Cardiology Flashcards
Describe the chest pain in stable angina.
- Brought on by exercise;
- Resolves with resting.
Describe the pain in pulmonary embolism
- Pleuritic in nature;
- Dyspnoea;
- Cough
- Tachycardia;
- Hypoxia
- Haemoptysis
- Leg swelling & other features of DVT.
Describe the pain in acute coronary syndrome.
- Pain for > 10min;
- Pain on rest or minimal exertion;
- Radiates to left arm and left jaw;
- Retrosternal pain (tightness, pressure);
- Diaphoresis;
- Dyspnoea;
- Nausea and vomiting.
Describe the pain and other symptoms of aortic dissection.
- Sudden tearing chest pain irradiating to the back in between the scapulas;
- Diaphoresis;
- Hypontension;
- Tachycardia;
- Different blood pressures and pulses in between arms;
- Abnormal or absent periphereal pulses.
Describe the symptoms of pericarditis.
- Pericardial friction rub
- Sharp pleuritic pain;
- Relieved by sitting forward;
- Worse with inspiration and body movements
- Fever;
- Cough;
- Similar to angina pain (but it changes with body position/movement unlike in angina).
What are the causes of pericarditis?
- (Post) viral infections: Coxsackie virus;
- Post MI: Dressler’s syndrome;
- Tuberculosis;
- Uraemia
- Trauma
- Connective tissue disease;
1st two are most important for the exam.
What is the ECG presentation in pericarditis?
Limb leads (I, II, III, aVL and aVF) and precordial leads (V2-V6)
* Concave ST elevation (saddle shape) of 0.5 - 1mm;
* PR depression
aVR lead
* ST depression
* PR elevation
Describe what is acute mitral regurgitation after MI.
- Seen 2-10 days after MI;
- Caused by papillary muscle dysfunction or partial rupture;
- (More) associated with inferior MI;
What are the symptoms of acute mitral regurgitation after MI?
- Dyspnoea;
- Haemodynamic instability.
Acute MR after MI
What is the 1st line for diagnosis?
Echocardiogram.
What is the treatment in pericarditis?
- NSAIDS: in most cases;
- Colchicine: prevents recurrence
Describe the management of adult tachycardia.
- ABCDE
Haemodynamically unstable tachycardia:
* Synchronised DC (direct shock) cardioversion
Haemodynamically stable tachycardia:
1. QRS ≥0.12 s (broad)
2. QRS <0.12s (narrow)
Broad QRS
* Regular: VT (amiodarone IV)
* Irregular: VF, Torsades de pointes, polymorphic VT, Wolff-Parkinson-White syndrome
Narrow QRS
* Regular: SVT
* Irrgular: AF
Describe ventricular tachycardia
- It is a broad complex (QRS) tachycardia;
- It impairs CO leading to hypotension, acute cardiac failure
- HR: 100 - 250 bpm
TREATMENT
1. With pulse:
Stable
* Amiaodarone
* Procainamide
* Lidocaine
* Flecainide
Unstable
Syncronised cardioversion
2. Without pulse:
Defribrillation
What is the function of anticoagulants?
They disrupt the coagulation cascade, reducing the frequency and extent of clot formation.
Describe the simplified coagulation cascade.
Intrisic pathway:
* Factor 9 ⟶9a
Extrinsic pathway:
* Factor 7⟶7a
Common pathaway:
* Factor 10⟶10a
* Prothrombin ⟶ Thrombin
* Fibrinogen ⟶ Fibrin
* CLOT FORMATION
Describe the pharmacology of warfarin
Class:
* Vitamin K antagonist.
MOA:
* ↓ the synthesis of vit K dependent clotting factors.
Use:
* Requires monitoring of INR;
* In VTE/PE requires rapid loading so bridge gap cover with LMWH until INR > 2 on two consecutive days.
* In AF slow loading so no bridge gapping with LMWH needed.
* Many interacion with medicines, food and herbals.
Reversal agent
* Vitamin K
* Prothrombin factor
* Fresh frozen plasma
Describe the pharmacology of DOAC’s:
-Apixaban
-Rivaroxaban
-Edoxaban
MOA: Factor Xa inhibitor.
Use:
* Baseline renal & liver function tests to start the administartion;
* No INR monitoring;
* Rivaroxaban needs to be taken with food to ↑ bioavailability.
Reversal agent:
* Andexanet alfa
Describe the pharmacology of DOAC’s:
* Dabigatran
MOA: Thrombin inhibitor
Use:
*Baseline renal & liver function tests to start the administartion;
* No INR monitoring;
* Needs to be taken with food to ↓ GI side effects.
Reversal agent:
* Idarucizumab
Describe the pharmacology of unfractioned heparin (UFH):
MOA:
* Inactivation of factor Xa
* Inactivaction of thrombin
* Inactivation of factor IXa
* Inactivation of 7a
Use:
* Imediate action after administration
* Short life
* Immediate reversibility
* Preferred on those at risk of bleeding
Reversal agent:
* Protamine
Describe the pharmacology of LMWH:
* Enoxiheparin
* Dalteparin
* Tinzaparin
MOA:
* Inactivation of factor Xa
* Inactivaction of thrombin
Use:
* Can be used SC
* Easier than UFH in terms of monitoring
* Can be used in pregnancy (doesn’t cross the placenta)
* Low risk of HIT
* Contraindicated in renal impairment (eGFR < 30 ml/min)
Reversal agent:
* Protamine
Name the causes of aortic stenosis.
1st world causes
- Degenerative calcification (older patient > 65YO);
- Bicuspid aortic valve (younger patients).
3rd world: Rheaumatic heart disease.
Symptoms of aortic stenosis
- Angina: ↓EF causing ↓ myocardial perfusion;
- Syncope: ↓EF causing ↓ cerebral perfusion
- Dyspnoea: fluid buildup
Describe the murmur of aortic stenosis
- Ejection systolic murmur
- Heard at 2nd intercostal space (right sternal border)
- Louder in expiration
- Radiates to the carotids
What is the investigation of choice in aortic stenosis?
Echocardiogram.
Describe the step by step classification of ACS
Ischaemic chest pain present
* Left sided, substernal or central;
* Radiates to the left arm, shoulder or jaw
* Can be silent MI in diabetic patients (without pain)
* Sweating
* Hypotension
12 lead ECG
ST elevation
* ST elevation MI (STEMI)
No ST elevation
* Measure troponin
Raised troponin
* Non-ST elevation MI (NSTEMI)
Normal troponin
* Unstable angina
Treatment for ACS upon arrival and confirmation
Dual antiplatelets aggregation
* AAS 300 mg
* Clopidogrel 300 mg
Anticoagulation
* Fondaparinux SC
* If on DOAC’s use LMWH (dalteparin/enoxiheparin) instead of fondaparinux
Antihypertensives
* ACEI
* Beta blockers
Statins
* Atorvastatin 80mg
STEMI: Describe the different ECG changes.
Inferior wall MI:
* ST elevation in lead II, III and aVF
* Coronary artery affected: Right Coronary Artery (80%) and Left Circumflex (20%)
Anterior wall MI
* ST elevation in leads V1-V4
* Coronary artery affected: LDA
Lateral wall MI:
* ST elevation in leads I, aVL, V5-V6
* Coronary artery affected: LCX
Posterior wall MI
* ST elevation in leads V7-V9
* Coronary artery affected: LCX and RCA
Describe the initial / immediate management for STEMI.
MONA
* Morphine IV
* O₂
* Nitrates (avoid in low BP and inferior wall MI)
* Antiplateletes (AAS 300 mg & consider clopidogrel 300mg)
Describe the definitive / GOLD standard management for STEMI.
Percutaneous coronary intervention:
* Within 12 h of symptoms onset
Thrombolysis:
* If PCI in not available within 120 min
* Perform within 12h of symptoms onset
* Alteplase or tenecteplase
Angiography with follow up rescue PCI: if persistent ST ↑ after thrombolysis.
Describe the long term management for STEMI.
- AAS for life
- Statins for life
- ACEi’s or ARB’s for life
- Beta blockers for 12 months
- Clopidogrel/Ticagrelor/Prasugrel for 12 months.
Define what is the CHA₂DS₂-VASc score
- It’s a score used to assess a person’s stroke risk.
- It used in AF to determine the most appropriate anticoagulation strategy.
Based on CHA₂DS₂-VASc score, when to offer anticoagulation treatment?
- When score is ≥ 2 (both men and women).
- When score is = 1(in men).
CHA₂DS₂-VASc score
≥ 65 YO or at least 1 comorbidity
Give DOAC.
CHA₂DS₂-VASc score
<65 and no comorbidities
Don’t give DOAC.
What is the management of AF with unstable vitals?
Signs of shock, syncope, acute cardiac failure or ischaemia.
Electric cardioversion.
What is the management of AF with stable vitals?
- Rate control (B-blockers)
- Rhythm control / chemical cardioversion
- Anticoagulation (CHA₂DS₂-VASc 1st)
Management of AF with stable vitals
Describe how rate control is done.
1st line:
* B-blockers: metoprolol/atenolol
OR
* (Rate limiting) Calcium channel blocker : Verapamil/Diltiazem
2nd line
If rate is refractory to 1st line
* Add digoxin
* If patient has heart failure digoxin is 1st line (or calcium channel blocker).
If patient has asthma choose calcium channel blockers
Management of AF with stable vitals
Describe how rhythm control (chemical cardioversion) is done.
- Amiodarone
- Flecainide
If patient on AF >48h, rate control and LMWH instead.
Management of AF with stable vitals
When to choose/do rhythm control (chemical cardioversion)?
Flecainide / Amiodarone
Patients that are:
- Symptomatic
- Young
- Presenting with lone AF for the 1st time.
Management of AF with stable vitals
When to choose/do rate control?
Patients that are:
* > 65 YO
* Stable and AF started > 48h (chemical cardioversion might cause thromboembolism)
* History of multiple failed cardioversions.
Management of AF with stable vitals
Anticoagulation (medications lines)
1st line:
* DOAC
2nd line
* Warfarin (if DOAC contraindicated).
What are the features of atrial myxoma?
Obstruction of MV
* Mid-diastolic murmur
* Dyspnoea
* Syncope
Embolisation
Arrhythmias
What is the Gold standard investigation in atrial myxoma?
Echocardiography.
What is the management of atrial myxoma?
Without embolisation
* Surgical removal
With embolisation
* Embolectomy
What are the symptoms of heart failure?
- Dyspnoea / orthopnoea / Paroxystic nocturnal dypnoea
- Fluid retention (ankle swelling)
- Fatigue
What are the causes of heart failure?
- Hypertension
- Valvular disease
- Alcohool
- MI
What are the investigations in heart failure?
- BNP (b-type natriuretic peptide)
- Echo (if BNP⬆︎).
What is the management of chronic heart failure with ⬇︎EF?
► 1st line
* ACE inhibitors / ARBs
OR
* B-blockers
then add
► 2nd line
* Aldosterone antagonist (spironolactone)
then add
► If refractory to all of the above meds
* SGLT₂ inhibitor (Dapagliflozin)
➜ If fluid overload
* Loop diuretics (furosemide)
➜ If atrial fibrillation
* Digoxin
Heart murmurs
Aortic stenosis
- Ejection systolic murmur
- 2nd intercostal space of right sternal border.
Ejection systolic because the LV is forcing blood through a stenotic valve during systole (the valve should be opened).
Heart murmurs
Aortic regurgitation
- Early diastolic murmur
- Left upper sternum border.
The LV pumps blood (ventricular systole) throught an opened AV, then the valve closes and ventricular diastole begins. The valve doesn’t close properly, hence the regurgitation in early diastole.
Heart murmurs
Mitral stenosis
- Mid-late dyastolic murmur
- Opening snap
- Apex
The LV receives blood from the atrium during dyastole (it needs to be relaxed to receive the volume). The inital stage of ventricular filling is passive, in mid to late dyastole, the atrium kicks (contracts) to deliver the rest of its volume. But there’s a stenotic valve that won’t completely open to let the blood flow normally. Hence a loud murmur in mid dyastole.
Heart murmurs
Mitral regurgitation
- Pan-systolic murmur
- Apex
- Radiates to the axilla
Pan-systolic means persisting through systole.
Systole begings when the MV closes, so that the LV can eject its content through the AV and not back through the MV.
So, in MR, the valve is somehow opened, during systole you will hear the back flow of blood through the MV.
Heart murmurs
Pulmonary stenosis
- Ejection systolic murmur
- 2nd intercostal space of left sternal border.
The RV contracts in systole to a stenotic valve (it should be opened). Hence the murmur being heard during systole.
Heart murmurs
Pulmonary regurgitation
- Early diastolic murmur
- 2nd intercostal space of left sternal border.
The RV relaxes in dyastole, the pressure drops. The valve doesn’t close properly, there’s no more pressure proppeling the blood flow forward so it backflows as soon as dyastole begins.
Heart murmurs
Tricuspid stenosis
- Diastolic rumble
- Lower left sternal edge
The RV receives blood from the atrium during diastole (it needs to be relaxed to receive the volume). The inital stage of ventricular filling is passive, in mid to late diastole, the atrium kicks (contracts) to deliver the rest of its volume. But there’s a stenotic valve that won’t completely open to let the blood flow normally. Hence a loud murmur in diastole.
Heart murmurs
Tricuspid regurgitation
- Pan-systolic murmur
- Lower left sternal edge
Systole begings when the TV closes, so that the RV can eject its content through the PV and not back through the TV.
So, in TR, the valve is somehow opened, during systole you will hear the back flow of blood through the TV.
Heart murmurs
Ventricular septal defect
- Pan-systolic murmur
- Left lower sternal border
Heart murmurs
Patent ductus arteriosus
- Continuous machinnery murmur
- Left infraclavicular area
Atrial flutter
- Sawtooth pattern of the P wave
- Regular R waves
- Treatment is the same is AF
Management of V-tach
►Stable patient (pulse present)
✿ Pharmacological cardioversion (amiodarone, flecainide, lidocaine)
➜ If above failed: synchronised cardioversion
►Unstable patient
✿ Pulse present: Electrical cardioversion
✿ No pulse: Defibrillation
Broad QRS / Regular / No P waves
Management of V-fib
Defibrillation.
Management of supraventricular tachychardia
► It is managed by RATE CONTROL
◘ Stable patients
➜ 1st line:
Valsava manoeuvres or carotid massage
➜ 2nd line:
-Adenosine 6mg IV bolus
-If failed: repeat 12mg adenosine IV
-If failed: repeat 18mg adenosine IV
➜ 3rd line:
Verapamil or B-blockers
➜ 4th line
Electrical cardioversion
◘ Unstable patients
➜ ELECTRICAL CARDIOVERSION
Prevention of episodes: B-blockers or radio ablation.
If asthmathic patient do not use adenosine or b-blockers. Only verapamil.
What are the causes of Torsades de Pointes?
- Long QT syndrome
- Electrolyte abnormalities:
-Hypomagnesemia
-Hypokalaemia
-Hypocalcaemia - Erhytromicin
- Antipsychotics
What is the management of Torsades de Pointes?
- Magnesium sulphates IV
- Correction of electrolyte abnormalities
- Stop the causative drug
- If it progresses to Vfib ➝ defibrillation.
What is familial hypercholesterolaemia?
Genetic inherited condition resulting in high levels of cholesterol in the blood.
When to suspect hypercholesterolaemia?
- Cholesterol > 7.5 mmol
- Personal of family history of premature coronary heart disease (before 60yo).
Describe 1st degree heart block
- PR interval > 0.2 sec (>5 small squares).
- There is conduction delay without interrumption from atria to ventricules.
Normal PR interval: 0.12 - 0.2 sec (3 to 5 small squares).
Name the causes of 1st degree heart block
- Increased vagal tone
- Electrolyte disturbances (hyperkalaemia)
- Inferior MI
- AV nodal blocking drugs (B-blockers, calcium channel blockers, digoxin, amiodarone)
- MV surgery
- Athlets
- As an isolated finding it is a benign entity that does not cause haemodynamic instability.
- No specific treatment is required for 1st degree heart block.
Name the types of 2nd degree heart block.
- Mobitz type I AV block (Wenckebach)
- Mobitz type II AV block
Describe the 2nd degree heart block Mobitz I (Wenckebach).
- Progressive prolongation of the PR interval, culminating in a non-conducting P wave.
What are the causes of Mobitz I (Wenckebach) AV block?
◉ Drugs:
* Beta-blockers
* Amiodarone
* Digoxin
* Calcium channel blockers
◉ ↑ vagal tone:
* Athletes
◉ Inferior MI
◉ Post cardiac surgery:
* MV repair
* Tretalogy of fallot repair
◉ Myocarditis
What is the treatment for Mobitz I (Wenckebach) AV block?
◉ Symptomatic:
* Atropine
◉ Asymptomatic:
* No treatment required
Describe the 2nd degree heart block Mobitz II.
- PR interval is constant
- P waves that do not conduct can be seen (dropped QRS).
What is the treatment for Mobitz II AV block?
➜ Initial treatment:
* Atropine
➜ Most appropriate treatment:
* Temporary pacing (until treated with a pacemaker)
Describe the 3rd degree (complete) heart block.
- No association between P waves and QRS complex.
- Atria and ventricles contract independently.
What are the causes of the 3rd degree (complete) heart block?
- Inferior MI
- Lyme disease
- AV nodal blocking drugs (b-blocker, calcium channel blockers, amiodarone, digoxin).
What is the treatment for 3rd degree (complete) heart block.
➜ Initial treatment:
* Atropine
➜ Most appropriate treatment:
* Temporary pacing (until treated with a pacemaker)
➜ Definitive treatment:
* Pacemaker
Name and describe the classification stages of hypertension.
◉ Stage 1 hypertension
- Clinic BP: >= 140/90 mmHg
AND
- Ambulatory or home blood pressure monitor: >= 135/85 mmHg
◉ Stage 2 hypertension
- Clinic BP: >= 160/100 mmHg
AND
- Ambulatory or home blood pressure monitor: >= 150/95 mmHg
◉ Stage 3 hypertension / Severe hypertension
- Clinic: Systolic >= 180 mmHg
OR
- Clinic: diastolic >= 120 mmHg
Describe the management treatment for stage 1 hypertension.
◉ Healthy patient
- Lifestyle changes only.
◉ Patient < 80 y.o.
➜ Treat if presenting with ≥1 of the following:
- Target organ damage
- Cardiovascular disease
- Renal disease
- DM
- A 10 year cardiovascular risk >= 10%.
Describe the management treatment for NON DIABETIC stage 2 hypertension.
◉ STEP 1
- < 55 yo: ACEi / ARB
- ≥ 55 yo: CCB (calcium channel blocker)
- African / afro-Caribbean: CCB
➜If BP still > 140/90, advance to step 2
◉ STEP 2
- < 55 YO: ACEi / ARB + CCB or thiazide-like diuretic.
- ≥ 55 YO:CCB + ACEi / ARB or thiazide-like diuretic.
- African / afro-Caribbean: CCB + ACEi / ARB or thiazide-like diuretic.
◉ STEP 3
- ACEi / ARB + CCB + thiazide-like diuretic.
Describe the management treatment for stage 2 hypertension with DIABETES.
◉ STEP 1:
1. ACEi / ARB
2. If black: ARB (less angiodema risk)
◉ STEP 2
- Add CCB or thiazide-like diuretic
◉ STEP 3
- ACEi / ARB + CCB + thiazide-like diuretic
Describe the BP targets on patients on antihypertensives.
Clinic BP targets:
- < 80 YO: < 140/90
- > 80 YO: < 150/90
DM
- Same as clinic
CKD + DM
- < 130/80
Describe the management of ABPM / HBPM results.
Stage 1 hypertension (BP ≥ 135/85)
- Offer lifestyle changes.
Stage 2 (BP ≥ 150/95)
- Start Rx
Describe the management of clinic BP results.
Stage 1 hypertension ≥ 140/90:
- Offer ABPM
NO STAGE 2
Stage 3 ≥180/120:
- Signs of target organ damage present: same day hospital referral.
- Absent signs of organ damage: start Rx.
Describe the presentation and symptoms of infective endocarditis.
➜ Fever + New murmur
* Congestive cardiac failure
* Janeway lesions: painless, erythematous lesions on palm or sole.
* Osler nodes: raised and tender nodes on the fingers.
* Roth spots: white spots on retina surrounded by hemorrhage.
* Splinter hemorrhage: on the nail beds.
What are the risk factors for infective endocarditis?
- Valvular heart disease
- Valve replacement
- IV drug user
- Dentristy procedures
What are the pathogens associated with causing infective endocarditis?
◉ Most common pathogens:
* S. aureus
* Streptococous
➜ Mitral valve is affected
◉ Injection drug users:
* S. aureus
➜ Tricuspid valve affected
What is the initial step on the management of infective endocarditis?
➜ 1st: Blood culture
➜ 2nd: Echo
Describe how the diagnosis of infective endocarditis is made.
◉ Modified Duke criteria
Diagnosis is made if:
➝ 2 major criteria
➝ 1 major + 3 minor criteria
➝ 5 minor criteria
► Major criteria:
* Positive blood cultures on 2 different occasions;
* Echo: showing abcess formation / new valve regurgitagion;
► Minor criteria:
* IV drug user / Predisposing heart condition;
* Fever ≥ 38ºC;
* Vascular phenomenon: embolus, splinther hemorrhage, janeway lesions;
* Immunological phenomenon: Roth spot, Osler’s nodes;
* Positive blood culture not meeting major criteria.
Describe the Rx of infective endocarditis.
► Native valve:
* Amoxicilin + Gentamicin
* MRSA: Vancomycin + Gentamicin
► Prosthetic valve:
* Vancomycin + Gentamicin + Rifampin
Describe the investigations done after a syncope episode.
- ECG (arrhythmias)
- Blood pressure (supine and standing/sitting)
- Blood glucose
Name what other investigation can be done in syncopal episodes when the main 3 are incoclusive.
Tilt table test.
Describe the ECG features of LBBB.
► Lead V6
* Broad complex QRS
* “M” shape QRS
* (Can also be seen in lead I and aVL).
► Lead V1
* Deep S wave in V1
* “W” shape S wave
➜ V6 is more important.
➜ V6: when placing the electrodes on the chest, V6 is located to the far left so remember LBBB=V6.
Describe the ECG features of RBBB.
► Lead V1
* “M” shape QRS complex
➜ V1: when placing the electrodes on the chest, V1 is located to the center right so remember RBBB=V1
What are the symptoms of Mitral regurgitation?
◉ Left ventricullar failure:
* Dyspnoea
* Orthopnoea
* Paroxymal nocturnal dyspnoea
➜ Signs of pulmonary congestion
◉ Right sided heart failure:
➜ With severe and chronic MR
* Oedema
* Ascites
✿Pansystolic/systolic murmur at the apex radiating to the axilla.
What is the cause of Mitral valve stenosis?
➜ Most commonly due to rheumatic fever.
What is the non-surgical Rx of patent ductus arteriosus?
- Indomethacin
- Ibuprofen
What is the investigation of choice on a STABLE patient with Abdominal Aortic Aneurysm (AAA)?
► Gold standard:
* CT angiography
What is the investigation of choice on an UNSTABLE patient with Abdominal Aortic Aneurysm rupture (AAA)?
- FAST scan.
What is the management of an UNSTABLE patient with Abdominal Aortic Aneurysm rupture (AAA)?
- IV fluids
- Emergency surgery / FAST SCAN
If surgery is an option than pick it, if not FAST.
Describe the 4 characteristics of TOF.
Congenital cyanotic heart disease
1. Pulmonary artery stenosis
2. Right ventricular hyperthrophy
3. Ventricular septal defect
4. Overriding of the Aorta (it overrides the VSD).
Right to left shunt, hence the cyanosis.
- Ejection systolic murmur (VSD doesn’t cause a murmur here).
- X-ray: boot shaped heart.
- Right to left shunt caused by the pulmonary stenosis.
Describe the management of troponin levels.
◉ Less than 3h of symptoms onset:
* > 30ng/L ⟶ treat as ACS
* < 12ng/L ⟶ repeat after 3h of symptoms onset
◉ More than 3h of symptoms onset:
* > 30ng/L ⟶ treat as ACS
* < 12ng/L ⟶ ACS unlikely ⟶Stable angina ⟶ Refer to cardiology outpatient
