Exam 2 Patho Lecture Notes
Cancer Biology and Cancer Epidemiology
Jimmy , 3 packs a day, 20 —-60 pack years
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Cancer Diagnosis due to the signs.
Inflammation is how cancer starts, release of ROS, radicals, cellular proteins, DNA damage, and over replicate and over proliferate and turn into cancer.
Treatment of cancer - CHemo, kills cancer cells. proliferate - replicate and rapidly reproducing cells, rapidly reproducing cells. Hair, Gi tract, changes to finger nails are all rapidly reprdoducing cells and that is why you have the side effects. they are not specific.
Radiation - beam to tumer, genetic abnormalties, shrink, gets smaller and perhaps dies.
Surgery - option at times but not all the time but you do often need additional treatment.
Stem cell transplant - liquid lymphoma , give you bone marrow from someone less , look this up.
look up insulin and potassium on how that works.
Infertililty is a problem with these treatments.
Most cancers but not all have rapidly reproducing cells.
Cancer isn’t always a tumor , you can have liquid cancers. abnormal growth of uncontrolled proliferation.
Benign tumors - low mitotic index
Malignant tumors - rapidly reproducing, not encapsulated, poorly differentiated, high mitotic index and spread distant whihc meens they metasticize. vary in shap and size which mean being polymorphic.
Classification and nomenclature
lipoma mentioned
Sarcoma , mescenhymal tissue, adenocarcinomas, ductal or glandular tissue and carcinoma tissues
Carcinoma in Situ - early stage cancer, it is an early stage cancer, not moved past the muscle layer and entered the bloodstream. It stayed in one specific area, wherever the lesion is.
Pap smears, squamous cell examples, they are not either malignant of benigh but will more than likely be benign if they are not addressed. Sometimes they are killed off by the body or invasive, muscle layer and connective tissue invaded. Look at the PP to refresh.
initiation - normal cell becomes a cancer cell.
tumor promotion - process by which cancer cells become more complicated due to epigenetics, genetics, and tumor environment- important
Progresssion - process to mestastisis all intertwined.
Genetic changes, multiple hits to the genetics of the cell to become invasisve. multiple genetic mechanisms.
Activation of the proto oncogene, whihc then turn into oncogene proton genes and oncogene.
Mutation of genes resulting in the loss or inactivity of gene products that would normally inhibit growth, which is when we would turn off out naturally suppressor gene.
Mutation of genes of over expression of products , prevention of apoptosis.
Genetic events are the primary basis .
4-7 hits of mutations to evetually develop into a cancer cell type. You can have changes to normal genes.
Point mutations where we start to have changes in the nucleotide base pairs the remember from biology with DNA. AG and CT
Chromosomal translocation
gene amplification - cause over expression of an oncogene that leads to cancer overtime
Normal colon cell - multiiple genetifc hits, inactivation of APC, ——Step 4 TP53 and activation of telemorase to sustain prliferative growth.
Tumor environment - development of cancer to wound healing ….look this up M1 and M2 macrophages
M1 inflammatiory ,kill bad things
M2 - Healing dispatches, promote new vessels, antiinflammatory state to allow healing
In cancer has a lot of M2 - TAMS to assist in blood, nutrietns and allow more cell to grow. This is where the analogy come in.
There are t lymphocytes but more M2 , creates an environment to thrive .
Hallmarks of Cancer
Sustained proliferative signaling - uncontrolled sustained proliferatation, secrete their own growth factors, HER2 growth fafctor breast cancer, alows more growth form the genetic
Proto Onco gen is normal non mutant cell that codes for cellular growth. Think of epithelial growth, skin flicks off and die all the time but can mutate to
Onco gene that direct protein synthesis and allow for that to continue to grow.
Tumor suppressing genes - antionco genes.
Evading suppressor genes - BRCA 1 and BRCA 2 - mutation in the tumor suppressor gene increases the odds of cancer. Examples of cancer stats on slide. P53 gene is the suicide gene, it tells certain cells in our body that they need to die. RBC is an example told by the P53 gene. It can be turned off which will enhance cancer.
Spoke about all the MD Anderson mumbo jumbo
Genomic instability - alteration in the genome, caretake genes start to go down. They are usually preparing damaged DNA but they go down.
STAR (Important) - Enabling Replication Immortality, telemeres are protective caps that that are held in place by telemorase. eventuallly they are supposed to fall off, it replicates and then a piece of telemorase falls off. But cancer activates and sustains telemorase which preserves the telemere on the chromososme and allows for continued replication. 90 % cancers have this.
Cellular Adaptation - Angiogenesis (growth of blood cells), these blood cells are porous pipes, it allows the cancer cellls to leak out and grow and more prone to bleed a lot. Brain tumor bleads, so a cough can cause bleeding. New blood vessel formed are
fragile
Reprogramming Metabolism - energy metabolism to allow prolfertive growth, expend energy without getting tired out, they can withstand oxygen and nutrient limiatations , maintain abnormal gene expression,
Resistance to destruction - P53 gene , promotion of inflammation , M2 (TAM) phenotype, block cytotoxic cells and natural kille rcells. secrete growth factors. The amoutn of TAMS is the lower of prognons.
Activating Invasion and Metastiasis - the spread of cancer from the primary site of origin to a distant site. It can leak out and start growing in a nearby area or spread through blood vessels or lymphatics. Occures inthe first cappilary bed but not always.
preferrential growth - Lungs to brain. lungs to heart, carotid to brain. High pressure and high velocity keeps from cancer forming in the lungs. Jimmy example, could be having seizures but it is related to lung cancer. Adenocarinoma from the lung by a biopsy of the brain. Many manifestation of cancer.
Manifestation of Organ Tropism - Colon to the hapatic portal vein in the liver and goes to the inferior vena cava to the lungs.
Prostate Cancer to the bone , direct metasitis to the liver…outlined in the slides
Inflammation - contributes to cancer by reactive oxygen species, increases the amount of free radicals, increases and promotes oxidative stress and starts to change the cellular proteins and promotes DNA damage, which promotes DNA Damag, which causes those genetic changes that contribute to cancer.
Mutiple inflammatory conditions that contribute to neoplasms. chronic inlamation of lungs , bronchitis, chron’s disease, ulcerative colitis , colon cancer. chronic pancreatis and pancreatic cancer.
Viruses and bacteria cause cancer , covid, sinusitis, causing inflammation
HPV and cancer - you probably have had HPV, body usually gets rid of it, but if not cancer can form. Chronic inflammation from the virus. Vaccination for HPV to prevent inflammation that will help not getting cancer. Now available for men. Hepatiis B and C, you can get liver cancer. Hepatocellular cancer due to no vaccination.
H. Pylori - bacteria that burrows into the lining of the stomach, changes the environment and causes chronic inflmation, chronic gastritis can also contribute to adenocarinoma inside the stomach.
Leading cause of death is heart disease, then cancer …..breast, then lung in ranking- women,
prostate then lung. Colon for both for 3rd.
Cancer Epigentics - study of gene expression or cellular phenotype, the way that cell genetics present itself caused by mechanisms other than changes and the underlying DNA sequence.
Examples : MRNA, Histones, Nutrition, lifestyle, and environment
Many years of promoting cancer, disease of aging usually but not always. Hormones, cigarettes, alcohol make things worse.
Read the skipped slides , it may be covered.
In Utero and Early Life Conditions - as a baby in the wound
Environment factors - radiation in bananas, lights, smoke detectors. UV radiation - importance of Sunscreen, UVA and UVB… Melanoma is the most aggressive . Alcohol conusmption - hepatitis, upper airway, pharyngeal gastric cancers, esophageal cancers, those type of things. Alcohol causes inflammation. how it metabolizes aldehyde, so at risk for hepatocellular carcinoma.
Sex - HPV, Hep C, HIV all contributers.
Physical activity resuces insulin and estrogen, promoters of cancer. It decreases inflammatory mediators, it increases gut motility to allow you to get rid of things.
Occupational Hazards -
Diet - gastric, colotic cancer..
Obesity - excess of any hormones, estrogen and insulin can create cancer.
Treatment of cancer
Clinical manifestation of cancer of Page 249 - paraneoplastic cancer syndrome , symptoms that are triggered by cancer but aren’t caused by the direct local effects of the tumor mass itself. Jimmy example, lung tumor, wheezing , but had overproduction of RBC or Hemoglobin, lung tumor causes this for more nutrition and glucose. Polycythemia is caused by cancer.
It wasnt the tumor that caused these signs like Jimmy but it could have a hormonal and possible immune function release.
Pg. 250 …..
Fatigue and pain - pressure , inflammation of tumor. Caution UP are manifestations , get them checked out. Fatigue is the most common. Sever fatigue , draw some labs , be proactive about it.
Cacexia - end stages of life, failure to thrive, starts to shut down, oxygen and nutrietnts move over to the tumor. overproliferating
WBC and RBC, Platelets changes - often times cancer patients have leukpenia and thrombocytopenia, low platelets because the body is fighting, sending macrophages over. or CHemo is killing this
oral ulcers, diarhea, etc. look these over.
Tumor Markers - substances produced by benign or malignant cells that are found on or in a tumor cell and maybe found in the blood , urine, and spinal fluid. It can be hormones, enzymes, genes, antigens, and antibodies as well.
Examples: Liver and germ cell tumors, secrete protein known as alpha feed, a protein or AFP and the blood. Prostate tumors secrete prostate specific antigen into the blood.
If the tumor marker there , it doesnt necessarily mean you have cancer but it is a screenign tool to identify high reisk of cancer diagnosed specific types of cancer.
Book states: K125 we see in pancrease, gallbladder, bile duct, and gastric cancers, calcitonin we see in thyroid cancers.
Draw these tumor markers to screen, prostate specific antigen , 50-55 men , draw PSA, 0 to 10 normal. But if you come in one year at 8 and then the next year you are at 15, you may have to take a further look. Monitor and go from there
So clninical treatment of cancer will start to hopefully drop markers of cancer. Like someone who has a PSA of 100, then 200, starts treatment, then 100 then 10. diagnosis, screening , and observing the clinical course of cancer.
How do we use this !!!! Test !
Stage 1 - Local not so good
Stage 2 - Regional - Left lung moved to right lung
Stage 3
Stage 4 - Bad
TNM Staging Systemv- Need to know this
Tumor
Lymphode
Metastasis
Know that T and M means how bad a cancer is. Organcs are different sizes in the body. A liver i smuch larger than the pancreas and thyroid.
A size is dependent on the organ itself, where it originated.
Tx - can’t be measured
T1 - not so bad, T 4 bad
N1- N3 - the more lymphnode chains involved.
Mx - can’t measure
M0 - has not metastisize
M1 - metastasize
Chemo - kills rapidly reproducing cell, goes after the crirical pathways of how the tumor started metastasizing.
REVIEW for EXAM: Induction, Adjuvant, Neoadjuvant, adn Salvage.
Salvage chemo - to keep cancer from growing , in ICU
Radiation - damaging the DNA
Brachytherapy - you will see this, radiation that is delivered nearby. Radioactive seeds that go into the urethra in the male and implant brachytherapy seeds inside of the prostate.
Pallitative surgery, remove some and see how it goes
surgery in advance - breast removal, uterus, etc. you can have micrometasticzie with surgery . They do a margin inspection for a pathologist to see if its all gone.
Immunotherapy - using our own immune system 1:23
Specialists take for example a cold virus that our body is familiar with and place it in a brain tumor and that is able to kill off cancer by recognizing .
Immune check point inhibitors - dont kill me, I’m normal ….turn off this to rapidly attacking the attack the cancer cells but the problem is attacking healthy cells.
Car T Cell - second line treatment of lypmphoma, train t- cells , they are pulled out of the blood , a pharmaceautical company trains those t-cells to go back and kill cancer. Kills all the lymphoma in your body, very expensive , and works very well. All individual .
Arcenic is used for cancer, poison,
metaports are used to deliver mediation…
7 rights of medication, imperative to do this all the time. allergies, always ask.
Cardiovascular System Lecture 1 - (Second Exam Lecture)
CD and Pulmonary are very important to know, the foundation of the course.
Cardio and Pulm relate a lot together.
The flow of blood through heart and lungs, deoxygenated through heart, lung, back to heart and out to the system
Know the arteries that go from the heart out to the systsm??????? They break off the Aorta
Clots - Left atrium appendage, shoots clot up to the brain, ie common through the carotid artery. research.
Right heart - pulmonary circulation
Left - to the rest of the body.
In the middle is the lungs, left and right heart
Right side of the blood, right ventricle, jugular venous distension. Where does the blood go if it cant be pumped through the right side of the heart. Especially laying flat, Edema, lower and upper exptremeties as well. Jugular venous pressure assessment? How much pressure is there ?
Hepatojugular reflex - back up on superior vena cava and inferior, this will back up blood into the liver. Push on liver, the blood pops out on neck vein, signaling right heart failure.
Left heart failure - poor perfusion distally, low ejection fraction. decreased perfusion can cause depression, less movement, less social interaction .
Electrical system of heart - each can generate their own heart rate. 60-100. Electricity to the pump to pump effectively —SA and AV Node….Pacemaker mentioned. Pump Issue? L. Vent. device drilled to pull blood from left ventricle to Aorta to act as pump system…Left ventricule devices lead to a heart transplant.
Heart wall, 3 layers. outside is the sac pericardial - in order to access you have to cut open the sack, move the tissues. …50 cc in the sac to help heart beat. mentioned all heart arteries, tricuspid and bicuspid valves …..Tenessee and Kentucky listening of heart sounds??? Doesn’t make sense to him.
Pressure of the heart , mgmt of cardiac issues. lower pressures in the atria and higher pressure in the ventricle. Systolic and diastolic pressure inside of the ventricles. So, higher pressure on on the left side of the heart, lower pressure on the right side and lower pressure .
RA 0-10 avg of 5.
RV 15-28 avg 24
Notice the same pressures being the same at the diastole
Situation - 70/30 patient BP, Central line in the neck, RA pressure measure (central venous pressure. was at 30 which is high 0-8 avg.
Assesss, recheck the BP to see, it was still low. Called the intern, who doesn’t know anything, 500 cc of saline, doesn’t make sense, called the second year intern, then called the 3rd year. Did not make sense, so he called the fellow for cardiovascular, called the attending physician, didn’t agree. Patient didn’t need anymore volume on the right side of the heart, he needed something to move the volume from right side to the left side. More squeeze to move it, dopamine did this but it is not used anymore. Dopamine increases beta contractility of the heart, makes it squeeze harder, its not used for volume. The volume may or may not help the BP, there are multiple strategies… Look this up.
You are the final stop, you do not have to fill a doctors order if you do not think this is correct. Document the hell of this, you will be covered.
Swanz Ganz Catheter into internal jugular entrance, sensors to measure pressures to all areas of heart… can’t measure effectively, indirect pressure of left atrium with the balloon.
Cardiac cycle, don’t have to know so much but really know systole and diastole, what occures during these cycles . coronary vessels, need to know what these feeds … Aorta , very important, many these feed offf of the Aorta.. When do the corornary arteries fill during systole or diastole? During DIastole - dont want to get blood at the same time it delivers. Where the cororanary vessels fill, open and closes with the aorta.. look this up
right coronary off the aorta, right side of the heart (right/left ventricle , SA Node 60-80 included. Brady cardia, 40-60 AV notde kicks on
Left main coronary artery,
Left anterior descending, left, front, and descending part of the heart, and septum.
Widow maker
Back the heart - posterior descending artery -
Collateral arteries - no example of this , our body trying ways to feed heart when having issues. Collateral artery formations? Know the important slide about all arteries. Slow accumulation of ischemia that will continure to maintain perfussion when needed.
Heat attack ? based on circulation. 12 lead EKG, electrical activity of the heart. Electrical activity in 12 pictures, there are only 10 wires. along different vectors, looking for ischemia, blood flow is limted in these areas, not enough oxygen so itll show on EKG
ST segmeent elevation - anterio septal MI example, old guy on the pp.
Inferior MI ST Segement
Different circulation in arteries lead to these 12 lead EKG ,
Conduction system of the heart slide - impulses of heart, come from SA Node- 60-100 that start the beat, travels prukinge fibers, a telephone wire that deliver the burst of electricity. If conduction goes off AV node 40-60, Prukingee 20-40 can kick on.
Heat has automaticity, can still beat on its own and has rhythmicity, normal sinus rhythym.
The Conduction of the heart slide - intrenodal bundles, note the pathway extending to the left atrium. SA node has branches that carry over to the left side of the heart, abnormal activity happens on this pathway. internodal pathways , abnormal beats. P - wave - atrial depolarization, ORA represents ventricular deporarization t - wave represent ventricular repolarization .
Know P, qrs, t and what is happening on your normal EKG
Q and S - positive vs negative items
Heart has nerves, sympathetic (gets it going) vs. parasympathetic nerves cannot repair.
Important stuff
Adrenergic Receptors - memorize Alpha 1, Alpha 2, Beta 1, and Beta 2
Number 1 - constriction
Number 2 - dilation
Alpha 1 - peripheral vasal constriction blood vessels , adrenergic agonist will cause vasoconstriction , phynylephrine , vasocontrict is when this is needed. So, Afrin nasal spray, congested with blood, mucus. it work as a nasal constriction.
Heart for Alpha 1… When BP is low, IV Push can shove the blood back to the heart and raise the BP by causing vasoconstriction. phenylephrine
Alpha 2 adrenergic receptors are located on the presynaptic neorons —-nerves, decrease tone, cause vasodilatioin. impact on heart.. Clonidine - adrenergic agonist, vasodilation to lower blood pressure. Can work on anxiety, detox from alcohol. Impacts on nerves, we do not give to the elderly, it affects their CNS too much, impacting the nerves.
Betal 1 adgrenergic receptors - increase heart rate, increase contraction - epinephrine helps increase heart rate and contraction.
Beta 2 - located in the peripheral blood vessels and smooth muscles, bronchiol smooth muscles, located in small blood vessels, as well as in your lung. Albetorol causes vasodilation of the lungs to assist you breath as an example.
Norepinephrine - is an Alpha 1 drug
Epinephrine - Alpha 1 but a very unique drug, many different drugs work on differett receptors , recongnize that they can act on Beta 1 receptors causing tackycardia. acts on a1, b1, and b2
0.3mg of epi pen, pediactrics, 0.15 mg dose…for beta 2 effect to keep breathing. 1 mg is the dose in cardiac arrest.
Antagonist - beta blocker, alpha 1 blocker, opposite effect.
Myocardial cell, like skeletal cells, remember that the sarcomere is the difference between two z-lines. Intercalated disks which allow for the rapid transmission of electrical impulses down those different muscle fibers. RECALL THIS INFORMATION, not tested
Myosin filaments and actin filaments
Know protein troponin!!! acts along with calcium to help bind the actin and myosin together to allow for appropriate muscle contractions. the elevation in blood stream means there is some heart stress , not necessarily heart attack
Factors of cardiac performance
NEED TO KNOW FOR EXAM!!
Preload - is fill , volume, pressure, 500 cc example, 30 ml of mercury in the right atrium. inside It is the fill, volume or pressure inside the ventricle. At the end of diastole, its the left ventricular end. Diastolic volume is one definition, one interpretation, one concept of what preload is. right before systole , right before you squeeze. VOLUME AND PRESSURE.
Dehydrated = low preload
Vs
Jugular venous distension - lower extremity edema, and a positve hepatic jugular reflex, your preload is probably high, especially on the right side.
Afterload- How hard does my heart have to beat against something to get that blood out? Its pressure, resistance, volume. How hard to do i have to push to get out of here.
Phynlyephrine, raises afterload, vosoconstriction, heart beats harder
septic shock - when pressure drops, bp goes down, nor epiphrine or epinephrine, we wouldn’t use phynylephrine.
If sclerosis or scarred aortic valve, every time my ventricle contracts, its beating against a closed valve.
Myocardial contractilty - how hard my heart is squeezing many different things can impact how hard my heart is squeezing.
-giant clot in pulmonary artery - blood can’t get to the other side
-myocardial contractility - if my heart is not getting perfusion from a big heat attack and my left interior descending artery is occluded. can’t contract. measured with stroke volume, preload, as well as ejection fraction. 55-65 % is the normal ejection fraction. That is how much blood you should be injecting.
If I don’t have volume, my blood pressure is low. Nausea, vomitting, diarrhea.
If I dont have afterload, my blood pressure is low
If I don’t have contractility, my blood pressure is low, so I can’t get blood to the rest of the body.
Cardiact out put Slide 1:25
Sroke volume X heart rate = cardiac output ——Important !!! look at slide
Heartrate - 100-120 for CPR , need this to squeeze, fill, increase preload and increase the output of the subsequent push.
Preload - in theory Frank Starling, the amount of fill that you provide to the heart, the stronger the subsequent contraction should be . The more volume I push into that chamber, the harder your heart should beat to get that out.
In most cases that is true but like a rubber band, this doesn’t always work, it fails. The more you fill the heart, it should work
You need to know preload, afterload, adn contractility for the exam!! need to apply these.
How does the heat rate generate ?
There are cardio excitatory and cardio inhibitory centers in our heart that allow us to maintain a normal heart rate.
Baro and chemo resceptors assist in this.
Structure of Blood Vessels slide - need to know this for exam.
Tunica Intima is essentially the endothelium , the small membrane that surround the endothelium is the basement membrane.
Endothelial dysfuntion and thickened basement membrane
Endothelium plays many differnt roles in our baody.
Arterial system has muscles that move the blood in the body
veins have valves.
Table 25.1 table. inflammation and immunity can crooss reference - hemostatic balance.
clotting blood due to damaged endothelium, permeation issues
Microcirculation - looking at capillary flow, alows for rapid exchange of items that play an important role. glucose trackers are here, example a finger stick. pulse oximetry .
Neuro control - Alpha 2 agonist ,
Rostrum ventral lateral medulla that controls your total peripheral vascular resistance of body as well.
Peripheral circulation - baroreceptors (in aortic arch and carotid arteries) - hepse sense changes in blood pressure based on those changes in pressure.
example: low bp, low stretch in aortic arch, low stretch and the carotid arteries, the bell receptors can actually release things to raise your bp like catecholamines, epinephrine, and nor epinephrine.
lay the person flat, dont put the head up. Hypotensive
Chemo receptors in medulla - these help sense changes in an oxygenation, when you become hypoxic or acidosis, these chemo receptors can release things that can raise you blood pressure. -emphasized these.
High ADH - High Water, Low ADH - low water
1: 42 Renin angiostensisn - aldosterone system -NEED TO KNOW THIS
Kidney—low bp, - renin- convert angio I—angio II in lungs — vasoconstrict (increases afterload and aldosterone), stimulates the release of aldosterone and antidiuretic hormone AKA vasopressin - both help allow you to retain more water, Aldosterone particularly also helps you retain more sodium. Both of these are interventions to help increase or decrease preoload. Increase preload, increase water and sodium. Feeds the kidneys more blood.
Cascade imporatnt due to patient’s medication.. IE ACE inhibitors, rennin blockers, ARB Blockers
ANP, BNP, and CNP, these are natural peptides. Help regulat sodium excretion, diuresis and also vasodilaton . water follow sodium. Regulate preload to alter your blood pressure. B
BNP - works similiar to ANP, except its not from your brain, its from your heart . When we have a BNP release, promotes water and sodium release to lower preload inside heart . BNP Lab , elevated peptide in blood stream , may have fluid overload. Heart failure
C-Type natriur peptide - is highly concentrated peptide in our endothelium and helps to mediate vasodilation and causes hypertensive episodes.
Mean arterial pressure (MAP) - in one cardiac cycle, the difference between arterial pressure and the venous pressure that drives that blood into the capillaries. This is the marker of what drives this pressure, drives that blood into the smaller spaces, drives blood into the smaller spaces, microciculation.
MAP is the number to titate vasopressors , two times the diastolic + systolic / 3
greater than 65 of 70-110 mmHG is normal
Your body can regulate itself if it can maintain pressure. 60-140 MAP , the amoutn of blood in heart will stay the same (ie perfusion) , you will recieve the same amount of blood .
when it drops or increases more, it can have ischemia or rupture. The body has to have a way to have a consistent flow.
Greater than 65 , body can sustain at the same rate. AUTOREGULATION CONCEPT.
Lymphatic - not testable!!!
Lymphcytes are important, lymphnodes
Lymphoma cancer, systemic manifestations - important.
Theres big vessels that your body uses for lymph movement.
Thorasic Duct —-Important, you can nick the duct and it will leak lymph fluid, can collapse the lung. the lymph system is important for these concerns.
Telemere shortening, things start to die off. alteration in pacemaker function and changes to vascular function, SGLT2, drugs that make you pee sugar water for disease conditions.
Not on test - assessment of cardiovascular function, but sensortum is the gold standard for assessment, how they look ? Can they speak, pale? Pink? Look at mucus membrane, pale , not good? feel pulse, thready pulse, is it strong?
X-Ray of Chest -Normal or Abnormal , congestion of fluid build up or something not functioning
Not testable - femoral and radial and go to the Aorta, coronary and see if there any occlussions or shoot dye into the ventricle to see the ejection rate. Baloon angioplasty
Alterations outside, to inside
Diseases of the veins
Vericous veins - valves , vein is pooling blood, trauma , venous distention, sitting or standing too much, causes venous blood to pull and wear the valves down.
develop swelling , increase of hydrystatic pressure. chronic venous inusfficiecies, causes ulcers.
risk factors for all of these vericous veins. thick vein of blood, damage to valves, high amounts of standings.
Change of color, hyperpigmintation, edema,
Its about prevention - stockings, help, but they will help, eventually you’ll get them. they are mor cosmetic, usually no medical reason to treat.
dermititis is the biggest reason to medically treat them. Cash, insurance wont pay for these, but there are stripping can be done for profound issueis. Its very invasive.
cosmetic is less invasive, glues can be used.
venous occlusion can cause spider veins, not as problematic as vericous veins.
Thrombus - blood clot , due to immobility, obesity, medical conditions, blood flow
bllood flow stasis, heart failure, hypercoagulate in cancer!!! big star - deep venous trombosis , oral contraceptives with smoking
3 factors and endothelial injury - know these!!! role in endothelial with appropriate coagulation . cancer, surgery, oral contraceptives and hormones for deep venous thrombosis.
DVT - Prevention is priority, anti coagulants ie heparin, warfarin, nomadic compression devices, squeeze calves.
Manifestations DVT - edema, blodd can’t make its way back to the heart. Pain, no colors but will probably hurt. If blue, that is an arterial problem, it should be ededemitus, need an ultrasound to see. 2:19
Ultrasound would be used , getting images
D-dimer test to see a clot is used, completely negative, but do do more tests if positive
Thromboemblolus - circulating throughout the body.
Thrombin inhibitors are used, warfarin, INR and PTT labs are used.
They squirt thrombyltic injection to break up a clot vs. a systemic medication to break up the clot
Ballon mechanism to pull out the clot, and they pull out the clot with the balloon
DVT NEED TO KNOW!!!! keep in mind that cancer, ortho, trauma, smoking and hormones play a role in DVT
SVC Syndrom - a progressive occlusion of the superior vena cava that leads to venous distension and the upper extremeties and the head. big head and big arms happen. look purple , looks weird due to venous pooling - its called plethoric appearance, progressive occulsion, poor movement of blood. Bronchogenic cancer pussing on superior vena cava syndrom is caused by. Also, a big ole clot in the actual in the lumen of the vessel, in this case, the superior vena cava. Nipple line and up.
Squirting thrombolytics at it is one way and common for SVC.
Does heparin break up blood clots? NO, it doesn’t!
Thrombolitics and your body breaks up blood clots due to also having thrombolitics, to bust up clots.
What is the purpose of starting heparin or warfarin and all thes other things? to prevent the clot from getting bigger. They prevent the dog pile and allow the body to catch up.
embolus - something that broke off from the clot and is circulating in the bloodstream. Examples are a thrombus, an air bubble. 55 zero to kill someone.
Air bumble can form by a central line being taken off and you take a breath in, IV, feeding tube.
Aggregate Fat - fat embolism
Bacteria - flick off in all types of places
Cancer -
Anything can cause an embolism …..26.3 Figuure
Pulmonary embolism - blood clot that travels to the lungs , most come from a DVT.. Deep Venous Trombosus
Symptoms are acute onset of short breath, chest pain, syncope - passing out. Hypoxia, can’t move right heart to lungs cus a clot is there. Tachycardia - right to left blood of heart is compromised. Hypotension - compensated by tachycardia. Right heart failure is the result of Pulm embolism.
Tachypnea, why? Hypoxia will happen, right to left of heart, and oxygen can’t get through …stuck on right side… Person starts breathing faster. Fever but not infection, inflammation caused by the body due.
Tachypnea - Respiratory Alkolosis, all CO2 blew out, PH goes.
Another example: Patient with respiratory alkolisis with an associated hypoxia? supplemental oxygen treatment still counts them as hypoxic.
Related to this: a patient has hypoxiat because they have pulmonary embolism and respiratory alkalosis. would it cause them to enter anaerobic respiration? So causes them to put them in acidosis ? can happen but they are about to die. you should enter that anerobic phase.
CT Scan and a contrast to find a clot, you look to see where the fluid stops or stalls to pinpoint the clot.
Right Heart failure in PE, EKG will identify the failure. You can perhaps see that they are having a PE.
Chest X ray - no you can’t identify a clot.
Right sides PE - R Pulm artery, you’ll leak into your pleural space and you can get a pleural effusion on the same side of your PE due to the blood not being able to get past.
Treatment, not tested…..
They send them home with these meds but we break them up. Thrombolitics are used in emergency situations - Thrombolysis to give you a systemic IV push . They make you bleed to death. It can kill you. They use a catheter directed thrombolysis rather than systemic.
Thrombectomies can be done to remove them but only at big medical centers.
Scarlet Ohara death, died of PE but it was linked to rectal cancer due to hyper coagulate abilities that it has. Some people don’t even know cancer and come in with a PE. Immediate cardiac surgery can pull the clot out but not common.
END of Lecture
Lecture Part 2 Cardio Vascular System
Slide 64
Diseases of the Arteries
Hypertension - primary hypertension, essential hypertension,
idiopathic hypertension, we havn’t a clue, all of these mean the same.
Stages of Hypertension Slide shown, elevated above 120 is hypertension. Review these levels.
Primary Hypertension
Genetic and environment are a factor. You can be skinny but you can still get it, diet, alcohol, but obesity and inflammation all cause it. But we don’t know, but genes is the biggest factor.
Other factors: endothelial dysfuntion, different hormones, obesity, insulin resistance, dietary sodium intake.
Salt all the time may be a contributing in the long term.
Positive family history, age, men are more likely younger than 55, women older than 55, Black , acohol (inflammation to hypertension), smoking/vaping, obesity, any nicotine intake. Vascular irritation . Surgeons won’t operate on you with nicotine use or make you stop. Insulin resistance.
Secondary Hypertension - something is causing
renal artery stenosis - most common, blood flow not getting to kidney’s , RAAS System is activated, then they get hypertension.
What caues it? Often times you are born with it , birth defect, developing a vascular problem.
Adrenal Corticol Tumors, release catecholomines, causing epi and nor epi increasing on BP.
Allergy medication, can make you hypertensive.
Complicated hypertension- Chronic hypertension is a chronic hypotensive damage to the blood vessels and you start to have smooth muscle changes, hypertrophy and hyperplasia with fibrosis of the Tunica intima aka endotherlium called vascular remodeling. VERY IMPORTANT HERE TO UNDERSTAND.
changes Size, shape, structure, and function
Hypertensive crisis- very elevated BP 180 past 200, and over 180, diabetes, renal disease, non compliance with meds, on a bunch of meds . Can lead to encephalopathy and life threating organ damage
ex
250/150 example comes into th ER , you do not give meds that drop to 120/80, they can stroke out and die, slowly IV infuse in ICU, oral meds, slow transition.
Manifestations - headache, silent killer, important to encourage screenings.
Embolic or hemoragic stroke - pressure on the brain blood vessel and you can get this stroke CVA , same thing.
Embolic type stroke - higher propensity of clotting with the pressure. Hypercoagulation causing blood clots to form in your brain. Embolic CVA.
Small vessels - in the back of eye , retina, higher propensity to burst. You can see inside of eye. Potential comp
Renal dysfunction or kidney failure. They can burst, vascular damage
Heart attack, work hard to pump blood, MI from high blood pressure.
Heart failure - muscle gets bigger and it can fail. It gets so enlarged, can’t fill and pump blood forward.
26.2 Table ——-Important, please look at this - Test
JNC 8 Recommendation - Clinical practice guidline, treats hypertension. DIastolic important - time when your heart is at rest, don’t want higher pressure in this case. Systolic can be high due to only anxiety, 1 number elevated only. Needs to be taken by a non provider, white coat hypertension. Multiple BP need to be done, manually is the best way.
Over 60, 150/90
Under 60 140/90
Let them ride with a bit of pressure
Modify your lifestyle , diet, salt, exercise, low fat…. sometimes that works, give an opportunity, lose weight, ect. no one does it usually
Medications - Thyazide diuretic is usually the first intervention. remove preload to lower the pressure method. Hydrochlorothiazide usually first or Northallerton. Black or Non Black. Black responds better to Calcium Channel Blocker. Non Black is usually an Ace Inhibitor, an ARB, or a Calcium Channel Blocker . Beta blockers not so much.
Hypotension - chronically like this. Orthosttic Hypotension AKA Postural Hypotension. Systolic 20 or 10 diastolic. within 3 minutes of standing, to compensate there may be some tachycardia. Older people need to sit first, then stand. Profound dehydration is another reason, not enough preload. Dizziness and syncpothy fainting is a possibility. Do not need an order to get this, just do the vitals for this.
3 part assessment for Orthostatic Hypotension
Vascular issues with the elderly, leading to pooling and basl dilation of their vasculature as well.
Acute Vs. Chronic - diarreaha, blood pressure, fluid loss, throwing up, all can lead to this.
Eat salty foods, raise the head of the bed, thigh high stockings - help contrict the blood to come back up (helps the drop in BP).
IV fluids give some volume , vasoconstriction meds
Menadrine - a medication used a lot in hospitals to assist around PT time.
Arterial Condition:
Bergers disease called Rambo, clots, AuTOIMMUNE Disease of the peripheral arteries, the burger is inflammed. Thrombi in smaller vessels in hands an feet, have thrombi overtime, get ulcerations, amputations, can lead to gangrene. Tobacoo, nicotine, vascular irratant. Thrombotic condition - anticoagulants may be needed.
Raynauds Phenomenon - Vasal spastic disorder of the small areteries and arterials on the hands and feet. vaso spasm, something is causing the spasm that loses blood flow.
example : tourniquet , we have learned that you can lose flow to limbs for hours. just because its blue , doesn’t mean its dying.
We don’t really know why this happens but they think it is due to seconday and systemic diseases such as : hypothyroidism, scleroderma (hardening connective tissue disorder), pulmonary hypertension. Manifestations are pallor, cyanosis, sensation of cold in your fingers and toes. Vasospastic disorder is what this is called.
Tip : Long time about a topic, you probably going to need to know it.
Arteriosclerosis - calcification Calcium and fat build up, why calcium? You start to lose calcium as you age and it sits in your arteries.
Chest X-Ray - shows a ring, an Aorta or a perfect white outline of Aorta, not normal, thick arteries, very hard, people will have hypertension.
Over time you can narrow the lumen there of you vessels and they can get hypoperfusion of the distal tissues so low perfusion to the tissues distal to where that occlusion is at. Can get these everywhere, eyes, fat, feet, hands, brain
Fat build up - lipid layden macrophages - accumulates right behind the vessel wall and the leading cause of coronary artery disease as well as cerebrovascular disease. Diabetes, hypertension, autoimmunte, LDL, VLDL , there are building up. HDL needs to be high because it has enough transport ability to take LDL to the liver for processessing. Statins to lower the LDL overtime. To raise HDL, exercise!!! Medications also raise HDL , but there are side effects. Need to get your heart rate up, low to moderate intensity is recommended for HDL.
How does the fat in your arteries actually happen?
There is fat inside of your blood lumen of your vessel. Its going to bounce around inside your blood vessel a little bit.
And when that happens you get an endothelial injury from the fat simply bouncing around inside of your bloodstream bouncing on the endothelial wall. Inflammation happens in the endothelium, cytokine release, cellular proliferatioin, and macrophage start to respond because of the inflamation inside the endothelium and eventually the macrophages and the lymphocytes will engulf that fat cell and goes underneath the endothelial layer, starts to form a pool of fat underneath the endothelium. Contributes to a narrow lumen, fibrous and complicated plaque can form.
Result is inadequate perfusion, ischemia, and necrosis
Other way to explain:
LDL enters endothelium—> oxidation of LDL monocytes and well as T Lymphocytes—>they start to engulf fat—→ a foam cell is formed —> a lipid pool is developed and overtime becomes fibrotic and can narrow the lumen.
VERY IMPORTANT !!!!!!!
What happens? Anureusism - plaque erosion in the vessel that make the vessel like an overinflated balloon. You can have an anureium anywere you have an artery, heart, brain, aorta.
Coronary artery disease - non enough profusion overtime.
50:34 Left off.
Atherosclerosis - Abnormal Lipid Panel and C- Reactive Protein - market of inflammation in body. Fat bouncing around causing inflammation in the blood vessel. contributes to MI and other conditions. BIG TEST QUESTION.
Satable angina - chest pain that goes away with rest
Intermittent Clautication -samething but in the arteries in the legs, it will hurt but with rest will go away.
Prince metals angina - upredictable chest pain as a result of chest spasms. Happens a lot at night, a charlie horse , most of the time is dehydration. but this is from the fat irritating the muscle inside that vessel. As a result to VASOSPASM. Vascular changes in skin in hyperperfusion.
Treatment - control cholesterol, decrease or stablize the plaque formation and restor blood flow overtime. Statins, exercise, anticoagulants (aspirin, antiplatelet).
Annuresym - fat build up causes wall to be w, eak. Atria can have an annureism . The fat plaque weakens the wall and hemorraging happens. Abdominal Aorta is a big spot for this and is assymptomatic, hypertension, smoking, and athelerosclorosis is the cause.
Triple A - common in elderly , significant triple A . Look what this is?
Manifestation - brain, heart, aorta, descending aorta,brocnhi, will cause dysphasia (swallow difficulties). Drop the blodd pressure, Beta blocker will be used in the ER to get that down. No smoking and high risk complicated surgery.
Atherosclerosis→ Anuerysm → Aortic Dissection
Aortic Dissection - tunica intima rips off the vessel and leaks in the lumen of the artery, emergency , eschemia, dizziness, hepertesion, . only way to fix is surgery, emergency surgery.
Complicated Vental surgery to fix this, must lay the persons head in ice to shut down the metaboilic demands of the brain and quickly go to work . These patient have a bit of a problem with keeping them call after this and getting off anesthesia, reprofusion back to the brain.
Peripheral artery disease - the same as coronary artery disease but everywhere else in your periphery. Diabets has a thicked basement membrane, prone to PAD and
Nitrates really popular , antiplatelet - aspirin , if you have Coronary Artery disease you probably have peripheral artery disease
Men are high risk, women post menopasual , and family history - things you can’t fix
dyslipedimai - high cholesterol, hypertension, cholesterol, smoking, fatty diet - risk factors
Markers - C Reactive Protein, elevated troponin I , Tropinin C —-PLEASE KNOW that troponin is the protein that helps by allowing calcium to bind and allow for the active myosin head to allow for contraction of the Sarcomere. The higher this is =more stress, possible heart attack.
Transient Myocardial Ischemia - heart is not getting enough blood transiently, when you have atherosclerosis and you manifest with stable angina, prince metals angian (spasm of the coronary vessels leading to not leading to adequate perfussion), silent ischemia or stressed induced ischemia .
Why do you get this? Fat, coronary spasms such as Prince Metals, and increase myocardial demand. Oxygen deficity of less than 20 minutes, more is a heart attack.
Hormones - post menopausal , lower estrogen , higher cardiac propensity, limit the risk factors as much as possible. Testeosterone can worsen the risk when elevated. Not regulated and it could mess with systemic manifestations of other diseases. Exogenous hormones should be regulated heavily, insurane does not cover.
Acute Coronary Syndrome - heart attack? which one?
memorize - 3 major things.
These are alway a review silide
Unstable Angina - minimal occluation - stil get blood flow, not enough , sustained, reversible due to blood still getting there.
fat-blood clot - red is the major
T - Wave Invesion, not enough oxygen, electrical activity has to go around , so the t wave is upside down, no necrosis yet but will get there but need treatment
Non ST Elevation Myocardial Infarction -
a rupture in the flat plaque, there is a severe occlusion of this vessel and you start to have necrosis, sub endocardial infaction, lack of perfusion.
ST Elevated Myocardial Infactions -
ST Segment elevation , complete and total occlusion of the corronary vessel from a piece of clot sitting on top of that fat plaque. The main patho physiologic issue in these conditions is a blood clot.
Treatment is addressing the blood clot
Subendocardial vs tranmuler is worse
NSTEMI- ST segment depression , often times none is seen
STEMI - ST Goes up , big changes
Stable to an unstable heart - see slide 98 !!!!!
Myocardial Infaction - clot in the coronary artery sitting on top of the myocardium. It is feeding the blood flow to the heart. Extended obstruction - mild site necrosis - NSTEMI, vs. STEMI - transmural full thickness associated with lack of perfussion. myocardial remodeling.
Review Myocardial thickness examples for heart attack slide - commit to memory
Clot forms - atherescloris underneath the endothelium and goes into the lumen, ruptures over time, the body puts a clot on it to stop the leakage, bleading etc. - Main pathophysiological issue. Treatments for blood clots on top of that FAT CAP.
I just want to reinterate the underlying pathophysiologic issue in Myocardial infaction is the rupture of that fat plaque in your body. then blood clot forming, needs to be addressed ASAP.
Slide 97 - Review on Manifstations - crusing substernal chest pain !! Elephant sitting on chest, huge amount of pressure.
Disparities of populations - women do not manifest in chest pain, pain down their arms, may be sensitized in the chest/breasts, atypical chest pain - pain in jaw or arm, abdomen. Example aunt, couging a lot, complaining about chest pain, throwing up, EKG , went to the hospital. Why was she throwing up? No blood, not beating well, all the blood went to the stomach to help process food, away from myocardium and that is what happened. Look at the EKG Slides. ST SEGMENT ELEVATION - a STEMI - Tombstone, fireamans hat, The tissue is not getting any flow at all, tissue is dying and becoming necrotic.
A large Q wave usually seen later - a necrotic dead tissue sign , an old MI had occured.
Why in a STEMI and NSTEMI different?
NSTEMI - no changes
Manifestations of MI include : Pallor, diephereses, nausea, fatigue, vommitting , ekg changes.
How do you know they are having a MI? these signs are the reason , don’t just use the EKG as a diagnostic factor. Key diagnostic factor for a STEMI is an elevated troponin level associated with the manifestations.
Stress test - ekg and makes you run, trying to get you to have chest pains to see if you have atheleclolerosis. Eschemia is going to happen and the T wave will flip. It show the ischemia that is going on.
Complications - left ventricular dysfunction, electrical instability, need the history of this patient, PQRST assessment.
Acute Myocardial Infaction - severe will cause necrosis but you can recover with myocardial stunting and you can eventually recover function overtime - Reperfusion injury
Chronic issue - sudden cardia death.
How do you treat MI? Evaluation, 12 lead EKG, electrical picture of you heart.
EKG, Chest E - Ray, Troponin leves , and manifistation of MI - NSTEMI
MONA - Morphin, oxygen, nitroglycerin, aspirn
Morphine - not used for pain, vasodilator , blood pressure goes down, dilate the vessel , the blood flow for more perfussion to heart . ST starts to drop.
Oxygen - titrate for 92 % and up
Nitroglycicerin - vasodilator , like morphine, 0.4mg sublingual underneat the tongue. Sublingual you have to swallow your spit down fo the pill to actually absorb.
Aspirin - platelet aggregation - prevents worsening 324 ot 325 mg , the most common baby aspirn is 81 mg (4 baby aspirin)
PCI vs. Thrombolytic and Heparin
Heparin - does this break up blood clots ? not it prevents them from getting bigger. So the doese of Heparin we give somebody is 5000 units of IV heparin adn start them on an IV infusion of Heparin to prevetn the clot from getting larger.
P2y12 inhibitos 75mg - 4 tablets
Glycoprotein - 3 inhibitors
All in the ER to get this handled.
Important for the nurse to get this done fast and rush them to the cath lab.
Metropolol - Beta blocker, beta adrengeric antagonist. but would this not let the heart beat as hard? The reason you use this . When do the coronary arteries fill ? during diastole . when you have a very anxious patient to allow more time for the heart to fill. There are only certain times to use this.
The connection is slowing down the heart rate to allow for more coronary perfusion when dealing with sever anxiety of a myocardial infarction.
PCI percautaneous coronary artery - stick a wire , inflate a balloon, and put a stent to allow flow through the bockage, adequat perfusion.
Underlying pathophysiolic issue is a blood clot, so you can also use fiber analytic medication to break up the blood clot.
You have to get this done within 90 minutes to get paid , this fiber analytics. The stents can be there the rest of your life but they can stop working in days, depends. Look at the blurry slide PCI and Fibronolytic agents.
TEST - ATHEREOSCLEROSIS, Myocardial Infarction, Acute Coronary Syndromes, Unsable Angina, STEMI, NON STEMI
Pericaditis - inflamation of the pericardium. Why inflamed all of a sudden? Infection, surgery, metabolic issues, immunologic issues like lupus, rheumatoid arthritis, vascular disorders.
Any surgery, lung, heart , etc, has to cut the pericardium open, its going to make it made and inflammed. This can cause complications. Wires are ofen seen in scans from prior sugeries. Supine position, they take a deep breath, lungs expand and casue the inflamation of pericardium rubbing on the sternum. You’ll here a friction sound with ausculation, sometime you can hear them
Treatment: Incense, NSAIDs, Steroids, and rest, and treat the underlying casue.
Pericardial Effusion is fluid accumilation, anything over 50 to 100 cc is classified as a pericardial effusion. Often its related to fluid overload. Body is trying to disperse fluid anywher it can. Cancers are a big cause.
Pericardial Effusion is GRADUAL .
Pericardial Tamponade is a SUDDEN accumulation of fluid or blood that alters the flow, trauma, neoplasms, the fluid around the heart, causing inflow and outflow in all cardiac chambers.
Right and left heart failure is pressent, manifestations of both. Jugular venous distenion, edema, hepatic magali, low shock volume, low cardiac outout. Blood can’t come in and the blood can’t come out. Just sitting inside the pericardial sac.
IMPORTANT CONCEPT: Pulses Paradoxes - abnormally large decrease in your blood pressure whenever you take a breath , the lungs hit the sac, pushing against it and even a bigger hit on outflow. a drop ofover 10 mm of mercury in systolic blood pressure when your patient is taking a breath.
Additionally, can’t fill during diastole when you have a breath , impaired left ventricular diastolic filling is what is causing the drop of more than 10 mm of mercury in your systolic blood pressure.
Look for a change in pressure in inspiration when there is tachycardia. can progress to cardiac arrest.
3 Signs - Bex Triad
Low blood pressue, impaired filling, right impaired outflow, muffled heart sound.
distension of the jugular veins
Why? Chest trauma, ruptured aorta after a heart attack, pappillary tear, caudate tendonai,
Only treatment is removal of fluid, stick a needle in the xiphoid process or cath lab or operating room.
Myocarditis - Covid 19 and vaccines, inflammation of the heart : infections, autoimmune disorders, toxins, medication. a lot of vaccines can cause this. arrithmias are the biggest complaints, chest pain, and heart faiilure. MRI, tropoinin, biopsy
Treatment : watch with time, Immune checkpoint therapy is a concern with myocarditis.
Cariomyopothies - eschemia, toxins, inherited traits. Myocardium starts to have issues.
NEED TO KNOW - Dilated cardiomyopathy , chronic
Dysrythmias are one of the most common presentations your see with this.
WHAT YOU NEED TO KNOW:
Ventricular Dilation - sometimes related to chronic ischemic heart disease
Chronic coronary artery disease- can cuas your ventricles to become more dilated. Often manifest with both diastolic and impaired systolic function, you eventually develop left sided heart failure as well.
Pregnancy - causes temporary dilated cardiomyopathy
Infections and toxins as well.
Ischemic heart disease - heart doesnt get enough flow and the contractility is decreased and so the preload is higher and that ventricle causes a stretching over time and allows it to just get bigger over time
Hypertrophic Cardiomyopathy - genetic condition associated with impaired systolic function. Most common in hypertension. It gets hypertrophic
Athletes - specific hypertrophic cardiomyopathy where the thickness and the intra ventricular septum and that contrbutes to arrythmias and sudden cardiac death with physical activity.
Heart sounds for athletes , any sort of abnormality, interventricular septum is thick
Echocardiogram is the best test, to rule out this.
Diastolic dysfuntion - impaired fillling and eventually right heart failure. idiopathic usually but may be related to sclerodema, sarcoidosis and amyloidosis
Protein deposits and tissues can cause lack of fill and chronic diastolic dysfuntion.
Slide on septum associated with athletes - sudden cardiac arrest
Valvular dysfuntion - Tenesse and kentucky ??? No sense
Supplemental course material - videos, heart attack, physiology , preload and after load, review supplemental material.
Stenosis - constricted and narrow, aortic stenosis murmor, loud , a flow of blood,
Regurgetation - Valve can’t close , blood is regurgitation
Murmur - Mitral stenosis and aortic regurgitation are examples of diastolic murmurs when the heart is at rest or when the valve should be typically closed. Systolic murmurs
Aortic stenosis - should be open, closed, open closed , when I have stenosis , perhaps calcification is sitting on my aorta. Hooo hooo hooo, during systoly and closed during diastole.
Mitro stenosis, this is the one that trips people up, Mitral valve sitting on the left atrium, left ventricles between that side. When is it open ? Diastole to allow filling , it will close during systoli ——NCLEX QUESTION
Aortic Stenosis in a valve- what happens when the blood can’t get out? Left ventricle !!! then left atrium, lungs, pulmonary edema and dyspnea on exertion. Why high afterload state , preload backs up. blood in lungs
Mitral Regurgetation - same things are the same , as aortic stenosis…
Review slide on most common stenosis .
Rheumatic heart fever - is a systemic manifestations of infection not local (swelling and redness is local), you can get systemic manifestations from other items wrong in your body.
Infammatory disease caused by a delayed immune response to a pharyngeal infection of group A. Streptococcus. Kids are more prone to this, it can become systemic, 5-9 years of age. Humoral and Cell mediated response that fight off the infection but this can stick on your valve and cause you to have valvular dysfunction.
M- Proteins - can cause systemic issues .
Fever, nodules on skin, corea, joint spaces - antigen antibody complexes and the immune response associated with the systemic infection that the body’s trying to fight off from strep. Treatement for this is a 10 day regimen of antibiotics, nsaid, the need for antimicrobials for up to give years to help fight off that strepoccal infection that’s been causing the rheumatic disease.
Valvular disorder is the biggiest issue due to this later in life.
Infective Endocarditis - Bacteria sticks on heart valves, collections causing murmors, can
also get from fungi, viruses , rickets, parasites. anywhere you have chronic bacteria entering your bloodstream, it can manifest to endocarditis. Iv drug users can cause this.
A fever that does not go away and a cardiac murmor are the two key items here.
Fever that does not go away : Endocarditis, HIV, and Lymphoma - systemic diseases and manifestations.
Heart Failure - inadequate perfussion to the tissues and the risk factors are ischemic heart disease and hypertension.
Systolic and diastolic heart failure - REMEMBER !!!!
Right sides and Left Sided Failure - REMEMBER !!
Systollic Heart Failure - inability to contract which results in a reduced ejection fraction. Inability to contract and decreasing cardiac output . Why ? Ischemic heart disease, hypertension can cause this.
Diastolic Heart Failure - inability to relax and fill appropriatly, but peserved ejection fraction but I cannot simply relax enough to fill.
Dr. Arrellano - Disagrees with this definition due to needing to have to generate adequate enough stroke volume for the ejection fraction to be preserved. Normally 55 to 65 % for systolic but remember in this context that diastolic is preserved.
Acute or chronic heat failure - MI or over time for chronic
Systolic less than 40%, contractility issues , can’t perfuse tissues with contractility , build up of preload.
High afterload state can cause systolic heart failure , beating against a closed system.
Reduce afterload (antihypertensives) and reduce preload (diuretics) - dialated to assist.
In shock, is the apposite, it is going against no resistance and the ejection fraction is 70 % or more.
Heart failure remodeling -changes of size, shape, structure, and physiology, how do you reverse that?
Beat blockers, ACE inhibitors, afterload adn preload reduction, thats how you treat it.
angiostensin 2 and afterload and how it plays a role in raising blood pressure, causes vaso constriction, ACE inhibitors.
So managing these medication closely is the best way to treat diastolic and systolic heart failure.
Diastolic Heart Failure - my heart can’t relax and is not filling appropriately , eventually causing issues on the left side.
Rigth heart has the innability to perfuse the left and essentially cause hypoxic pulmonary disease.
Right heart is beating to get it to the lungs, so it can get it to the lungs.
Read slide about Peripheral edeam.
Reduce afterload and reduce afterload the treatment.
The additional slides are the same concepts , look over them .
The following slides are over Arrhythmias, don’t need to know but you do need to know about 🇦
Normal sinus Rhythm, ST segment elevation and T wave invesion.
Last Lecture - Pulmonary Lecture - Dr. Hanneman
Pulmonary and Cardiovascular go together, so connected.
A, B, C, - you can not have one without both. Pulomonary and circulation go together.
Nose and mouth to the larynx - Upper Respiratory System
Upper Airway - Warms the air we breath in 37 degrees C in the body. Normally, we have to devote water to assist in humifying. Crustation will form without this.
Filtering is importatnt - Cedar Allergies, levels are so high, how do we apply this to the bedside???
Atelectasis can happen, so this is important.
Water for refliltertion for humidifier, mechanical ventilators…. focus on the concepts. How am I going to prevent complications in this patient at all tyimes.
Cricoidotomy - emergency upper airway obstruction , used in an emergency.
No rise or fall of the chest situation - so she did cricoidotomy, she stuck a pen in there, started doing rescue breaths. saved his life.
Airway anatomy - right mainstem bronchi - 20-25 degrees - aspiration pneumonia happens here. Common in children…. right lung , harder against the left lung.
left mainstream bronchi - 45 Degree Angle - harder for fluid to get there.
Choking story from texans game, checking for aspiration pneumonia after that.
Carina - right and left of the trachea - parasympathetic component - constricts - causes people to cough, don’t want to mess with it. Don’t want the tip of a tracheaotomy because that will irritate it. 5-8 cm above the carina for placement. needs to be some room for movement. Or reposition the tube for the Carina.
Distal airways - big differnce in this , vasocontriction
Obstructive lungs diseases - Asthma
COPD - Chronic bronchitis and emphysema - not reversable diseases
Mechanics of Breathing
Elastic properties
-Elastic Recoil - Lung tissue, introverts (place themselves almost invisible), RIb cage extroverts. - Happened in open surgery.
Elastin same as elastic in the rubber band
Emphysema - loss of elasticity , eats away of lung tissue itself. The elastic is difficient. Lungs stay hyperinflated due ot elastic recoil. Works with complianc
Compliance - distend and fill the lung with air. or put air externally, has to be able to expand, stretch, pressure and volume inserted in.
Most diseases have to do with low compliance.
There will be resistance with the low compliance and to disted the lungs.
High compliance - ONLY EMPHYSEMA!!! lose elastin, alveolar units including the septum, can’t recoil. The elasticity of the recoil is damaged. TOO easy to get air in. There is no objections and the smalllest amount of pressure will fill lungs.
Airway resistance - obstruction of the airways - carina , change in pressure with flow of air. If the patient has bronchoconsriction , walls are going to close in. More difficult getting air in and mainly air out. Usually we don’t have problems breathing out because there is dilation breathing out, comes out passively. Breathing in is different, work involved.
Going to have trouble breathing, especially air out.
Work of breathing - important , always be subjectively paying attention , if you notice an increase of work of breathing, there needs to be intervention, body will tire out and go into respiratory arrest.
Frank Starling - Volume and Pressure Relationship.
X - disteding pressure
Y- volume
Normal Compliance curve - really little pressure for 1 liter , goes up in 2, 3,4 L of water. There is a plateau for the lungs and how much volume into the lungs.
High Compliance (frank starling curve)- IV Vasopressors , vasoconstriction causing pressure, more stroke volume.
Fibrosis - stiff tissue around the airways, minimum volume of air for higher pressure.
Both compliant curves - larger amount of air or blodd according to pressure. They all plateau , doesn’t matter of pathological , normal. There is a limitation affected bythe plateu.
REALLY IMPORTANT CONCEPTS!!!
Vasodilation of blood vessells and Vasoconstriction on airway - Anaphylaxis - Review these .
Airway resistance - comparison of infant (4mm), vs adult (8mm)
Big difference when it comes to edema and airway resistance , reversing broncho resistance, you will hear wheezing , what is causing it?
Respiratory Distress - intercostal muscles, not normal part of respiration. Asynchrony between stomah and chest when having problems breathing .
Severe respiratory rate video, distress going into respiratory arrest
Oxyhemoglobin dissociation curve
SaO2 - Y access - they don’t work optimally , arterial blood drawn
SpO2 - Pereferial , continuous measure, it is not
Core has blood shunted there, shift protection to the organs. Extremities are the peripheral , not priority for protection.
SaO2 Slide - Increased Affinity, normal, decreased affinity. - only - the affinity for the blood to bind to hemoglobin. Oxygen binds to hemoglobin 97% of the time.
Oxygen bind to the hemoglobin in RBC, RBC take the oxygen to the tissues of the body. Hemoglobin releases oxygen to the body and returns for more.
Oxyhemoglobin dissociation curve - Releasing oxygen at the tissue level.
The pink part of the curve (top part) has an increased affinity - did not want to release the lucy oxygen and the tissue are going to die - hypoxia will occur, tachycardia will compensate, lungs will underperform, liver will stop metaboliing.
Take a lood ath this Powerpoint on Oxyhemoglobin. Left vs. Right Side Curved. INCREASED AFFINITY WILL BE BETTER - Release the oxygen to the tissues is the most important.
You have to check the patients items such as orientated, mental function, brain function, heart rate, color, respiration rate. If you notice patients breathing, you must take time to analyze what is going on??
Hypothermia and acute alkolosis -
SPO2 - is not everything, you must stop to explore to see if they do not have tissue hypoxia that could lead to death .
Important Slide : Acute Respiratory Failure : 50/50 Rule —-Need Youtube Video
PaO2 equal or less than 50 mmHg
and or
PaCO2 equal or greater than 50 mmHg with PH equal
Chronic Respiratory failure - Chronic CO2 retainers, gets acute problem like aspiration pneumonia
Hypoxemia - not enough oxygen to the tissues …..
Acute respiratory failure - mid 50s , less than or equal to 60 = Hypoxemia
What is compensation in the blood gas exchange.. PH in 7.25 would not have a big compensation.
Look over this with everything you got about compensation with PH, Bicarbonate…..
Ventilation V /Perfusion Q Defects
4 panels shown - the exam only has 3 panels.
Normal V/Q -
Low V/Q - doen’t pick up the entire oxygen because the aveoli is blocked. Low VQ in relation to low blood being deoxygenated.
Shunt (very low),, alveoli is collappsed, worse hypoxemia , ARDS, ulmonary Edema, bad Pneumonia
High V/Q - normal ventilation - blood clot problem, that reduces the blood flow, the entire left lung is not getting any oxygen, the problem is perfusion is low
Pulmonary Hypertension Slide - Cor pulmonale caused by lung problems due to right side heart failure…..
Pulmonary Embolism Slide - Venous stasis , vessel injury, Hypercoagulability.
Hypoxemia and Hypoxia relationship,
Alveolar Capillary Membrane Slide -
Type 2 cells - Surfactant assists the alveoli from collapses.
basement membranes…
Plumonary edama in the interstital space - cause the distance of the capillary and alveolar and wall and can really disrupt gas exchange. Oxygen is less diffusable than carbon dioxide, you’ll have hypoxia first.
Alveolar Surface Tension Slide -
Pulmonary Edema Slide VIDEO THIS - 3 main mechanisms but Cardiogenic and Non Cardiogenic Edema (something other than the heart).
Non cardiogenic edema is due to capillary leak , onctotic pressure shifts, albumin walks its way and now you have a higher pull in the oncotic pressure .
Pulmonary Edema Cont (cont) - problems with the inte
ABG - Hypoxemia, Hypercapnia, Respiratory then to Metabolix Acidosis.
ACUTE RESPIRATORY DISTRESS SYNDROME SLIDE
-most serious pathological conditoin
- Manifestations are important - intractable hypoxemia - irreversible , you can not budge the PaO2,
ARDS Pathogenesis Slide -
ARDS Con.. Slide
Atelectasis - collapse of impaired surfacant … Clinical Manifestations
Atelectatic Lung Tissue Slide-
Pleural Effusion - Slide
very different concept , not talking about the lung , its the pleural that is attached to the lung . Visceral and Pareital attach to the chest. Pleura inside this , normally have space but there is very little fluid in there. absess can drain into the pluera space, you wil increase the pressure . build up pressure on the lungs.
Local atelectasis. Hydrostatic pressure … white out will show on the
Manifestations - Pleural Effusion cont. Slide
Pneumothorax - air in the pluero space, break in the chest wall.
Tension Pneumothorax Slide - life threatening, everytime the ventilator 500 mL of air, every 6 seconds air comes in. It can not get out of the left lung. The tension is not ventilating the left lung, pushing the lung into the right side, which pushs the right lung to the rib, heart, cardio pulmonary arrest will follow.
Asthma Pathophysiology Slide
Look at the flow chart
COPD Disease
Bronchitis - Edema, chronic is a lot more excessive mucus
Emphysema - The srtructure is dirrent
Lost of elastin and alveoli destroyed, no pressure buidl up , recoil issue
2 additional ribs and teh spaces increase in the hyperinflated chest.
Chronic bronchitis and Emphysema
The work of breathing is so much but can’t do anything else but breathing. Emphysema tend to be thin.
Hypoxemia Mechanisms V/Q , problems
Restrictive vs. Obstructive Diseases Slide
Look at the differences
ABG Interpretation Practice - Review , pehaps video