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Cardio Flashcards

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1
Q

Medical co-morbidities increase the risk of atherosclerosis and should be carefully managed to minimise the risk

A
  • Diabetes
  • Hypertension
  • Chronic kidney disease
  • Inflammatory conditions e.g. RA
  • Atypical antipsychotic medications
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2
Q

end result of atherosclerosis

A
  • Angina
  • Myocardial infarction
  • Transient ischaemic attacks
  • Strokes
  • Peripheral arterial disease
  • Chronic mesenteric ischaemia
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3
Q

scoring system that estimates the percentage risk that a patient will have a stroke or myocardial infarction in the next 10 years

A

QRISK

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4
Q

CVD primary prevention medication and indications

A

Atorvastatin 20mg to all patients with:
- CKD (eGFR < 60 ml/min/1.73 m2)
- T1DM for>10 years or are 40+ yrs
- QRISK >10%

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5
Q

how do statins reduce cholesterol production

A

in the liver by inhibiting HMG CoA reductase

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6
Q

blood test after starting a statin

A
  • check lipids 3 months after starting statins and increasing the dose to aim for a greater than 40% reduction in non-HDL cholesterol
  • LFTs within 3 months of starting a statin and again at 12 months. Can cause slight increase in ALT and AST initially. Ok so long as <3x normal
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7
Q

rare and significant side effects of statins

A
  • Myopathy
  • Rhabdomyolysis
  • Type 2 diabetes
  • Haemorrhagic strokes (very rarely)
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8
Q

medication that interacts with statins

A

macrolides (erythro/calrithromycin)

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9
Q

other cholesterol lowering drugs

A
  • Ezetimibe: inhibits the absorption of cholesterol in the intestine. Can combine with bempedoic acid, a drug that reduces cholesterol production in the liver.
  • PCSK9 inhibitors (e.g., evolocumab and alirocumab) are monoclonal antibodies that lower cholesterol.
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10
Q

Secondary prevention of CVD

A

4A’s
A – Antiplatelet medications (e.g., aspirin, clopidogrel and ticagrelor)
A – Atorvastatin 80mg
A – Atenolol (or alternative BB) titrated to the max tolerated dose
A – ACE inhibitor (commonly ramipril) titrated to the max tolerated dose

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11
Q

medication post MI

A

dual antiplatelet treatment with:
- Aspirin 75mg daily (continued indefinitely)
- Clopidogrel or ticagrelor (generally for 12 months before stopping)

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12
Q

Management of familial hypercholesterolaemia involves:

A
  • Specialist referral for genetic testing and testing of family members
  • Statins
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13
Q

what is angina

A

caused by atherosclerosis affecting the coronary arteries, narrowing the lumen and reducing blood flow to the myocardium

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14
Q

Immediate sx relief for angina

A
  • GTN: vasodilation
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15
Q

Long term sx relief for angina

A
  • Beta blocker (e.g., bisoprolol)
  • Calcium-channel blocker (e.g., diltiazem or verapamil – both avoided in heart failure with reduced ejection fraction)
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16
Q

Medications for secondary prevention of angina

A

4As mnemonic:
A – Aspirin 75mg once daily
A – Atorvastatin 80mg once daily
A – ACE inhibitor (if diabetes, hypertension, CKD or heart failure are also present)
A – Already on a beta blocker for symptomatic relief

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17
Q

Vessels used in CABG

A
  • Saphenous vein (harvested from the inner leg)
  • Internal thoracic artery, also known as the internal mammary artery
  • Radial artery
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18
Q

Two coronary arteries branch from the root of the aorta

A

Right coronary artery (RCA)
Left coronary artery (LCA)

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19
Q

RCA curves around the right side and under the heart and supplies

A
  • Right atrium
  • Right ventricle
  • Inferior aspect of the left ventricle
  • Posterior septal area
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20
Q

left coronary artery becomes the

A

Circumflex artery
Left anterior descending (LAD)

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21
Q

circumflex artery curves around the top, left and back of the heart and supplies the

A

Left atrium
Posterior aspect of the left ventricle

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22
Q

left anterior descending (LAD) travels down the middle of the heart and supplies the:

A

Anterior aspect of the left ventricle
Anterior aspect of the septum

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23
Q

patients at risk of silent MI

A

diabetics

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24
Q

ECG changes in STEMI and NSTEMI

A

STEMI: LBBB and ST elevation
NSTMI: ST depression, T wave inversion

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25
Anatomy of heart
Left coronary artery, Anterolateral view, leads I, aVL, V3-6 Left anterior descending, Anterior, V1-4 Circumflex, Lateral view, I, aVL, V5-6 Right coronary artery, Inferior view, II, III, aVF
26
reasons for troponin rise
- MI - Sepsis - PE - CKD - myocarditis - aortic dissection
27
Causes of ACS
- Left atrium likely to cause clot (embolism)- can cause MI or stroke. Coronary embolism from AF - Plaque rupture MC cause ACS- 95% - SCAD: spontaneous coronary artery dissection. Younger women 30-50. blood in subintimal space, bruised artery causing bleeding and dissection. - Cocaine induced vasospasm can cause ACS
28
how to classify STEMI
- > 1 lead that are next to each other - ST elevation - Chest leads need more than 2mm in 2 or more leads next to each other, because they are anatomically closer together. In v1-6 - Limb leads need more than 1mm in 2 or more leads next to each other. - New left bundle branch block: counts as a STEMI. Can’t always see ST segments. There are 2 sub branches, so to have LBBB is most likely STEMI because both are blocked - Posterior STEMI: ST elevation at back means needs ST depression in the front v1-3. Dominant R wave in v1-3 more likely to be posterior STEMI.
29
Mx of ACS
1. 10mg metaclopramide and morphine 2. 300mg aspirin- stop platelets sticking together in plaque rupture. 3. Only give oxygen if not stable 4. Give clopidogrel (same dose as aspirin) or ticagrelor (used more often now. 180mg) both anti platelets 5. Send off for PCI <2hrs or thrombolysis >2hrs Give unfractionated heparin for stent operation: better than LMWH because can give protamine to reverse it if necessary + short half life
30
discharging medication with ACS
1. aspirin 75mg 2. clopi 75mg or ticagrelor (dual antiplatelet with aspirin) 3. 80mg atorvastatin for secondary prevention 4. Bisoprolol 2.5mg/1.25mg and build up slowly to 10mg (to prevent VF post infarct. Main cause of death post MI) 5. ACEi- give ramipril 1.25/2.5 mg exactly like bisoprolol. Has same max dose 10mg as bisoprolol (reduce HF by 1/3. So want to prevent HF, prevents atherosclerosis too) all for life exc clopi stop after 1 yr
31
Mx of NSTEMI
1. 10mg metaclopramide 2. Morphine 3. 300mg aspirin- stop platelets sticking together in plaque rupture. 4. Give clopidogrel (same dose as aspirin) or ticagrelor (used more often now. 180mg) both anti platelets 5. Recheck chest pain, give GTN if yes
32
why does GTN work in NSTEMI but not STEMI
vessel is not fully blocked so can be used, because GTN works by reducing after load, less work for the heart to push against (e.g. reducing 180 to 120). Can also reduce preload, overall reducing the amount of blood the heart needs. In an NSTEMi because vessel is not totally occluded reducing the amount of blood needed can solve the ischaemia, whereas in STEMI vessel is totally occluded so will have no impact. GTN can cause shock. It can never work in a STEMI patient so giving them GTN can make them more likely to go into shock. Nitrates given to NSTEMI and unstable angina only.
33
Do NSTEMI go to cathlab
yes but not emergency if no ongoing chest pain give fondaparinux Would not give early in case they need to go to cathlab and need heparin. Do not give to STEMI or NSTEMI/unstable angina with ongoing chest pain.
34
what is the GRACE score
6-month probability of death after having an NSTEMI 3% or less = low risk >3%= med/high risk (PCI within 72hrs)
35
complications of MI
DREAD D – Death R – Rupture of the heart septum or papillary muscles E – “oEdema” (heart failure) A – Arrhythmia and Aneurysm D – Dressler’s Syndrome
36
Dressler's syndrome
- post MI syndrome - occurs 2 – 3 weeks after acute MI - caused by a localised immune response that results in inflammation of the pericardium - presents with pleuritic chest pain, low-grade fever and a pericardial rub on auscultation. - ECG (global ST elevation and T wave inversion), echo (pericardial effusion)
37
Mx of Dressler's syndrome
- NSAIDs (e.g., aspirin or ibuprofen) - severe= steroids - Pericardiocentesis may be required to remove fluid from around the heart
38
types of MI
Type 1: Traditional MI due to ACS Type 2: Ischaemia secondary to increased demand or reduced supply of oxygen (e.g. secondary to severe anaemia, tachycardia or hypotension) Type 3: Sudden cardiac death or cardiac arrest suggestive of an ischaemic event Type 4: MI associated with procedures such as PCI, coronary stenting and CABG “ACDC” mnemonic: Type 1: A – ACS-type MI Type 2: C – Can’t cope MI Type 3: D – Dead by MI Type 4: C – Caused by us MI
39
causes of pericarditis
- Idiopathic - Infection (e.g., tuberculosis, HIV, coxsackievirus, Epstein–Barr virus and other viruses) - Autoimmune and inflammatory conditions (SLE) - Injury to the pericardium (e.g., after myocardial infarction, open heart surgery or trauma) - Uraemia secondary to renal impairment - Cancer - Medications (e.g., methotrexate)
40
Mx of pericarditis
NSAIDs colchicine to prevent recurrence
41
what is cardiac tamponade
Pericardial effusion is large enough to raise the intra-pericardial pressure--> squeezes the heart and affects its ability to function-->reduces heart filling during diastole, decreasing cardiac output during systole. This is an emergency and requires prompt drainage of the pericardial effusion to relieve the pressure.
42
presentation of pericarditis
- Low-grade fever - Chest pain - Pericardial rub on auscultation The chest pain is: - Sharp - Central/anterior - Worse with inspiration (pleuritic) - Worse on lying down - Better on sitting forward
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Ix in pericarditis
- Blood tests: raised inflammatory markers - ECG: Saddle-shaped ST-elevation, PR depression - Echo: pericardial effusion
44
cardiac output equation
CO = SV x HR
45
triggers of acute left ventricular failure
- Iatrogenic (e.g., aggressive IV fluids in a frail elderly patient with impaired left ventricular function) - Myocardial infarction - Arrhythmias - Sepsis - Hypertensive emergency (acute, severe increase in blood pressure)
46
presentation of acute LVF
- SOB worse lying flat - Type 1 respiratory failure picture (low oxygen without an increased carbon dioxide). - Cough with frothy white or pink sputum - Raised RR, reduced O2, tachycardic - 3rd heart sound - Bilateral basal crackles (sounding “wet”) - Hypotension in severe cases (cardiogenic shock)
47
Mx of acute LVF
SODIUM S – Sit up O – Oxygen D – Diuretics I – Intravenous fluids should be stopped U – Underlying causes need to be identified and treated (e.g., myocardial infarction) M – Monitor fluid balance
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HF w reduced and preserved ejection fraction percenages
reduced = <50% preserved = >50%. issue with LV filling during diastole
49
Causes of heart failure
- Ischaemic heart disease - Valvular heart disease (commonly aortic stenosis) - Hypertension - Arrhythmias (commonly AF) - Cardiomyopathy
50
presentation of HF
- raised JVP - SOB, worse on exertion - Cough, which may produce frothy white/pink sputum - Orthopnoea - Paroxysmal nocturnal dyspnoea - Peripheral oedema - Fatigue
51
what is paroxysmal AF
intermittent AF and palpitations still need to do chadsvasc and consider apixaban anticoagulation
52
what is Paroxysmal nocturnal dyspnoea
suddenly waking at night with a severe attack of shortness of breath, cough and wheeze
53
classification system to grade the severity of symptoms related to heart failure
New York Heart Association (NYHA) Class I: No limitation on activity Class II: Comfortable at rest but symptomatic with ordinary activities Class III: Comfortable at rest but symptomatic with any activity Class IV: Symptomatic at rest
54
Mx of HF
BNP 400–2000 ng/litre =echo by 6wks > 2000 ng/litre = echo within 2 wks diuretics ABAL” mnemonic: - A: ACEi/ARB titrated as high as tolerated - B: BB titrated as high as tolerated - A: Aldosterone antagonist if sx not controlled with A and B (reduced EF) - L: Loop diuretics
55
side effects of ACE inhibitors and aldosterone antagonists
hyperkalaemia
56
surgical procedures fo chronic heart failure
- Implantable cardioverter defibrillators continually monitor the heart and apply a defibrillator shock to cardiovert the patient back into sinus rhythm if they identify a shockable arrhythmia. If pt had VT/VF - Cardiac resynchronisation therapy (CRT) used in severe HF with EF < 35%. Biventricular (triple chamber) pacemakers, with leads in the right atrium, right ventricle and left ventricle. The objective is to synchronise the contractions in these chambers to optimise heart function. - Heart transplant
57
causes of hypertension
- primary or secondary (ROPED) - Renal disease (MC secondary) (renal artery stenosis) - Obesity - Pregnancy/pre-eclampsia - Endocrine (conn's - Drugs
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diagnosis of hypertension
Stage 1: > 140/90 clinic, 135/85 home Stage 2:>160/100 clinic, 155/95 home Stage 3: >180/120 clinic
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tests for end organ damage in hypertension
- fundoscopy - urine albumin:creatinine - ECG - bloods
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Mx of hypertension
- lifestyle - A: ACE inhibitor - B: Beta blocker - C: Calcium channel blocker - D: Thiazide-like diuretic - ARB: Angiotensin II receptor blocker Step 1: Aged under 55 or type 2 diabetic of any age or family origin, use A. Aged over 55 or Black African use C. Step 2: A + C. Alternatively, A + D or C + D. Step 3: A + C + D Step 4: A + C + D + fourth agent (see below) 4. < 4.5 mmol/L spironolactone. > 4.5 mmol/L alpha blocker (e.g., doxazosin) or a beta blocker
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treatment target of hypertension
<80y/o = 140/90 >80 y/o = 150/90
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Mx of accelerated (malignant) hypertension
Sodium nitroprusside Labetalol Glyceryl trinitrate Nicardipine
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Erb's point
Third ICS on the left sternal border and is the best area for listening to heart sounds (S1 and S2).
64
Murmur grades
Grade I: Difficult to hear Grade II: Quiet Grade III: Easy to hear Grade IV: Easy to hear with a palpable thrill Grade V: Audible with stethoscope barely touching the chest Grade VI: Audible with stethoscope off the chest
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valvular causes of hypertrophy
- Mitral stenosis causes left atrial hypertrophy - Aortic stenosis causes left ventricular hypertrophy - Mitral regurgitation causes left atrial dilatation - Aortic regurgitation causes left ventricular dilatation
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Aortic stenosis
- most common valvular heart disease - ejection-systolic, high-pitched, crescendo-decrescendo character - radiates to the carotids as the turbulence continues into the neck - Slow rising pulse - exertional syncope - "whoosh dub"
67
causes of aortic stenosis
- Idiopathic age-related calcification (MC) - Bicuspid aortic valve: young - Rheumatic heart disease
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aortic regurgitation
- incompetent aortic valve, allowing blood to flow back from the aorta into the left ventricle - early diastolic, soft murmur - apex diastolic “rumbling” murmur. This is caused by blood flowing back through the aortic valve and over the mitral valve, causing it to vibrate. - Collapsing pulse - Wide pulse pressure - head bobbing - quincke sign (nails) - HF and pulmonary oedema - "dub whoosh"
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causes of aortic regurgitation
- Idiopathic age-related weakness - Bicuspid aortic valve - Connective tissue disorders, such as Ehlers-Danlos syndrome and Marfan syndrome
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mitral stenosis
- narrowed mitral valve restricting blood flow from the left atrium into the left ventricle - mid-diastolic, low-pitched “rumbling - loud S1 due to thick valves requiring a large systolic force to shut, then shutting suddenly. There is an opening snap after S1 - Malar flush - Atrial fibrillation
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causes of mitral stenosis
Rheumatic heart disease Infective endocarditis
72
Mx of mitral stenosis
- Asymptomatic: regular echo - Symptomatic: percutaneous mitral balloon valvotomy or mitral valve surgery (commissurotomy, or valve replacement) - if also AF need warfarin
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mitral regurgitation
- blood flows back from the left ventricle to the left atrium during systolic contraction of the left ventricle. The leaking valve causes a reduced ejection fraction and a backlog of blood waiting to be pumped through the left side of the heart, resulting in congestive cardiac failure - 2nd MC - pan-systolic, high-pitched “whistling” - third heart sound - HF and pulmonary oedema - Atrial fibrillation
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Causes of mitral regurgitation
- Idiopathic weakening of the valve with age - Ischaemic heart disease - Infective endocarditis - Rheumatic heart disease - Connective tissue disorders, such as Ehlers-Danlos syndrome or Marfan syndrome
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tricuspid regurgitation
- pan-systolic murmur. - split second heart sound due to the pulmonary valve closing earlier than the aortic valve, as the right ventricle empties faster than the left ventricle - Raised JVP with giant C-V waves (Lancisi’s sign) - Pulsatile liver (due to regurgitation into the venous system) - Peripheral oedema - Ascites
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Causes of tricuspid regurgitation
- Pressure due to left-sided heart failure or pulmonary hypertension (“functional”) - Infective endocarditis - Rheumatic heart disease - Carcinoid syndrome - Ebstein’s anomaly - Connective tissue disorders, such as Marfan syndrome
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pulmonary stenosis
- narrowed pulmonary valve, restricting blood flow from the right ventricle into the pulmonary arteries. - ejection systolic murmur loudest in the pulmonary area with deep inspiration - widely split second heart sound (LV empties faster than RV) - Raised JVP with giant A waves (due to the right atrium contracting against a hypertrophic right ventricle) - Peripheral oedema - Ascites
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causes of pulmonary stenosis
usually congenital and may be associated with: - Noonan syndrome - Tetralogy of Fallot
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tetralogy of fallot
congenital condition where there are four coexisting pathologies: Ventricular septal defect (VSD) Overriding aorta Pulmonary valve stenosis Right ventricular hypertrophy
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types of prosthetic valves
- Bioprosthetic valves - 10yr lifespan. “Porcine” - Mechanical valves- lifespan (well over 20 years) but require lifelong anticoagulation with warfarin. The INR target range with mechanical valves is 2.5 – 3.5
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complications of mechanical heart valves
- Thrombus formation - Infective endocarditis - Haemolysis causing anaemia
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Transcatheter Aortic Valve Implantation (TAVI)
treatment for severe aortic stenosis catheter into the femoral artery inflating a balloon to stretch the stenosed aortic valve and implanting a bioprosthetic valve in the location of the aortic valve
83
organisms for IIE in prosthetic valve
gram-positive cocci organisms: Staphylococcus Streptococcus (viridans) Enterococcus rarer pseudomonas, HACEK, fungi
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RF for infective endocarditis
- Intravenous drug use - Structural heart pathology (VHD, prosthetic, pacemaker, congenital, HOCM) - Chronic kidney disease - Immunocompromised - Hx of infective endocarditis
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most common organism in IE
staph aureus staph epidermididis if valve replacement 1-2 months
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criteria to diagnose infective endocarditis
Duke's criteria (1maj +3min or 5minor) Major criteria are: 1. Positive blood cultures 2. Specific imaging (e.g. a vegetation on echo) Minor criteria are: 1. Predisposition (e.g., IVDU or heart valve pathology) 2. Fever above 38°C 3. Vascular phenomena (e.g., splenic infarction, intracranial haemorrhage and Janeway lesions) 4. Immunological phenomena (e.g., Osler’s nodes, Roth spots and glomerulonephritis) 5. Microbiological phenomena (e.g., positive cultures not qualifying as a major criterion)
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Mx of infective endocarditis
IV broad spec abx (amox +/- gentamicin) 4 weeks for OG heart valves 6 weeks for prosthetic valves surgery if no response to abx, large vegetation
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Hypertrophic obstructive cardiomyopathy (HOCM)
- left ventricle becomes hypertrophic - Asymmetrically affect the septum of the heart, blocking the flow of blood out of the left ventricle = left ventricular outflow tract (LVOT) obstruction. - assoc with HR and MI - bisferiens pulse (feel 2 pulse beats)
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Mx of HOCM
A-E - Amiodarone - BB or verapamil - Cardioverter defibrillator (for those at risk of sudden cardiac death or ventricular arrhythmias) - Dual Chamber Pacemaker - Endocarditits prophylaxis - Surgical myectomy - Alcohol septal ablation (shrink the obstructive tissue)
90
things to avoid with HOCM
- Intense exercise, heavy lifting, deydration - ACEi - nitrates
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types of cardiac myopathy
- dilated - alcohol induced - restrictive - arrhythmogenic - Takotsubo: LV dysfunction and weakness following severe emotional stress (broken heart syndrome) - HOCM
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AF
arrhythmia, disorganised electrical activity of atria - irregularly irregular ventricular contractions
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Causes of AF
SMITH - Sepsis - mitral valve pathology - IHD - Thyrotoxicosis - Hypertension (+alcohol and caffeine)
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differentials for irregularly irregular pulse
AF ventricular ectopics (disappear when HR is high)
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Mx of AF
rate or rhythm control anticoagulation to prevent strokes
96
Rate control for AF
all patients with AF should have rate control as first-line, except with: - A reversible cause - New onset atrial fibrillation (within the last 48 hours) - Heart failure caused by AF - Symptoms despite being effectively rate controlled 1. BB 2. CCB 3. Digoxin
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rhythm control for AF
offered to patients with: - A reversible cause - New onset atrial fibrillation (within the last 48 hours) - Heart failure caused by AF - Symptoms despite being effectively rate controlled 1. Cardioversion immediate if unstable or <48hrs. Use flecainide or amiodarone or electrical or delayed >48hrs, use electrical, anticoagulate for 3 weeks 2. Long-term rhythm control using medications (BB, dronedarone, amiodarone)
98
Mx of paroxysmal AF
pill in the pocket (flecainide)
99
ablation for AF
when can't tolerate rhythm or rate control - left arterial ablation - AVN ablation + pacemaker
100
CHADSVASC
C – Congestive heart failure H – Hypertension A2 – Age above 75 (scores 2) D – Diabetes S2 – Stroke or TIA previously (scores 2) V – Vascular disease A – Age 65 – 74 S – Sex (female) 1 consider, 2 give
101
Anticoagulants in stroke prevention in AF
DOAC Warfarin 2nd line
102
ORBIT score
risk of major bleeding in patients with atrial fibrillation taking anticoagulation O – Older age (age 75 or above) R – Renal impairment (GFR less than 60) B – Bleeding previously (history of gastrointestinal or intracranial bleeding) I – Iron (low haemoglobin or haematocrit) T – Taking antiplatelet medication
103
Normal electrical signal pathway in heart
SAN-->atria -->AVN-->bundle of his-->purkinje fibres ventricles
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what is supraventricular tachycardia
electrical signal re-entering atria from the ventricles, causing narrow complex tachycardia
105
narrow complex tachycardias
QRS <0.12 or <3 small squares 1. Sinus tachycardia 2. Supraventricular tachycardia 3. Atrial fibrillation 4. Atrial flutter
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sinus tachycardia
- normal P wave, QRS complex and T wave - not an arrhythmia - due to sepsis or pain
107
Atrial fibrillation
- absent p waves - narrow QRS complex tachycardia - irregularly irregular ventricular rhythm
108
Atrial flutter
- around 300bpm - saw tooth patten - QRS regular - often 2 atrial contractions to one ventricular contraction 2:1, 3:1 or 4:!
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Supraventricular tachycardia
- looks like QRS followed immediately by T wave - there are p waves but often buried in the T waves - regular rhythm - abrupt onset - can appear at rest with no cause
110
3 main types of SVT
1. atrioventricular nodal re-entrant tachycardia: re-entry point back through AVN. MC. 2. Atrioventricular re-entrant tachycardia: re-entry point is an accessory pathway. WPW syndrome 3. Atrial tachycardia: signal originates in the atria but not in SAN
111
Wolff Parkinson White Syndrome
- extra electrical pathway connecting the atria and ventricles - pre excitation syndrome - can have no sx or SVT - Short PR interval, wide QRS, delta wave
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Mx of Wolff Parkinson White syndrome
- radiofrequency ablation of accessory pathway
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possible consequence of WPW + A fib/flutter
- polymorphic wide complex tachycardia- emergency - can lead to VF and cardiac arrest
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medications contraindicated in WPW syndrome
anti-arrhythmic medications (e.g. BB, CCB, digoxin and adenosine) reduce conduction through AVN and promote conduction through the accessory pathway
115
Mx of SVT w non life threatening features
continuous ECG monitoring 1. vagal manoeuvres 2. adenosine 3. verapamil or BB 4. synchronised DC cardioversion
116
Mx of SVT with life threatening features
- synchronised DC cardioversion under sedation - IV amiodarone if DC shocks are unsuccessful
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what are vagal manoeuvres
stimulate vagus nerve increasing PNS activity, slowing heart activity - valsalva manoeuvre (blow into syringe) - carotid sinus massage - diving reflex
118
Half life of adenosine
<10 seconds
119
When to avoid adenosine
- asthma - COPD - HF - heart block - severe hypotension - potential atrial arrhythmia with underlying pre-excitation
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dose of adenosine
6mg, 12mg, 18mg
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what to use instead of adenosine if contraindicated
IV verapamil
122
synchronised DC cardioversion
- timed with ventricular contraction - used in pt with a pulse
123
when to use shock with no synchronicity
- pulseless VT - VF
124
paoxysmal SVT and mx
recurrent episodes of SVT Mx: BB/CCB/amiodarone or radiofrequency ablation
125
what is radiofrequency ablation
done in cath lab + sedation burns abnormal electrical pathway
126
shockable rhythms
- ventricular tachycardia - ventricular fibrillation
127
non-shockable rhythms
- pulseless electrical activity (all except VF/VT) - asystole (no significant electrical activity)
128
Broad complex tachycardia
QRS > 0.12s or 3 small squares
129
Types of broad complex tachycardia
1. VT or unclear cause (amiodarone) 2. polymorphic VT e.g. torsades de pointes (IV mag sulph) 3. AF with bundle branch block (treat same as AF) 4. SVT with bundle branch block (treat as SVT)
130
prolonged QT interval
- >440ms men or 460 female - represents prolonged repolarisation of myocytes
131
torsades de pointes
- "twisting of spikes" - looks like VT but QRS twists around baseline - height of QRS gets progressively smaller than larger and repeat - will terminate spontaneously or turn to VT
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Causes of prolonged QT (torsades)
- long QT syndrome (inherited) - Medications (antipsychotics, citalopram, flecainide, sotalol, amiodarone +macrolides) - Electrolyte imbalances (hypokalaemia, hypomagnesaemia and hypocalcaemia - hypothermia
133
Mx of prolonged QT interval
- stop meds that prolong and correct electrolytes - BB - pacemakers or implantable cardioverter defibrillators
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acute Mx of torsades de pointes
- correct cause - magnesium infusion - defibrillation if turns to VT
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What are ventricular ectopics
- premature ventricular beats caused by random electrical discharges outside the atria - common - more common with heart conditions - otherwise normal ecg
136
what is Bigeminy
when every other beat is a ventricular ectopic.
137
Mx of ventricular ectopics
- nothing in health people - specialist in pt has heart diseases or FH - BB
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First degree heart block
- delayed conduction through AVN - prolonged PR interval >0.2s (1 big square) - every P waves followed by QRS
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Second degree heart block
- some atrial impulses do not make it through AVN to ventricles - some p waves not always followed by QRS complexes - Mobitz type 1 and 2
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Mobitz type 1
- Conduction through the AVN takes progressively longer until it finally fails, after which it resets, and the cycle restarts. - increasing PR interval till p wave has no QRS
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Mobitz type 2
- intermittent failure of conduction through the AVN, with an absence of QRS complexes following P waves - PR interval normal - risk of asystole
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3:1 block
set ratio of P waves to QRS complexes
143
2:1 block
-2 P waves for each QRS complex - hard to tell if it is mobitz type 1 or type 2
144
Third degree heart block (complete)
- no relationship between P waves and QRS complexes - risk of asystole
145
Causes of bradycardia
- medications (BB) - heart block - shock sinus syndrome
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what is shock sinus syndrome
- Many conditions that cause dysfunction in the SAN - Often caused by idiopathic degenerative fibrosis of the SAN - Can result in sinus bradycardia, sinus arrhythmias and prolonged pauses.
147
Asystole
absence of electrical activity in the heart (resulting in cardiac arrest). Risk of asystole in: - Mobitz type 2 - Third-degree heart block - Previous asystole - Ventricular pauses > 3s
148
Mx of unstable patients and those at risk of asystole
- IV atropine (1st line) - Inotropes (e.g., isoprenaline or adrenaline) - Temporary cardiac pacing - Permanent implantable pacemaker
149
Options for temporary cardiac pacing
- transcutaneous pacing - transvenous pacing
150
side effects of atropine
- pupil dilation - dry mouth - urine retention - constipation
151
Indications for a pacemaker
- Symptomatic bradycardias (e.g., due to sick sinus syndrome) - Mobitz type 2 heart block - Third-degree heart block - Atrioventricular node ablation for atrial fibrillation - Severe heart failure (biventricular pacemakers)
152
What are single chamber pacemakers
- lead in either RA or RV - RA if issue with SAN - RV if issue with AVN
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What are dual chamber pacemakers
- leads in both RA and RV - coordinates contraction of atria and ventricles
154
What is a Biventricular (Triple-Chamber) Pacemaker
- in severe HF - leads in RA, RV, LV - cardiac resynchronisation therapy
155
what are implantable cardioverter defibrillators
- continually monitor heart and apply a shock if they identify VT or VF - used in pt with previous cardiac arrest, HOCM, long QT syndrome
156
ECG changes with a pacemaker
A line before each P wave = a lead in the atria. A line before each QRS = a lead in the ventricles. Therefore: - A line before either the P wave or QRS complex but not the other = single-chamber pacemaker - A line before both the P wave and QRS complex = dual-chamber pacemaker
157
side effects of BB
bronchospasm cold peripheries fatigue sleep disturbances, including nightmares erectile dysfunction
158
side effect of continuous nitrates
development of tolerance, which results in reduced therapeutic effects.
159
medication contraindicated in aortic stenosis
nitrates due to risk of profound hypotension
160
Ix for stable angina
1st line: CT coronary angiography
161
what is coarctation of the aorta
narrowing of the descending aorta M > F
162
associations of coarctation of the aorta
Turner's syndrome bicuspid aortic valve berry aneurysms neurofibromatosis
163
signs of coarctation of aorta
- elevated blood pressure - radiofemoral delay - CXR: notching of the ribs in the mid- clavicular line
164
Beck's triad of cardiac tamponade
- hypotension - elevated JVP - muffled heart sounds
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Mx of cardiac tamponade
urgent pericardiocentesis
166
Classification of aortic dissection
tanford classification type A - ascending aorta, 2/3 of cases type B - descending aorta, distal to left subclavian origin, 1/3 of cases DeBakey classification type I - originates in ascending aorta, propagates to at least the aortic arch and possibly beyond it distally type II - originates in and is confined to the ascending aorta type III - originates in descending aorta, rarely extends proximally but will extend distally
167
Ix for aortic dissection
- CT angiography of the chest, abdomen and pelvis is the investigation of choice - CXR widened mediastinum - Transoesophageal echocardiography (TOE) for more unstable patients
168
Mx of aortic dissection
Type A - surgical management, control BP to a target systolic of 100-120 mmHg whilst awaiting intervention Type B conservative management bed rest reduce blood pressure IV labetalol to prevent progression
169
Takayasu's arteritis
- large vessel vasculitis. - causes occlusion of the aorta - absent limb pulse - assoc with renal artery stenosis
170
Mx of Takayasu's arteritis
- steroids
171
ECG in hypercalcaemia
short QT interval
172
ECG in hypothermia
J wave
173
ECG signs of hypokalaemia
prolonged PR interval prominent U waves ST depression long QT small or absent T waves
174
side effects of thiazide diuretics
hypercalcaemia and hypocalciuria
175
Left ventricular heart failure heart sounds
gallop rhythm s3
176
Normal heart sounds
- S1) closure of the mitral and tricuspid valves - (S2) aortic and pulmonary valve closure
177
Heart sounds S1
- closure of mitral and tricuspid valves - soft if long PR or mitral regurgitation - loud in mitral stenosis
178
Heart sounds S2
- closure of aortic and pulmonary valves - soft in aortic stenosis - splitting during inspiration is normal - loud in pulmonary hypertension
179
Heart sounds S3
- caused by diastolic filling of the ventricle - normal if < 30 years old (may persist in women up to 50 years old) - heard in left ventricular failure (e.g. dilated cardiomyopathy), constrictive pericarditis (called a pericardial knock) and mitral regurgitation
180
Heart sounds S4
- may be heard in aortic stenosis, HOCM, hypertension - caused by atrial contraction against a stiff ventricle - therefore coincides with the P wave on ECG - in HOCM a double apical impulse may be felt as a result of a palpable S4
181
Medication to be avoided in HOCM
- ACEi (can reduce afterload and worsen LVOT) - nitrates - inotropes
182
how to identify LBBB and RBBB
WiLLiam and MaRRoW - in LBBB there is a 'W' in V1 and a 'M' in V6 - in RBBB there is a 'M' in V1 and a 'W' in V6
183
Causes of RBBB
- normal with increasing age - right ventricular hypertrophy - chronically increased right ventricular pressure - e.g. cor pulmonale - pulmonary embolism - myocardial infarction - ASD (ostium secundum) - cardiomyopathy or myocarditis
184
Complications of MI
- cardiac arrest - cardiogenic shock - chronic heart failure - tachyarrhythmias - bradyarrhythmias - pericarditis - LV aneurysm - LV free wall rupture - VSD - acute mitral regurgitation
185
Pericarditis post MI
within first 48hrs
186
Dressler's syndrome
- within 2-6 weeks - fever, pleuritic pain, pericardial effusion and a raised ESR - Mx = NSAIDs
187
Left ventricular aneurysm
- ischaemia weakens myocardium - associated with persistent ST elevation and left ventricular failure - bibasal crackles - presence of a S3 and S4
188
LV free wall rupture
- within 1-2 weeks post MI - acute heart failure secondary to cardiac tamponade (raised JVP, pulsus paradoxus, diminished heart sounds). - Mx = Urgent pericardiocentesis and thoracotomy
189
VSD post MI
- within the first week - acute heart failure associated with a pan-systolic murmur - Mx = surgery
190
acute mitral regurgitation post MI
- More common with infero-posterior infarction - due to ischaemia/ rupture of the papillary muscle - Acute hypotension and pulmonary oedema may occur - Early-to-mid systolic murmur - Mx = vasodilator therapy + emergency surgical repair
191
side effects of warfarin
- haemorrhage - teratogenic, can be used in breastfeeding - skin necrosis: biosynthesis of protein C is reduced -->temporary procoagulant state after initially starting warfarin, normally avoided by concurrent heparin administration --> thrombosis may occur in venules leading to skin necrosis - purple toes
192
Medication contraindicated in ventricular tachycardia
- verapamil - can precipitate cardiac arres
193
Acute heart failure mx
- IV loop diuretics - oxygen - vasodilator (nitrates) - CPAP if respiratory failure
194
Chronic heart failure drug mx
- ACEI AND BB 1ST LINE - Aldosterone antagonist - SGLT2 inhibitors - Ivabradrine, nitrate, digoxin, CR therapy
195
Brugada syndrome
- inherited AD, result in cardiac death - convex ST segment elevation > 2mm in > 1 of V1-V3 followed by a negative T wave - partial RBB - the ECG changes may be more apparent following the administration of flecainide or ajmaline - this is the investigation of choice in suspected cases of Brugada syndrome
196
Mx of Brugada syndrome
- implantable cardioverter defibrillator
197
Raised INR
- 5-8 + no bleeding = Withhold few doses, reduce maintenance. Restart when INR <5 - 5-8 +minor bleeding = stop warfarin. Vit K slow IV. Restart when INR <5 - >8, no bleed/minor bleed = Stop warfarin. Vitamin K (oral/IV) no bleeding/if risk factors for bleeding or minor bleeding. Check INR daily. - Major bleeding, (including intracranial haemorrhage) = Stop warfarin. Give prothrombin complex concentrate. If unavailable, give FFP. Also give vitamin K IV.
198
signs of right-sided heart failure
- raised JVP - ankle oedema - hepatomegaly
199
Ix for PE
- CTPA - V/Q scan in renal impairment
200
Tests before starting amiodarone
- CXR - TFT - LFT - U+E
201
Takotsubo cardiomyopathy
- apical ballooning - induced by severe stressful triggers - "octopus trap" - bottom of the heart (the apex) does not contract and therefore appears to balloon out. However, the area closer to the top (the base) continues to contract (creating the neck of the octopus trap).
202
Rheumatic fever
develops following an immunological reaction to a recent (2-4 weeks ago) Streptococcus pyogenes infection.
203
How to diagnose rheumatic fever
2 major/1 major + 2 minor (+strep inf) Major - erythema marginatum - Sydenham's chorea: late feature - polyarthritis - carditis and valvulitis (eg, pancarditis) regurgitant murmur - subcutaneous nodules Minor - raised ESR or CRP - pyrexia - arthralgia - prolonged PR interval
204
which part of the heart is affected in ST elevation with third-degree heart block and slow junctional escape rhythm.
inferior aspect it supplies RCA which gives off the AVN artery. so ischaemia can lead to 2nd/3rd degree heart block
205
Nicorandil is most useful in the management of
angina
206
Wellen's syndrome
- caused by high-grade stenosis in the left anterior descending CA - patient's pain may have resolved by presentation and cardiac enzymes may be normal/minimally elevated
207
ECG changes in Wellen's syndrome and Mx
- biphasic or deep T wave inversion in V2-3 - minimal ST elevation - no Q waves - Mx = medical emergency, requiring urgent PCI as per ACS protocol
208
digoxin therapy ECG features
- down-sloping ST depression ('reverse tick', 'scooped out') - flattened/inverted T waves - short QT interval - arrhythmias e.g. AV block, bradycardia
209
where is the lesion in complete heart block following a MI
RCA
210
side effects of GTN spray
Hypotension + tachycardia + headache.
211
Eisenmenger syndrome
reversal of left to right shunt
212
Buerger's disease
- small/medium vessel vasculitis - strongly associated with smoking. Features: - extremity ischaemia - intermittent claudication - ischaemic ulcers - superficial thrombophlebitis - Raynaud's phenomenon
213
Mechanical valves - target INR
aortic: 3.0 mitral: 3.5
214
Murmur assoc with Marfan's
Aortic regurgitation
215
Commonest cardiac defect in Down syndrome
AVSD, rather than ASD
216
ASD examination findings
ejection systolic murmur, louder on inspiration Fixed split S2
217
VSD examination findings
pansystolic murmur hear best on left lower sternal edge palpable thrill
218
Best place for insertion of PCI
Radial access is preferred to femoral access for primary PCI
219
Pulmonary stenosis examination findings
ejection systolic murmur louder on inspiration
220
important cause of falls in the elderly
RBBB +left anterior or posterior hemiblock + 1st-degree heart block = trifasicular block
221
Dextrocardia ECG signs
inverted P wave in lead I, right axis deviation, and loss of R wave progression
222
Mx of aortic stenosis
- asymptomatic = observe pt - symptomatic = valve replacement - asymptomatic but valvular gradient > 40 mmHg and with features such as left ventricular systolic dysfunction = consider surgery (surgical or transcatheter depending on performance status)
223
what are premature ventricular beats
caused by early depolarisation of the ventricular tissue leading to an early contraction. The symptoms are usually brief and self- limited, and the patient may not require any specific treatment. However, it is important to exclude underlying cardiac disease. - thumping palpitations or a sensation of a sudden jump in the heart
224
difference between premature ventricular beats and premature supraventricular beats
can also present as thumping palpitations or a sensation of a sudden jump in the heart but the ECG shows three broad-complex ectopic beats suggesting a ventricular origin
225
surgical intervention for chronic distal aortic and bilateral common iliac occlusive disease.
Aorto-bifemoral bypass graft bypasses the occluded aortic and iliac vessels with a synthetic graft to restore blood flow to the legs
226
causes of dominant R waves in V1
- Normal in children and young adults - Right Ventricular Hypertrophy - Right Bundle Branch Block - Posterior Myocardial Infarction (ST elevation in Leads V7, V8, V9) - Wolff-Parkinson-White (WPW) Type A - Incorrect lead placement (e.g. V1 and V3 reversed) - Dextrocardia - Hypertrophic cardiomyopathy - Dystrophy (duchenne)
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