liver capillaries are the most permeable and muscle capillaries are the least  Transcapillary Exchange  Diffusion = gasses and other lipid soluble molecules  J = PS (Co - Ci)  Bulk flow = moves water and small lipid insoluble molecules (dependent on capillary structure)  Vesicular Transport = translocates large molecules across endothelium Movement of Substances  Small molecules can move easily  Diffusion is dependent on flow  Large molecules cannot move as easily  Diffusion is dependent on capillary permeability  If you have a lot of edema (swelling) the distance between the capillaries increases making diffusion less dependent on flow and more dependent on diffusion ability of the molecule (the molecule cannot travel the increased distance as easily). The same goes for areas with low capillary density  Filtration and Absorption  Magnitude and direction of filtration and absorption is equal to the difference in hydrostatic and osmotic pressures in the capillary and its surrounding fluid (interstitial fluid)  Hydrostatic pressure depends on blood pressure and is different on arteriole and venous sides  Hydrostatic pressure is the pressure pushing fluid out of the capillary  On one side filtration is high and the other side absorption is high  Arteriole = High filtration  A change in diameter (constriction or dilation) changes hydrostatic pressure  Constriction ---> lower hydrostatic pressure and therefore less filtration  Dilation ----> high hydrostatic pressure and therefore more filtration  Venous = High absorption  Increase venous pressure ---> increased hydrostatic pressure decrease absorption  Decrease venous pressure -----> decrease hydrostatic pressure and increase absorption Factor Governing Osmotic Forces  Oncotic pressure of the capillary is the force keeping fluid in the capillary based on concentration of plasma proteins inside the capillary  Concentration of plasma proteins such as albumin  Albumin has a negative charge at normal blood pH ---> large oncotic pressure  Balance Between Forces  Starling forces govern filtration and absorption (NFP >0 is filtration and NFP < 0 is absorption)  NFP = k(outward forces - inward forces)  NFP = k(Pc + Pi + 𝜋i) - (𝜋c + 𝜋i)  Pi is usually zero and 𝜋i is ONLY an inward force if it is a NEGATIVE number  Therefore usually NFP = k((Pc + 𝜋i) - 𝜋c)  In this example at the arteriole end:  NFP = (32 + 2) - 25    At the venule end:  NFP = (15 +2) – 25    Disturbances in the Starling Forces  When filtration exceeds drainage ----> edema (swelling)  Increase hydrostatic pressure in the capillary  Causes the fluid to be pushed out of the capillary into the interstitial space  Decreased Plasma Protein  No force keeping the fluid in the capillary so it accumulates in the interstitial space  Increased capillary permeability ----> increased oncotic pressure in the interstitial space  Fluid is easily leaving the capillary and the oncotic pressure in the interstitial space is keeping the fluid from entering the capillary Oxygen Delivery  Arterial blood flow x arterial oxygen content = oxygen delivery  Hemoglobin bound oxygen and rate of blood flow determine O2 delivery  Since at normal PO2 hemoglobin is almost 100% bound by O2, the best way to increase O2 delivery is by increasing flow  If you have a condition like anemia (low RBC) then the best way to increase O2 delivery will be to increase hemoglobin  O2 delivery will decrease with decreased flow and decreased O2 content of the blood  This graph shows the binding affinity of oxygen and hemoglobin which is a determinant of the amount of O2 available in the blood  CADET face right is the mnemonic for conditions that shift the curve right decreasing O2s affinity for hemoglobin  CO2, acidity (decreased pH), 2,3 DPG (BPG), Exercise, increased temp   Lymph blockage Nephrotic syndrome or any other disease decreasing capillary oncotic pressure  Dehydration is the opposite of edema  Increased capillary oncotic pressure  Fluid leaves the interstitial space Venous System  Low pressure, volume reservoir system  This allows the veins to adjust preload  High compliance (C = volume / pressure)  As compliance increases, venous resistance decreases  As blood volume in the veins increases, venous resistance increases  As stroke volume increases venous resistance decreases  Gravity can cause the blood to pool in lower extremities  Reduces cardiac output  Supine = more uniform distribution of blood in veins resulting in more return of blood to the heart and lower pressure in the veins  Standing = reduces volume in thoracic vessels, increasing the pressure in the veins and reducing the blood return to the heart, therefore lowering CVP  Varicose Veins: Overstretched veins due to excess venous pressure causes weakness in the valves resulting in edema on standing Venous Return  As you breathe in:  Chest wall expands and diaphragm flattens  There is a decrease in intrapleural pressure of the lungs and an increase in transmural pressure of the SVC, IVC, RA and RV  This increases venous return to the heart  As you breathe out the opposite happens  Valsalva Maneuver:  EXHALING forcefully against a closed glottis  Phase 1: aortic pressure increases and heart rate decreases reflexively  Phase 2: aortic pressure falls ----> decreased venous return and CO and HR increases reflexively  Phase 3: normal respiration resumes  Phase 4: aortic pressure increases due to return of CO to normal, SVR stays elevated due to SNS activation but eventually returns to normal Central Venous Pressure  CVP = pressure in the Vena Cava near the right atrium of the heart reflecting amount of blood returning to the heart  Factors affecting CVP  Decreased CO (heart does not pump well) ----> fluid will back up in veins and increase CVP  Arterial dilation ----> decreased in SVR ----> more blood delivered to venules ---> fluid in venous side increases ----> increased CVP  Postural changes ----> squatting down or reclining back ----> decreased pressure in the veins ----> increase the amount of blood returning to the heart---> increased CVP 34: Peripheral Vascular Controls and Special Circulations (Panavelil)  33: Lymphatic and Venous System Function (Benmerzouga)   Lymphatics  Collects fluid and protein and returns it to the circulation  Overlapping endothelial cells create valves that help move flow  Lymph Flow  Comes from interstitial fluid  High protein content  120 ml/hr rate of flow is proportional to pressure in interstitium  If something affects pressure in interstitium it will affect lymph flow (for these think about things that are increasing the force pushing fluid into interstitium or holding fluid in interstitium ----> your outward forces)  Increased Hydrostatic pressure in capillary  Decreased oncotic pressure in capillary  Increased oncotic pressure in interstitium  Increased capillary permeability  Flow is also increased by lymphatic pump and external factors that cause compression (ex: skeletal muscle contraction)  Lymphatic pumps are due to smooth muscle contraction on expansion of capillary Edema  Edema forms due to disruption of the Starling Forces  Increased capillary hydrostatic pressure  Increased capillary permeability   Autoregulation of blood vessels  The overall goal is to maintain constant flow to organs, local compensations are used to counteract the systemic changes  A rise in arterial pressure transiently increases the flow to that organ, but that increased flow will quickly return to normal via autoregulation.  Autoregulation is possible between the systolic pressure range 70mmHg-175mmHg(essentially all the time), but in circumstances where systolic is outside this range, we lose our ability to compensate  Compensatory mechanisms:  Metabolic hypothesis: metabolic by-products are vasodilators, metabolic tissues will vasodilate the arterioles approaching them(this counteracts the transiently increased flow due to increased pressure)  Myogenic control: increased transmural pressure causes VSM contraction(vasoconstriction) decreased transmural pressure causes VSM relaxation(vasodilation) Metabolic Hypothesis  The blood flow to an organ matches it’s O2 demand, as demand increases, flow increases, this is active hyperemia  In times following occlusion, where no flow caused an O2 debt accumulation, the blood flow will be increased, this is reactive hyperemia  Accumulation of metabolites in the infarcted tissue will vasodilated the arterioles, flow is 4-7x greater when reperfusing the tissue  Most active metabolites in vasodilation: Low PO2, high PCO2, low pH, lactate, ADP, adenosine, histamine, ATP, K+  Coronary circulation is more sensitive to PCO2 and adenosine  Systemic circulation is more sensitive to just PCO2  Most active metabolites in vasoconstriction: Epi, Norepi, angiotensin 2, Vasopressin, Prostaglandin F, Urotensin 2, Thromboxane A2, Serotonin Non-metabolic Vasoconstrictors/dilators   Vasoconstriction: Endothelin 1 is a potent vasoconstrictor released from damaged endothelium, endothelin pulls the damaged vessel together aiding the clotting process  Increased ions that lead to vasoconstriction: Ca  Vasodilation: ANP, bradykinin, prostacyclin, prostaglandin E, Nitric Oxide  Increased ions that lead to vasodilation: K, Mg, H, CO2, anions like citrate and acetate Circulation in various tissues  Coronary circulation: almost completely controlled by autoregulation, has alpha and beta receptors but ANS has a minor role. Increased metabolic demand will lead to vasodilation of coronary arteries, mediated by adenosine, low pH, low O2  Cerebral circulation: like coronary circulation, cerebral flow is mainly controlled by metabolites inducing autoregulation.  High CO2, high H+, low O2 cause vasodilation of cerebral arteries increasing flow. If these metabolites are senses in the brainstem, vasodilation of the brain vessels, vasoconstriction of body vessels to shunt blood to brain  Cutaneous circulation: ANS is most important mediator, solely sympathetic. Cold environments, and situations like hemorrhage stimulate sympathetic response in skin leading to vasoconstriction via A1 receptors  White reaction: stroking the skin gently will activate mechanoreceptors to vasoconstrict, creating a white line as the object is dragged  Triple response: inducing a inflammatory reaction by rubbing firmly on the skin, redness and swelling due to capillary dilation, increased permeability and extravasation  36: Respiratory System Physiology (Mayrovitz)     35: Cardiovascular Controls and Reflexes (Benmerzouga)      Reflexes that control MAP: baroreceptors  In the aortic arch and the carotid sinus, there are baroreceptors that monitor blood pressure  If blood pressure increases, it is sensed by these baroreceptors, they depolarize and transmit this information to the nucleus tractus solitarius(NTS) and then to the medulla, from the medulla vagus will slow the HR, decrease contractility, slow conduction velocity  If blood pressure decreases they hyperpolarize, that is transmitted to the NTS then the medulla as well, sympathetic input to the heart will increase dromotropy, chronotropy and lusitropy  Glossopharyngeal nerve transmits signals from the carotid sinus, vagus nerve transmits signals from the aortic arch Reflex control on CO+MAP: chemoreceptors  Peripheral carotid bodies and aortic bodies have chemoreceptors that monitor blood pH, PCO2, and PO2. If there are hypoxic, hypercapnic, acidic conditions, glomus cells in these bodies will depolarize, sending a signal to the NTS then medulla to increase ventilation, and increase cardiac output.  Central chemoreceptors are found in the medulla itself, and they mainly respond to PCO2, they can respond to acidic conditions. When PCO2 is increased in the csf, the central chemoreceptors depolarize, increasing ventilation and increasing cardiac output RAAS and ANP  MAP control via the secretion of peptides, and interactions between the heart, blood vessels, and kidneys  RAAS: low perfusion to the kidney leads to secretion of renin by juxtaglomerular cells, renin is an enzyme that converts circulating angiotensinogen to angiotensin 1, angiotensin 1 gets converted to angiotensin 2 by ACE, angiotensin 2 has target tissue effects like increasing aldosterone, vasoconstriction, and increasing ADH. Net result: increased BP  ANP: peptide released by the right atria in response to high venous return (stretch sensitive) and increased right atrial pressure. ANP dilates the afferent arteriole to the renal glomerulus, constricts efferent arteriole, and reduces reabsorption. Net result: increasing flow to the kidney, increasing filtration(fluid loss) to lower blood pressure Valsalva Maneuver  Phasic response of HR to bearing down(increasing intrathoracic pressure)  1. Immediately after bearing down, increased intrathoracic pressure compresses the aorta, and increases pressure sensed by the baroreceptors in aortic arch. The signal is sent to the medulla and there is reflexive bradycardia  2. Increasing intrathoracic pressure also compresses the vena cava to the point venous return decreases. Less preload will lead to less stroke volume and drop P. The drop in BP is sensed by baroreceptors to reflexively increase HR and vasoconstriction  3. Patient takes a breath, decreasing the intrathoracic pressure  4. Combination of the effects of step 2 and 3(increased heart rate vasoconstriction, and decreased thoracic pressure) cause an overshoot in BP sensed by baroreceptors, leading to reflex bradycardia again Cushing’s Reflex  Reflexive increase in MAP when intracranial pressure increases.  Perfusion pressure is MAP-ICP, to maintain perfusion to brain following trauma/edema/tumor/collapsed vein  Increased MAP is sensed by baroreceptors and HR is reflexively decreased  Net result: high BP low HR in response to increased ICP Hemorrhage  Loss of blood decreases venous return and activates sympathetics  Low blood volume decreases perfusion to organs, as a result PCO2 builds up in tissues, acidifying them, activating chemoreceptors  Increased vasoconstriction, inotropy, chronotropy  Increased ventilation  Increased kidney reabsorption   Conducting zone = Trachea down to terminal bronchiole  No gas exchange ---> “dead space” Respiratory zone = Respiratory bronchioles to alveolar sacs  Gas exchange happens here  Acinus = region supplied by primary respiratory bronchiole (respiratory zone)  Terminal respiratory unit = 3 acini Metrics  Diameter of the airway decreases with increasing functional capacity  Cross sectional area increases with increasing functional capacity  Respiratory zone = smaller individual diameters but larger cross sectional area  Small airways have larger resistance to flow Alveoli  Made up of Type 1 and Type 2 alveolar epithelial cells  Type 1 = tight junctions (regulate what goes in and comes out)  Type 2 = Produce surfactant  More alveoli towards apex of lungs  Forces on the alveoli:  2 inward forces: elastic recoil (think rubber band, when it’s stretched out it recoils back faster) and surface tension (works opposite surfactant and tires to close alveoli) Gas Exchange interface  Membrane sandwich between capillary endothelium and alveolar epithelium  Increase the membrane ---> reduce ability of gas to diffuse  Normal = 0.5 micrometers  Capillaries can be recruited as needed to increase gas exchange Ventilation - Perfusion - Diffusion: An overview  Conducting zone = Vt = tidal volume x respiratory rate  PO2 = (Patm - 47)FIO2  FIO2 is 0.21 or 21%  Respiratory zone = Va = (TV - ADS) x RR  ADS is the anatomical dead space = 1mL/lb  Average person = 150 mL