Cardiology Flashcards

Question

12 Lead EKG Intrepretation

Answer 1

* Primary focus is on L Ventricle because if it fails, it is the biggest problem * Walls of the heart that may be impacted * Inferior II, III, aVF * Anterior V3, V4 * Posterior * Lateral V5, V6, I, aVL * Impact to any one Coronary Artery could impact in some way the L Ventricle

Answer 2

II III aVF

Answer 3

V5 V6 I aVR

Answer 4

* begins at the apex of the heart and ascends along the anterior longitudinal sulcus to the base of the ventricles. * It then curves to the left in the coronary sulcus, and reaching the back of the heart and returns the blood to the atrium

Answer 5

* Three types of cells: Nodal Cells, Conducting Cells, Contracting Cells * SA Node - Sino Atrial & AV Node - Atrio Ventricular Node are made of nodal/pacemaking cells * Purkinje Cells - Conducting cells * Internodal Pathways * Underneath AV Node are purkinje fibers * Bundle of HIS splits into * Parallel structures called L/R Bundle Branches * Bundle Branches are the terminal fillaments of purkinje fibers

Answer 6

* ***_cardiac muscle contracts in absence of neural or hormonal stimulation_*** * Does not require body or brain to tell it what to do, because of the SA & AV cells * Will beat without the influence of SA/AV nodes

Answer 7

**Initiate & distribute** electrical impulses which lead to cardiac muscle contraction SA node sends message to conduction system which is relayed to contaction system, which tells heart to squeeze. There is critical relationship between conduction and contraction; when one of the parts fails ⇒ the heart fails.

Answer 8

* Found in the walls of the R Atrium * considered to be official pacemaker of the hear * generates action potential at inherrent pacing rate of 80-100 min

Answer 9

* distribute contractile stimulus to atria and send impulse to AV Node * inherrent pacing rate of 60-80 bpm

Answer 10

* Located in the floor of R Atrium * Slows the conduction rate to allow blood to flow into Ventricle

Answer 11

* Considered the AV Junction * Inherent pacing rate is 40-60 bpm

Answer 12

* Job is to distribute stimulus/AP to the ventricles * inherrent pacing rate 20-40 bpm

Answer 13

Electrical Function leads to Mechanical function

Answer 14

**Local** - isolated local event ie shunting from fluid in lungs **Neural** - Brain exerting control over body systems **Endocrine** - to be discussed at later date

Answer 15

1. Increase in metabolic demand; increase in O₂ uptake into cells = increase in pressure gradient * **exercise** creates an increase in demand for O₂ to do work = heaver breathing = increased pressure gradient 2. Increase in CO₂ capillaries near peripherial tissues; arterial smooth muscle relaxation ⇒ increased blood flow * vasodialation ⇒ allows for more blood to pass through to pick up CO₂ to be expelled 3. Shunting - relating to lungs/alveoli * ie Congestion/fluid in alveoli * shunted toward the alveoli with high PO₂ * air entering lungs is shunted toward capillaries with high PCO₂

Answer 16

1. Pons & Medulla: * increase in CNS stimulation * ie. increase in body temp ⇒ increase in rate of breathing because of impact on pons & medula and their dictated response 2. Reflexes * **baroreceptors** - * free nerve endings in walls of distensible organs * Stretching causes distortion of dendrites (nerve endings) ⇒ changes route of AP formation * **Hering-Breuer Reflexes** * inflation/deflation reflex - prevents overexpansion/total collapse of lung * Increase in BP ⇒ decrease in Respiratory rate and vice versa * **chemoreceptors** - located in carotid and aortic bodies - monitor PCO₂ & PO₂ concentrations * Primary respiratory drive - increased PCO2 = increased respiration rate * Secondary (Hypoxic) respiratory drive - decreased PO2 = increased respiratory rate; seen in pt's with COPD 3. Higher Centers or cerebral cortex ⇒ concious control of breathing; physical manipulation of breathing needs; reverts to automatic when not being thought about.

Answer 17

acidosis - 7.35 \< WNL \< 7.45 alkalosis

Answer 18

Changes in pH ⇒ * disruption in stability of cell membranes * decrease in pH (increase in [H⁺] = denaturation of proteins (non-functional) * inactivation of critical enzymes * Problems or changes with pH/[H+] concentration are fixed with Buffers

Answer 19

composed of Salt + Weak Acid stabilize pH by removing or replacing H+ ions either Take H+ out of solution so that they are bound to something else and not contributing to acidosis or rearranges chemical compounds so that the H+'s are occupied \* does not have to have anything to do with a base or H+

Answer 20

1. Protein buffer sustem - ie Hb; amino acids/proteins in blood may function as buffers by binding H+ and removing them from solution 2. Carbonic Acid Buffer system 3. Phosphate Buffer System - Reversible reation between H⁺ + HPO₄ ⇔ H₂PO₄^2-, stabilizes pH of Urine by removing H+ from solution.

Answer 21

Samples of blood values directly from artery vs veins provides more accurate representation of how sick patient is * pH = 7.35-7.45 * PCO₂ = 35-45 * PO₂ = 70-100 * HCO₃ = 22-26 * SaO₂ \> 90%

Answer 22

Primary Respiratory Problem * hypoventilation * increased CO₂ * not breathing * Narcotic OD H⁺ + HCO^-₃ ⇔ H₂CO₃ ⇔ H₂O + ***CO₂*** increase in ***CO₂***by default results in decrease in pH (increase in H+)& Increase in HCO^-₃ \*\*patients who are not breathing sufficently will have disturbance in pH associated with not breathing * CO₂ increases ⇒ body then converts CO₂ into carbonic acid ⇒ which makes more H⁺ and bicarbonate

Answer 23

Hyperventalation Syndrome H⁺ + HCO^-₃ ⇔ H₂CO₃ ⇔ H₂O + ***CO₂*** \*\*pt who is hyperventilating is depleting CO₂ , causing reaction to move left to right results in decrease in ***CO₂***, causing Increase in pH (decrease in ***H+***) & decrease in ***HCO^-₃*** to H₂O and CO₂

Answer 24

* DKA * Sepsis - Lactic acidocis * ASA OD * TCD OD * Chronic Renal Failure ***H⁺*** + ***HCO^-₃*** ⇔ H₂CO₃ ⇔ H₂O + ***CO₂*** decrease in pH (increase in ***H+*** in blood) as a result of the different disease processes; ie if blood becomes acidic proteins denature and critical enzymes become inactive Body compensates by driving reaction to right and increasing production of ***CO₂*** by default Respiratory rate increases decrease in HCO^-₃ \*Most important because pt is breathing fast (tachypnea) for any number of reasons, but provider fails to recognize that the patient is critically ill

Answer 25

* Tums OD * Vommiting H⁺ + HCO^-₃ ⇔ H₂CO₃ ⇔ H₂O + ***CO₂*** Increase in pH (decrease in H+), HCO^-₃ (decrease in ***CO₂***) Vommiting reduces your stomach acid which is Hydrogen Ions, increases HCO^-₃, and decreases available CO₂

Answer 26

Metabolic Acidosis Tachypnea in presence of clear lung sounds or no obvious respiratory distress usually indicates DKA Sepsis - Lactic Acid ASA OD TCA OD Chronic Renal failure

Answer 27

* maintain/stabilize pH all the time * dynamic effort by body constant shifting to: * if there is a decrease in avaliable H+ available ⇒ then released from appropriate buffer system * if there is an increase in avaliable H+ then more will be taken up

Answer 28

* Respiratory - Fast Compensation * Renal - Slow Compensation Buffers are compensation effort by body, when they fail/resources used up ⇒ disease

Answer 29

Problems with CO2 = Respiratory Problems with BiCarb (HCO^-₃) = Metabolic

Answer 30

* The SA/AV nodes do not have a steady state/ resting potentials * Pacemakers drift between depolarized to repolarized in fashion similar to sine wave * Leak channels are responsible for changing of ions that are present; once one cell depolarizes primarily due to gap junctions cells near by depolarize and influences other cells ie the Atria * SA's depolarization sends wave of depolarization down internodal pathways to AV where it slows and sends wave on to Purkinje Fibers which then spreads across to the ventricles

Answer 31

depolarization ⇒ repolarization ⇒ plateau ⇒ depolarization ⇒ rest Resting Potential for Atria is 80mV Resting Potential for Ventricles is 90mV

Answer 32

* Resting Phase/Potential * -90mV * Threshold is -75mV * Resting portential maintained by NA+/K+ Pump * Resting phase is associated with Diastole

Answer 33

* Rapid depolarization Phase (3-5ms) * prepotential activated by SA/AV Node * leading to rapid entry of Na+ ions causing a change in membrane potential to +30mV

Answer 34

* Repolarization Phase (175ms) * Na+ reaches approximate equilibrium and Na channels close and are inactivated until return to relative refractory period (approx -60mV) * K+ channels open and repolarization

Answer 35

* Plateau Phase (75ms) * Ca²⁺ exchanged for Na+ maintains membrane potential at 0mV * Major difference between what Ca²⁺ is used for in Neurons and what it is used for in cardiac/muscle cells * Ca²⁺ arrives for sarcoplasmic reticulum and T-Tubules because it is in higher concentration in ECF and stored in sarcoplasmic reticulum * Entry of Ca²⁺ makes muscle contraction possible, ie:troponin⇒topomyosin⇒actin/myosin b * Ca²⁺arrival is critical to linking **conduction** and **contraction**

Answer 36

* Rapid/Main Repolarization phase (50ms) * Ca²⁺ channels close * K+ Channels exit enabling rapid repolarization * Cell returns to resting phase/potential (-90mV) where Na/K pump works to maintain membrane potential

Answer 37

* **Absolute** - Period of time from when Na+ channels are inactivated until they are just closed and can be opened again which is around -60 mV * generally long absolute period in cardiac vs skeletal isn't as possible for tetany (sustained contraction), allows heart muscle to relax befor contracting again * **Relative** - from -60 to -90mV during relative refractory where Na+ is closed but is able to be opened again

Answer 38

* Topomyosin - microfiliment located on actin filament * Troponin - Binding site for Ca²⁺ on Tropomyosin which unlocks binding site for Myosin to cause crossbridge-powerstroke-muscle contraction * Actin - Thin micro filaments containing toponin and tropomyosin * Myosin - Thick micro filament, has head that binds to Actin to produce muscle contraction; has both ADP and Pi * ADP and Pi - located on Myosin, Pi released when myosin forms Crossbridge (links with Actin) ADP expended during Powerstroke * ATP links with Myosin to release Actin which causes ATP to break down into ADP + Pi and heads return to resting

Answer 39

* Consists of Actin and Myosin not touching * Myosin has ADP + Pi attached to binding head * Actin's Myosin Binding sites are blocked by Tropomyosin which has troponin (Ca²⁺) binding sites on them

Answer 40

* Calcium is delivered from sarcoplasmic reticulum and from ECF via the T-Tubules * Ca²⁺ binds to troponin causing tropomyosin to reveal myosin binding sites * ***Corresponds to plateau phase of Ventricular action potential; as Ca²⁺ arrives to cause muscle contraction***

Answer 41

* Once Myosin binding sites are revealed on Actin; Myosin heads release Pi molecule as they bind to Actin toform cross bridge formation. * ADP is expended as Myosin head pulls themselves along Actin causing muscle to contract (shortening muscle) * Affinity to the arrival of a new ATP molecule causes Myosin to release and return to it's resting phase, which breaks ATP down into ADP + Pi * If calcium is still present, cycle will repeat; increased calcium causes prolonged muscle contraction * When ATP runs out it is not possible to seperate the Actin and Myosin, Hence rigamortis a couple hours after death due to lack of O2, runs out of glucose, runs out of ATP.

Answer 42

* When heart muscle has block in coronary artery * Muscle not recieving nutrients it becomes * irritable * ischemia not enough O2 * injury * infarc - tissue death * With no ATP = No Na/K Pump = wrong membrane potential ⇒ shifting of fluids ⇒ cells to lyse ⇒ contents released into bloodstream ⇒ changes what you see on EKG ⇒ perhaps ST elevation = MI * even if there is no ST elevation, pt may still be having MI, revealed via analysis of cardiac enzymes (Troponin, myoglobin, CK(MB))

Answer 43

* Heart is relaxed both A & V are resting * Pulmonary circulation returns from lungs & Systemic circulation returns from body and begin to passively fill ventricles as much as it can before atrial systole

Answer 44

* phase following atrial depolarization the atrium will contract * 70% of returning blood has passively filled ventricle, remaining 30% will be pushed into ventricles during contraction. * Approximatley 130mL remain in Atria following contraction

Answer 45

* AV Valves close⇒ increasing pressure (bp rises) ⇒ when BP is \> Aorta/Pulmonary Trunk Pressure ⇒ Blood is expelled into circulation * Then returns to Atrial/Ventricular diastole, blood passively fills from circulation

Answer 46

electrical function

Answer 47

**EDV** - Amount of blood in Ventricles after **Atrial** contraction last moment of ventricular diastole ie the maximum amount of blood they will recieve (130mL) **ESV -** Amount of blood remaining in ventricles after **Ventricular** contraction (50mL)

Answer 48

Amount of blood actually pumped out of heart in single beat 70-80mL for healthy adult

Answer 49

SV divided by EDV % of blood ejected from single heart beat Normal ejection fraction runs between 60 and 70%

Answer 50

SV x HR amount of blood pumped out of heart each minute * changes to EDV or ESV ⇒ change in SV ⇒ CO * neural or hormonal stimulation ⇒ changes in HR ⇒ changes in CO

Answer 51

* Atrials are incompetent * Atrias quiver rather than push blood from Atria to Ventricles * 30% of blood that doesn't get pushed into ventricles is called Atrial Kick * Blood pools in Atria and doesn't circulate, * Pooling blood can clot ⇒ when shocked, clot can begin to circulate causing clots in pulmonary circulation or systemic circulation

Answer 52

* Increase in the opening or likelihood of opening of Na⁺ and Ca²⁺ channels ⇒ increase in the influx of positive ions ⇒ results in muscle contraction * Increase in rate at which depolarization occurs = an increase in heart rate * Example of SA node involvement

Answer 53

* Muscarinic - ACh Receptor linked to K+ channels * Binding ACh ⇒ Opens K+ channels ⇒ exit of K+ from cell ⇒ hyperpolarization ⇒ slows the rate of spontaneous depolarization * example of effect on AV node

Cardiology Flashcards

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