Week 2 CVS I Continued Lecture Notes PDF

CVS I Continued Lecture Notes September 18, 2023 8:56 AM The cell quiz 21 questions Sometimes there are pathology questions on the quiz Isovolumetric contraction and relaxation: - All 4 valves closed - Volume of blood is not changing during phase (no blood coming in or going out) - During contrac...

CVS I Continued Lecture Notes September 18, 2023 8:56 AM The cell quiz 21 questions Sometimes there are pathology questions on the quiz Isovolumetric contraction and relaxation: - All 4 valves closed - Volume of blood is not changing during phase (no blood coming in or going out) - During contraction phase: ventricles contracting and building up pressure ○ Hear S1 - as AV valves close - Relaxation phase: ventricles are relaxing and pressure falls ○ Hear S2 - as SL valves close Week 2 Page 1 EDV - volume present in the ventricles ESV - volume left in ventricles at the end of the contraction. The volume of blood is not emptied completely b/c will have increased risk of creating bubbles, which we want to avoid entering through circulation Stroke Volume (SV) - volume ejected from the ventricles every beat ex. (EDV - ESV) = (120-50) = 70ml Late diastole: - Ventricles are filling, and the atria are pushing blood through the AV vales, which allows blood to fill the ventricles Atrial Systole: - Atria then contracts and pushes a little more blood into the ventricles = atrial kick - AFib = loss of coordination of the atria Week 2 Page 2 Systole: - Isovolumetric ventricular contraction, all 4 valves are closed, ventricles are starting to contract and generate pressure, papillary muscles are also starting to contract, but not enough pressure yet to open SL valves - So ventricles will contract and generate pressure to overcome pressure of the SL valves - Pulmonic valve 20mmHg and aortic valve over 120mmHg - Isovolumetric = same volume - As pressure increases, SL open and blood flows into systemic or pulmonary circulation - Blood ejected = SV Early Diastole: - Isovolumetric relaxation, pressure will drop in ventricles and SL valves will close, and the AV valves are still closed, too. - The ventricles will relax and pressure must decrease enough so that it's pressure is lower in the ventricles than atria - Blood will never move from area of low pressure to high pressure (only high to low pressure) Week 2 Page 3 Ventricular volumes: - Ventricular volume increasing in diastole - Little bump is the atrial kick, up to 20% of SV, usually 10% - Period where there is 0 change in ventricular volume, as ventricle contracts, blood leaves ventricles = ESV - Then Isovolumetric relaxation - Ventricular pressures: - Pressures are low in atria Week 2 Page 4 - ECG and Heart Sounds: - S1 - AV valves closing - S2 - SL valves closing Dicrotic notch - SL valve has closed and hear the turbulence around this Week 2 Page 5 Cardiac output: - Volume of blood ejected from LV into aorta every minute - Determined by SV (blood volume per beat) x HR(# of beats/min) - L/min - Gives us an idea of supply and demand of the body - Cardiac reserve = diff between max CO and CO at rest --> athletes can show a diff of up to 500 800% difference in CO - Problems if max CO = resting CO, leads to cardiovascular disease, heart doesn't have extra capacity for heart to exert any energy - Influences of SV: - Preload: - Afterload: - Contractility: - ^ work independently or together, can have diff combinations of them working together in different amounts, all of this creates the capacity to meet the demands of the body Week 2 Page 6 Preload: - Amount of stretch required on the ventricles as you push volume into the ventricles - The more the muscle is stretched, the greater the force of contraction (to a point) Week 2 Page 7 - The more the muscle is stretched, the greater the force of contraction (to a point) - Ex. If put 130ml in ventricle, the heart will stretch and contract to keep its normal volume after ejection. But can't accommodate 1000ml, so it allows volume to a point. This is what is seen in HF pts. If give HF pts too much fluid, it worsens the BP. - According to Frank starling law: Inc in preload should increase CO - Normal contracting myocardial cells should contract Muscle cells short and they conduct electricity Ionotropic agents and inc ability to contract cardiac muscle ANS hormones (Epi, NE, DA) will rev up ability of the heart to work Digitalis increases contractility, effective in early HF pts - not late HF pts Negative inotropes: CCB, dec ability of the heart to contract Ex. Anoxia, inc CO, acidosis, high K+, anaesthetics (halothane) limit heart to work well and will also limit ATP to work Week 2 Page 8 - The resistance the heart has to pump against - Ex. Pushing the door against a strong wind - #1 of inc afterload/inc resistance is HTN, ventricular has to overcome the high pressure in the systemic circulation/aorta Week 2 Page 9 - Exercise - will help CO be more efficient, utilizes O2 better - Hormones (Epi, TH, Ca2+) - ANS - Function: to bring the nutrients and get rid of waste to the heart muscle - Smallest circulation - Have an arterial supply and venous return system and dumps waste into general circulation - Diastolic pressure more impt for function of coronary circulation - Most of blood flow to heart is in the diastolic phase - Blood is pushed to organs during the systolic phase, but the heart gets its blood during the diastolic phase Week 2 Page 10 - Blood flow starts in epicardium, and move through the myocardial layer, and then the subendocardial plexus - During diastole, get blood flow to heart - Coronary blood flow is fastest while heart is contracting - HR doesn't affect blood flow to heart - Coronary arteries don't carry blood to fibrous pericardium - 80% of people are L side dominant, majority of blood supply of heart is on the L side Week 2 Page 11 - RCA blockage - pacemaker - L main artery -->LAD(majority of anterior LV supply) + circumflex (lateral and posterior supply) - Blockage in L main = widow maker, impacts most of LV circulation Week 2 Page 12 - Venous circulation returns to coronary sinus via great cardiac vein and gets dumped into RA - Veins and arteries begin on surface and then go deeper into heart and then overlap Week 2 Page 13 - Veins and arteries begin on surface and then go deeper into heart and then overlap - As ppl age, people develop anastomoses of arteries and veins, starting at the age of 50yo, to get around areas that are slow - Thus MI at 40yo have more profound dysfunction, than an 80yo, b/c 40 yo haven't yet developed anastomoses - 1 nuclei (skeletal has multiple nuclei), centered 25% of cytosol is mitochondrial space (more than skeletal muscle) Larger than skeletal muscle Intercalated discs - cross-bridging attaching cardiac cells, allowing the cells to function as a unit GJ allows conduction to travel fast Sarcoplasmic reticulum - sequesters Ca 2+, and pulling Ca 2+ for contraction Week 2 Page 14 Arrangements, nuclei, hormonal influence - TH and ANS hormones influence - ***KNOW THIS ^ FOR MIDTERM*** Week 2 Page 15 - Unit of contraction Sarcolemma Transverse tubule - move Ca2+ See video of contraction Inside sarcomere, thin and thick filaments arranged for max capacity for contraction M line (holds myosin) Z line(holds actin) No need to know bands But know what overall moves and doesn't Week 2 Page 16 - Actin and myosin don't shorten, they only slide past each other - Actin pulls closer together and the overall cell contracts - The H zone and I zone shortens, but the filaments don't shorten - No shortening of A band (myosin filament) Week 2 Page 17 - Head on myosin has 2 binding sites --for actin and ATP - No power stroke unless has the ATP - Binding sites on actin for myosin, and initially they are covered with tropomyosin(a regulatory protein) - Troponin also has binding sites and binds Ca2+ and tropomyosin 1. When troponin binds ca2+, it will move the tropomyosin out of the way 2. Now the actin binding site is exposed 3. ATP on the myosin, and myosin can now bind the actin 4. Power stroke 5. And myosin will come closer together 6. Sarcomere shortens and creates a contraction - Don't need to know bands, but know process of actin and myosin binding and creating power stroke Week 2 Page 18 - Troponin = intracellular regulatory protein The cell is surrounded by PM, and it's semi-permeable A regulatory protein should be inside the cell A loss of integrity of the cell membrane causes troponin to be released into circulation Troponin T (used by most hospital organizations as a cardiac marker for MI) Troponin I & T are unique to cardiac muscle T - binds to tropomyosin I - inhibitory on cardiac muscle C - ca2+ bound in cardiac and skeletal muscle, thus not as specific No difference between CK and CPK (diff terminology) CK - enzyme found in muscle cells, released, if levels rising, have large muscle damage ○ Used to use isoenzymes: CKMB unique to cardia muscle and CKMM (skeletal) and CKBB (brain muscle)--> don't use this clinically Week 2 Page 19 - Heart muscle has certain component of cells that have automaticity--thus doesn't need outside source to start contraction - Main pacemaker = SA node - Develops its own APs Week 2 Page 20 - Develops its own APs - Has an unstable resting membrane potential - pacemaker potential is not flat As soon as AP finished, it moves towards threshold, and then will continue to fire APs - Epi increases the HR - It increases the AP slope, thus less time to reach threshold, and thus inc rate of APs - ACh dec the AP slope, which will take longer for the AP to reach the threshold, thus it will take Week 2 Page 21 - ACh dec the AP slope, which will take longer for the AP to reach the threshold, thus it will take longer between APs - Know the cardiac electrical pathway - If SA node not working, the AV node can generate APs, but only between 40-60bpm Week 2 Page 22 - If SA node not working, the AV node can generate APs, but only between 40-60bpm - Lag between SA node to AV node, different pathways to AV node P wave - atrial depolarization QRS - ventricular depolarization T wave - ventricular repolarization Week 2 Page 23 - Atrial repolarization is hidden in the QRS wave, thus don't see this Week 2 Page 24 - Absolute refractory period: plateau phase associated with Ca2+, there is no other electrical response that can hit the cardiac muscle at this time, which helps to protect the heart from entering an arrhythmia, thus can't get tetany - Skeletal muscle has NO refractory phase, thus you CAN get tetany Week 2 Page 25 - Medications can influence this - Ex. CCB, BB, digoxin can elongate the plateau phase Week 2 Page 26