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Finals > Cardio > Flashcards

Cardio Flashcards

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
Q

Anatomy of heart

A

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

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26
Q

reasons for troponin rise

A
  • MI
  • Sepsis
  • PE
  • CKD
  • myocarditis
  • aortic dissection
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27
Q

Causes of ACS

A
  • 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
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28
Q

how to classify STEMI

A
  • > 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.
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29
Q

Mx of ACS

A
  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

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30
Q

discharging medication with ACS

A
  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

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31
Q

Mx of NSTEMI

A
  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
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32
Q

why does GTN work in NSTEMI but not STEMI

A

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.

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33
Q

Do NSTEMI go to cathlab

A

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.

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34
Q

what is the GRACE score

A

6-month probability of death after having an NSTEMI
3% or less = low risk
>3%= med/high risk (PCI within 72hrs)

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35
Q

complications of MI

A

DREAD
D – Death
R – Rupture of the heart septum or papillary muscles
E – “oEdema” (heart failure)
A – Arrhythmia and Aneurysm
D – Dressler’s Syndrome

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36
Q

Dressler’s syndrome

A
  • 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)
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37
Q

Mx of Dressler’s syndrome

A
  • NSAIDs (e.g., aspirin or ibuprofen)
  • severe= steroids
  • Pericardiocentesis may be required to remove fluid from around the heart
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38
Q

types of MI

A

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

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39
Q

causes of pericarditis

A
  • 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)
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40
Q

Mx of pericarditis

A

NSAIDs
colchicine to prevent recurrence

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41
Q

what is cardiac tamponade

A

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.

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42
Q

presentation of pericarditis

A
  • 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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43
Q

Ix in pericarditis

A
  • Blood tests: raised inflammatory markers
  • ECG: Saddle-shaped ST-elevation, PR depression
  • Echo: pericardial effusion
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44
Q

cardiac output equation

A

CO = SV x HR

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45
Q

triggers of acute left ventricular failure

A
  • 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)
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46
Q

presentation of acute LVF

A
  • 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)
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47
Q

Mx of acute LVF

A

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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48
Q

HF w reduced and preserved ejection fraction percenages

A

reduced = <50%
preserved = >50%. issue with LV filling during diastole

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49
Q

Causes of heart failure

A
  • Ischaemic heart disease
  • Valvular heart disease (commonly aortic stenosis)
  • Hypertension
  • Arrhythmias (commonly AF)
  • Cardiomyopathy
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50
Q

presentation of HF

A
  • raised JVP
  • SOB, worse on exertion
  • Cough, which may produce frothy white/pink sputum
  • Orthopnoea
  • Paroxysmal nocturnal dyspnoea
  • Peripheral oedema
  • Fatigue
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51
Q

what is paroxysmal AF

A

intermittent AF and palpitations
still need to do chadsvasc and consider apixaban anticoagulation

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52
Q

what is Paroxysmal nocturnal dyspnoea

A

suddenly waking at night with a severe attack of shortness of breath, cough and wheeze

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53
Q

classification system to grade the severity of symptoms related to heart failure

A

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

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54
Q

Mx of HF

A

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

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55
Q

side effects of ACE inhibitors and aldosterone antagonists

A

hyperkalaemia

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56
Q

surgical procedures fo chronic heart failure

A
  • 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
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57
Q

causes of hypertension

A
  • primary
    or secondary (ROPED)
  • Renal disease (MC secondary) (renal artery stenosis)
  • Obesity
  • Pregnancy/pre-eclampsia
  • Endocrine (conn’s
  • Drugs
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58
Q

diagnosis of hypertension

A

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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59
Q

tests for end organ damage in hypertension

A
  • fundoscopy
  • urine albumin:creatinine
  • ECG
  • bloods
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60
Q

Mx of hypertension

A
  • 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)

  1. < 4.5 mmol/L spironolactone. > 4.5 mmol/L alpha blocker (e.g., doxazosin) or a beta blocker
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61
Q

treatment target of hypertension

A

<80y/o = 140/90
>80 y/o = 150/90

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62
Q

Mx of accelerated (malignant) hypertension

A

Sodium nitroprusside
Labetalol
Glyceryl trinitrate
Nicardipine

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63
Q

Erb’s point

A

Third ICS on the left sternal border and is the best area for listening to heart sounds (S1 and S2).

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64
Q

Murmur grades

A

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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65
Q

valvular causes of hypertrophy

A
  • 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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66
Q

Aortic stenosis

A
  • 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”
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67
Q

causes of aortic stenosis

A
  • Idiopathic age-related calcification (MC)
  • Bicuspid aortic valve: young
  • Rheumatic heart disease
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68
Q

aortic regurgitation

A
  • 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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69
Q

causes of aortic regurgitation

A
  • Idiopathic age-related weakness
  • Bicuspid aortic valve
  • Connective tissue disorders, such as Ehlers-Danlos syndrome and Marfan syndrome
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70
Q

mitral stenosis

A
  • 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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71
Q

causes of mitral stenosis

A

Rheumatic heart disease
Infective endocarditis

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72
Q

Mx of mitral stenosis

A
  • 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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73
Q

mitral regurgitation

A
  • 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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74
Q

Causes of mitral regurgitation

A
  • 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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75
Q

tricuspid regurgitation

A
  • 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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76
Q

Causes of tricuspid regurgitation

A
  • 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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77
Q

pulmonary stenosis

A
  • 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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78
Q

causes of pulmonary stenosis

A

usually congenital and may be associated with:
- Noonan syndrome
- Tetralogy of Fallot

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79
Q

tetralogy of fallot

A

congenital condition where there are four coexisting pathologies:

Ventricular septal defect (VSD)
Overriding aorta
Pulmonary valve stenosis
Right ventricular hypertrophy

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80
Q

types of prosthetic valves

A
  • 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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81
Q

complications of mechanical heart valves

A
  • Thrombus formation
  • Infective endocarditis
  • Haemolysis causing anaemia
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82
Q

Transcatheter Aortic Valve Implantation (TAVI)

A

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

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83
Q

organisms for IIE in prosthetic valve

A

gram-positive cocci organisms:

Staphylococcus
Streptococcus (viridans)
Enterococcus

rarer
pseudomonas, HACEK, fungi

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84
Q

RF for infective endocarditis

A
  • Intravenous drug use
  • Structural heart pathology (VHD, prosthetic, pacemaker, congenital, HOCM)
  • Chronic kidney disease
  • Immunocompromised
  • Hx of infective endocarditis
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85
Q

most common organism in IE

A

staph aureus
staph epidermididis if valve replacement 1-2 months

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86
Q

criteria to diagnose infective endocarditis

A

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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87
Q

Mx of infective endocarditis

A

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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88
Q

Hypertrophic obstructive cardiomyopathy (HOCM)

A
  • 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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89
Q

Mx of HOCM

A

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)
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90
Q

things to avoid with HOCM

A
  • Intense exercise, heavy lifting, deydration
  • ACEi
  • nitrates
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91
Q

types of cardiac myopathy

A
  • dilated
  • alcohol induced
  • restrictive
  • arrhythmogenic
  • Takotsubo: LV dysfunction and weakness following severe emotional stress (broken heart syndrome)
  • HOCM
92
Q

AF

A

arrhythmia, disorganised electrical activity of atria
- irregularly irregular ventricular contractions

93
Q

Causes of AF

A

SMITH
- Sepsis
- mitral valve pathology
- IHD
- Thyrotoxicosis
- Hypertension
(+alcohol and caffeine)

94
Q

differentials for irregularly irregular pulse

A

AF
ventricular ectopics (disappear when HR is high)

95
Q

Mx of AF

A

rate or rhythm control
anticoagulation to prevent strokes

96
Q

Rate control for AF

A

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
97
Q

rhythm control for AF

A

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
Q

Mx of paroxysmal AF

A

pill in the pocket (flecainide)

99
Q

ablation for AF

A

when can’t tolerate rhythm or rate control
- left arterial ablation
- AVN ablation + pacemaker

100
Q

CHADSVASC

A

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
Q

Anticoagulants in stroke prevention in AF

A

DOAC
Warfarin 2nd line

102
Q

ORBIT score

A

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
Q

Normal electrical signal pathway in heart

A

SAN–>atria –>AVN–>bundle of his–>purkinje fibres ventricles

104
Q

what is supraventricular tachycardia

A

electrical signal re-entering atria from the ventricles, causing narrow complex tachycardia

105
Q

narrow complex tachycardias

A

QRS <0.12 or <3 small squares
1. Sinus tachycardia
2. Supraventricular tachycardia
3. Atrial fibrillation
4. Atrial flutter

106
Q

sinus tachycardia

A
  • normal P wave, QRS complex and T wave
  • not an arrhythmia
  • due to sepsis or pain
107
Q

Atrial fibrillation

A
  • absent p waves
  • narrow QRS complex tachycardia
  • irregularly irregular ventricular rhythm
108
Q

Atrial flutter

A
  • around 300bpm
  • saw tooth patten
  • QRS regular
  • often 2 atrial contractions to one ventricular contraction 2:1, 3:1 or 4:!
109
Q

Supraventricular tachycardia

A
  • 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
Q

3 main types of SVT

A
  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
Q

Wolff Parkinson White Syndrome

A
  • extra electrical pathway connecting the atria and ventricles
  • pre excitation syndrome
  • can have no sx or SVT
  • Short PR interval, wide QRS, delta wave
112
Q

Mx of Wolff Parkinson White syndrome

A
  • radiofrequency ablation of accessory pathway
113
Q

possible consequence of WPW + A fib/flutter

A
  • polymorphic wide complex tachycardia- emergency
  • can lead to VF and cardiac arrest
114
Q

medications contraindicated in WPW syndrome

A

anti-arrhythmic medications (e.g. BB, CCB, digoxin and adenosine) reduce conduction through AVN and promote conduction through the accessory pathway

115
Q

Mx of SVT w non life threatening features

A

continuous ECG monitoring
1. vagal manoeuvres
2. adenosine
3. verapamil or BB
4. synchronised DC cardioversion

116
Q

Mx of SVT with life threatening features

A
  • synchronised DC cardioversion under sedation
  • IV amiodarone if DC shocks are unsuccessful
117
Q

what are vagal manoeuvres

A

stimulate vagus nerve increasing PNS activity, slowing heart activity
- valsalva manoeuvre (blow into syringe)
- carotid sinus massage
- diving reflex

118
Q

Half life of adenosine

A

<10 seconds

119
Q

When to avoid adenosine

A
  • asthma
  • COPD
  • HF
  • heart block
  • severe hypotension
  • potential atrial arrhythmia with underlying pre-excitation
120
Q

dose of adenosine

A

6mg, 12mg, 18mg

121
Q

what to use instead of adenosine if contraindicated

A

IV verapamil

122
Q

synchronised DC cardioversion

A
  • timed with ventricular contraction
  • used in pt with a pulse
123
Q

when to use shock with no synchronicity

A
  • pulseless VT
  • VF
124
Q

paoxysmal SVT and mx

A

recurrent episodes of SVT

Mx: BB/CCB/amiodarone or radiofrequency ablation

125
Q

what is radiofrequency ablation

A

done in cath lab + sedation
burns abnormal electrical pathway

126
Q

shockable rhythms

A
  • ventricular tachycardia
  • ventricular fibrillation
127
Q

non-shockable rhythms

A
  • pulseless electrical activity
    (all except VF/VT)
  • asystole (no significant electrical activity)
128
Q

Broad complex tachycardia

A

QRS > 0.12s or 3 small squares

129
Q

Types of broad complex tachycardia

A
  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
Q

prolonged QT interval

A
  • > 440ms men or 460 female
  • represents prolonged repolarisation of myocytes
131
Q

torsades de pointes

A
  • “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
132
Q

Causes of prolonged QT (torsades)

A
  • long QT syndrome (inherited)
  • Medications (antipsychotics, citalopram, flecainide, sotalol, amiodarone +macrolides)
  • Electrolyte imbalances (hypokalaemia, hypomagnesaemia and hypocalcaemia
  • hypothermia
133
Q

Mx of prolonged QT interval

A
  • stop meds that prolong and correct electrolytes
  • BB
  • pacemakers or implantable cardioverter defibrillators
134
Q

acute Mx of torsades de pointes

A
  • correct cause
  • magnesium infusion
  • defibrillation if turns to VT
135
Q

What are ventricular ectopics

A
  • premature ventricular beats caused by random electrical discharges outside the atria
  • common
  • more common with heart conditions
  • otherwise normal ecg
136
Q

what is Bigeminy

A

when every other beat is a ventricular ectopic.

137
Q

Mx of ventricular ectopics

A
  • nothing in health people
  • specialist in pt has heart diseases or FH
  • BB
138
Q

First degree heart block

A
  • delayed conduction through AVN
  • prolonged PR interval >0.2s (1 big square)
  • every P waves followed by QRS
139
Q

Second degree heart block

A
  • 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
140
Q

Mobitz type 1

A
  • 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
141
Q

Mobitz type 2

A
  • intermittent failure of conduction through the AVN, with an absence of QRS complexes following P waves
  • PR interval normal
  • risk of asystole
142
Q

3:1 block

A

set ratio of P waves to QRS complexes

143
Q

2:1 block

A

-2 P waves for each QRS complex
- hard to tell if it is mobitz type 1 or type 2

144
Q

Third degree heart block (complete)

A
  • no relationship between P waves and QRS complexes
  • risk of asystole
145
Q

Causes of bradycardia

A
  • medications (BB)
  • heart block
  • shock sinus syndrome
146
Q

what is shock sinus syndrome

A
  • 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
Q

Asystole

A

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
Q

Mx of unstable patients and those at risk of asystole

A
  • IV atropine (1st line)
  • Inotropes (e.g., isoprenaline or adrenaline)
  • Temporary cardiac pacing
  • Permanent implantable pacemaker
149
Q

Options for temporary cardiac pacing

A
  • transcutaneous pacing
  • transvenous pacing
150
Q

side effects of atropine

A
  • pupil dilation
  • dry mouth
  • urine retention
  • constipation
151
Q

Indications for a pacemaker

A
  • 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
Q

What are single chamber pacemakers

A
  • lead in either RA or RV
  • RA if issue with SAN
  • RV if issue with AVN
153
Q

What are dual chamber pacemakers

A
  • leads in both RA and RV
  • coordinates contraction of atria and ventricles
154
Q

What is a Biventricular (Triple-Chamber) Pacemaker

A
  • in severe HF
  • leads in RA, RV, LV
  • cardiac resynchronisation therapy
155
Q

what are implantable cardioverter defibrillators

A
  • 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
Q

ECG changes with a pacemaker

A

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
Q

side effects of BB

A

bronchospasm
cold peripheries
fatigue
sleep disturbances, including nightmares
erectile dysfunction

158
Q

side effect of continuous nitrates

A

development of tolerance, which results in reduced therapeutic effects.

159
Q

medication contraindicated in aortic stenosis

A

nitrates due to risk of profound hypotension

160
Q

Ix for stable angina

A

1st line: CT coronary angiography

161
Q

what is coarctation of the aorta

A

narrowing of the descending aorta
M > F

162
Q

associations of coarctation of the aorta

A

Turner’s syndrome
bicuspid aortic valve
berry aneurysms
neurofibromatosis

163
Q

signs of coarctation of aorta

A
  • elevated blood pressure
  • radiofemoral delay
  • CXR: notching of the ribs in the mid- clavicular line
164
Q

Beck’s triad of cardiac tamponade

A
  • hypotension
  • elevated JVP
  • muffled heart sounds
165
Q

Mx of cardiac tamponade

A

urgent pericardiocentesis

166
Q

Classification of aortic dissection

A

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
Q

Ix for aortic dissection

A
  • CT angiography of the chest, abdomen and pelvis is the investigation of choice
  • CXR widened mediastinum
  • Transoesophageal echocardiography (TOE)
    for more unstable patients
168
Q

Mx of aortic dissection

A

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
Q

Takayasu’s arteritis

A
  • large vessel vasculitis.
  • causes occlusion of the aorta
  • absent limb pulse
  • assoc with renal artery stenosis
170
Q

Mx of Takayasu’s arteritis

171
Q

ECG in hypercalcaemia

A

short QT interval

172
Q

ECG in hypothermia

173
Q

ECG signs of hypokalaemia

A

prolonged PR interval
prominent U waves
ST depression
long QT
small or absent T waves

174
Q

side effects of thiazide diuretics

A

hypercalcaemia and hypocalciuria

175
Q

Left ventricular heart failure heart sounds

A

gallop rhythm s3

176
Q

Normal heart sounds

A
  • S1) closure of the mitral and tricuspid valves
  • (S2) aortic and pulmonary valve closure
177
Q

Heart sounds S1

A
  • closure of mitral and tricuspid valves
  • soft if long PR or mitral regurgitation
  • loud in mitral stenosis
178
Q

Heart sounds S2

A
  • closure of aortic and pulmonary valves
  • soft in aortic stenosis
  • splitting during inspiration is normal
  • loud in pulmonary hypertension
179
Q

Heart sounds S3

A
  • 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
Q

Heart sounds S4

A
  • 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
Q

Medication to be avoided in HOCM

A
  • ACEi (can reduce afterload and worsen LVOT)
  • nitrates
  • inotropes
182
Q

how to identify LBBB and RBBB

A

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
Q

Causes of RBBB

A
  • 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
Q

Complications of MI

A
  • cardiac arrest
  • cardiogenic shock
  • chronic heart failure
  • tachyarrhythmias
  • bradyarrhythmias
  • pericarditis
  • LV aneurysm
  • LV free wall rupture
  • VSD
  • acute mitral regurgitation
185
Q

Pericarditis post MI

A

within first 48hrs

186
Q

Dressler’s syndrome

A
  • within 2-6 weeks
  • fever, pleuritic pain, pericardial effusion and a raised ESR
  • Mx = NSAIDs
187
Q

Left ventricular aneurysm

A
  • ischaemia weakens myocardium
  • associated with persistent ST elevation and left ventricular failure
  • bibasal crackles
  • presence of a S3 and S4
188
Q

LV free wall rupture

A
  • 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
Q

VSD post MI

A
  • within the first week
  • acute heart failure associated with a pan-systolic murmur
  • Mx = surgery
190
Q

acute mitral regurgitation post MI

A
  • 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
Q

side effects of warfarin

A
  • 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
Q

Medication contraindicated in ventricular tachycardia

A
  • verapamil
  • can precipitate cardiac arres
193
Q

Acute heart failure mx

A
  • IV loop diuretics
  • oxygen
  • vasodilator (nitrates)
  • CPAP if respiratory failure
194
Q

Chronic heart failure drug mx

A
  • ACEI AND BB 1ST LINE
  • Aldosterone antagonist
  • SGLT2 inhibitors
  • Ivabradrine, nitrate, digoxin, CR therapy
195
Q

Brugada syndrome

A
  • 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
Q

Mx of Brugada syndrome

A
  • implantable cardioverter defibrillator
197
Q

Raised INR

A
  • 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
Q

signs of right-sided heart failure

A
  • raised JVP
  • ankle oedema
  • hepatomegaly
199
Q

Ix for PE

A
  • CTPA
  • V/Q scan in renal impairment
200
Q

Tests before starting amiodarone

A
  • CXR
  • TFT
  • LFT
  • U+E
201
Q

Takotsubo cardiomyopathy

A
  • 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
Q

Rheumatic fever

A

develops following an immunological reaction to a recent (2-4 weeks ago) Streptococcus pyogenes infection.

203
Q

How to diagnose rheumatic fever

A

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
Q

which part of the heart is affected in ST elevation with third-degree heart block and slow junctional escape rhythm.

A

inferior aspect
it supplies RCA which gives off the AVN artery. so ischaemia can lead to 2nd/3rd degree heart block

205
Q

Nicorandil is most useful in the management of

206
Q

Wellen’s syndrome

A
  • 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
Q

ECG changes in Wellen’s syndrome and Mx

A
  • 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
Q

digoxin therapy ECG features

A
  • down-sloping ST depression (‘reverse tick’, ‘scooped out’)
  • flattened/inverted T waves
  • short QT interval
  • arrhythmias e.g. AV block, bradycardia
209
Q

where is the lesion in complete heart block following a MI

210
Q

side effects of GTN spray

A

Hypotension + tachycardia + headache.

211
Q

Eisenmenger syndrome

A

reversal of left to right shunt

212
Q

Buerger’s disease

A
  • small/medium vessel vasculitis
  • strongly associated with smoking.

Features:
- extremity ischaemia
- intermittent claudication
- ischaemic ulcers
- superficial thrombophlebitis
- Raynaud’s phenomenon

213
Q

Mechanical valves - target INR

A

aortic: 3.0
mitral: 3.5

214
Q

Murmur assoc with Marfan’s

A

Aortic regurgitation

215
Q

Commonest cardiac defect in Down syndrome

A

AVSD, rather than ASD

216
Q

ASD examination findings

A

ejection systolic murmur, louder on inspiration
Fixed split S2

217
Q

VSD examination findings

A

pansystolic murmur
hear best on left lower sternal edge
palpable thrill

218
Q

Best place for insertion of PCI

A

Radial access is preferred to femoral access for primary PCI

219
Q

Pulmonary stenosis examination findings

A

ejection systolic murmur louder on inspiration

220
Q

important cause of falls in the elderly

A

RBBB +left anterior or posterior hemiblock + 1st-degree heart block = trifasicular block

221
Q

Dextrocardia ECG signs

A

inverted P wave in lead I, right axis deviation, and loss of R wave progression

222
Q

Mx of aortic stenosis

A
  • 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
Q

what are premature ventricular beats

A

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
Q

difference between premature ventricular beats and premature supraventricular beats

A

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
Q

surgical intervention for chronic distal aortic and bilateral common iliac occlusive disease.

A

Aorto-bifemoral bypass graft
bypasses the occluded aortic and iliac vessels with a synthetic graft to restore blood flow to the legs

226
Q

causes of dominant R waves in V1

A
  • 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)

Finals (26 decks)

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