Cardiovascular Emergencies and 12 Lead EKGs Condell Medical
- Slides: 145
Cardiovascular Emergencies and 12 Lead EKG’s Condell Medical Center EMS System April 2007 Site Code #10 -7200 E-1207 Prepared by: Sharon Hopkins, RN, BSN, EMT-P
Objectives Upon successful completion of this program, the EMS provider should be able to: – understand the normal anatomy & physiology of the cardiovascular system – describe anatomical changes to the heart during ischemic episodes – differentiate presentations of patients with cardiorespiratory complaints
–describe lead placement for obtaining a 12 lead EKG –recognize ST elevation on the 12 lead EKG – identify and appropriately state interventions for a variety of dysrhythmias – actively participate in discussion of case presentations – successfully complete the quiz with a score of 80% or better
Cardiovascular System u This system is composed of the heart and blood vessels Delivers oxygenated blood to all cells Transports hormones throughout the body Transports waste products for waste disposal u The heart is a pump – right pump is under low pressure – left pump is under high pressure
Components of Circulatory System À Functioning heart Á Sufficient blood volume Intact blood vessels If any one of the above 3 are not working properly, the patient may be symptomatic and could be in need of intervention
Blood Flow Through The Body u Systemic circulation Left ventricle Aorta arteries arterioles capillaries venules veins Right atrium
Superior vena cava Right atrium Right ventricle Aorta Left atrium Left ventricle
Myocardial Blood Flow u The heart is a muscle (myocardium) u 3 layers epicardium - smooth outer surface myocardium - thick middle layer, responsible for cardiac contraction activity endocardium - innermost layer of thin connective tissue u Myocardial blood flow – via coronary arteries immediately off aorta – heart is the 1 st structure to receive oxygenated blood - it’s that important!
Coronary Arteries ªLeft main coronary artery –left anterior descending coronary artery (LAD) supplies left ventricle, septum –circumflex coronary artery supplies left atrium, left ventricle, septum, part of right ventricle ªRight coronary artery (RCA) supplies right atrium & ventricle
Coronary Blood Flow
Influences of Heart Function u Preload – pressure under which a ventricle fills; volume of blood returning to fill the heart u Afterload – the resistance the ventricle has to pump against to eject blood out of the heart – the higher the afterload the harder the ventricle has to work u Ejection fraction (EF) – percentage of blood pumped by the ventricle with each contraction (healthy >55%) – damage to heart muscle decreases EF
Problems That Affect & Afterload Preload Afterload u increased oxygen u arteriosclerosis demand increases induced high B/P volume of blood can cause left returning to heart ventricle to become exhausted & stop u temporarily not a working efficiently problem u heart enlarges when preload remains increased (Frank. Starling law)
Problems That Decrease Ejection Fraction (EF) u Myocardial infarction (MI) u Congestive heart failure (CHF) u Coronary artery disease (CAD) u Atrial fibrillation u Cardiomyopathy u Anemia u Excess body weight u Poorly controlled blood pressure
CO = SV x HR u CO - cardiac output – amount of blood pumped by the heart in one minute (normal 5 -6 L/min) u SV - stroke volume – amount of blood pumped out by either ventricle in a single contraction (normal 60 -100 ml) u HR - heart rate – number of cardiac contractions per minute (normal pulse rate 60 -100/min)
CO = SV x HR A change in stroke volume or heart rate will affect cardiac output u SV and HR = CO – ie: compensatory mechanism u SV and steady HR = CO – ie: preload = afterload (ie: shock in patient taking beta blockers) u SV and HR = CO – ie: patient with symptomatic tachycardia u steady SV and HR = CO – ie: patient with symptomatic bradycardia
Coronary Artery Disease (CAD) u Leading cause of death in USA – Narrowing or blockage in coronary artery decreasing blood flow – Atherosclerosis - thickening & hardening of the arteries due to fatty deposits in vessels – Plaque deposits build up in arteries uarteries narrow uarteries become blocked ublood clots form u Overtime, CAD can contribute to heart failure & dysrhythmias
Collateral Circulation u Development of new blood vessels to reroute blood flow around blockage in a coronary artery u New arteries may not be able to supply enough oxygenated blood to heart muscle in time of increased demand u Ischemia occurs when blood supply to the heart is inadequate to meet the demands
Coronary Artery Disease (CAD) Plaque in a coronary artery breaks apart causing blood clot to form and blocks artery
Defining Acute Coronary Syndrome u Types of CAD related to sudden rupture of plaque inside a coronary artery unstable angina non-ST segment elevation MI (NSTEMI) ST segment elevation MI (STEMI) u Length of time blood flow blocked and amount of damage determines type of acute coronary syndrome
Symptoms of Cardiovascular Problems u Breathing problems – Shortness of breath (SOB) – Paroxysmal nocturnal dyspnea (PND) usuddenly awakens with shortness of breath – Orthopnea udyspnea when lying down – Breath sounds uare clear or not clear?
u Peripheral edema – excess fluid found in tissues of the most dependent part of the body upresacral area in bedridden person ufeet and ankles in someone up and about u Syncope – fainting when cardiac output falls – fainting while lying down is considered cardiac in nature until proven otherwise u Palpitations – sensation of fast or irregular heartbeat u Pain
Initial Impression u Not necessarily important to know exactly what to “name” the patient’s problem (diagnosis) u Important to identify signs and symptoms that need to be treated u Important to recognize the possible medical condition the signs and symptoms may be representing u Important to determine the right treatment approach
Patient Assessment: OPQRST of Pain Symptoms u Onset – Sudden or gradual? – Anything like this before? u Provocation or palliation – What makes it better/worse? – What was the patient doing at the time? u Quality – What does it feel like (in patient’s own words)?
u Radiation – From where to where? u Severity – How bad is it on a scale of 0 -10? u Timing – When did it start – How long did it last? – Continuous or intermittent?
Vital Signs: Tools for Pt Assessment u Heart rate – too fast uventricle does not stay open long enough to adequately fill – too slow urate too slow to pump often enough to maintain an adequate volume output u Blood pressure – could be elevated in anxiety and pain – low in shock – serial readings (trending) tell much
u Respirations – Abnormally fast, slow, labored, noisy? Clear - hear breath sounds enter & exit Crackles - pop, snap, click, crackle ufluid in lower airways Rhonchi - rattling sounds; resembles snoring umucus in the airways Wheezes - whistling sound; initially heard on exhalation unarrowing airways (ie: asthma) ¨Absence of sound - not good!!!
u Pulse oximetry (Sa. O 2) – Measures percent of saturated hemoglobin in arterial blood – <95% indicates respiratory compromise – <90% indicates dire problem – Need to evaluate reading with patient’s clinical presentation do they match?
Inaccurate Sa. O 2 Readings Hypotensive or cold patient (falsely low) Carbon monoxide poisoning (falsely high) Abnormal hemoglobin (sickle-cell disease) (falsely low) Incorrect probe placement (falsely low) Dark nail polish (falsely low) Anemia (falsely high - whatever hemoglobin patient has is saturated)
u EKG monitoring – Indicates electrical activity of the heart – Evaluate mechanical activity by measuring pulse, heart rate and blood pressure – Can indicate myocardial insult and location K ischemia - initial insult; ST depression L injury - prolonged myocardial hypoxia or ischemia; ST elevation L infarction - tissue death –dead tissue no longer contracts –amount of dead tissue directly relates to degree of muscle impairment –may show Q waves
ST depression ST elevation Q wave
Acute Coronary Syndrome Variety of events that represent acute myocardial ischemic pain (plaque rupture) ¬Unstable angina u. Intermediate severity of disease between stable angina and acute MI; tissue ischemia Non-Q wave infarct (NSTEMI) u. No ST elevation but MI is present with tissue necrosis (death) ®Q wave infarct (STEMI) u. ST elevation MI with tissue necrosis (death) u. Usually a large/significant infarct
Initial Treatment Acute Coronary Syndrome u Regardless of the end diagnosis, all patients treated initially the same – IV-O 2 -monitor-vital signs-history – aspirin – nitroglycerin – morphine if necessary – 12 lead EKG obtained & transmitted u Treatment fine-tuned as more diagnostic information is obtained
Acute Myocardial Infarction u Coronary blood flow deprived so that portion of muscle dies – occlusion by a thrombus (blood clot superimposed on ruptured plaque) – spasm of coronary artery – reduction in blood flow (shock, arrhythmias, pulmonary embolism) u Location and size of infarct depends on which coronary artery is blocked & where – left ventricle most common
AMI Signs & Symptoms u Chest pain - most common especially in men – lasts >15 minutes – does not go away with rest – typically felt beneath sternum – typically described as heavy, squeezing, crushing, tight – can radiate down the arm (usually left), fingers, jaw, upper back, epigastrium u Pain not influenced by coughing, deep breathing, movement
Atypical AMI Signs & Symptoms Persons with diabetes, elderly, women, and heart transplant patients u Atypical presentation - from drop in cardiac output (CO) – sudden dyspnea – sudden lose of consciousness (syncope) or near-syncope – unexplained drop in blood pressure – apparent stroke – confusion – generalized weakness
Atypical AMI Signs & Symptoms Women – nausea – lightheadedness – epigastric burning – sudden onset weakness – unexplained tiredness/weakness u Women at greater risk – symptoms ignored (by patient & MD) – under-recognized – under-treated
Congestive Heart Failure u Heart unable to pump efficiently u Blood backs up into systemic system, pulmonary system or both – Right heart failure umost often occurs due to left heart failure ucan occur from pulmonary embolism ucan occur from long-standing COPD (esp chronic bronchitis) – Left heart failure umost commonly from acute MI ualso occurs due to chronic hypertension
Right Heart Failure u Blood backs up into systemic circulation – gradual onset over days to weeks – jugular vein distension (JVD) – edema (most visible in dependent parts of the body) from fluids pushed out of veins – engorged, swollen liver due to edema – right sided failure alone seldom a life threatening situation u Field treatment most often symptomatic u More aggressive treatment needed when accompanied with left heart failure
Left Sided Heart Failure u Heart unable to effectively pump blood from pulmonary veins u Blood backs up behind left ventricle u Pulmonary veins engorged with blood u Serum forced out of pulmonary capillaries and into alveoli (air sacs) u Serum mixes with air to produce foam (pulmonary edema)
Progression Left Heart Failure u Think “left - lungs” u Impaired oxygenation – compensates by respiratory rate u Fluid leaks into interstitial spaces – auscultate crackles u interstitial pressure narrows bronchioles – auscultate wheezing u Dyspnea & hypoxemia panic release of adrenaline increased work load on heart
Left Heart Failure u Sympathetic nervous system response – Peripheral vasoconstriction uperipheral resistance (afterload) increases uweakened heart has to pump harder to eject blood out through narrowed vessels ublood pressure initially elevated to keep up with the demands and to pump harder against increased vessel resistance udiaphoretic, pale, cold skin
Asthma or Heart Failure? Asthma Left heart failure u younger patient u older patient u hx of asthma u poss hx heart problems u unproductive cough u orthopnea u meds for asthma u recent rapid weight gain u wheezing u cough with watery or foamy fluid u accessory muscles being used u meds for heart problems u wheezing u JVD u Pedal or sacral edema
Which Came First - CHF or AMI? u Often hard to determine which came first and triggered the development of the other problem Heart failure poor perfusion & hypoxemia myocardium suffers from inadequate blood & oxygen supply acute myocardial ischemia acute coronary syndrome AMI poor pumping performance of heart acute failure of left heart pump left heart failure u Not unusual to see the AMI patient in pulmonary edema - watch for it!
Cardiogenic Shock u Heart extensively damaged; it can no longer function as a pump u 25% of heart damage causes left heart failure u >40% of the left ventricle is infarcted, cardiogenic shock occurs u High mortality rate
Signs & Symptoms Cardiogenic Shock u Altered level of consciousness – confusion to unconsciousness u Restless, anxious u Massive peripheral vasoconstriction – pale, cold skin, poor renal perfusion u Pulse rapid and thready u Respirations rapid and shallow u Falling blood pressure
Treatment Goals Acute Coronary Syndrome u Goals – early recognition of a possible cardiac problem – minimize size of infarction – reduce myocardial oxygen demand – decrease patient’s fear & pain (minimizes sympathetic discharge) – salvage ischemic myocardium – prevent development of dysrhythmias – improve chances of survival
Acute Coronary Syndrome u Oxygen – may limit ischemic injury u Aspirin - 324 mg chewed – blocks platelet aggregation (clumping) to keep clot from getting bigger – chewing breaks medication down faster & allows for quicker absorption – hold if patient allergic or for a reliable patient that states they have taken aspirin within last 24 hours
u Nitroglycerin 0. 4 mg sl every 5 minutes – dilates coronary vessels to relieve vasospams – increases collateral blood flow – dilates veins to reduce preload to reduce workload of heart – if pain persists after 2 doses, move to Morphine u Morphine - 2 mg slow IVP – decreases pain & apprehension – mild venodilator & arterial dilator ureduces preload and afterload – 2 mg slow IVP repeated every 2 minutes as needed, max total dose 10 mg
Treatment Goals Congestive Heart Failure u Goals – improve oxygenation – decrease workload of the heart (ie: preload & afterload)
Treatment Stable Acute Pulmonary Edema (B/P>100) u Nitroglycerin - 0. 4 mg sl – Vasodilator to create venous pooling – Reduces preload & afterload – Maximum 3 doses (repeated every 5 minutes) u Consider CPAP - use if indicated u Lasix - 40 mg IVP – Diuretic - excess fluid excreted via kidneys – Venodilating effect to pool venous blood – Dose to 80 mg IVP if patient on Lasix
u Morphine - 2 mg slow IVP – Venodilator to increase pooling of blood – Anxiolytic to calm anxious patient – May repeat 2 mg dose every 2 minutes – Maximum total dose 10 mg u Albuterol - 2. 5 mg/3 ml nebulizer – Wheezing may indicate bronchoconstriction from excessive fluid – Bronchodilator could be helpful u Hypotensive side effects – Treatment used (NTG, Lasix, Morphine, CPAP) can all cause venodilation B/P
Treatment Unstable Acute Pulmonary Edema (B/P<100) u Contact Medical Control u CPAP on orders of Medical Control u Consider Cardiogenic Shock Protocol u If wheezing (indicating bronchoconstriction), contact Medical Control for Albuterol order – if patient needs to be intubated, Albuterol to be delivered via in-line
Treatment Goals Cardiogenic Shock u Goals – Improve oxygenation – Improve peripheral perfusion – Avoid adding any workload to the heart
Treatment Cardiogenic Shock u Oxygen via nonrebreather mask – BVM if respirations ineffective – Intubation may become necessary u Positioning – Supine if lungs are clear – Head somewhat elevated if pulmonary edema is present (semi-fowler’s) u IV/IO fluid challenge in 200 ml increments if lung sounds are clear – The shock may include a hypovolemic component
Treatment Cardiogenic Shock u Cardiac monitor – Arrhythmias are likely u. May cause hypotension decreasing cardiac output u Dopamine Infusion - maintain B/P >100 – Effects dose related & dependent on clinical condition of patient – 5 - 20 g/kg/min has beta influence on the heart u. Increases contractility strength of heart u. To a lesser degree increases heart rate
u Dopamine cont’d – Doses >20 g/kg/min u. Alpha stimulation predominate & vasoconstriction my negatively affect circulation u Extravasation - leaking out of vessels – Can cause tissue necrosis – Report IV infiltration to ED staff & document u Dosing - start at 5 g/kg/min – Refer to table in SOP page 13 OR – Take patient’s weight in pounds, take 1 st 2 numbers, & subtract 2 (ie: 185 pounds: 18 - 2 = 16 gtts/min to start drip)
EKG Monitoring & 12 Lead EKG’s u Goal EKG monitoring – Identify a disturbance in the normal cardiac rhythm – Arrhythmias caused by u. Ischemia u. Electrolyte imbalances u. Disturbances or damage in electrical conduction system u Goal of obtaining 12 lead EKG – Early recognition Acute Coronary Syndrome u Treat clinical condition, not the monitor!
12 Lead EKG’s u Obtain and transmit to Medical control when you are following the Acute Coronary Syndrome SOP u Many patients can be monitored by a Lead II but not all patients need a 12 lead. u Some patients experiencing angina or an acute MI will not yet have any EKG changes indicated on the 12 lead.
A normal EKG DOES NOT necessarily mean there is nothing acute going on!
Cardiac Conduction System u SA node - dominant pacemaker – upper right atrium – blood supply from RCA u Internodal pathways – to spread electrical impulse thru-out atria u AV node in region of AV junction – in 85 -90% of people, blood supplied by RCA to AV node – in 10 -15% of people, blood supplied by left circumflex
Conduction System cont’d u bundle of His u Right and left bundle branches u Purkinje fibers - through ventricular muscle ª Changes in electrolyte concentrations influence depolarization and repolarization sodium (Na+), potassium (K+), calcium (Ca++), Magnesium (Mg++)
Conduction System L l Left bundle branches
EKG Wave Forms u. P wave – depolarization of atria u PR interval – depolarization of atria & delay at AV junction – normal PR interval 0. 12 - 0. 20 seconds u QRS complex – depolarization of ventricles – normal QRS complex <0. 12 seconds u. T waves – repolarization of ventricles (and atria)
EKG Wave Forms
The J Point J point - end of QRS complex & beginning of ST segment u ST segment elevation - evaluated 0. 04 seconds after J point u
Acute Myocardial Infarction Acute myocardial infarction (AMI) is part of a spectrum of disease known as acute coronary syndrome (ACS) u ACS – Larger term to cover a group of clinical syndromes compatible with acute myocardial ischemia – Chest pain is due to insufficient blood supply to the heart muscle that results from coronary artery disease (CAD) – Clinical conditions include unstable angina to non-Q wave MI and Q wave MI u
Preparation for 12 Lead EKG u Patient preparation – Relatively hairless surface clip hair if necessary so electrodes adhere – Clean and dry skin surface gently rub skin area with gauze pad w need to remove skin oils & dead skin if diaphoretic patient wipe with towel/gauze or use antiperspirant deodorant spray u Patient positioning – Preferably flat; if elevated note on EKG
12 -Lead Placement u Utilizes 10 electrodes attached in specific locations u 4 standard limb leads RA (right arm) LA (left arm) LL (left leg) RL (right leg) u Limb leads should be placed on limbs
Precordial Chest Leads For every person, each precordial lead placed in the same relative position V 1 - 4 th intercostal space, R of sternum V 2 - 4 th intercostal space, L of sternum V 4 - 5 th intercostal space, midclavicular V 3 - between V 2 and V 4, on 5 th rib or in 5 th intercostal space V 5 - 5 th intercostal space, anterior axillary line V 6 - 5 th intercostal space, mid-axillary
Precordial Leads
Lead Placement u The more accurate the lead placement, the more accurate the 12 -lead interpretation u 12 -leads are often evaluated on a sequential basis, each interpretation considering the previous one u V 4 -6 should be in a straight line
12 Lead Printout u Standard format 81/2 x 11 paper u 12 lead views printed on top half I a. VR V 1 V 4 II a. VL V 2 V 5 III a. VF V 3 V 6 u Additional single view of rhythm strips usually printed on bottom half u Machines can analyze data obtained but humans must interpret data
Limb Leads (Bipolar) Lead I - views the left (lateral) side of heart Lead II - views the bottom (inferior) side of heart Lead III - another inferior view of the heart
Limb Leads (Unipolar) u a. VR - view from right arm u a. VL - lateral view from left arm u a. VF - inferior view from left leg
Precordial (Chest) Leads Views the septal, anterior, & lateral portions of the
Heart in the Thoracic Cavity
Myocardial Insult u Ischemia – lack of oxygenation – ST depression or T wave inversion – permanent damage avoidable u Injury – prolonged ischemia – ST elevation – permanent damage avoidable u Infarct – death of myocardial tissue – may have Q wave
Evolution of AMI A - pre-infarct B - Tall T wave C - Tall T wave & ST elevation D - Elevated ST, inverted T wave, Q wave E - Inverted T wave, Q wave F - Q wave
ST Depression u Can indicate ischemia electrolyte abnormality rapid heart rate digitalis influence reciprocal changes to ST elevation u ST depression measurement – 1 mm (1 small box) below baseline measured 2 mm (2 small boxes) after end of QRS
ST elevation is more significant so should be looked for in opposite leads when depression noted
T Wave Inversion T wave represents ventricular repolarization – Normally upright in all leads except V 1 and a. VR Inverted T waves tend to represent ischemia Note T wave inversion a. VL, V 4 -6
ST Segment Elevation u Finding indicates injury or damage u Injury probably due to occluded coronary artery u Muscle can still be salvaged u If corrective intervention not taken in timely manner, tissue necrosis/death is likely (infarction) TIME IS MUSCLE!
Significant ST Elevation u ST segment elevation measurement – 0. 04 seconds after J point u ST elevation – > 1 mm (1 small box) in 2 or more contiguous chest leads (V 1 -V 6) – >1 mm (1 small box) in 2 or more anatomically contiguous leads u Contiguous lead – limb leads that “look” at the same area of the heart or are numerically consecutive chest leads
Contiguous Leads u Inferior wall: II, III, av. F u Lateral wall: I, a. VL, V 5, V 6 u Septum: V 1 and V 2 u Anterior wall: V 3 and V 4 u Posterior wall: V 7 -V 9 (leads placed on the patient’s back 5 th intercostal space creating a 15 lead EKG)
ST Segment Elevation
u u Coved shape usually indicates acute injury Concave shape is usually benign if patient is asymptomatic
Groups of EKG Leads u Inferior wall - II, III, a. VF u Septal wall - V 1, V 2 u Anterior wall - V 3, V 4 u Lateral wall - I, a. VL, V 5, V 6 u a. VR is not evaluated in typical groups u Standard lead placement does not look at posterior wall or right ventricle of the heart - need special lead placement for these views
Pathological Q Waves - Infarction u Death of tissue u Pathological Q wave – >0. 04 seconds wide or – 1/ of R wave height 3 – when seen with ST elevation indicates ongoing myocardial infarction u Remember: ST segment probably single most important element on EKG when looking for evidence of AMI
Pathological Q Wave
Acute MI Locator Table
Common Complications of AMI u V 1 -2: septal wall - infranodal heartblock, BBB u V 3 -4: anterior wall - LV dysfunction, CHF, BBB, 3 rd degree HB, PVC’s u I, a. VL, V 5 -6: lateral wall -LV dysfunction, AV nodal block in some u II, III, a. VF: inferior & posterior wall LV - hypotension, sensitivity to Nitroglycerin & Morphine
Reciprocal Changes u Changes seen in the wall of the heart opposite the location of the infarction u Observe ST segment depression u Usually observed at the onset of infarction u Usually a short lived change u Lead Reciprocal changes II, III, a. VF I, a. VL, V 5, V 6 II, III, a. VF V 1 -V 4 V 7 -V 9
Practice Identifying ST Segment Elevation > 1 mm (1 small box) in 2 leads from any group or 2 or more contiguous leads (>2 mm (2 small boxes) in limb leads considered alternative elevation by some) measured 0. 04 seconds after J point
Practice Identifying Leads Showing ST Elevation Evaluate the top 3 rows of the 12 -lead EKG Additional rows run rhythm strips
Think Pattern Recognition Inferior Wall MI
Think Pattern Recognition Lateral Wall MI
Think Pattern Recognition Anterior Wall MI
Think Pattern Recognition Septal Wall MI
Test Yourself What pattern would indicate an anterior/septal wall MI?
ST Elevation II, III, a. VF Inferior Wall Involvement
ST Elevation V 5, V 6, a. VL - Lateral
ST Elevation V 1 -V 4 - Ant/Septal
ST Elevation II, III, a. VF, V 6 Inferior & Lateral Wall
ST Elevation I, a. VL, V 2 -6
ST Elevation II, III, a. VF
Case Discussion #1 u 66 year-old male presents with “indigestion” for past 2 hours, frequent belching, nausea, paleness, diaphoresis, left arm discomfort u Vital signs – 102/76 HR 98 RR 20 u What Sa. O 2 98% is your impression and what initial treatment is indicated?
Case #1 u Impression: possible AMI u SOP: Acute Coronary Syndrome u Treatment: – IV-O 2 -monitor-pulse ox – Vitals stable – History unremarkable – Aspirin chewed (any contraindications? ) – Nitroglycerin sl (ask about Viagra use) – Morphine if pain unrelieved after 2 NTG – 12 lead to ED for interpretation
Case #1 12 -Lead
Case #1 u Impression of 12 lead? – no ST segment elevation noted u Does lack of ST segment elevation change field treatment for this patient? – Normal EKG does not preclude that acute myocardial event is occurring – Acute Coronary Syndrome SOP to be followed
Case Discussion #2 u 77 year-old female with history of CABG, hypertension, cholesterol, and long standing diabetes u Presents with vague complaints of not feeling well, very tired & no energy over the last day u Meds: – Aspirin, Isoptin, Toprol, Hydrochlorothiazide, Lipitor, Glucophage
Case #2 u Vitals: 110/72 HR-72 RR-18 Sa. O 2 97% u Monitor (lead II rhythm strip):
Case #2 u What is your initial impression? u Need to at least consider possible MI u Remember: – women, elderly, and long standing diabetics report the most atypical complaints u Remember: – a lead II only looks at one view of the heart – a normal EKG does not rule out AMI
Case #2 u Treatment: – IV-O 2 -monitor-vitals – Aspirin appropriate? – Nitroglycerin indicated? – 12 lead EKG necessary? – What about antidysrhythmic for the PVC’s? ucall Medical Control for guidance uoxygen is often enough to suppress PVC activity
Case #2 u Aspirin – if patient reliable and took own dose within last 24 hours, can omit, document why omitted and when taken u Nitroglycerin – patient not having chest pain. Defer to Medical Control for orders – no contraindications noted (B/P >100; no viagra type drug used within past 24 hours - ask, don’t assume!) u 12 lead should be obtained on high index of suspicion
Case #3 u 81 year-old female complaining of shortness of breath for past 2 days. Unable to tolerate lying flat; JVD noted u History of CHF, angina, arthritis, and mild COPD u Vitals: 126/92 HR-170 RR-24 Sa. O 2 97% u Medications: nitroglycerin PRN, – Lasix 40 mg daily – Potassium – Aspirin, one daily – Proventil inhaler PRN
Case #3 - What is this rhythm?
u Rhythm Case #3 Rapid atrial fibrillation u Initial impression? Rapid atrial fibrillation u heart rate ineffective pumping cardiac output u Treatment initiated IV-O 2 -monitor-vitals-history u Goal of therapy - slow down heart rate u Is patient stable or unstable? – Stable - B/P >100, alert & cooperative
Case #3 u ALS Treatment – If Diltiazem not available, then what? u Verapamil – 5 mg IVP slowly over 2 minutes – If no response after 15 minutes and B/P remains >100, repeat 5 mg slow IVP u Carefully monitor patient for development of further deterioration and increased difficulty breathing u Position of comfort - usually sitting up
Verapamil / Isoptin® Action u Calcium channel blocker u Slows conduction thru AV node to control ventricular rate u Relaxes vascular smooth muscle u Dilates coronary arteries
Verapamil Indications u Alternative to Diltiazem/cardizem u SVT not responsive to 2 doses of Adenosine - to terminate rhythm u Stable rapid atrial flutter/fibrillation to control heart rate Dosing u 5 mg IVP slowly over 2 minutes u If no response after 15 minutes and B/P >100, may repeat Verapamil 5 mg IVP slowly over 2 minutes
Verapamil Side Effects u Headache, dizziness u B/P from vasodilation u nausea & vomiting Contraindications u B/P u Wide complex tachycardias of uncertain origin u Heart block without implanted pacemaker u WPW, short PR & sick sinus syndromes
Case #4 u 32 year-old male patient with complaints of chest tightness, shortness of breath, and just not feeling well for past 2 days. Also states sore throat and ear pain. Very anxious & scared. u No history, no meds u Jogs 2 -3 miles 5 times per week u Vitals: 110/70 HR-68 RR-20 Sa. O 2 98% u Lungs clear; skin warm, dry & pink
Case #4 u Initial impression Cardiac? Musculoskeletal (what has patient been doing)? Viral illness (sore throat & ear pain)? u What treatment would you begin? Cardiac - can give Aspirin but call Medical Control for NTG or Morphine Normal EKG cannot rule out ACS process
Case #5 u 68 year-old male called 911 due to non -radiating chest discomfort (not relieved with 3 of the patient’s own nitroglycerin) with some minor shortness of breath u History: – stable angina – GERD – hypertension (controlled with medications) – Type II diabetic (recently diagnosed)
Case #5 u Allergies - aspirin u Medications – nitroglycerin PRN – isordil – nexium – verapamil – glucophage u Vital signs – 136/78 HR-78 RR-18 Sa. O 2 99% u What is your initial impression & what treatment is initiated?
Case #5 Initial impression: acute coronary syndrome u IV-O 2 -monitor-vitals & history u Lead II EKG strip: u
u You have just hooked the patient for a 12 lead EKG and they grabbed their chest and became unresponsive
Case #5 u What is this rhythm strip? u What action needs to be taken by EMS?
Case #5 u Confirm no breathing, no pulse u Begin CPR until the defibrillator is ready and is charged to maximum joules u Clear the patient & deliver 1 shock u Immediately resume CPR for 2 minutes (5 cycles of 30: 2) u Check rhythm, defibrillate u Meds: vasopressor (Epinephrine) antidysrhythmic (choose 1) u 1 shock in between meds & 2 min CPR
VF/Pulseless VT Meds u Epinephrine 1 mg every 3 -5 minutes IV/IO for duration of arrest u Antidysrhythmic: Amiodarone 300 mg IV/IO 1 st dose OR Lidocaine 1. 5 mg/kg IV/IO 1 st dose u Repeat dose antidysrhythmic x 1 in 5 min: Amiodarone 150 mg IV/IO OR Lidocaine 0. 75 mg/kg IV/IO
Antidysrhythmics in VF/VT u Amiodarone to the vein) needs to be diluted (irritable – total of 20 ml syringe (med mixed with saline) – rapid push in VF/VT (slow if pt has pulse!) u Lidocaine - – if unsuccessful defibrillation ucontact Medical Control for 3 rd dose order – if defib successful & bolus given < 10 min, begin drip 2 mg/min (30 mcgtts) – if defib successful & bolus given >10 min, give Lido 0. 75 mg/kg IV/IO & start drip
Case #5 The patient was defibrillated twice and received 1 dose of epinephrine u After the 3 rd shock, 2 minutes of immediate CPR resumed u After 2 min of CPR, what is the rhythm? u
Case #5 u Rhythm: sinus rhythm u EMS action? – Determine if there is a pulse (yes!!!) – Reevaluate airway, breathing, circulation-B/P – Medications: ubecause no antidysrhythmic were given, need to call Medical Control for direction if Lidocaine, usually 0. 75 mg/kg IV/IO if Amiodarone, 150 mg diluted into 100 ml bag D 5 W; run thru mini-drip tubing; run piggyback at rapid drip over 10 minutes u. May not want any antidysrhythmic given
Medication Administration u 6 medication rights right patient right medication (check 3 times) right dose right time right route right documentation (time, drug, dose, route, response)
ETT Route u Endotracheal tube route is discouraged, not eliminated. u Absorption found to be unpredictable u ETT route L - Lidocaine E- Epinephrine A- Atropine N - Narcan u Double the calculated amount for the IV/IO route
SOP Test u Will be given during May, 2007 CE u Similar to November, 2006 SOP exam u Will test knowledge of entire SOP u Start to review revised SOP’s now u No Jeopardy before the May test
Bibliography u American Heart Association Guidelines CPR ECC 2005 u Beasley, B. , West, M. Understanding 12 Lead EKG. Pearson Ed, 2001. u Caroline, Nancy. Emergency Care in The Streets, Jones & Bartlett, 2008. u Page, B. 12 -Lead EKG, Pearson, 2005. u Phalen, T, Aehlert, B. The 12 -Lead EKG in Acute Coronary Syndromes, 2006. u www. clevelandclinic. org u www. nhlbi. nih. gov/health/dci/Diseases
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- Environmental emergencies emt
- Chapter 23 gynecologic emergencies
- The term "behavioral crisis" is most accurately defined as:
- Chapter 18 neurologic emergencies
- Chapter 16 respiratory emergencies
- Leukostasis symptoms
- Chapter 35 geriatric emergencies
- Chapter 13 handling emergencies
- Chapter 12 behavioral emergencies
- Chapter 32 environmental emergencies
- Psychiatric emergency
- Qut security emergency extension number
- Immunologic emergencies
- A 41 year old man presents with slow irregular breathing
- Anatomy and physiology unit 7 cardiovascular system
- Cardiovascular system diseases and disorders chapter 8
- Burlington aprons
- Difference between medical report and medical certificate
- Blood vesel
- Riesgo cardiovascular por perimetro abdominal
- Azoulay maniobra
- What makes up the circulatory system
- Rutas integrales de atencion en salud
- Pithed model
- Fresenius national cardiovascular partners
- Cardiovascular/lymphatic system it's totally tubular
- Cardiovascular drift
- Structure of blood vessels
- Cengage chapter 5
- Chapter 46 the child with a cardiovascular alteration
- Chapter 26 the child with a cardiovascular disorder
- Chapter 25 assessment of cardiovascular function
- Figure 11-9 is a diagram of the hepatic portal circulation
- Figure 11-8 arteries
- Chapter 11 the cardiovascular system
- Lesson 11 cardiovascular system
- American board of cardiovascular medicine
- Advanced cardiovascular life support
- Receptores sensoriales
- Circulatory system tissue
- Hypertensive atherosclerotic cardiovascular disease
- Vasos sanguineos
- Cardiovascular research institute basel
- Introduction of cardiovascular system
- Halimbawa ng cardiovascular endurance
- Cardiovascular system
- Salud cardiovascular
- Mapeh grade 7 health
- Salud cardiovascular
- Cuestionario aha/acsm
- Chapter 7 cardiovascular fitness
- Chapter 13 cardiovascular system
- Rosita rodriguez
- Aparato cardiovascular
- Sistema cardiovascular
- Pequena circulação e grande circulação
- Cardiovascular disorders
- Prairie cardiovascular consultants springfield il
- Amit pursnani
- Blood vessels
- Sistolw
- Chapter 11 the cardiovascular system figure 11-2
- The cardiovascular system includes the
- Veias
- Sistema cardiovascular quiz
- Cardiovascular disease risk factor
- Cardiovascular endurance frequency
- Sistema cardiovascular
- Clinica cardiovascular santa maria
- Major arteries
- Onda p
- Bhf glasgow cardiovascular research centre
- Chapter 26 the child with a cardiovascular disorder
- Chapter 19 the cardiovascular system blood vessels
- Cmqcc cardiovascular toolkit
- Ptal california medical board
- Gbmc medical records
- Torrance memorial map
- Cartersville medical center medical records
- How can anger and revenge lead to fights
- Solubility chart
- Body of news report
- Astonisher lead examples
- Was ist eine opportunity
- Secondary headline
- Net ionic equation vs total ionic equation
- Relieving prism
- Lead sheet symbols and figured bass
- Staccato lead in journalism
- Strong leads in narrative writing
- Signal phrases
- Where you lead me i will follow
- Lead time in community medicine
- Weichert lead network
- Pica jopo sting
- Outer fringe vision
- Lead quote
- Lead free control plan
- What is anecdotal lead
- Lead tipped whip
- Einthoven triangle
- Example of clincher sentence
- Narrative lead
- Learn to lead chapter 6
- Army applemdt
- Transvenous vs transcutaneous pacing
- Latent heat of lead
- Contoh gambar piramida terbalik
- Example of summary lead
- Lead time bias vs length time bias
- Iodide solubility
- Relazione finale dad scuola dell'infanzia
- Lead time in community medicine
- Length bias vs lead time bias
- R on t wave
- Length bias vs lead time bias
- Efes final expense
- Mcs weebly
- Contoh lead reportase
- Match pace lead
- Lead time bias คือ
- Lead(ii)nitride
- Rop formula
- Catenation property
- Lead passive voice
- Short sentence lead
- Know yourself to lead yourself
- Blood lead concentration
- Lead poisoning children
- Qu es una noticia
- Lead chamber process
- Easi lead placement
- Feature leads examples
- Michigan lead safe home program
- Jira project lead