Physio Reinforce Concepts Pt6 PDF

Pulse and blood pressure 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 Pulse pressure increases if there is ● ● ● increased rate of left ventricular ejection increased stroke volume decreas...

Pulse and blood pressure 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 Pulse pressure increases if there is ● ● ● increased rate of left ventricular ejection increased stroke volume decreased aortic compliance HTN Classification: If systolic and diastolic measurements are in two different classifications, stage the patient in the worse category Autoregulation 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 Metabolic hypothesis: metabolic by-products are vasodilators, metabolic tissues will vasodilate the arterioles approaching them. 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 ● Most active metabolites in vasodilation: Low PO2, high PCO2, low pH, lactate, ADP, adenosine, histamine, ATP, K+ 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 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 Reflexes on MAP If blood pressure increases, it is sensed by baroreceptors in the carotid and aortic sinus, 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 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: 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 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 ● Sheer stress ○ Cardiac Flow/Resistance ○ ● Flow is smallest in single vessels and greatest in organs with vessels in parallel ○ ● ● Remember: R total = R1 + R2 + R3 (in series) and 1/R total = 1/R1 + 1/R2 + 1/R3 ■ Less total resistance means greater flow!! In arterioles there is the greatest pressure lost bc they have high resistance (P = Q x R) Types of Pressure in a vessel ○ ○ Perfusion pressure is the pressure upstream vs the pressure downstream ■ This is the pressure in a longitudinal direction and drives flow through a vessel Transmural Pressure is the pressure inside minus outside of the vessel ■ Across the wall of the vessel (bc you paint murals on walls) ● The blood moves faster at the center of the vessel and slower near the walls of the vessel bc the walls of the vessel increase resistance and that lowers flow If you lower flow, you are lowering velocity (remember you can rearrange your formulas Q = U x A) Pulmonary Artery Wedge Pressure ○ ○ ○ Estimate of pressure in the LEFT atrium Insert a balloon into the pulmonary artery via a Swanz-Ganz Catheter PVR = (MAP - PAWP) / CO ■ Remember PAWP is just replacing LAP in this equation!! EQUATIONS: ● ● ● CO = SV x HR ● 𝚫P = Q x R ● ● ● TPR = SVR = (MAP - CVP)/CO PVR = (MAP - LAP)/CO Velocity of blood is = Q / A PP = Ps - Pd MAP = Pd + 1/3 PP EKGs ● ● ● ● The limb leads create a triangle on the body called Einthoven’s Triangle ○ The average wave should be moving toward the PMI of the heart (down and to the left) ● If the dipole is moving toward the electrode (positive) it will be a positive deflection on the EKG ● If the dipole is moving away from the electrode (negative) it will be a negative deflection on the EKG ● Ventricular depolarization happens Endo to Epi and ventricular repolarization happens Epi to Endo MEA Finding MEA a step by step approach: ○ Determine which lead is most isoelectric (which one looks like the straightest line with the smallest positive and negative deflections ○ Looking at the circle graph, find which lead is perpendicular to the lead that is most isoelectric ○ Look at the EKG and see if that lead is more positive or more negative ○ If it's more positive the MEA is its positive direction on the circle graph OR if only 2 leads are given, use the thumbs up approach ○ If your left thumb is lead 1 and your right thumb is lead 2 ○ Thumbs up means the lead is more positive and thumbs down means the lead is more negative ○ If BOTH thumbs are up its a normal axis ○ If the LEFT thumb is up and the right is down then its a LEFT axis deviation ○ If the RIGHT thumb is up and the left thumb is down then its a RIGHT axis deviation Wigger’s and PV loop Diagrams ● Change in contractility ○ PV Loop Changes ● Decreasing afterload ○ ○ ○ ○ ○ Remember afterload is the pressure the heart needs to overcome to eject blood MAP is a good estimate of afterload The end systolic volume decreases along the PIP line The SV (width) increases The preload is unchanged ● ○ ○ ○ Change in contractility ○ ○ ○ ○ Contractility is the slope of the PIP line As you change contractility the slope of the line changes This increases or decreases ESV The SV is increased or decreased as well Contractility is the slope of the PIP line As you change contractility the slope of the line changes This increases or decreases ESV The SV is increased or decreased as well Heart Sounds ● S1 = inlet valves closing ○ ○ ○ ● S2 = outlet valves closing ○ ○ ○ ● Ventricular relaxation End of T wave Beginning of isovolumetric relaxation on PV loop (2) S3 = Early Diastole ○ ○ ○ ○ ● Onset of ventricular systole QRS complex Onset of isovolumetric contraction of PV loop (4) Rapid filling Heard in a volume overloaded state or in high artial pressure In between T wave and following p wave During early filling on PV loop (right after 3)) S4 = Atrial systole ○ ○ ○ ○ Atrial contraction Head in LVH or RVH or in a stiff ventricle state During p wave End of filling on PV (right before 4) loop (4) Pulse Waves ● Pulse wave speed is inverse to Compliance ○ ● Pulse reflections mostly happen at arterial branch point ○ ● ● ● Siffer vessels (arteries) have higher pulse wave speed We are hitting many different walls at many different directions Pulse is the sum of forward and backward waves 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 Ankle Brachial Index ○ Take blood pressure in the arm and in the leg and divide the systolic pressures ○ Ankle/brachial = ABI ○ Tells you how much if any blockage there is in a peripheral vessel Microcirculation ● Small molecules can move easily ○ ● ● ● ● ● Diffusion is dependent on flow Large molecules cannot move as easily ○ Diffusion is dependent on capillary permeability 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 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) ● ● ● Oxygen Binding curve CADET Face Right With a right shift - it is harder for O2 to bind and easier for Hb to unload O2 onto tissues ● Lymphatics ● ● Lymph Flow 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 ● ● 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 ● 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