Critical Care Exam 1 ECG INTERPRETATION Normal conduction o SA node intrinsic pacemaker 60 100 2nd AV node 40 60 perkinje fibers 15 40 Due to MI heart ischemia no oxygen LOWER CO no atrial contraction stimulus below blood NOT pumped efficiently into ventricles o Electrical stimulus impulse SA node AV node bundle of His bundle branches 1 on RIGHT 2 on LEFT perkinje fibers vesicular posterior an terior ventricles mechanical stimulus Starts in right atrium goes to left atrium via intra atrial pathways stimulates left and right P wave atrial depolarization contraction SA node firing PR Interval o Start of P wave to start of QRS wave o Atrial depol to ventricle depol onset impulse travel from SA to AV with brief delay to let atria empty o Normal intact CONDUCTION o Prolonged blocked conduction QRS ventricle depol bundle branches depolarize and stimulate vents o Impulse travels through bundle branches and perkinje fibers o Electrical stimulation mechanical activity o Different NORMAL variations o Atrial repolarization occurs within QRS complex after atrial depol J Point end of QRS complex returns to isometric line o Area that shows MI or heart ischemia ST segment start at J point to start of T wave o Normal flat and at isometric baseline within 1 box mm o 3 mm ST ELEVATION MI or STEMI o 3 mm ST DEPRESSION heart ischemia or MI further lab work 12 lead SOB chest pain increased heart enzymes CKMB troponin non STEMI T wave ventricles repolarize rest QT Interval start of QRS to end of T wave o Ventricular cycle start of vent depol to end of vent repol o Prolonged with premature next cycle V FIB Presence of U wave hypokalemia ECG Graph Paper o 1 box 0 04 sec q 5 boxes 20 seconds o Measure left to right time o Measure up and down voltage height in mm ST elevation dep 3 Rs o Rate count QRS complexes in 6 second strip Determine by 1500 of small boxes btwn complexes o Regularity consistency between intervals P to P R to R o Rhythm determine PR QRS QT intervals P to P regular R to R regular Normal rate consistent or vary Normal Intervals o PRI 0 12 0 20 sec 3 5 boxes Prolonged first degree AV block taking too long for electrical impulse to leave AV node Biphasic P wave half above and half below isometric line o QRS 12 LESS than 3 boxes Prolonged bundle branch block taking too long for the electrical im pulse to travel down bundle branches Conduction prolonged to perkinje fibers WIDE complex Indicates new or old MI left ventricular hypertrophy o QT less than HALF of R to R interval usually around 0 35 0 44 R on T phenomenon prolonged QT and next impulse is on T wave V FIB not efficient cardiac arrest Varies according to HR shorter with increased HR Bradycardia Tx o Assess pt BP LOC resp rate pulse ox o Give ATROPINE 0 5 mg IV if symptomatic hypotensive dizzy lightheaded Give additional 0 5 mg dose if first doesn t work o Tx with transcutaneous pacemaker if atropine does NOT work Tachycardia Tx o Check pt and treat cause pain anxiety fever hypoxemia o Treat cause pain meds antipyretics anxiolytics o Tx with beta blockers calcium channel blockers if you can NOT identify cause and pt still has tachycardia Artifact electrical interference d t pt movement or contact with another electrical devise o Tx check pt immediately and fix leads INVASIVE HEMODYNAMICS delivery of nutrients to body Measures BF through cardiovascular circuit determines perfusion oxygenation Needed for interventions medical nursing pharmacological Cardiac Output best indicator of the condition of heats contractile ability in otropic volume of blood ejected by heart into circulation in 1 minute o Normal 4 8 L at rest 4 6 L o CO SV x HR Cardiac Index CO body surface area o Normal 2 2 4 L min m2 o Lower 2 2 for 300 lb symptomatic cool clammy SOB hypotensive Stroke volume amount of blood ejected by left vent during each systole Normal o Preload blood volume and amount of stretch placed on muscle fibers PRIOR 60 70 ml to systole Frank starling max volume to create max stretch best contraction until certain point overstretch BAD Increases CO in some cases up to certain point Stretch on heart fibers filling pressure LVEDP and RVEDP filling pressures fom blood volume Assess CVP RVEDP PA diastolic PCWP LVEDP Elevated increases SV ventricular work myocardial oxygen require ments all adverse consequences for CC pts From volume overload Ivor vent mus fiber damage vent dys function valvular defects stenosis regurgitate insufficiency cardiac tamponade fluid in pericardial space can t fill nor mally vasoconstriction systemic pulmonary HTN Left side symptoms orthopnea dyspnea dry cough crackles S3 backflow from L vent L atrium pulm veins congested lung tissue HF pulm edema Right side symptoms JVD edema HJR HOB 45 and push on liver distended neck veins o Continued backflow from lungs o Cor pulmonale isolated right HF lung dis pulm HTN Reduction therapy directly reduce blood volume diuretics o Promote vasodilation nitrates calcium channel blockers beta blockers Decreased decreases SV vent work myocardial oxygen require ments excessive inadequate contractile response From hypovolemia hemorrhage third spacing excessive diure sis inappropriate vasodilation dis Rx S S altered LOC less O2 to brain decreased UO decreased vi tal organ perfusion tachycardia hypotension dry cool skin dry mucous mem poor skin turgor test on chest wall least affected by env o High preload also affects forward perfusion LOC Enhancement therapy volume adm crystalloids colloids blood trenbelemburg position o Vasoconstrictor NE levophed increase volume in central circulation effective FIRST replace volume o Afterload pressure ventricle has to pump against to eject blood increased vent wall tension or stress Determined by vascular resistance best indicated by SVR Aorta pulm artery vasoconstrict wall tenstion resistance with con traction heart works harder to move blood into sys Assess MAP most accessible SVR need invasive catheter to know CO PVR right side of heart Elevated increase pressure and heart workload O2 consumption From vasoconstriction high SVR HTN septic shock increased aortic impedance diseased aortic valve atherosclerotic plaque less BF hypoxia pain hypothermia catecholamine release CC pts physically stressed increase cathecholamines Reduction therapy vasodilators reduce without hypotension o Continuous IV drips nitroprusside nicardipine o ACE inhibitors ARBs non selective beta blockers Decreased no forward flow in aorta from vent systole From vasodilation low SVR
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