Cardiology Flashcards

Question

Bradycardia - Secondary Causes

Answer 1

**Critical** 1. Hyperkalaemia 2. Ischaemia 3. Drugs - Brady bunch 4. CNS - raised ICP - deep TW inversions **Emergent** 1. Hypothermia 2. Myxodema coma 3. Infection - myocarditis, endocarditis. lyme's, travel - dengue, malaria, typhoid, legionnaries 4. OSA **Special** 1. Post cardiac / valve surgery 2. Ruptured viscus / ectopic - paradoxical bradycardia with vagal response

Answer 2

* Slightly prolonged QRS (may not be >120ms) * rS complexes in leads II, III, aVF (Dep going away) * qR complexes in leads I, aVL (Dep going towards) * Left Axis Deviation (LAD)

Answer 3

* Slightly prolonged QRS * rS complexes in leads I and aVL (Dep going away) * qR complexes in leads II, III and aVF (dep going towards) * Right Axis Deviation (RAD) * Absence of RVH or prior lateral MI

Answer 4

* Bradycardia * Renal failure * AV block * Shock * Hyperkalaemia Treatment aims 1. Calcium 2. Fluid resus - consider normal bicarb 3. K+ Mx - usual methods +/- frusemide or dialysis if anuric 4. Adrenaline - cardiogenic shock

Answer 5

1. 3d and 2d AV block + 1. Symptomatic bradycardia / arrhythmia 2. Symptomatic bradycardia secondary to drugs for dysrrhythmia Mx 3. AF with pauses \>5s 4. Catheter ablation of AV node 5. Post-op AV block not expected to resolve 6. NMD (dystrophies) 2. Symptomatic bradycaradia + 2⁰ AV block 3. Persistent 3⁰ AV block 4. Chronic tri or bi-fascicular block with intermittent type II 2⁰ block or 3⁰ block 5. 3⁰ and 2⁰ AV block with exercise

Answer 6

Usually within 6-8 weeks Usually a lead issue or programming issue Consider PPM lead infection + endocarditis if pt has fever LBBB normal, RBBB abnormal - consider lead displacement Magnet does not turn off PPM - turns of sensing or inhibition function Causes of malfunction: 1. **Failure to capture** - No pacing spikes or spike not followed by an atrial/ventricular complex * Lead fracture / displacement or insulation break * Exit block * Battery depletion 2. **Inappropriate sensing** - Spikes occur prematurely or not at all * Undersensing - - fails to register deoplarisation (flushing toilet) * Lead fracture / displacement or insulation break * Inadequate endocardial contact * Low voltage P waves and QRS complexes * Oversensing - detecting signals other than that for the chamber =\> witholding pacing * Extra-cardiac signals - artefact, myopotentials * TW or PW sensing 3. **Inappropriate pacemaker rate** * ****Battery depletion * Ventriculo-atrial conduction + pace-maker mediated tachycardia * 1:1 response to atrial dysrhythmias

Answer 7

Bridge to transplant or destination therapy All anticoagulated and can presnet with GIH or ICH Can dvp acquired Von Willebrand's PLT dysfunction Dysrrhythmias frequent so pts have AICD LVAD * Some - No palpable pulse or BP * MAP with art line with BP cuff - constant flow indicates MAP * Assess other vital for perfuson status * Shock may be RVF - deviced does not support RV - consider dobutamine, dopamine * Compressions NOT HELPFUL - confirm absence of pump function and fix malfunction * Some have backup hand pump TAH * ECG asytole as no native cardiac activity * Defib / pacing and chest compressions NOT HELPFUL

Answer 8

5 letter code First 3 anti-bradycardia function Last 2 additional functions 1. Chamber paced - A/V/D/O 2. Chamber sensed - A/V/D/O 3. Response - Trigger/Inhibit/Dual/O 4. Programability - P/M/R/C/O 5. Anti-tachcardia functions Pacing, shock, dual, rate modulation Common Pacing codes 1. VVI - TV pacing mode Paces and senses ventricle No electrical impulse sensed = pace @ a pre-programmed rate Electrical impulse sensed = pacing inhibited Asynchronous pacing 2. VVIR As above but rate adaptive mechanism to meet patients physiological needs 3. DDD Ventricular pacing and sensing If SA and AV node functioning then pacemaker will just sense if not then PPM will tkae over 4. DDDR Same as above except has a rate-adaptive mechanism 5. VOO Licence to kill - PPM not sensing Mode for surgery (asynchronous pacing) Ventricle paced at a pre-programmed rate Sensing not interfered with by diathermy etc Need to monitor for R on T with diathermy -> torsades de pointes

Answer 9

1. Infection 1. Usually S. aureas 2. Haematoma 3. PTx 4. Pericarditis 5. Thrombophlebitis 1. 30-50% 2. NB SVC obstruction 6. Skin erosion * Replace unit and ABx 7. Pacemaker syndrome

Answer 10

Functions - cardioversion, defibrillation, pacing Indications 1. VF/VT with no transient or reversible event 2. Spontaneous sustained VT 3. Syncope of undetermined origin + induced and sustained VF/VT (EP study) 4. Non- sustained VT + CVD + refractory to class I antiarrhythmic Causes of shock delivery to patient * Increase VF / VT (ischemia / electrolyte disturbance / drug effect) * Displaced or break in ventricular lead * Recurrent non-sustained VT * Sensing and Shock of SVT * Oversensing T-waves * Sensing non-cardiac signals Causes of syncope * Recurrent VT with slow shock strength (lead problem / change in defib threshold) * Hemodynamically significant SVT * Inadequate backup pacing for bradyarrythmias Admit patient * Haemodynamically unstable * \> 2 shocks in one week * Correctable cause * Infection * Disruption of mechanics

Answer 11

Most commonly seen with SAH, Haemorrhagic CVA * Deep symmetrical (Giant) TWI throughout * QT prolongation * Bradycardia Others * Flat T waves * ST elevation or depression * ↑ U wave amplitude * Rhythm disturbances - ST, Junctional, PVCs, AF

Answer 12

1. Bradydysrrhythmias 2. Tachydysrrhythmias 3. Cardiogenic shock 4. LV free wall rupture 5. Septal rupture 6. Papillary muscle rupture → MR 7. Pericarditis 8. Embolic or Haemorrhagic stroke 9. Hyperglycaemia 10. Iatrogenic 1. AntiPLT, Anticoag, antifibrinolytis complications 2. Pseudoaneurysm from arterial cath

Answer 13

Depends on HR + gender (M - 440ms, F - 460ms) Short if \<350ms Congenital * Lange-Nielson - recessive + deaf * Romano-Ward - dominant + no deafness Acquired * Idiopathic * Electrolytes - low K, Mg, Ca * Clinical conditions * AMI * Hypothermia * Raised ICP * Severe Bradydysrrhytmias i.e. CHB with escape rhythm * Drugs - by the anti-drugs * Biotics * Dysrrhytmics * Emetics * Fungals * Neoplastics * Psychotics Significance = dvpt of… Polymorphic VT Monomorphic VT VF

Answer 14

Definition * 3 or more episodes of sustained VT (\>30s) within 24 hrs Arrest - Defibrillate Conscious + unstable = DCCV Conscious + unstable * Rx underlying cause * Consider * Intubation * Deep sedation - propofol * Arterial line - labile haemodynamics * Anti-arrhythmics (loading + infusion) * 1st line - Amiodarone up to 900mg loading in 24 hrs * 2nd line - BB - propanolol 0.15mg/kg over 10mins or esmolol 0.3-0.5mg/kg IV * 3rd line - lignocaine 1-1.5mg/kg bolus * MGSO4 + electrolyte replacement * Double defibrillation (if \> 5 shocks not reverted) * Stellate ganglion block * ECMO

Answer 15

Arrest - defibrillate Conscious - DC cardiovert MGSO4 - 10mmol over 10-15 minutes Treat underlying bradyarrhythmia by shortening QT interval * Atropine * Isoprenaline * Overdrive pacing 90-120bpm Avoid class Ia, Ic and III anti-dysrrhythmics Treat underlying cause * Correct electrolytes * Warming hypothermic pt

Answer 16

The ACSss * Acute Coronary Ischemia * ACS * Variant Angina * Cocaine * Coronary Embolism/Vasculitis * Comorbidities * Renal, failure, sepsis, ARDS\< Stroke, SAH * Systemic shock states * Distributive (sepsis, CO, burns) * Cardiogenic (myocarditis, mycocardial contusion, cardiomyopathy

Answer 17

Absolute * Previous ICH or Haemorrhagic CVA * Ischaemic CVA in last 3/12 * Intracranial neoplasm * Internal bleeding * Suspicion of aortic dissection or pericarditis Relative * Ischaemic CVA \> 3/12 ago * Severe uncontrolled HTN \> 180/110 * Recent trauma last 2/52 * Prolonged CPR \> 10 mins * Major surgery last 3/52 * Oral anticoagulant use * Known bleeding diathesis or hepatic dysfunction * Recent internal bleeding in last 4 /52 * Neoplasm with inc bleedin risk * Recent organ biopsy or vascular puncture

Answer 18

Predictor of adverse outcomes at 14 days and or severe ischaemia requiring urgent PCI 1. Age \> 65 years 2. At least 3 coronary risk factors 3. Prior angio show \> 50% stenosis 4. ST segement deviation 5. \>2 episodes of angina in last 24 hours 6. Aspirin use in last 7 days 7. Inc cardiac biomarkers Point for each parameter Limitations: 1. Score of 0-1 has cardiac event rate of up to 2% 2. Score 7 cardiac event rate of up to 41% 3. No weights of factors in score 4. Angio result may be unknown 5. Most predeictive power is biomarker elevation

Answer 19

* Hypoechoic fluid in peri-cardial sac - > 2cm = large > 500ml + * RV (early)diastolic collapse * RA (late)systolic collapse * IVC dilation w/ no variation in respiration * Sonographic alternans (swinging)

Answer 20

Serum levels \>3mmol/l symptomatic Calc: Sx: Stones, Bones, Moans, Groans Signs: ECG - short QT interval Mx Excretion - IVF - LOOP diuretic (thiazide makes worse) - Dialyse Osteoclast inhibition (dec Ca release) - Bisphosphonate - Pamidronate 90mg IV - Calcitonin - PRN for cardiac dysrhythmias - takes 24-48 hrs to work

Answer 21

Brugada pattern - Type 1 + Clinical signs **Brugada Pattern** Coved ST segment elevation \>2mm in \>1 of V1-V3 followed by a negative T wave **Clinical signs** * Documented ventricular fibrillation (VF) or polymorphic ventricular tachycardia (VT). * Family history of sudden cardiac death at \<45 years old . * Coved-type ECGs in family members. * Inducibility of VT with programmed electrical stimulation . * Syncope. * Nocturnal agonal respiration.

Answer 22

Valve is too small, narrow or stiff Most common isolated valve lesion M\>F 4:1 Disease of age RF * Congenital biscupid valve 50% * Calcific AS 25% * RhF - rare 15% * Coarctation of aorta Symptoms * Angina * Increased O2 demand - LVH * Reduced O2 suppley to coronary arteries - LVH * Postural dizziness * Syncope * due to fixed stroke volume * SOB Signs * Pulse - slow rising, sustained and small volume * BP - Reduced SBP and pulse pressure * Palpation * Apex - hyperdynamic, displaced * Thrill - base of heart, aortic region is severe * HS * S4 * Split S2 * Soft or absent S2 * Occasionally early ejection click - indicated mobile valve * Murmur * Harsh ESM, 2nd RICS with radiation to carotids * Accentuated by leaning forward and breath held in expiration Complications * Exertional syncope * Angina * IE * LVF - late * Sudden death * Heyde's syndrome = AS + GI angiodysplasia, vWF syndrome (shear stress) Mx * CVS RF modification * CCF Mx - AVOID B Blockers but cautious use of * Digoxin, ACEi, Diuretics * Surgery * AVR 25% 1 yr mortality w/out surgery * TAVI * Aortic balloon valvotomy - temporising measure in unstable pt

Answer 23

Symptomatic AS (potential to be sick) - IV Fluids: overall, AS is preload dependent, and these patients may require IVF resuscitation to maintain cardiac output - Inpatient admission for echo + evaluation for surgery for AVR _Patients with severe AS and failing LV (currently really sick AS), consider the following_: * Nitroprusside may dec afterload, improve systolic and diastolic function and dec myocardial ischaemia * Inotropes - dobutamine * Early consultation w/ cardiology for balloon dilatation for temporising measure * Ultimately need AVR

Answer 24

Preload dependent * Higher preload for normal systolic function * Avoid diuretics and BB or CCB and GTN Rate * Aim HR 50-60 * Slower rate allows hypertrophic LV to relax in diastole Rhythm * Maintain SR * Do not cope with AF =\> loss of diastolic filling time Contractility * Increased contractility mechanism to adjust to valve narrowing * Avoid BB or CCB Afterload * Afterload fixed - stenosis in AV not peripheral ciculation * Avoid hypertension * More important to avoid hypotension - if DBP falls to low then coronaries will not have enough filling pressure - keep DBP high

Answer 25

Retrograde flow of blood from AV to LV during diastole Causes * Primary Valve * Bicuspid, IE, RhF, vasc dx, degen aortic valve dx * Aortic root disruption * Marfan's, HTN, congential * Aortitis - syphilis, RA, Ank spond, GCA, Takayasu * Acute * Bacterial endocarditis * Type A dissection * Thoracic trauma Complications * IE * LHF * Angina Symptoms * Initially nil * Exertional SOB, angina, palpitations Signs * Pulse * Collapsing /Waterhammer * **Corrigans** - prominent carotid pulsation * **Quincke's** - visible pulsation of nail bed with light compression * **de Musset's** - head bob with each heart beat * **Muller** - systolic uvula pulsation * BP * SBP mildly increased * DBP reduced * PP increased * Palpation * Apex - Hyperkinetic, displaced * Thrill - Occ left sternal edge * HS - soft 2nd HS * Murmur * Early decrescendo diastolic murmur * Valve lesion - left sternal edge * Root lesion - right sternal edge * Accentuated sitting up and expiration * Austin Flint murmur - mid diastolic murmur at apex sitting forward and expiration * Femoral artery murmurs * **Traube's** - pistol shot femoral pulses * **Duroziez's** - sys and dias murmur over partially occluded distal femoral Mx * Acute * Inotropes + vasodilators titrated to BP * Chronic * Vasodilators * Ace inhibitor * BB * Surgery

Answer 26

Preload * Highly preload dependent =\> forward flow * Avoid GTN Rate * Keep HR higher - 90bpm * Regurgitant flow occurs in diastole = keep diastolic time shorter Rhythm * Cope with AF Contractility * Needs to be high to maintain CO * Avoid BB, CCB * Dobutamine Afterload * Higher the afterload = \> more regurgitation into LV * CCB if not decompensated CCF * Sodium nitroprusside - only for decompensated as decreases preload and afterload

Answer 27

* **Deeply inverted or biphasic T waves in V2-3 (may extend to V1-6)** * **ECG pattern present in pain-free state** * Isoelectric or minimally-elevated ST segment (\< 1mm) * No precordial Q waves * Preserved precordial R wave progression * Recent history of angina * Normal or slightly elevated serum cardiac markers

Answer 28

**Clinical significance** * Critical LAD stenosis * High risk for anterior wall MI within the subsequent days to weeks * Require invasive therapy * Poor prognosis with medical Mx and may suffer MI or cardiac arrest if inappropriately stress tested

Answer 29

* R in V5/V6 + Sin V1 \> 35mm * R in aVL \> 11mm * Max R + max S in precordial leads \> 45mm * Lots of others

Answer 30

Repolarisation abnormality increases specificity * ST depression in I + aVL or V4-6 * Asymmetrical inverted T waves in leads above * STE V1-3 +/- aVR * QRS widening (non-specific IVCD)

Answer 31

No great methods but consider… * Symmetrical TWI in I/aVL/V4-6 * Horizontal ST depression * Excessive discordant STE in V1-3

Answer 32

High-risk individuals to whom antibiotic prophylaxis should be provided are as follows [4,5]: * Prosthetic valves * PMHx IE * Cyanotic CHD * 6/12 months post cardiac surgery + prosthetic material * Aortic regurgitation Procedures indicated * Dental * Implanted cardiac devices * Procedure in infected/colonised tissue Antibiotic Regime * Amoxycillin 2g PO 60 mins before procedure * Clindamycin 600mg PO if penicillin allergic

Answer 33

_Acute_ - Type Aortic dissection or endocarditis or blunt chest trauma AR → dec stroke volume → compensatory tachycardia to maintain CO Stiff LV → inc LV pressure → prevents forward flow from LA → pulmonary congestion Severe AR → progressive hypotension, peripheral vasoconstriction, and cardiogenic shock. Mx _Treatment:_ Definitive treatment for severe acute AR is immediate surgical intervention In ED: * Intubate if necessary * Nitroprusside → afterload reduction, decreased LV preload, and results in reduced regurgitant volume * Dobutamine: inotrope → inc contractility and SV * Add in nitroprusside to increase forward flow and temporize the patient * ABx for suspected endocarditis _Treatment Pitfalls:_ NO Beta blockers - decrease reflex tachycardia, but that tachycardia is currently maintaining their cardiac output. Decreased HR will worsen AR due to more time in diastole

Answer 34

Acute: IE, papillary muscle rupture, trauma Chronic: MV prolapse, Rh HD, Cardiomyopathy, LVF, connective tissue disorders, congenital, DXT Clinical * Chest - pan-systolic, blowing, high pitched murmur * ECG - P mitrale, RAD, LVH strain, AF * CXR - LVH, LA dilation, APO Severity - regurg fraction * Mild \<30% * Mod 30-50% * Severe \>50% Mx * Fast (forward flow) and loose (dec afterload) * Dobutamine * Sodium nitroprusside

Answer 35

6 week risk of MACE Score: * 0-3 = \<2%, D/C home * 4-6 = 12-16.6%, admitted * \>7 = 50-65%, early invasive measures

Answer 36

Formulae 1. Bazett's * QTc = QT (msec) / √RR (s) * Overcorrects for fast HR (\>100) and undercorrects for slow HR (\<60) - unreliable outside these ranges 2. Framingham * QTc = QT + 0.154(1-RR) 3. Hodges * QTc = QT + 1.75(HR-66) 4. Half R-R Rule * QTc should be \< 1/2 R-R rule = **unreliable** 5. QT Nomogram * Best method in context of drug toxicity * Median of 6 readings

Answer 37

Frequency of LVF CXR findings in descending order 1. Dilated upper lobe vessels 2. Cardiomegaly 3. Interstitial oedema 4. Enlarged pulmonary artery 5. Pleural effusion 6. Alveolar oedema 7. Prominent SVC 8. Kerley B Lines

Answer 38

* T wave inversion in right precordial leads V1-3, in absence of RBBB (85% of patients) * Epsilon wave (most specific finding, seen in 50% of patients) * QRS widening in V1-3 (> 110ms) * Prolonged S wave upstroke of 55ms in V1-3 * Ventricular ectopy of LBBB morphology, with frequent PVCs > 1000 per 24 hours * Paroxysmal episodes of ventricular tachycardia (VT) with LBBB morphology (RVOT tachycardia)

Answer 39

## Footnote AF w/ RVR, rapidly conducting accessory pathways exist that can carry atrial impulses to the ventricle at rates exceeding 250 bpm. AV nodal blocking agents cause both faster and preferential conduction through these accessory pathways, which can result in extremely rapid ventricular response rates and deterioration to ventricular fibrillation. For these reasons, AV nodal blocking agents are contraindicated in preexcitation AF.

Answer 40

* Rate 140-180 bpm in adults, > 220 suggest accesory pathyway * Kids - >220 bpm infants and >180 small children * Regular NCT * Occ RBBB w/ abberant conduction * P waves variable * Typical (90%) - buried in QRS complex * Atypical (10%) - retrograde or inverted in INF leads, positive P wave V1r * Rate related ST depression * QRS alternans - phasic variation assoc w/ AVNRT and AVRT * STE aVR 70% sensitive and specific for accessory pathway SVT

Answer 41

1. Synchronsied DC shock if unstable a. 1-2J/kg in children STABLE 2. Vagal manoeuvres a. Neonates, <6mo - facial immersion ice water 5-10s, ice-cold face cloth or ice slurry bag over face 15-30s b. Older infants - ice slurry c. Older / Adults - modified valsalva 3. Drugs a. Adenosine 100mcg/kg b. Sotalol 0.5-1.5mk/kg or verapamil - NOT for infants c. Verapamil 5mg over 5mins / flecainide 2mg/kg over 30mins d. Amiodarone 5mg/kg IV

Answer 42

Subtypes of AVNRT 1. **Slow-Fast** (80-90%) i. Slow AV nodal pathway for anterograde conduction and Fast AV nodal pathway for retrograde conduction 2. **Fast-Slow** (10%) i. Fast AV nodal pathway for anterograde conduction and Slow AV nodal pathway fpr retrograde conduction 3. **Slow-Slow** (1-5%) i. Slow AV nodal conduction for anterograde conduction and slow left atrial fibres for retrgrade conduction **Summary of AVNRT subtypes** No visible P waves? –> Slow-Fast P waves visible after the QRS complexes? –> Fast-Slow P waves visible before the QRS complexes? –> Slow-Slow

Answer 43

Supraventricular rhythm - usually benign 3 or more sites of atiral ectopy Not amenable to DCCV Causes 1. **COPD** - hypoxia, hypercapnoea, acidosis 2. CVD - IHD/CCF/HTN 3. Metabolic - hypo K/Mg 4. Drugs - sympathomimetics, digoxin 5. Sepsis Mx 1. Rx underlying cause 2. Rate control if sustained RVR 3. Ablation V node

Answer 44

3 or more P wave morphologies Rate > 100 bpm N QRS Irregular Isoelectric baseline between P waves COPD - RVH

Answer 45

Cardiac IHD Valvular disease Cardiomyopathy Pericarditis / Myocarditis CVD - HTN, Obese, ASD Atrial myxoma Non-Cardiac Sepsis Electrolyte disurbance PE Drug and alcohol intoxication Thyrotoxicosis Lung Cancer

Answer 46

**RHYTHM** Lone AF w/ clear onset < 48 hrs Young < 65yrs Pt Preference Significantly symptomatic Assoc HF HD unstable No/few comorbidities Unlikely to revert spontaneously - i.e. required DCCV before **RATE** Age > 65 yrs Onset > 48 hrs 90% revert w/ Rx if < 48 hrs duration 50% revert > 48hrs Presence of CCF Previous episodes AF Failed antiarrhythmic therapy Structural cardiac lesions Dilated LA Secondary AF

Answer 47

3 classifications we care about: 1. Hypertensive emergency = BP > 180/110 +acute target-organ dysfunction (clinical or Ix) 2. Poorly controlled chronic HTN (no end organ dysfunction) - Some drugs can elevate BP i.e. steroids, NSAIDs, stimunlants, decongestants, appetite suppressants 3. Newly elevated BP - not an ED diagnosis Pathophysiology ● Macrocirculation ○ High SVR (due to peripheral arteriole back up from SNS and RAAS activation) increase LV mass ○ LVH - Diastolic dysfunction ○ Elevated LA end diastolic pressures ■ Acute SVR rise = Flash pulmonary edema ■ Chronic = LVH - leads to ischemia (outgrowing blood supply) and eventual thinning of myocardium ○ Thus end with big floppy bag of systolic dysfunction ● Microcirculation ○ Critical luminal narrowing - occlusion and ischemia ○ “Silent” ischemic episodes lead to primary cause of chronic end organ damage ○ Lumen thinning - aneurysm and rupture ■ Results in tissue edema, fibrinoid necrosis, and MAHA

Answer 48

BP > 180/110 + and organ dysfunction ❏ Abrupt rise in BP overwhelms autoregulation = endothelial injury ❏ Post injury, a major vascular smooth muscle relaxant (NO) is decreased ❏ Further increase of SVR = downward spiral that maintains elevated BP ❏ Left unchecked, this leads to terminal arteriole dilation and rupture **BP >180/110 +** *HA / Blurred vision AMS / Seizures Focal Neuro Deficits Chest pain / SOB Renal failure*

Answer 49

General principles for lowering BP rapidly in the ED: 1. Blood pressure should almost never be rapidly lowered (except in aortic dissection). 2. Lower pressure by no more than 25%, to avoid ischemia in organs auto-regulated to higher BP. 3. Therapies that correct the cause (e.g. phentolamine if the BP is elevated by catecholamines) will be most effective. 4. Monitor the symptoms to determine whether the BP has been adequately lowered. BP Targets Ischaemic Stroke <220/120 Ischaemic Stroke w/ thrombolysis >185/110 ICH <180/90 SAH <160/90 Pre-eclampsia < 140/90 Aortic DIssection BP <120/80 and HR 60

Answer 50

MAJOR HTN Congential Heart Disease Aortic stenosis - bicuspid aortic valve, coarctation aorta CT disease - Marfan's, Ehlers-Danlos OTHER Iatrogenic - post-cardiac surgery, balloon dilatation for coarctation Cocaine Pregnancy Inflammatory - Vasculitis - GCA, Takayasu Weight lifting

Answer 51

Widened mediastinum (52-75%) Dilatation aortic arch (31-47%) Obliteration aortic knuckle Double density of aorta (suggesting true and false lumen) Localised prominence along aortic contour Distortion L main bronchus NGT / Tracheal devation to R Calcium sign (>6mm betw/ intimal calcium and outer aortic wall Pleural effusion L > R Cardiomegaly Changes in configuration oarta subsequent xrays (47%)

Answer 52

Consider Aortic dissection with CP + CVA CP + paralysis CP + hoarseness (recurrent laryngeal nerve) CP + limb ischemia

Answer 53

Stanford Type A: 62% involves **ascending** aorta +/- descending **Surgery** usually indicated Type B: 38% Involves **descending** aorta (beyond Left subclavian artery only. Medical Mx w/ BP control. Older pts, heavy smokers w/ chronic lung disease w/ atherosclerosis and HTN. DeBakey 1: Entire aorta affected 2: Confined to the ascending aorta 3: Descending aorta affected distal to subclavian artery 3a: thoracic aorta only 3b: abdominal aorta involved

Answer 54

Leaking or ruptured aorta End organ ischaemia Extension despite medical Mx Refractory pain Severe uncontrolled HTN

Answer 55

Pseudoaneurysms, are abnormal outpouchings or dilatation of arteries which are bounded only by the tunica adventitia, the outermost layer of the arterial wall True aneurysms, which are bounded by all three layers of the arterial wall. Pseudoaneurysms typically occur when there is a breach in the vessel wall such that blood leaks through the inner wall but is contained by the adventitia or surrounding perivascular soft tissue. Causes: Iatrogenic - angiogram, Trauma Vasculitides AMI - LV false aneurysm

Answer 56

Complications anytime post-op ● Infection - difficult to diagnose! ○ Graft contamination ○ Adjacent infectious spread ○ Hematogenous seeding ● Aortoenteric fistula (AEF) ○ Consider with GI bleeding + PMHx AAA surgery ● Pseudoaneurysm (anastomotic aneurysm) ○ Arise from the leaking anastomosis site Delayed Complications: 1. Infection 2. Ischemic complications a. Spinal cord ischemia b. CVA c. Extremity ischemia d. Visceral ischemia (Celiac/SMA/Renal) e. Post implantation syndrome (fever, leukocytosis and reactive inflammation, can get uni/bilateral reactive pleural effusions - SIRS to the max) 3. Aortoenteric fistula 4. Pseudoaneurysm (anastomotic aneurysm) 5. Chylous Ascites / Chylothorax 6. Endo Leak i) Blood flow outside graft lumen - BUT contained within the aneurysm sac ii) up tp 20% of patients who have had repair! iii) Grade I-IV

Answer 57

Acute limb threatening ischaemia Aterial occlusion cause severe symptoms when there is no collateral circulation Femoral 45% > Iliac 20% > Popliteal 10% RF Age > 60, M>F Embolic - AF, IVDU Thrombotic - HTN, DM, Hyperlipdaemia, smoking Iatrogenic - recent arterial cannulation, Bier's block Trauma - endothelial injury Symptoms / Signs 6 P's - pain, pallor, pareasthesia, paralysis, perishingly cold, Pulseless Cyanosis Late signs - pain, tense swelling and tender muscle belly > 12 hrs of symptoms leads to irreversible limb ischaemia Ix ABPI (>1.0 normal, <0.9 aterial Dx, 0.5-0.9 claudication, <0.5 rest pain) Vascular USS DSA, CTA, MRA Mx Analgesia Heparin Correct aggravating factors - dehydration, sepsis, arrhythmias, MI) Urgent revascularisation - Thrombus extraction - Thrombo-aspiration - Surgical thrombectomy - +/- bypass grafting

Answer 58

Ankle-Brachial Pressure Index Highest Ankle systolic / Highest Brachial systolic 1.0-1.3 Normal 0.9 Mild Dx 0.5-0.8 Moderate Dx - Claudication <0.4 Severe Dx - Rest Pain

Answer 59

Neuro 1. ICH ever 2. SOL 3. CVA, dementia, CNS damage w/in 1 yr 4. HI or brain surgery 6 months Trauma 1. Major surgery, trauma or bleedin last 6 weeks 2. Traumatic CPR within 3 weeks Haem 1. Internal bleeding last 6 weeks 2. Known bleeding disorder Other 1. Suspected aortic dissection or pericarditis

Answer 60

CVS 1. Uncontrolled HTN 180/110 2. Infective endocarditis 3. Intra-cardiac thrombi Neuro 1. TIA 6 months 2. Dementia GI 1. Acute pancreatitis 2. Active PUD 3. Advanced liver disease Resp 1. Cavitating TB Vasc 1. Puncture non-compressible vessel 2 weeks Bleeding risk 1. NOAC / warfarin 2. Previous thrombolysis

Answer 61

1. VF or sudden cardiac death survivors 2. VT-associated syncope not caused by MI or other correctable cause 3. Risk of SCD - Long QT, HOCM, Brugada 4. Cardiomyopathy 5. Minimally symptomatic VT with EF <35% 6. Dysrhythmia resistant to anti-arhythmics or if anti-arrhythmics contra-indicated

Answer 62

**Primary Valve Failure** 1. Acute - tearing or broken component - sudden death, APO, MI 2. Chronic - calcification or thrombus - HF, unstable angina, haemolytic anaemia Mx Major haemodynic instability -> valve replacement Afterload reduction - GTN Inotropic support - dobutamine IABP **Thromboembolism** Caged > single leaflet > bileaflet 15% within 5 yrs implant, greatest risk first 3 months Mitral > others Subtherpaeutic anti-coagulation **Metallic Valve thrombosis** Mx Anti-coagulate Thrombolytic therapy Surgical replacement **Endocarditis** **Haemolytic Anaemia** MAHA - low grade 70%, severe 5% **Complications of Anti-coagulation** Bleeding Skin necrosis Atheromatous Cholesterol embolism Recurrent thrombosis Teratogenic effects

Answer 63

Risk Factors Prosthetic valves - 30% Worldwide is Rh Fever IVDU Organisms Staph no most common cause Strep species - viridans (dental), bovis Enterococcus (older esp > 60yrs) Predisposition **Structural** - Rh HD, MV prolapse, Prosthetic valves, CHD, Cardiomyopathy, Previous IE **IDVU** - mostly RHS lesions **FB** - PPM, CVC **Immunosuppression** / DM **Poor dental hygiene** Complications Destruction of valve + acute severe HF Conduction Abnormality Septic emboli - Unexplained CVA - Septic arthritis - Organ abscess - CNS, lung, hepatic, splenic - Organ infarction - Generalised sepsis Immune - glomerulonepritis

Answer 64

QRS >0.12s Slurred S wave I, aVL, V5, and V6 (Depolarization moving away from these leads) RSR’ in V1 and V2 with R’ > R (Depolarization moving toward these leads) Causes 1. IHD 2. RVH 3. PE 4. Cardiomoypathy 5. RHD 6. CHD 7. Myocarditis 8. Lenegre-Lev Disease (degenerative fibrosis) DDx Brugada syndrome

Cardiology Flashcards

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