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Cardio BEH2131

PAC (premature atrial contraction) Ectopic beat 1.Generated by atrial focus outside SA node or very high AV junction. 2.Earlier than next contraction. 3.May/may not be conducted through AV node (depend on refactoriness). 4.Different P wave morph dep on site. 5.Cause irregular pulse. 6.P-R <0.20sec. 7.Have compensatory pause. X
PVC (premature ventricular complex) Ectopic beat 1.Generated in Ventricles 2.Wide QRS complex >0.12sec. 3. Earlier than next contraction in underlying rhythem. 4.P wave disassociation. 5.Cause irregular pulse. 6.Often compensatory pause. 7.Three in a row= VT X
Af (atrial fibrillation) 1.Irregularly irregular. 2.Multiple ectopic sites in atria. 3.No P wave. 4.Conduction to AV node is ramdom. 5.Controlled=<100bpm 6.Uncontrolled=>100bpm 7.QRS norm/wide. 8. ANY RHYTHM THAT IS IRREGULAR IS Af UNTIL PROVEN OTHERWISE. 9.DANGER-formation of clot.(use of warfarin as anticoagulant). X
Normal Sinus Rhythm 1.Reg. 2.60-100bpm. 3.P wave upright/rounded. 4.QRS 0.06-0.12sec. 5.P wave>>QRS>>T wave. X X
Sinus Brady 1.Reg. 2.<60bpm. 3.P wave upright/rounded. 4.QRS 0.06-0.12sec. 5.P wave>>QRS>>T wave. X X
Sinus Tachy 1.Reg, 2.>100bpm. 3.P wave upright/rounded. 4.QRS 0.06-0.12sec. 5.P wave>>QRS>>T wave. X X
Sinus Arrhythmia 1.Irregular R-R by >0.04sec. 2.60-100bpm. 3.caused by change in vagal tone due to inspiration/expiration. 4.increase HR inspiration. 5.Decrease HR expiration. X X
Junctional Rhythm 1.Reg. 2.40-60bpm. 3.P wave(not present\ different morph\ retrograde) 4.QRS normal 0.06-0.12sec. 5.P-R <0.12sec. 6.T wave follow every QRS. X X
Junctional Bradycardia 1.Reg. 2.<40bpm. 3.P wave(not present\ different morph\ retrograde) 4.QRS normal 0.06-0.12sec. 5.P-R <0.12sec. 6.T wave follow every QRS. X X
Accelerated Junctional rhythm 1.Reg. 2.60-100bpm. 3.P wave(not present\ different morph\ retrograde) 4.QRS normal 0.06-0.12sec. 5.P-R <0.12sec. 6.T wave follow every QRS. X X
Junctional Tachycardia 1.Reg. 2.>100bpm. 3.P wave(not present\ different morph\ retrograde) 4.QRS normal 0.06-0.12sec. 5.P-R <0.12sec. 6.T wave follow every QRS. X X
AIVR (accelerated idioventricular rhythm) 1.Reg. 2.Ventricular rate 40-100bpm. 3.P waves absent. Dissociated P wave>>3rd Deg AV block. 4.QRS>0.12sec. X X
Ventricular Standstill 1.Abscence of ventricular electrical activity. 2.P waves present. X X
VT (Ventricular Tachycardia) 1.Usually reg. 2.>100bpm. 3.P wave if present not associated to QRS. 4.P-R interval-NIL. 5.QRS-Wide, Bizarre, ST segment opposite direction of QRS. 6.>3 consecutive beats. 1.AV dissociation. /independent P wave. /capture of fusion beats. 2.Sustained VT >30 sec. 3.Non Sustained <30 sec. 4.Monomorphic or polymorphic. 5.Can produce output. CAUSE /Ischemia /disease /infection /electrolyte disturbance /Drugs/medication
Ventricular Fibrillation 1.Chaotic 2.nondiscernible rate 3.irregular /Coarse or fine /will NEVER produce output. /talking pt CANNOT be in VF. X
AF (Atrial Flutter) 1.240-360bpm(norm 300bpm) 2.P wave absent. 3.Sawtooth pattern 4.macro-reentry circuit activity within atrium. 5. ventricles fire at a relative rate to atrial firing rate. eg 3:1(atrial rate:ventricle rate). X X
SVT (AVNRT- AV node reentry tachycardia) 1.Reg. 2.Narrow QRS complex <0.12sec. 3.Normal T wave. 4.P wave may be before after or buried in QRS. 5.Reentry circuit in AV node. X X
STEMI ECG Change 1.Normal ECG prior to MI. 2.Hyperacute T wave(0-30min). 3.Marked ST Elevation w/hyperacute T wave(0-6hr). 4.Marked ST Elevation w/T wave inversion(6-12hr). 5.Pathological Q wave, less ST Elevation, terminal T wave inversion(necrosis). Q wave(>0.04sec or >25% R wave)(12-24hr). 6. Pathological Q wave, T wave inversion(necrosis and fibrosis)(>24hr) 7.Pathological Q wave, T wave revert upright.(months-yrs) X
nSTEMI ECG Change 1.ST depression. OR 2.Symmetrical T wave inversion. 3.OR both. X X
AMI ECG Change 1.Ischemic Zone Change(T wave inversion/Hyperacute T wave). 2.Injury Zone Change(ST Elevation). 3.Infacted Zone Change(Pathological Q wave). X X
ECG Square -Horizontal(time). \small. \large. -Vertical(mV). -print speed. HORIZONTAL\\ -Small \0.04sec -Large \0.20sec -5Large=1sec. -300Large=1min VERTICAL\\ -Large \0.5mV X
Absolute Refractory Period Begin in Phase 0(start Q) >> half way phase 3(half Twave) \cell is unable to initiate another action potential X X
Relative Refractory Period Half way Phase 3(half Twave X X
P wave -<0.10sec -<3mm X X
P-R interval -0.12-0.20sec X X
Q wave -First neg deflection. -<0.04sec(less than one small square). -<25% of R wave. X X
R wave -First positive deflection. X X
S wave -First negative wave after R wave. X X
QRS complesx -0.06-0.12sec X X
T wave -<5mm. -0.10-0.20sec X X
U wave <2mm. X X
Q-T interval -Depend in HR -<half of RR X X
S-T Segment -End QRS>>start T. ->0.20sec. ->1.0mm X X
ACS Prodrome PAIN(heaviness, tightness, burning, indigestion-like, pressure). IN(chest, shoulder, jaw, back, arm, epigastrium). \Nausea. \Diaphoresis. \SOB. \Palpitations. \Tiredness. \Lethargy. X
Automaticity The ability of a cardiac cell to spontaneously depolarise without external stimulus. X X
Paroxymal Sudden, unnexpected occurance. X X
Antipyretic Drug reducing fever X X
DCCS Direct current counter shock X X
Prodrome Preliminary symptom; indicating onset of disease. X X
Hypokalaemia \Slow onset. \K+ lost>>intracellular K+ move to interstitial space to maintain RMP. \can be caused by Insulin OD(insulin promote K+ uptake) \Leads to loss of skeletal muscle and smooth muscle tone. \can precipitate(torsades, PEA, asystole) \CAUSE-(Malnutrition, Starvation, Anorexia nervosa). \SIGNS+Symp(inability to think/comrahend, forget words, stutter, profound muscle weakness, chronic tiredness and fatigue). \CARDIAC ISSUE(Brady, Tachy, Prolong QT, Heart palpitations, Fainting/near Fainting, Chest tightness). ECG CHANGE-(Prolong PR, Slightly peaked P wave, ST depression, Shallow T wave, Prominent U wave).
Hyperkalemia \Increase K+ level>>cell less negative/partially depolarised>>myocardial cells increase automaticity. NORMAL K+ 3.5-5.0mEq/L CAUSE-(MEDICAL\ renal impairment. \OD on K+ med[slow K]. \PT lethargic, muscle weakness, ECG changes, can lead to VF.)\\\(TRAUMATIC-major burn>>leakage of intracellular K+. -cruch syndrome. -Rhabdomyolysis[muscle meltdown]). ECG CHANGE \\MILD(5.5-6.5mEq/L) Peak T, prolong PR. \\MODERATE(6.5-8.0mEq/L ) loss P, Prolong QRS, ST elevation Ectopic beats and escape rhythms. \\SEVERE(>8mEq/L) Progressive wide QRS, Sine wave, Vfib, asystole, axis deviation, BBB, Fascicular block.
Brugada Syndrome (SCD) \\SADS(sudden adult death syndrome). \\precipitates VF in healthy Pt. \\Most common in male of Asian origin. \\Genetically inherited. \\Complex ECG change. \\Often diagnosed from autopsy due to structural abnormality in RVent. X
Prolong QT syndrome (SCD) \\Delayed repolarisation of heart. \\QT seg prolong if >440ms(male) OR >460ms(women). \\QT seg >500ms>> increase risk of torsards de points. \\QT seg abnorm short if <350ms. RULE OF THUMB- Normal QT less than half of preceding RR interval. X
SCD (Sudden Cardiac Death) //Spontaneous generation of non-perfusing rhythm. //usually VF //Over 30=ACS //NON ACS Causes: Long QT, Cardiomyopathy, sick sinus, brugada syndrome, Aortic dissection, SUDEP. X X
Systolic (pumping problem) inability heart to contract to provide enough blood flow forward. X X
Diastolic (filling problem) inability of the left ventricle to relax normally, resulting in fluid backup into the lungs. X X
Left-sided (heart failure) inability of the left ventricle to pump enough blood, causing fluid backup into the lungs. X X
Right-sided(heart failure) inefficient pumping of the right side of the heart, causing fluid build up in the abdomen, legs, and feet. X X
EJECTION FRACTION SV = EDV-ESV EF(ejection fraction) = SV/(EDV x 100) X
Causes of HF \\CAD-STEMIS NSTEMIS \\Cardiomyopathy \\Hypertension \\Valvular heartdisease \\Myocarditis \\Congenitalabnormalities \\Arrhythmias(fastandslow) \\Diabetes \\Chronicanaemia X X
When the heart stops pumping what happens? //Arterial End—Blood filtrates out due to capillary hydrostatic pressure greater than blood osmotic pressure. //Mid Capillary—No net movement. //Venous end—REABSORBTION cap hydrostatic P less than blood colloidal osmotic P.
LVF //INC pulmonary P. //Hydrostat P VS oncotic P //cause fluid shift from pulmonary capils>interstitium>> alveoli>>>ALVEOLAR FLOODING. X X
Acute Pulmonary Oedema //When CO drops despite systemic resistance, so that blood returning to L.atrium exceeds that leaving LV. >> INC pulmonary P>>CAPIL HYDRO P in lung is > oncotic P of blood. X X
RVF //peripheral oedema. //Hepatosplenomegaly. //Jugular vein Distension //Ascites(collection of fluids in abdo). X X
SIGNS/SYMPTOMS of HEART FAILURE //SOBOE //Unexplained COUGH(APO). //crackles(APO). //DECR Spo2. //INC resp distress. //DECR urine output(dec. kidney>>inc. fluid retention). //Dizziness. //Confusion. //Lower leg OEDEMA. //Abdo Pain. //Nausea. X X
Cardiogenic Shock //Persistant hypotension and tissue hypoperfusion caused by cardiac dysfunction in presence of adequate intravascular volume and LV filling pressure. ACS CAUSEs //AMI. //Cardiomyopathy. //Sepsis. //Dysrhythmia leading to impaired diastolic filling. NON ACS Causes. //pulmonary embolus. //Cardiac tamponade(Fluid in pericardial sac). //Valvular Disorder.
Aortic Aneurysm //An enlargement of arterial wall creating false lumen. //saccular(bulging one side). //fusiform(uniform bulging). //Dissecting(tear creating sac) X X
Pericarditis //inflammation and swelling of pericardial sac. //pain on inspiration. //fever. //altered perfusion. //abnormal ECG. //SHARP,STABBING chest pain. //Concave ST seg + ST elevation X X
NEW BORN (Age/HR/RR/BP) Birth- 24hr. //HR:120-160 //RR:40-60 //BP:N/A X
INFANT (Age/HR/RR/BP) <1 //HR:100-160 //RR:20-50 //BP:>70 X
SMALL CHILD (Age/HR/RR/BP) 1-8yr //HR:80-120 //RR:20-35 //BP:>80 X
LARGE CHILD (Age/HR/RR/BP) 9-14YR //HR:80-100 //RR:15-25 //BP:>90 X
Foetal circulation //liver not needed>>DUCTUS VENOSUS bypass liver //lungs not needed>>FORAMEN OVALE + DUCTUS ARTERIOSUS X
Which ventricle is more dominant in Foetal and newborn? //RIGHTSIDE X X
How is CO maintained in peads? //Peads less able to alter STROKE VOLUME(preload/afterload) thus they INC HR to maintain a stable CO. X X
Circulating Volume //ADULT 65-70mL/kg (70kg=4.5-4.9L). //PEADs 80-90mL/kg. /NEW BORN 3.5kg=280-315mL. /SMALL CHILD 13kg=1-1.2L. X X
PEAD Cardiovascular Assessment //RED Flags: //cyanosis. //lethargy. //onset poor feeding. //Aponeas. X X
CENTRAL CAPILLARY REFILL TIME is the greatest indicator of perfusion //normal <2sec X X
SpO2 sats(pead) //should be >94% X X
PEAD Congestive Cardiac Falure //L.Side stop work. R.Side kinda stop work>>blood pooling. //Presentation is often vague and non-specific. X X
PEAD Cardiac Arrest //Initial presenting Rhythm: Asystole 74% >> PEA 18% >> VF/VT 7% (92% UNSHOCKABLE RHYTHMS) //ROSC 22.8% //Survival 7.7% VS ADULT //initial rhythm: VF 46% >>PEA 27.1% >>Asystole 25% >> VT 0.5% (47.3% shockable/52.6% NONSHOCKABLE)
Pead Arrest—think resp!! RESP RESP HYPOXIA
When do you start compressions in PEAD arrest? //<60bpm and/or UNRESPONSIVE/not breathing effectively. //15:2. //4j/kg every 2min. X X
Sick Sinus Syndrome //Abnormal sinus node function>>Brady/cardiac insufficiency. //Tach Brady Syndrome. //CAUSE: Ischemic heart disease, scarring of conduction system due to age, cardiac surgery. X
Types of Pacing //External. //Transvenous. //Implantable X X
Transveneous Pacing //Temporal. //for life threatening/unstable Brady. //Electrode advanced under fluoroscopy to place electrode. X X
Implanted Pacemaker Types //Fixed rate. //Demand. X X
Pacemaker Types //Atrial. //Ventricular. //Dual chambered. X X
VVI (Pacing mode) //electrode in vent>vent sensed> if impulse detected pacemaker inhibited>if no impulse then pacemaker pulse at pre-set rate X X
VVIR-(Pacing mode) //electrode in vent>vent is sensed>Pacing inhibited if impulse detect>if NO pulse then paced to match physiological need. X X
DDD-(Pacing mode) //Dual chamber electrodes>Dual chambers sensed>if either atrium/vent not conveyed then pacemaker take over. X X
DDDR-(Pacing mode) //Dual chamber electrodes>Dual chambers sensed>if either atrium/vent not conveyed then pacemaker paced with rate-adaptive mechanism. X X
Pacemaker Rate modulation Pacemaker sense //Resp rate/min volume. //Blood pH X X
Failure to sense (Pacemaker Problem) //Pacemaker fail to sense heart own impulse >> Inappropriate pacing times. X X
Failure to capture (Pacemaker Problem) //paced stimulus DOES NOT result in myocardial depolarisation. X X
Failure to place (Pacemaker Problem) //impulse not paced (can be due to poor electrode placement) X X
Can you Diagnose STEMI from ECG of pt with Vent. Paced rhythm? //NO. //HOW THEN? //Through HISTORY and ULTRASOUND.
Implantable Defib Indications IF PT. //had prior VF or VT arrest. //had at least on eps. Of VT. //had prior heart attack >> increased risk for sudden cardiac/death. //has hypertrophic cardiomyopathy (myocardial wall thickening) X X
Implantable Defib (specs) Implantable Defib //high energy defib at 35-40joules. //low energy as low as 2 joules <10 joules //leads biphasic. X X
Prodrome //premonitory symptom. //symptom indicating onset of disease. X X
ACS Prodromal Symptoms //Heavy, tight, burning, pressure like PAIN. //PAIN in chest, shoulder, jaw, back, arm, epigastrium. //Nausea. //Diaphoresis. //Dizziness. //SOB. //Tired, lethargic. X X
SCD (Sudden Cardiac Death) //Spontaneous generation of non-perfusing rhythm. //usually VF //Over 30=ACS //NON ACS Causes: Long QT, Cardiomyopathy, sick sinus, brugada syndrome, Aortic dissection, SUDEP. X X
Challenge of CPR: EET //Value of EtCO2 /measure efficiency of treatment post arrest >> INCR CO indicated by INCR EtCO2. /measure CPR EFICIENCY in same manner. /Effective CPR=EtCO2 of ~30mmHg. /predict survivor: IF EtCO2 >15mmHg THEN 71% chance survival. IF EtCO2 <10mmHg at 20 min arrest THEN NO SURVIVOR. X
Challenge of CPR: DCCS (Direct Current Counter Shock) //Terminates arrhythmia allowing higher pacemaker to resume conduction. //Transthoracic Impedance>>AFFECT DELIVERY of ENERGY: Chest size, pad size, pad position, impedance decrease with repeated shocks. //AFFECT DEFIB>>Cardiomyopathy, Electrolyte imbalance, Drug toxicity, 82% energy lost, 72% of vent mass require depolarisation to override VT/VF X
Four Challenges of ROSC //Brain injury. //Myocardial Dysfunction. //Systemic ischemia/reperfusion response. //Ongoing precipitant pathology. X X
Initial post ROSC care Initial post ROSC care //Optimise cardiac function>systemic perfusion> brain perfusion. //Measures to -prevent reoccurrence. //Measures to improve long term neurological intact survival. //Transport. //Try identify cause of arrest. X X
3 Principles of preventing reperfusion injury //Hypothermia. //Hypertension. //Haemodilution. To reduce cerebral metabolic demand> Reduce microvascular emboli> Reduce Ca2+ influx into cerebral vasculature/neurons> Reduce pattern of impaired cerebral autoregulation. X
4H/4T //Hypoxaemia. //hypovolaemia. //hyper/hypokalaemia. //hyper/hypothermia. //Tension Pneumothorax. //Tamponade. //Toxins. //Thrombosis(pulmonary/coronary) X
Cause of arrhythmia? //I-schemia/Infarct. //D-isease. //I-nfection. //E-lectorolyte disturbance. //D-rugs/Medications. X X
Long QT Syndrome //Delayed repolarisation of heart. //can lead to TORSADES DE POINTS. //COMPLEX!! //Prolong if (MEN >440ms)(WOMEN >460ms) >500ms risk torsades. //abnormal short if <350ms //NORMAL QT less than half preceding RR interval. X
Bragada Syndrome //AKA SADS(Sudden Adult Death syndrome) or SUDS(Sudden Unexplained Death Syndrome). //Precipitates VF in otherwise health Pt. //most common in males of Asian. //Genetic inherited.
AMI Diagnosis //History. //ECG. //Blood Enzymes. ECG Changes: //Ischemia=ST depression/T wave inversion. //Injury=ST Elevation. //Infarction=Pathological Q wave. X
STEMI //Occurs when thrombus is completely occlusive. //Myocardial necrosis results from interruption to myocardial blood supply. ECG Criteria: //ST Elevation in 2 or more leads. //ST Elevation of >1mm or >2mm in chest leads. //New left Bundle branch block. X
UA //Episodic angina that has a changes pattern. //New onset angina. //more frequent, easily provoked, difficult to relieve. //occurring at rest. //no evidence of myocardial injury or necrosis. X X
ACS //Characterized by coronary plaque disruption, with superimposed thrombus formation ranging from superficially adherent thrombus interrupting coronary blood flow to total occlusion>> >>compremising myocardial perfusion, leading to ischemic necrosis and eventually AMI //STEMI-ECG CHANGE. //nSTEMI/UA-No ECG change but Increase troponin.
Cardiovascular Risk Factors NON-Modifiable Risks: /AGE-risk double each decade >55. /SEX: Male>Female. /FAMILY HISTORY- Increased risk if 1st deg blood relative had CVD/Stroke before 55. /ETHNICITY- Indian, srilankan, Aboriginals. Modifiable risks: /BEHAVIORAL-tobacco,low exercise, diet, high alcohol, shift work. /BIOMEDICAL-hypertension, high blood chol, over weigh/obese, depression. X
Heart Valves LEFT AV- Bicuspid/mitral LEFT SL- AORTIC RIGHT AV- Tricuspid RIGHT SL- pulmonary X
SA node inherent rate 60-100bpm X X
AV node inherent rate 40-60bpm. delays action potential from SA node by 0.06-0.12sec X X
what are the 5 phases of cardiac cell activity? Cardiac cycle begins at Phase 4 where cells are at rest. /0- rapid influx of sodium ions throu channels in cardiac cells. K+ ions slowly begin to exit the cell and depolarization occurs, altering the electrical charge present in the cell. /1- Na+ influx decreases while K+ continues to exit the cell slowly. /2- begins movement of calcium into the cell while potassium continues to leave the cell. .3- calcium movement ceases with continued outflow of potassium.
PJC (premature junctional complex) Ectopic beat 1.generated by irritable focus within AV junction. 2.Earlier than underlying rhythem. 3.May/may not be conducted through AV node (depend on refactoriness). 4.Will have abnormal P wave morph. 5.QRS norm/abnorm morph. 6.P-R <0.12 sec (~3 sqr) 7.Have compensatory pause. X
IVR (Idioventricular Rhythm--Slow VT) 1.reg. 2.Ventricle rate <40bpm. 3.P waves absent. Dissociated P wave>>3rd Deg AV block. 4.QRS>0.12sec. X X
Created by: Gt_cockatoo