Cardiology_Medicine Flashcards
(95 cards)
IHD - Types? Definition? Dx? Mx?
Stable angina - chest pain on exertion relieved by rest
- Path - mismatch in O2 supply and demand to the myocardium
- Ix: CT-angiogram
- Mx:
- B-blockers - reduces HR req for activity –> reduced likelihood of mismatch in O2 supply & demand
- GTN spray - reduce myocardial preload + reduces strain
- RF modification –> reduced risk of progression
Acute coronary syndrome - Sx caused by sudden reduced BF to the myocardium
- Dx:
- ST-elevation = STEMI
- Troponin raised = NSTEMI (+ dynamic T-wave inversion, ST depression)
- Unstable angina pectoris (pain at rest) = ischemia NOT infarct
- Generic ACS Mx - MONA BASH
- ALL immediate:
- 5-10mg Morphine IV + Nitrates (GTN spray)
- Dual antiplatelet therapy (DAPT) - 300mg Aspirin STAT + 300mg Clopidogrel STAT (or 180mg PO Ticagrelor)
- ALL long-term:
- Continue DAPT
- 1 year: 75mg OD Aspirin + 75mg OD Clopidogrel (or 90mg BD Ticagrelor)
- >1yr - 75mg OD Aspirin
- B-blocker (1.25-10mg Bisoprolol OD)
- ACEi (1.25-10mg Ramipril OD)
- Statin (80mg Atorvastatin OD)
- Continue DAPT
- ALL immediate:
- STEMI Mx: establish coronary reperfusion ASAP
- Sx <12hrs: PCI BUT if no PCI within 2hrs Dx –> thrombolysis (e.g. tPA - tissue plasminogen activator)
- Sx >12hrs: invasive coronary angiography ± PCI if needed
- PCI:
- If having PCI give Prasugrel (instead of Clopi/Ticagrelor)
- PCI accessed via radial (or femoral) artery, guidewire passed via X-ray guidance into the affected coronary artery AND IV unfractionated heparin during the procedure –> stent inserted impregnated with an anti-proliferative agent (e.g. Tacrolimus - to prevent adverse tissue reaction) –> takes longer for endothelialization of stent so DAPT needed for 1yr
- If PCI with stents inserted –> DAPT 12 months
- NSTEMI Mx:
- 2.5mg SC Fondaparinux (direct factor 10a inhibitor)
- Risk stratify - GRACE criteria (& others)
- High risk = invasive coronary angiography (within 48-72hrs)

Angiography & PCI
- Access usually gained through radial artery (or femoral) –> guide wire passed up through axillary artery –> subclavian artery –> relevant coronary artery
- Guidewire passed via X-ray guidance into the affected coronary artery
- IV unfractionated heparin during the procedure
- PCI - stent inserted impregnated with an anti-proliferative agent** (e.g. Tacrolimus - to prevent adverse tissue reaction) –> takes longer for endothelialization of stent so **DAPT needed for 1yr

Heart failure def? Pathophysiology? Categories & Causes? Ix? Mx?
Def: pumping of blood by heart insufficient to meet the demands of the body
Pathophysiology:
- RHF - right side of the heart pumps deoxygenated blood from the body to the lungs to be reperfused - if the RH is not pumping effectively you get the fluid collection in the peripheries = PERIPHERAL OEDEMA
- LHF - left side of the heart pumps oxygenated blood from the lungs to the body - if the LH is not pumping effectively you pooling of blood in the lungs = PULMONARY OEDEMA
- Reduced CO –> shock, tachycardia, AKI
- CO = SV*HR
- Ejection fraction = SV/End-diastolic Volume
Categories:
- HF w/ preserved ejection fraction (left ventricular >50%) = inadequate filling of ventricles during diastole (from ventricular stiffness)
- Causes of ventricular stiffness:
- Volume overload (valve regurg)
- Pressure overload (HTN)
- Decreased distensibility (constrictive pericarditis)
- Causes of ventricular stiffness:
- HF w/ reduced ejection fraction (left ventricular <40%) = inadequate emptying of ventricles during systoles (from outflow obstruction/impaired contractility)
- Causes of outflow obstruction/impaired contractility:
- MI, Cardiomyopathy, Arrythmia
- Causes of outflow obstruction/impaired contractility:
Ix:
- Bedside: ECG - detects if anything precipitating HF (arrhythmia/ischaemic event)
- Bloods: ABG (if resp compromise from pul oedema), troponin (ACS), BNP (HF screening)
- Imaging: CXR (visualise pul oedema, cardiomegaly), ECHO (valvular abn/regional wall mov abn)
Mx: MON BA (out of MONA BASH)
- Immediate:
- Sit the patient up (reduce venous return to heart –> less strain)
- O2 15L/min NRM
- Medical:
- IV furosemide (loop diuretic) - remove excess fluid + venous dilation (reduce preload)
- Nitrates (GTN/Isosobide Mononitrate) AND Morphine - reduce preload on the heart
- Long-term:
- Reduced ejection fraction - prognostic benefit:
- B-blocker (bisoprolol) - reduce strain on heart, do not give acutely if severe HF as will kill them
-
ACEi - reduce strain on heart
- After the above if LVEF <35% & Sx –> mineralocorticoid antagonist e.g. spironolactone
- 3rd line - by specialist: Sacubitril/Valsartan (entresto), Ivabradine & CRT
- SGLT2 inhibitors (dapagliflozin)
- RF modification - poor glycaemic control/high cholesterol
- Sx (diuretics)
- Reduced ejection fraction - prognostic benefit:

How does heart failure look on CXR?
Pulmonary oedema (fluffy alveolar shadowing = bilateral perihilar consolidation = batwings distribution) ±:
- Kurly B-lines (peripheral septal lines)
- Cardiomegaly (thoracic ratio >0.5)
- Upper lobe venous diversions (tubes going up towards apex instead of lines)
- Pleural effusion (costo-phrenic blunting)

Atrial fibrillation (AF)
- Def? Causes? Ix? Mx?
Def: rapid, chaotic, and ineffective atrial electrical conduction
- ECG def: irregularly irregular narrow complex tachycardia with no p waves
Causes: idiopathic, cardio (IHD, valvular disease, cardiomyopathy), resp (PE, pneumonia), hyperthyroidism, alcohol
Ix: ECG (absence of p-waves, irregularly irreg rhythm)
Mx:
- Haemodynamically unstable (≤90 BP, chest pain, acute HF) –> DC Cardioversion
OR
- Rate control –> B-blocker (bisoprolol) OR rate-limiting CCB (verapamil - asthma)
OR
- Rhythm control - ONLY if clear reversible cause
- Sx onset <48hrs –> DC/chemical cardioversion (amiodarone/flecanide)
- NOTE: IV heparin started prior to cardioversion
- Sx onset >48hrs –> anticoagulate for 3wks –> elective cardioversion (also anticoag for 4wks after)
- Sx onset <48hrs –> DC/chemical cardioversion (amiodarone/flecanide)
AND
- Stroke risk - CHADS-Vasc Vs Orbit/HAS-BLED score –> DOAC (Apixaban)
- If metallic heart valve –> warfarin INR 3-3.5
- Otherwise DOAC
- NOTE: if incidental non-symptomatic AF - normal rate, no other RFs, CHA2DS2-VASc 0 –> anticoagulation not recommended
-
CHF, HTN, Age ≥75rs (2), DM, Stroke (2), Vascular disease, Age 65-74, Sex - female
- Score 1 - consider; ≥2 - DOAC/Warfarin needed
- Lifetime risk = annual risk x estimated years of life left (up to 80 yrs e.g. if 60 then x annual risk by 20)
Types of anticoagulant
Heparins
- LMWH (SC) - VTE prophylaxis BUT bad for renal function
- UFH (SC/IV) - GOOD for renal function as a rapid reversal BUT heparin-induced thrombocytopenia (hypercoag state) risk needs APTT ratio monitoring
DOACs - oral + no monitoring BUT bad for renal function e.g. Apixaban (BD), Rivaroxaban (OD)
Vit K antagonist = Warfarin if weight extremes, reduced renal function or AF w/ MS/mechanical heart valve BUT INR monitoring + drug interactions
Virchow’s triad to determine anticoag vs antiplatelets
1) Stasis - coag factor activation–> venous clot (AF, DVT/PE)
* Anticoags (DOAC/Hep/Warfarin) are most effective as coag factors cause clot
2) Vessel wall injury - plaque rupture - thrombogenic material release –> platelets activated –> arterial thrombosis (MI, stroke)
* Antiplatelets (Aspirin/Clopidogrel) most effective as platelets cause clots
3) Hypercoagulability - does not change acutely
SVT - Def? Types? Presentation - case example? Mx?

Def: regular narrow-complex tachycardia with no p-waves + supraventricular origin
Junctional types:
- AVNRT - local re-entry circuit within AV node
- AVRT - re-entry circuit between atria and ventricles –> after SVT termination = delta wave = WPW syndrome:
- Assoc w/ HOCM
- Avoid digoxin, verapamil, amiodarone (reduce conduction down SAN –> worsen retrograde conduction –> risk of VT)
- Can use B-blocker/flecainide instead
Case example: 23yrs, 1-hr palpitations + SoB, 2 similar episodes prev following alcohol, this time severe chest pain
Mx:
- Unstable tachycardia (<90 BP/chest pain/acute heart failure) –> synchronised DC Cardioversion
-
Vagal manoeuvres (increase parasympathetic stim via vagus nerve to slow conduction via AV node)
- Valsalva manoeuvre (blow out through nose while pinching + shut mouth) - breath through 50ml syringe
-
Adenosine 6mg –> 12 mg –> 12mg
- NOTE: if adenosine CI (e.g. asthma) –> VERAPAMIL (rate-limiting CCB)
- Other:
- IV B-blocker/amiodarone/digoxin
- Synchronised DC Cardioversion

Key heart murmurs?
Accentuation manoeuvres?
Causes?
Left vs right heart valve abn epidemiology?
Mx?
Key murmurs:
-
AS = ejection systolic + radiates to carotids, slow rising pulse, narrow pulse pressure, heaving apex beat
- Sound: Wooooshhh
- Severe AS - absent/soft 2nd heart sound, reversed splitting of 2nd HS, heaving apex beat
- A longer murmur is worse (small space for blood to pass through = takes longer)
-
MS = mid-diastolic + LLP, malar flush, AF, loud/palpable S1 “tapping” apex, pul HTN (loud P2 - pul thrill)
- Sound: Wooosh de (loud S1) de (early diastolic snap)
-
AR = early diastolic + sitting forward (LLSE), collapsing pulse, wide pulse pressure, displaced apex
- Sound: de woooshhhh
- Severe AR –> Austin-flint murmur = ‘Rumbling mid-diastolic murmur’
- Best heard at apex, caused by blood flowing back through aortic valve and over mitral valve
- Shorter murmur is worse (quicker to flow back through large hole)
-
MR = pan-_systolic_ + radiates to left axilla, AF, displaced thrusting apex, LVF/pul HTN
- Sound: Woooooshhh (holosystolic)
- NOTE: same pattern for pulmonary & tricuspid (pul stenosis & tricuspid regurgitation = systolic)
- TR - pulsatile liver
- PS - radiates to back, assoc w/ Noonan’s (AD, webbed neck, wide-spaced eyes etc.)
Accentuation manoeuvres:
- R-sided murmurs (tricuspid + pulmonary) –> louder on INspiration = blood goes IN to right-side of heart
- L-sided murmurs (aortic + mitral) –> louder on EXpiration = blood EXits left-side of heart
- AS radiates to the carotids + louder on leaning forward + listen on right sternal edge
- MS louder on turning to the left, MR radiates to axilla
Causes:
- AS (stenosis/sclerosis): senile calcification (aortic valve)
- MR: IHD (papillary-muscle dysfunction post-MI), Infective endocarditis, cardiomyopathy, RHD
- AR: acute (infective endocarditis, aortic dissection), chronic (CTD, RHD, HTN, congenital)
- MS: rheumatic heart disease (RHD)
Left vs Right valve abn:
- Left = more common as higher pressure system, more likely in damaged valves, commonly Strep Viridans
- Right = more common in IV drug users –> tricuspid valve is first valve reached, commonly S. aureus
Management:
- AS:
- C: 6-monthly ECHO, exercise-stress test if asymptomatic
- M: RF optimisation (statins, HTN, DM), HF Sx (diuretics, ACEi)
- S: Based on severity/comorbid - STS-PROM (surgical risk calc)
- If severe AS:
- Medically fit (req midline sternotomy & cardiopul bypass) = Surgical aortic valve replacement (SAVR)
- Not fit = Transcatheter aortic valve replacement (TAVR)
- Acutely Sx/cardiogenic shock = Balloon valvuloplasty
- If severe AS:
- MR:
- M:
- ACEi ± B-blockers (as HTN worsens MR)
- Tx AF & anti-coagulate
- Diuretic (if refractory to surgery)
- S: for acute MR (post-MI, chordae tendinae rupture), asymptomatic LVEF <60%, symptomatic LVEF >30%
- Valve _R_epair > _R_eplacement
- M:
- AR:
- M: asym + Reassurance (good prog)
- Unfit for surgery/waiting - ACEi & vasodilators (e.g. hydralazine)
- S: acute/Sx/severe = surgery
- Valve _R_eplacement > _R_epair
- M: asym + Reassurance (good prog)
-
MS:
- C: asymptomatic - Monitor
- M:
- AF Tx, anti-coagulate & diuretics (if Sx/severe)
- S: Sx/severe - can do balloon valvuloplasty/replacement
- Valvuloplasty = lateral thoracotomy scar
- Do not do percutaneously if persistent left atrial thrombus/rigid calcified valve –> need open heart surgery (CABG, concurrent severe MS)

MI location based on ECG
- Inferior – right coronary artery (2,3, aVF foot)
- Anterior – left anterior descending artery (V1-2)
- Lateral – circumflex artery (1 ,aVL, V5/6)
- Posterior - ST depression in V2-4, abnormal R wave in V2

Infective endocarditis - RFs? Ix? Dx criteria? Mx?
Acute vs subacute bacterial endocarditis - what hearts affected? who are commonly affected? What bacteria most likely?
Def: infection of heart valves (typically mitral/aortic or tricuspid in IVDU)
RFs: bacteraemia (long-term lines, IVDU, dental work), abn valves (prosthetic, RHD), prev endocarditis, VSD, piercings
Presentation: low-grade fevers, night sweats
- Exam:
- Splenomegaly
- Splinter haemorrhages, osler’s nodes, Janeway lesions, petechiae, Roth spots (eyes)
- Chronic = clubbing (rare, mostly acute now)
Ix:
- Urine dip - haematuria
- Serial BCs (x3 but start empirical abx), ESR
- Transoesophageal Echo (TOE - vegetations)
Dx: DUKE’S CRITERIA (2 major OR 1 major + 3 minor OR 5 minor):
- Major: +ve BC (typical organism), new regurg murmur/veg on echo
- Minor: RF, fever (>38), embolic (vascular) phenomena, immune phenomena, +ve BC (another organism)
- Mx: IV abx for 6wks – fluclox/vanc/gent
Acute in structurally normal heart – In IV drug user the first valve met is tricuspid valve, commonly S. aureus (also most common cause in prosthetic valve endocarditis)
Subacute in structurally abn heart – mitral & aortic valves more commonly affected as high pressure system, more likely damaged valves, commonly Strep Viridans (overall most common cause of endocarditis)
ECG Important Considerations
- Make sure to compare to a previous ECG = dynamic changes (acute)
- Coronary infarcts commonly present as T-wave inversion/RBBB/LBBB, not always with ST-elevation/depression
NSTEMI Mx? Scoring? Ix?
Immediate:
- Aspirin PO stat AND Ticagrelor OR Clopidogrel PO stat
- Fondaparinux SC
On discharge (give all despite BP/HR):
- Aspirin for life
- Ticagrelor OR Clopidogrel for 1 year (2 needed for 1 year as stent impregnated with Tacrolimus
- Ramipril (ACEi) - titrate up to 10mg
- Atorvastatin
- Bisoprolol (B-blocker) - titrate up to 10mg
Scoring Risk: GRACE score
Ix if high risk: cathlab for angiogram (will be started on IV unfractionated heparin instead of fondaparinux as procedure is very thrombogenic) –> PCI (stent)
Heart failure key consequences x2
1) Reduced CO (SV*HR) –> shock, tachycardia, AKI
2) Congestion –> pulmonary oedema + peripheral oedema
Acute HF vs ACS

Irregularly irregular heart rhythm - Dx? Ix? Mx?
AF - narrow complex tachycardia with no p-waves
Ix:
- ECG, Echo (valve check)
- Bloods - U&E, Mg (QT interval), Troponin (ischaemic), TFTs
Mx:
- Haemodynamically unstable –> DC cardioversion
- Rate control - Bisoprolol 2.5mg OD (max 10mg, can use rate-lim CCB)
- Rhythm control - if clear reversible cause: <48hrs = DC/chemical cardioversion (flecanide/amiodarone); >48hrs = anticoag 3-4wks (clot may have formed)
- Stroke risk Mx - CHADS-Vasc Vs HAS-BLED/ORBIT - Apixabab 5mg BD (DOAC, can use Warfarin)

How do you calculate ejection fraction? What are the different types of HF based on ejection fraction?
Ejection fraction = SV/End Diastolic Volume
HF w/ preserved EF: >50% - inadequate filling of stiff ventricles
- Causes: volume overload (valve regurg), pressure overload (HTN), decreased distensibility (constrictive pericarditis)
- No drugs w/ prognostic benefit, Mx Sx w/ diuretics
HF w/ reduced EF: <40% - inadequate emptying of ventricles from outflow obstruction or impaired contractility
- Causes: MI, cardiomyopathy, arrhythmia
Types of anticoagulant
- Heparins
- LMWH (SC) - VTE prophylaxis BUT bad for renal function
- UFH (SC/IV) - GOOD for renal function as a rapid reversal BUT heparin-induced thrombocytopenia (hypercoag state) risk needs APTT ratio monitoring
- DOACs - oral + no monitoring BUT bad for renal function e.g. Apixaban (BD), Rivaroxaban (OD)
- Vit K antagonist = Warfarin if weight extremes, reduced renal function or AF w/ MS/mechanical heart valve BUT INR monitoring + drug interactions

Virchow’s triad + anticoagulants vs antiplatelets
1) Stasis - coag factor activation–> venous clot (AF, DVT)
* Anticoags are most effective as coag factors cause clot
2) Vessel wall injury - plaque rupture - thrombogenic material release –> platelets activated –> arterial thrombosis (MI, stroke)
* Antiplatelets most effective as platelets cause clots
3) Hypercoagulability - does not change acutely
Bibasal crackles indicates what? Ix? Mx?
Fluid overloaded with pulmonary oedema = acute heart failure
HF = pumping of blood by heart isn’t meeting body demands
Ix:
- Bedside - ECG
- Bloods - ABG, troponin, BNP
- Imaging - CXR, Echo (further down the line)
Acute HF Initial Mx:
- Immediate: sit patient up, O2 15L/min NRM
- Medical: IV furosemide (higher dose if on LT Tx), GTN, Morphine IV
- If no improvement: repeat furosemide (after 15mins) –> consider CPAP
Long-term HF Mx:
- Reduced ejection fraction - prognostic benefit:
- B-blocker (bisoprolol) - reduce strain on heart
- ACEi - reduce strain on heart
- SGLT2 inhibitors (dapagliflozin)
- RF modification - poor glycaemic control/high cholesterol
- Sx (diuretics)
ECG changes in IHD
ST-elevation
Ischaemic changes
- Dynamic T-wave inversion
- ST depression

What heart condition is malar flush associated with?

Mitral stenosis
Key features of mitral stenosis
- Malar flush
- Middle-aged female
- AF
- Tapping apex beat (palpable/loud first heart sound)
- Quiet blowing mid-diastolic murmur –> accentuate leaning to left and listening over mitral area while holding breath exhaled –> if can’t be heard then would get the patient to do exercise
Complications of MI
FAP (failure, arrhythmias, pericarditis)
Arrythmias (incl. VF)
Heart failure
Pericarditis
- Early - positional chest pain day after MI –> give NSAIDs
- Late - Dressler’s syndrome - immune response @6wks (fever, pleuritic chest pain, pericarditis/pericardial effusion)






