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Cardiac #1
Patho
| Question | Answer |
|---|---|
| Apex is formed __ by left ventricle and is the ___ ___ intercostal space | 2/3, left, 5th |
| is the right atrium posterior of anterior? | anterior |
| ___ is a thin projection at the top of the anterior surface | auricle |
| fossa ovalis is remnant of | foramen ovailis |
| air tends to collect at the __ and __ junction | SVC and RA |
| IVC, SVC, or Coronary sinus has the lowest Sv02 | Coronary sinus 80% venous return from the coronary circulation |
| what are two ways the fossa ovalis can remain open or reopen? | RAP> LAP or positive pressure |
| which valves is the largest? | tricuspid |
| T or F do both ventricles perfuse through the entire cardiac cycle? | False; only the right ventricle |
| which valve is difficult to visualize on TEE | pulmonary valve |
| what causes a aortic dissection | the shearing effect of the ligamentum arteriosum which is attached to the aorta |
| which is the most common site to develop blood clots? | Left auricle |
| what allows for expansion of the L atrium to take in larger volume | left auricle |
| blood entry into the left artium is via | four pulmonary veins |
| the left ventricle is only perfused during? | Diastole |
| What can develop from a inferior MI? | Mitral regurg. secondary to papillary damage from ischemia |
| papillary muscles stablize? | chordae tendinea |
| Sv02 is highest when returning from the OR vs. open awakening? T or F | true |
| Tricuspid, Mitral, and Aortic valves have how many cusp? | T(3) M(2) A(3) |
| what is defined as critical stenosis | less than 1 cm2 |
| this coronary artery is dominant in 20% of individuals | LCA |
| what is the sinus of valsalva | where the LCA arises from left aortic sinus |
| how is the LM branched out? | LM-LAD-D1,D2 LM-Lcirc.-OM1,OM2 |
| is the R or L more susceptible to myocardial infraction? | Left |
| the RCA orignates from the | right aortic sinus |
| the R or L CA supplies the SA and AV nodes | RCA |
| if the RCA becomes occluded you will experience tachyarrythmias? | false; commomly causes bradycardias |
| coronary flow is balanced in __% of pts | 30 |
| ventricle size __ the risk for ischemia? | increase |
| L ventricle drains to the ____ found in the found in the right atrium? | coronary sinus |
| where are retrograde catheters placed? | coronary sinus |
| these drain deep muscle to RA and RV | thebesian veins |
| some direct drainage from the RV wall into __? | RA |
| where is the attachment points for the ductus venosum? | it turns into ligamentum venosum. Attached to the left branch of the portal vein within the pora hepatis of theliver. |
| what is know as the widow maker? | LMA |
| occlusion of the RCA: leads, area | II, III, aVF inferior wall |
| occlusion of the LAD: leads, area | V1-V2 anterior wall |
| occlusion of the circ: leads, area | V4,V4,V6 lateral wall |
| if you have lead changes in II,II,aVf you would expect what type of rhythm? | Bradycardia; RCA supplies the SA/AV node |
| if you see ST depression in leads V1-V2 you would expect what? | Anterior wall ischemia |
| ST elevation in leads V4,V5,V6 | lateral wall injury |
| the presents of Q waves | infarct |
| this has a zero reference point, T-P segment is the reference line | the J point |
| ST depression may or may not have T wave inversion | ischemia |
| ST segment elevation, with or without loss of R wave | injury |
| what are some causes of inverted T waves | Conduction defects, Hypertrophy, Ischemia, Pericarditis, SAH, Subendocardial infarction. CHIPSS |
| causes of short QT | hypercalcemia |
| causes prolonged QT | ischemia, drugs, low: Ca, Mag, K |
| what makes cardiac muscle contraction take place? | Ca influx of Ca causes mov't of tropomyosin, allowing attachment of myosin head to the actin filament therefore allowing contraction |
| what relaxes muscle contraction? | ATP; binds to myosin and breaks hold |
| What terminates muscle contraction | re-uptake of Ca |
| if you have a pt with 2nd degree type II block why shouldn't you put them to sleep? | when placed on positive pressure it causes the RA to stretch and increase PVR which can turn into 3rd degree. caution in pt with SA node disease as well. |
| what part of the sarcomere moves during contraction? | Z-lines move as the myosin heads pull the actin |
| where is the CA located inside the cell? | sarcoplastmic reticulum in the mitochondria |
| CPP equation | ADP-LVEDP aortic diastolic pressure |
| which ventricle has the least compliance | left |
| where does sympathetic myocardial innervation take place | right stellate ganglion supplies the coronary sinus and AV node left stellate ganglion innervates the ventricle, distributed throughtout the entire heart |
| where does the parasympathetic myocardial innervation take place | primarily distributed in the atrium and specialized conduction system. SA and AV node. Vagus nerve |
| what is preload? | the sarcomere length just prior to contraction, importance of sarcoma length, pressure volume curves mimic this |
| how is preload measured | can't be measured except with rapid echo, indirectly as the LVEDV/LVEDP |
| what is preload | load that the muscle must do once contraction begins |
| what does afterload depend on | ventricular intracavity presure, wall thickness, chamber radius, geometry of the ventricle, vascular load, ventricular load |
| how is afterload measured | no measured but calculated |
| what is contractility | ability of the heart to contract with force |
| how is contractility assessed | echo, SV |
| what is normal SV? | 60ml (65%EF) 3L/min at rest LVEDV 120-140 |
| what causes decreases in slope 4 | vagal stimulation, positive airway pressure, acute hyperkalemia, arrythmias |
| increases in slope 4 | art.hypoemia, hypercarbia, catecholamines, sympat. drugs, acute hypokalemia, hyperthermia, HTN, |
| what part of the EKG is considered the health of the AV node | PR interval |
| what electrolyte is decreased by stress and bacteria | mag |
| which dysrhythmia a pacemaker is indicated | Second degree AV block type II |
| bifascicular block is also | a third degree block |
| esmolol should not be given to which pts | ST, PSVT with unknown cause, need to dx cause first |
| what is considered irregular, irregular | A.fib |
| this rhythm has a pathway of kent | WPW |
| what med shouldn't you give a WPW pt | verapamil |
| this access. pathway is inside the AV node, short PR interval | lown-ganong-levine syndrome |
| causes of PVCs | lt. anesthesia, vagal, art. hypoxemia, hypercarbia, MI, SNS activation, hypokalemia, hypomagnesemia, drugs, mechanical irritation (caffeine, ETOH, dig tox,local tox, volatile) |
| how would you tx a pt that starts having lots of PVC's? | is pt receiving O2, cancel case, indication for list of possible causes, consider cause and treat. |
| how do you monitor ischemia | 1)TEE, 2)PA cath,3)EKG |
| what causes prolonged QRS | hypertrophy, cardiac dilation, purkinje syst. block, cardiac injury |
| what cause changes in QRS ht/width(voltage) | increase voltage:hypertrophy decrease voltage:myopathies,tamponade,pleural effusions, COPD, pneumothorax, BBB |
| how do you dx a RBBB | (-)lead I, (+) lead aVF vector analysis or bunny ears in V1 |
| how do you dx a LBBB | (+)lead I, (-) lead aVF vector analysis or bunny ears in lead I |
| why is it important to to dx R or L BBB | if placing a PA cath, if you have a LBBB you can knock out the R side and end up with complete block (SC pacer pads at bedside) |
| how do you treat neurogenic and spinal shock? | ABC's, IVF therapy, vasopressors, inotropes, corticosteroids, monitor for acidosis, evaluate level of injurt |
| how would you treat hypovolemic shock? | ABC's, evaluate and tx cause, intubate if in full shock, if not in full shock assess bld gases and ability to maintain airway, IVResuscitation, vasopressors, DON'T put in trendelenburg, A/L needed |
| what are the five important variables to ascertain shock? | CO, SVR, PAOP, CVP, SvO2 |
| SMART stands for? | stabilize, monitor, assess, review, treat |
| how are hypovolemic and neurogenic shock different? | hypovolemic:hemorrhagic or nonhemorrhagic due to electrolyte loss #1 Diarrhea Neurogenic: spinal cord injury |
| what drugs should be avoided in WPW | Verapil, Ketamine, Pancuronium and others that increase HR |
| what organs get affected by HTN | HTN leads to MSOF (multisystem organ failure) Cardiac-CHF Renal-CRF Neurogenic-CVA Liver-why not? |
| what is the difference b/n primary and secondary HTN | Primary HTN: unknown(90% pts) Secondary HTN:Drugs, renal disease, pyelonephritis, glomerulonephriitis, diabetic nephropathy, vascular disease, coarchtation of the aorta, hyperadrenocorticism, primary aldosteronism, intracranial HTN, pheochromocytoma |
| what is malignant HTN | hypertensive crisis: diastolic>130mmHg results in damage to retinal vessels (papilledema), |
| what med should be avoided in HTN crisis | ACE Inhib |
| what is a key concept in shock? | perfusion |
| with shock when should you give bicarb? pH___ | <7.20 |
| what is a sign of flank bruishing? | retroperitoneal hemorrhage |
| where is LVEDP and LVEDV located on the press. vol. curve | look on the pressure-vol. curve LOL! |
| complications of thiazides diuretics | low:K,Mag,lithium clearance high:Ca, glucose, cholesterol, uricicemia dermatitis, alkalosis, photosensitivity |
| complications of K-sparing diuretics | hyperkalemia hyponatermia megablastic anemia dermatitis |
| compilations of clonidine | sedation, orthostatic HypoTN, bradycardia, impaired glucose tolerance, rebound HTN, dry mouth |
| complications of beta blockers | CHF, bradycardia, bronchospasm, sedation, rebound angina, parasthesias, impotence masking of hypoglycemia, raynauds phenomena |
| complications of ACE inhibitors | hyperkalemia, proteinuria, cough, fetal death, dermatitis, ANGIOEDEMA |
| complications of hydralazine | reflex tachycardia lupus like syndrome, fever |
| what is the final common pathway in shock | organ regional bld flow disturbances, lack of cellular oxygenation, leads to ATP depletion and eventually cell damage and death |
| what symptoms do you always get with shock | Neuro:mental status changes, miosis(overdose), mydriasis Cardiac:↑HR, ↓BP,↓contract., new murmurs, dysrhythmias,↑JVP(RHF), ↓JVP(hypoTN), disparate perip. pulses(aortic diss) Resp:↑RR,Pedema, hypoxia Renal:oliguria Skin:cool, clammy lactic acidosis, fever |
| What is the most important thing to remember when you manage anybody in shock? | ABC's |
| How do you differentiate b/n anaphlaxtic shock and neurogenic shock | you can't |
| how can you dx carogenic shock? | CI must be less than 2L/min/m2 PAOP must be greater than 17-20 mm Hg |
| what kind of shock is left ventricular MI? | cardiogenic shock |
| what is considered impedance to ventricular filling | pericardial tamponade |
| what is considered impedance to ventricular outflow | massive pulmonary embolism |
| what is the txment for anaphylaxis shock | vol. expansion, epi early, diphenhydramine, steroids |
| what is considered trauma without hypovolemia | Burns, crush injuries |
| what causes the fast Na channels to remain inactivated in pacemaker cells | the max negative voltage -60 |
| what is Na intra, extra, and equilibrium potential | 144, 7, +81 |
| what is K intra, extra, and equilibrium potential | 4, 151, -97 |
| what is Cl intra, extra and euilibrium potential | 114, 4, -90 |
| during phase 2 of the cardiac action potential what occurs | plateau phase 2:1 ca influx 1 enters K efflux 2 leave |
Created by:
melbacs