Copy of Module 3 EKG-circulatory shock.docx

Pathophysiology I (PA521) Exam 3 Objectives CIRCULATORY SHOCK: Describe the characteristics of the compensated, decompensated, and irreversible stages of shock. Compensated stage Neurohormonal mechanisms are activated to maintain CO and BP such that vital organ perfusion is maintained = ta...

Pathophysiology I (PA521) Exam 3 Objectives CIRCULATORY SHOCK: Describe the characteristics of the compensated, decompensated, and irreversible stages of shock. Compensated stage Neurohormonal mechanisms are activated to maintain CO and BP such that vital organ perfusion is maintained = tachycardia, peripheral vasoconstriction, decreased urinary output, cutaneous vasoconstriction Decompensated stage Tissue hypoperfusion and onset of worsening circulatory and metabolic derangement, including acidosis In prolonged hypoxic state, compensatory mechanisms are overwhelmed, anaerobic intracellular metabolism takes over= lactic acid formation= lowers tissue pH which blunts vasomotor response= arterioles dilate and blood begins to pool in the microcirculation= worsened CO Signs of organ dysfunction (brain kidneys, heart) and DIC; may be reversible with aggressive intervention 15-25% blood volume lost Irreversible stage Cell and tissue injury is so severe that death is inevitable Leakage of fluid and protein into extracellular space (edema) Metabolic acidosis= mitochondrial dysfunction and cell death Severe tissue ischemia from inadequate blood flow Damage to capillary endothelial cell of kidneys, liver, and lungs Bacterial invasion in GIT Acute renal insufficiency= oliguria Describe the compensatory responses that occur in nonprogressive shock: tachycardia, increased TPR Decreased CO= tachycardia (increased HR) to make up for the decreased blood TPR is increased from peripheral vasoconstriction why is the skin pale, cool, and moist? Compensatory reflex for decreased CO and BP= cutaneous vasoconstriction in order to pump most of blood to vital organs. Skin is then cold, pale, and moist what happens to the renal, GI, GU, and skeletal muscle circulations? Increased TPR in renal, skeletal muscles, and visceral circulations what happens to the cerebral and coronary circulations? Coronary and cerebral vessels are less sensitive to vasoconstricting neurohormones due to wanting to maintain brain and heart perfusion why does decreased urinary output occur? Renal has increased TPR and vasoconstriction to keep water in body Identify the following causes for the types of shock: cardiogenic: AMI, CHF, arrhythmias, massive PE, cardiac tamponade, venous obstruction Most common cause is LV dysfunction and necrosis as result of AMI From Reduced cardiac output or depressed systolic cardiac function (EF<20%) NOT CAUSED BY REDUCED BLOOD VOLUME (HYPOVOLEMIA) hypovolemic: hemorrhage, diarrhea, dehydration, heat stroke, burns, trauma Shock secondary to profound decrease in blood volume caused by fluid loss from the vascular compartment= severely reduced intravascular volume MOST COMMON cause is hemorrhage secondary to trauma Treat with IV fluids or possible blood transfusion Hemorrhagic factors GI bleed Trauma Internal bleeding/hemorrhage Nonhemorrhagic factors Burns dehydration= vomiting, diarrhea sequestration= ascites, third-space accumulation septic: g- infection with release of endotoxin Endotoxemia due to gram-neg or other overwhelming infection Septic shock= persistence of severe sepsis despite adequate fluid resuscitation sepsis= life threatening organ dysfunction caused by dysregulated host response to infection Severe sepsis= organ dysfunction, hypoperfusion, or hypotension Only shock that produces a fever neurogenic: general anesthesia, cerebral ischemia, overdoses of CNS depressants Increased vascular capacity with no loss of blood volume Increased vascular capacity to such an extent that normal blood volume cannot fill circulatory system Caused by sudden loss of vasomotor tone= massive venodilation= decreased VR due to venous pooling anesthesia= depressed vasomotor center= vasomotor collapse Cerebral ischemia (over 5-10 min)= inactive vasomotor neurons Overdose of CNS depressants= depressed vasomotor center anaphylactic: IgE-mediated type I hypersensitivity; role of histamine Aka systemic inflammatory response syndrome? (SIRS) Inflammatory cytokines are produced by the body in response to ischemia, injury, or infection ????? State the three major events in the pathogenesis of shock. Common chain of events regardless of etiology Decreased CO Decreased tissue perfusion Hypoxic cell injury Explain the concept of the “vicious cycle” and how it leads to irreversible shock: endothelial damage= increased vascular permeability= increased exudation of fluid from circulation decreased circulating blood volume- caused by above increased anaerobic glycolysis and lactic acid production- due to above decreased renal perfusion- caused by decreased blood flow. Inability to excrete H- metabolic acidosis-due to inability to excrete H- hypoxic injury to cardiac cells= decreased contractility= decreased CO and perfusion Describe the effects of shock states on body temperature. Explain the mechanism and clinical features of septic shock. Septic shock caused by bacteria Proinflammatory mechanisms “endotoxin shock” direct= bacteria directly enter bloodstream and trigger inflammatory response indirect= bacteria can release endotoxins that binds to circulating defense cells (macrophages, dendritic cells)= trigger for inflammatory cytokines Procoagulant mechanisms Presence of cytokines and endothelial injury triggers release of tissue necrosis factor (TNF)= increased risk of thrombus which can lead to hypoperfusion and tissue ischemia Normal homeostatic mechanisms are dysfunctional in septic patients (fibrinolysis) Clinical features usually presents within 24-hours of bacteremia Fever, chills, N/V/D, vasodilation, endotoxin effects (anaphylaxis, depression of contractility), and disseminated intravascular coagulation (DIC) DIC a rare but serious condition that causes abnormal blood clotting throughout the body's blood vessels Increases thrombin and fibrinogen= microvascular thrombosis Fibrinolytic system then activated= leads to hemorrhage Increase platelet aggregation and deposition in microcirculation= thrombocytopenia= hemorrhage Describe the role of the following therapies in the treatment of shock: replacement therapy (whole blood or plasma), plasma expanders, glucocorticoids. Overall goal is to increase CO Replacement therapy= IV fluids and PRBCs Used for hypovolemic patients, PRBCs/blood tranfusion good for hemorrhagic Plasma expanders Used for hypovolemic patients Glucocorticoids Steroids stabilize lysosomal membrane and prevent release of enzymes Glucocorticoids and antihistamines have been used as adjunctive therapy when no response to other pharmacologic agents Antihistmamine + EPI good for anaphylactic shock State which types of shock may be effectively treated by sympathomimetics and explain why sympathomimetics have little to no value in hemorrhagic shock. Inotropic agents or vasopressors used when volume resuscitation is inadequate to maintain perfusion neurogenic= counters depression of SANS anaphylactic= produces vasoconstrictor effect to oppose vasodilatory effects of histamine sympathomimetics= EPI, NE, phenylephrine, dobutamine, dopamine Sympathomimetics have no value to hemorrhagic shock since SANS is already maximally active State the two drug therapies effective in anaphylactic shock and explain why they are effective. Antihistamine + EPI good for anaphylactic shock. produces vasoconstrictor effect to oppose vasodilatory effects of histamine HEART SOUNDS, VALVULAR DISEASE: Define the terms “stenosis” and “regurgitation”. Stenosis Leaflets adhere to each other such that flow is blocked Narrowing of valve orifice that impedes the forward flow of blood Regurgitation Leaflets are destroyed by scar tissue and won’t close Allows backflow Explain the mechanisms for production of the four types of heart murmurs, and state the descriptions of these murmurs (systolic or diastolic, duration, crescendo or decrescendo, shape of tracing): aortic stenosis Loud systolic crescendo-decrescendo murmur Blood ejected through stenotic valve at high velocity which causes severe turbulence and severe vibrations= loud murmur Heard best at RSB 2nd ICS, can hear in carotids aortic regurgitation Pandiastolic murmur Blood flows backward into LV and mixing with residual blood mitral stenosis 2 murmurs Mid Diastolic murmur occurs during rapid passive filling stage= decrescendo Presystolic murmur occurs during atrial contraction= crescendo LA does not have high enough pressure to cause high velocity= low rumbling mid diastolic murmur during first ⅔ of diastole mitral regurgitation Pansystolic murmur Backflow of blood from LV into LA during systole Describe how stroke volume (SV) and cardiac output (CO) are affected in aortic stenosis and in aortic regurgitation. SV and CO both decreased in AR and AS explain the compensatory responses LVH due to increased LV workload. Muscle mass of LV may increased up to 4-5x Increased blood volume Low CO= low BP and decreased renal perfusion RAAS will decrease renal perfusion to increase BP explain what ultimately happens to LV function and left atrial pressure (LAP) Ultimately, the compensatory responses are not enough to meet metabolic demands After time, LV will become dilated, LAP will increase, then pulmonary edema will follow state the consequences for the pulmonary system. Leads to pulmonary edema Explain why angina is frequently an outcome of either aortic stenosis or regurgitation. AS High intraventricular pressure increases workload of heart= compressed coronary vessels with little to no coronary blood flow during systole LVH may have deficiency coronary circulation Greatly decreased pulse pressure AR DBP may fall very low due to regurgitation= inadequate coronary blood flow Particularly damaging for subendocardial muscle which receives no flow in systole Describe the effects of aortic stenosis on intraventricular pressures. Very high intraventricular pressures may develop (200mmHg at rest, 400mmHg during activity) in order to eject blood through the narrowed orifice= compressed coronary vessels Describe how pulse pressure is affected in aortic stenosis and in aortic regurgitation. AS: ventricular systolic pressure much higher than arterial systolic pressure AR: arterial pressures have wide pulse pressures: 180/50 Systolic pressure increased due to backflow increases next SV Very low diastolic arterial pressure Explain how LAP is affected in both mitral stenosis and regurgitation, and why atrial arrhythmias may occur in these conditions. Stenosis impedes the filling of ventricles so that a pressure gradient develops between atria and ventricles during diastole= high atrial pressure and lower ventricle pressure Regurg allow blood to flow from the ventricles to atria during systole= high atrial pressure Consequences: Increased LAP up to 40mmHG= pulmonary edema LA dilation= can cause disruption of electrical circuits= AFIB State the compensatory mechanisms in both mitral stenosis and regurgitation. Decreased renal perfusion activates RAAS= increase blood volume to increase VR= help to restore CO Hypertrophy of right side of heart NORMAL EKG: Describe the charges on the inner and outer membrane surfaces of excitable cardiac cells in the following states: polarized, depolarized, repolarized. Polarized (resting state) Inner surfaces of atrial and ventricular muscle fiber membranes (sarcolemma) are negatively charged with a resting membrane potential of -85 to -95 mV Outer membrane surface is positively charged Depolarized Due to action potential, membrane reverses its charge Interior becomes positively charged and outer surface is negatively charges Repolarized Recovery from state of depolarization Outer membrane positively charged For each fo the following components of the electrocardiogram (EKG), describe a) the electrical event represented; b) the resulting contractile state of the tissue; c) beginning and ending points when applicable: P wave Atrial depolarization just prior to atrial contraction PR interval Normal range 0.12-0.20 Begins at start of P wave ends at start of QRS complex This is the time for conduction through atria, AV node, AV bundle, and bundle branches PR segment End of P wave to start of QRS Used to determine baseline of EKG QRS complex Ventricular depolarization prior to ventricular contraction Beginning of Q wave to end of S wave Normal 0.06-0.12 ST segment From end of QRS to start of T wave Entire ventricle is depolarized. This is the time between depolarization and repolarization J point Point at which QRS complex ends and ST segment begins T wave Ventricular repolarization QT interval Beginning of QRS to end of T wave (onset of ventricular depolarization to end of ventricular repolarization) Reflects action potential duration in ventricular muscle cells normal=0.35 sec Define the terms “isoelectric line” and “action potential duration” and explain how they are represented on the EKG. Isoelectric line= no deflection from baseline is recorded in the EKG. this is when all parts of ventricles is at same electrical potential (completely depolarized) State the condition that must exist with regard to polarization state in order for deflections from baseline to occur on the EKG. In order for current to flow and reach the body surface (and be recorded on EKG), the muscle must be partly polarized and partly depolarized= therefore, current must be flowing Describe the relationships between electrical and mechanical activity in the P wave, QRS complex, and T wave. State the direction of current flow on the outer membrane surface of excitable cardiac cells, and the direction (anatomical regions) of the net averaged current flow in the heart. Be able to explain: the diagrams in the Notes that summarize direction of depolarization and current flows for ventricular depolarization (R wave) and repolarization (T wave) the rationale that explains why the R wave and the T wave have the same polarity in the EKG Explain why the Q and S waves cause negative deflections on the EKG. Q wave is negative due to initial depolarization of the left side septum before the right side. This created a weak, momentary direction of current flow from left to right before the usual base-to-apex depolarization S wave is negative because just before depolarization is complete, the average current flow is reversed: flowing apex to base Know the names for the bipolar limb leads Lead I: RA (-) and LA (+) 0 degrees Lead II: RA (-) and LL (+) 60 degrees Lead III: LA (-) and LL (+) 120 degrees augmented unipolar limb leads aVR: LA (-), LL (-), and RA (+) 210 degrees aVL: RA (-), LL (-), and LA (+) -30degrees aVF: RA (-), LA (-) and LL (+) 90 degrees precordial leads V1 V2 V3 V4 V5 V6 State which of the 12 EKG leads fits the following descriptions and explain the reasons: the bipolar lead that gives the strongest positive QRS deflection Lead II gives strongest positive QRS deflection because its vector axis of 60 degrees is closest to the axis of mean vector which is 59 degrees the augmented unipolar lead that gives a negative QRS deflection aVR because the positive is on the right arm while negative is on the left side. Ventricular depolarization occurs in the opposite direction. the twp precordial leads that give negative QRS deflections V1 and v2 exhibits negative QRS since the chest electrode is nearer to the base of the heart than the apex the two precordial leads that give positive QRS deflections. V5 and V6 are oriented over the left side of the heart, since depolarization wave moves from base (right) to apex (left), the QRS is positive VECTOR ANALYSIS OF EKG: Remember all the details concerning the representation of currents in the heart by vectors: the head (or arrow) of the vector always points towards the positive direction, that is, the direction in which the excitable cells still have positive charges on their outer membrane surfaces and are waiting to be depolarized (or have been repolarized) the tail (or origin) of the vector always points towards the negative direction, that is, the direction in which the excitable cells have negative charges on their outer membrane surfaces; this corresponds to the depolarized state the mean QRS vector for ventricular depolarization is in a direction from base (upper right) to apex (lower left) with the origin at the AVN Explain the terms frontal plane and horizontal plane and list the EKG leads which are represented in each plane. Explain the statement “in the ventricles, last depolarized is first repolarized”. Typically, first depolarization is first to repolarize but after depolarization occurs, the ventricular muscle contracts causing compression of blood vessels that perfuse the heart= reduction in blood flow. Blood flow reduction is greatest at the base of the heart. Blood flow is needed to repolarize ( which base does not have yet) so the apex repolarizes first. This is why repolarization is an upward reflection on the EKG Locate the sites in the EKG where the following events occur: beginning of repolarization Occurs at the ST segment repolarization is 50% complete Occurs at the peak of T wave completion of repolarization Completed in T-P interval Explain the statement “in the atria, first depolarized is first repolarized”, and describe the atrial T wave. Depolarization begins in SA node and spreads in all directions- then SA node is first to repolarize Atrial T wave is a negative deflection because of this (not usually seen because of QRS State examples of disease conditions in which either left or right ventricular hypertrophy occurs. Discussed below with R and L axis deviation Explain why the axis of the mean vector for the heart shifts towards a: hypertrophied ventricle. Greater amount of muscle on the hypertrophies side generates larger currents More time is required for the depolarization wave to travel through the hypertrophied ventricle; therefore, the normal ventricle depolarizes far ahead of the hypertrophied side= axis deviation Left axis deviation= LVH Caused by HTN, AS, AR, congenital heart conditions -15 degrees Right axis deviation= RVH Caused by PS, tetralogy of Fallot, interventricular septal defect, increased pulmonary vascular resistance (pulmonary HTN) 170 degrees bundle branch blocked ventricle. If one bundle branch is blocked, the cardiac impulse travels through the normal ventricle long before the abnormal ventricle; therefore, depolarization of the two ventricle does not occur at the same time QRS prolonged in both Left axis deviation in LBBB RV becomes negative while LV remains positive. Vector will point to positive (LV) -50 degrees Right axis deviation in RBBB LV depolarizes far ahead of RV= strong vector toward positive (RV) 105 degrees Describe how the QRS complex is altered in bundle branch block, and the separation of peaks often observed. QRS prolonged Double R peaks Define the term “isoelectric lead” in the horizontal plane under normal conditions, and which precordial leads become the isoelectric lead in right or left axis rotation. V2 is normally negative V3 and V4 are approximately equal in positive and negative deflection (isoelectric QRS leads) Isoelectric lead= positive of QRS and negative of QRS are equal heights If isoelectric in V1 or V2= right axis deviation If isoelectric in V5 or V6= left axis deviation Define the term “current of injury” and explain its most common cause. Injury to the heart muscle may cause partial or total depolarization at the injured site to occur all the time with current always flowing from the area of injury (depolarized) to the normal muscle (polarized). Injured portion of muscle is negative since it is partially or totally depolarized all the time Causes Mechanical trauma Infectious disease Local ischemia (MOST COMMON) Infarct area which has lost its perfusion is electrically neutral and cannot depolarize; the mean QRS vector points away from the infarcted area since it cannot contribute to the mean vector for depolarization State whether a current of injury can be detected in the following during: the T-P interval Repolarization is completed when repolarization is complete Depolarization Flows from ischemic area toward rest of ventricle. All ventricular muscle becomes negative when depolarization is complete and no current flows including current of injury when depolarization is complete Repolarization occurs and becomes complete except permanently injured Define the “J point”, how it is used to determine current of injury, and how current of injury is related to the ST segment. J point is a zero reference potential for analyzing current of injury Located at the beginning of the ST segment Determine the exact point at which the depolarization wave just completes its passage through the heart (at end of QRS). all parts of the muscle, normal or injured, are depolarized and no current is flowing Zero voltage exists at this J point which is the junction point of the QRS wave and the ST segment J point is where there is no charge, if at any point the J point is not on the same line as the T-P segment, then a current of injury exists: will see a ST segment shift (elevation or depression) Explain how the mean vector is deviated in the presence of infarcted cardiac muscle. Infarct area which has lost its perfusion is electrically neutral and cannot depolarize; the mean QRS vector points away from the infarcted area since it cannot contribute to the mean vector for depolarization Explain why T-wave inversion occurs in: bundle branch block BBB causes slow conduction When conduction of the depolarization wave through the ventricles is greatly delayed, the T wave is of the opposite polarity (inverted) to the QRS complex ischemia at the apex of the heart Most common cause of prolonged depolarization When ischemia occurs, the time for depolarization for this area increases out of proportion to any other area If the apex required an abnormally long period for depolarization, then repolarization will not occur in the usual apex to base sequence Base will repolarized before apex and vector for repolarization would point from apex toward base= inverted T EKG IN ISCHEMIA & INFARCTION State the: two principal EKG findings during an ischemic episode in a patient with stable angina May appear normal but if not: Significant Q waves suggest previous MI ST segment depression T wave inversion the usual EKG findings occurring in unstable angina patients during nonischemic periods and during ischemic episodes Nonischemic periods May be normal Exhibit nonspecific ST segment T wave changes May exhibit Q waves from previous MI Ischemic periods ST segment deviations T wave changes (flattening or inversion) usually transient Persistence of T wave changes after 12 hrs indicate non-q-wave MI the principal EKG change occurring in variant (Prinzmetal’s) angina Vasospastic angina? ST segment elevations during ischemia Prolonged, severe ST elevations may results in MI, conduction disturbances, or Vtach May be asymptomatic and detectable by holter EKG Describe the evolutionary changes in the EKG that take place during Q-wave MI. Presence of significant Q waves enables the diagnosis of MI Disregard aVR Q wave indicated necrosis Evolutionary changes Tall T wave (hyperacute) ST segment elevation (acute) Appearance of abnormal Q waves Decrease ST elevation with beginning of T wave inversion (days 1-2) Isoelectric ST segment with symmetrical T wave inversion Q waves persist, ST and T normal Describe how the ST segment is usually altered during acute transmural and subendocardial infarctions. Transmural infarcts Abnormally tall T waves (hyperacute) followed by T-wave inversion Subendocardial infarctions Type of non-Q-wave infarction that does not extend through gull thickness of LV wall An exploring electrode is separated from the injured area by normal epicardial layer Epicardial layer becomes electrically more negative that the injured subendocardium at the end of depolarization= a relatively negative potential= ST segment depression Describe how the ST segment is altered during: Pericarditis ST segment elevation that is flat or concave that resolves with time. digoxin (digitalis) therapy ST segment depression exercise-induced ischemia ST segment depression For the following types of AMIs, state the most common EKG findings: anterior infarction Q waves in V1, V2, V3, or V4 Due to occlusion of anterior descending branch of left coronary artery lateral infarction Q wave in I and aVL Due to occlusion of circumflex branch of left coronary artery ARRHYTHMIAS: List the principal causes and describe the EKG characteristics and treatments for sinus tachycardia and sinus bradycardia. Sinus tachycardia EKG rate>100 bpm Originates from SA node Normal EKG waveforms Caused by: sympathetic stimulation Any decline in BP significant enough to elicit reflex tachycardia Circulatory shock Drug-induced (vasodilators) thyrotoxicosis Conditions which elicit compensatory sympathetic responses HF AMI Treatment Treat underlying cause Negative chronotropic agents (decrease HR) BB CAUTION: HF patients may be dependent on sympathetic drive for CO. may need to start BB at lower dose a titrate up Sinus bradycardia EKG rate<60 bpm Regular rhythm originating from SA node Normal waveforms Caused by: vagal stimulation Parasympathetic stimulation decreases HR Carotid sinus syndrome Atherosclerosis causes excessive sensitivity of carotid sinus baroreceptors Mild pressure applied to the neck elicits a strong baroreceptor reflex causing intense vagal stimulation= extreme bradycardia or even decreased CO Treatment: If CO is inadequate, pacemaker required Describe the characteristics and EKG features of SA nodal block and sick sinus syndrome (SSS), and describe how these conditions are treated. SA nodal block EKG Sudden disappearance of P waves, atrial standstill Caused by: Usually not ischemia related Fibrosis, cardiomyopathy of SA node Iatrogenic (digoxin, CCB, BB, some antiarrhythmics) If atrial systole permanent, AV node will take over= normal QRS with normal T Wave of same polarity If atrial systole is temporary, There will be 1 or more missed cycles with no P waves followed by SA node resuming pacemaker activity If pause is long enough, overdrive suppression will disappear and an AV nodal rhythm may appear as an escape rhythm Treatment Pacemaker is symptomatic (dizziness, syncope, HF) Sick sinus syndrome (SSS) SA nodal dysfunction associated with unresponsive atrial and junctional automaticity foci, which also fail to function as pacemakers EKG: Irregular rhythm with marked sinus bradycardia and no escape mechanisms in any supraventricular foci Etiology: Elderly with heart disease Young, well condition subjects with PNS hyperactivity Treatment Pacemaker if symptomatic List the four types of atrioventricular (AV) block. 1st degree block Lengthens interval between atrial and ventricular depolarizations= prolonged PR interval in all cycles Second degree Some atrial depolarization (p wave) are allowed to pass to ventricles while others are blocked= “dropped beat” Second degree type 1 (wenckebach) This occur IN the AV node Abnormal conduction in AV node, usually due to parasympathetic excess or drugs that intensify vagal effect Progressive lengthening of the PR interval with each beat until an impulse cannot be conducted= last p wave stands alone Second degree type 2 (mobitz II) This occurs BELOW the AV node= AV conduction system block May be blocked within bundle of his or bundle branches Will have widened QRS if blocked within bundle branch Produces a series of normal P wave conductions preceded by p waves that fail. Each repeating series has consistent P:QRS ratio=regular rhythm like 2:1, 3:2, 3:1 Differentiate between type 1 and type 2 Type 1: long PR, normal QRS Type 2: normal PR, wide QRS 3rd degree AV dissociation Complete block in upper AV node Automaticity in AV junction escape overdrive suppression and pace the ventricles- 40-60bpm, will have normal QRS Complete block of AV or bundle of His Ventricles must pace themselve= 20-40 bpm with wide QRS Wide QRS is due to automaticity foci in ventricles depolarizing their site first and the other side of ventricle is depolarized much later. They do not contract together. Will still have P waves Atrial depolarizations are independently paces by SA node but are not conducted to ventricles= P waves are dissociated from QRS complexes State the principal EKG feature of first-degree heart block. See above For Wenckebach & Mobitz: where the AV block occurs See above the EKG changes that are observed See above how PR interval and QRS width are used to distinguish these cases See above Treatment. Pacemaker if symptomatic Describe the three types of 3rd-degree AV block with regard to the: location of AV block resulting pacemakers which emerge EKG changes relationship of SAN-generated P waves to the ventricular rhythm See above Describe the condition of Stokes-Adams syndrome and its treatment. Complete heart block that comes and goes (paroxysmal) results in periodic syncope Av block occurs and ventricles stop 5-30 seconds due to overdrive suppression= syncope. Ventricular pacemaker begins= 15-40 bpm Treat with pacemaker Explain the EKG features of right and left bundle branch block (RBBB and LBBB) in terms of the depolarization timing and sequence in the ventricles. BBB= one bundle branch conducts normally while the other bundle branch is blocked. This delays depolarization to the ventricle supplied by the blocked bundle branch. Depolarization in blocked branch proceeds very slowly through ventricular muscle until it can stimulate the blocked branch below site of block If it eventually gets through an depolarizes at a different spot and creates RR’= incomplete BBB RBBB. Left contracts normally when right contraction is delayed. LBBB. vice versa May be extra info: Fascicles: RBBB, anterior LBBB, posterior LBBB Bifascicular block= complete block in 2 out of 3 fascicles RBBB+ anterior LBBB RBBB+ posterior LBBB Anterior LBBB + posterior LBBB= LBBB Trifascicular block= intermittent block in at least 1 fascicle Describe the EKG features of RBBB in leads V1 and V2 and LBBB in leads V5 and V6. RBBB Distinct in right chest leads RsR’ in V1 and V2 LBBB Distinct in left chest leads RR’ in V5 and V6 Treatment: pacemaker Explain the mechanisms of atrial, junctional, and ventricular escape beats and rhythms, and the associated EKG changes. Escape beats= an automaticity focus transiently escapes overdrive suppression to emit one beat Atrial Transient SA nodal block causes SA nose to miss one cycle= atrial automaticity focus to escape overdrive suppression and produce an atrial escape beat Atrial focus is suppressed when SA node resumes EKG P wave of different shape P wave inverted if the focus is very low in the atrium due to retrograde atrial depolarization Junctional Same at above but atrial response is absent which allows junction to take control EKG Pause of electrical activity for 1 cycle Normal QRS with no p wave Ventricular transient , excessive parasympathetic stimulation depresses automaticity of SA node, atrial foci, and junctional foci. Leaving ventricular foci to take control EKG Pause of electrical activity for 1 cycle Enormous QRS with inverted Twave Define the term “retrograde atrial depolarization” and be able to identify the arrhythmias that: can generate retrograde atrial depolarization Atrial escape beat/rhythm Junctional escape beat/rhythm PAC PJC PAT PJT produce inverted P’ waves due to retrograde atrial depolarization. Atrial escape beat/ rhythm Junctional escape beat/rhythm Can occur before, during, or after QRS PAC PJC PAT PJT Explain why an inverted T wave occurs with a ventricular escape beat or rhythm and be able to identify all the arrhythmias in which inverted T waves occur. All arrhythmias with inverted T waves Ventricular escape beat/rhythm For premature contractions occurring in the atria (PAC), AV bundle (PJC), and ventricles (PVC) describe:: the mechanism of the premature beat Caused by an ectopic focus which spontaneously fires a premature single stimulus (area of local ischemia, mechanical irritation from plaques, chemical irritation like drugs, or cardiac cath causing mechanical stress) associated EKG changes PAC Etiology Occurs in healthy people and athletes often Triggered by excessive adrenergic stimulation (adrenal gland stimulation, pheochromocytoma), drug induced sympathetic stimulation (caffeine, cocaine, amphetamine), hyperthyroidism, excessive parasympathetic blockade, digoxin toxicity, ischemia, hypoxia EKG Abnormal P wave that occurs too soon, can be superimposed on T wave If foci is near SA node= upright p wave If foci is low in atrium= inverted p wave Normal QRS PAC may also depolarize SA node, this resets the SA node to resume pacing= one normal cycle length after PAB PJC Same triggers as PAC EKG Normal QRS P wave before, during, or after QRS SA node resets its pacing with each retrograde atrial depolarization= may produce gaps of empty baseline PVC Etiology Ischemia (MOST COMMON)= decreased CO, hypovolemia, cardiogenic shock, coronary insufficiency, myocardial infarction hypoventilation= airway resistance or obstruction (asthma, COPD), pneumothorax, PE, low O2 content (high altitude, suffocation) Hypokalemia Mitral valve prolapse EKG From foci of ventricle wide, high voltage QRS p wave absent If QRS is upright, PVC is mainly downward the mechanism of SAN resetting (in PAC and PJB) PAB can reset SA control if depolarizes SA node PJB can reset SA control if it causes retrograde atrial depolarization (inverted P wave) For a PVC, state the: most common trigger= ischemia reasons for widening and inversion of the QRS complex (compared to normal QRS)= control from random foci in ventricle= ventricles don’t depolarize at the same time. Can be inverted if foci is upward. reasons for T wave inversion- after PVC, T wave has potential of opposite polarity to QRS Slow conduction causes first depolarized to be first to repolarize when it is normally last to depolarize is first to repolarize in the ventricles morphologic features of unifocal PVC’s and multifocal PVC’s Isolated unifocal PVC QRS normal, stray impulse from infarcted or ischemic areas Multifocal PVC Multiple ventricular automaticity foci where each foci produces their own PVC State the two major features of paroxysmal tachycardias. Begin and end suddenly Irritable automaticity foci in atria, junction, or ventricle Adrenergic stimulation= atrial and junctional foci Hypoxia, hypokalemia= ventricular foci FYI: Classified as PSVT (PAT, PVJ, or AVNRT) or PVT For paroxysmal atrial tachycardia (PAT) and paroxysmal junctional tachycardia (PJT): describe the EKG changes state the consequences of matching the ventricular rate to the rate of the ectopic focus PAT Atrial rate= 100-180 bpm Irregular rhythm Normal QRS P wave can be inverted If ventricular rate= atrial rate, CO and coronary perfusion are greatly reduced PJT rate= 150-250 bpm P wave before, during, or after QRS P wave can superimpose on T wave P wave can be inverted QRS normal- can be widened Describe the characteristics and EKG features of ventricular tachycardias, and distinguish between nonsustained and sustained VT and the preferred treatments in each case. 120-200 bpm Caused by cardiomyopathy or digoxin toxicity, can initiate VFIB EKG 3 or more PVCs in a row Av dissociation SA depolarization may happen randomly= normal QRS (capture beat) Fusion of capture beat with PVC-beat to produce a “fused” QRS complex that does no resemble other (fusion beat) Nonsustained Vtach Less than 30 sec without hemodynamic instability treatment= amiodarone, lidocaine, and procainamide Sustained Vtach More than 30 seconds WITH hemodynamic instability DC cardioversion followed by amiodarone for maintenance Describe the mechanism of multifocal atrial tachycardia (MAT) and define the term “protective entrance block”. List the EKG features of MAT. Like wandering pacemaker but faster HR Pacemaker activity “wanders” from SA node to nearby atrial automaticity foci Common in patients with COPD and digoxin toxicity patients with heart disease Atrial automaticity foci develops “protective entrance block” Resistance to overdrive suppression from any other focus No single focus can dominate pacemaking Each focus paces at its own inherent rate; combine multiple foci produce a rapid irregular rhythm EKG Atrial rate> 100 bpm At least 3 atrial foci involved (3 or more different p wave morphologies) Irregular ventricular rhythm For atrial fibrillation (AF): explain the mechanism for each explain how the P waves differ in each case describe the EKG features explain the resulting effects on ventricular rate and cardiac output explain the approaches to treatment. For atrial flutter: explain the mechanism for each explain how the P waves differ in each case describe the EKG features explain the resulting effects on ventricular rate and cardiac output explain the approaches to treatment. Explain the reentry mechanism and “circus movement” that may result in ventricular fibrillation (VF). Reentry mechanism Numerous parasystolic ventricular foci produce impulses which depolarize only small surrounding portions of ventricular muscle, resulting in rapid, ineffective twitching three conditions that promote impulse reentry Long impulse pathway, such that the initially stimulated portion is out of its refractory period when the impulse returns (occurs in dilated hearts) Decreased conduction velocity (purkinje blockage, ischemia, hyperkalemia) Shortened refractory period (drugs) Effective refractory period of re-entered region must be less than the propagation time around the long pathway EKG features Single ventricular automaticity focus. Rate 250-350 bpm Smooth, rapid series of similar appearing waves effects on cardiac function No real pumping