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Cardio Flashcards

1
Q

How to do ECG rate?

A

300/number of squares in R-R interval
OR
Number of QRS X6 (10 sec strip)

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2
Q

Normal ECG axis and how to calculate

A

-30 - +90
Look at leads I and aVF If these are both positive then axis is between -30 and +90

Also Leads I and II leaving returning rule for L and R deviation

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3
Q

What is P-wave & what increases & makes absent

A

This is atrial depolarisation

Inc = Cor pulmonale, PE
Absent = AF
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4
Q

What is PR interval
Prolonged = ?
Shortened = ?

A

Time from atrial to ventricular depolarisation (120-200ms)

Prolonged = AV block, digoxin, hypokalaemia, rheumatic fever, sarcoidosis (RF and Sarc give AV node fibrosis)

Shortened = Accessory pathway e.g. WPW (assoc with Delta wave - upstroke on QRS due to retrograde impulse activity).

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5
Q

QRS breadth

Narrow =
Broad =

A

Normally 80-120ms

Narrow = normal HIS/Purkinje

Broad = ventricular ectopic, accessory pathway (non His-Purkinj)

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6
Q

What is R-wave progression?

A

This is normal phenomenon where QRS become more positive

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7
Q

What can cause tall T-waves

A

Hyperacute STEMI

Hyperkalaemia

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8
Q

What can cause inverted T-waves

A 
Ischaemia
Digoxin toxicity
SAH
PE
Brugada syndrome
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9
Q

What can cause prolonged QT (interval over 500ms)?

Why is this important?

A

Citalopram
Antipsychotics
Macrolides (erythromycin)
Genetic

Risk of arrhythmias (longer relative refractory period means ectopics can cause arrhythmias)

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10
Q

First 4 steps in ECG interp

A

Patient name
Rate
Rhythm
Axis

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11
Q

Leads for Circumflex occlusion?

A

Leads I, V5, V6

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12
Q

Leads for Right coronary occlusion?

A

Leads II, III, aVF

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13
Q

Leads for LAD occlusion?

A

V1-V4

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14
Q

What are some causes of an irregular tachycardia

A

VF
Torsades (give Mg Sulphate)
AF+WPW (can be seen in association)

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15
Q

What can cause Left axis deviation

A

LBBB
WPW with right sided accessory pathway
hyperkalaemia
ASD

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16
Q

Causes of right axis deviation

A

RV hypertrophy

lung disease: cor pulmonale, PE

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17
Q

ST elevation causes

What causes prolonged ST elevation

A

MI
Pericarditis
LV aneurysm (cause of persistent STEMI)
Prinzmetals angina

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18
Q

ST depression causes

A

Can be seen secondary to abnormal QRS (LVH, RBBB/LBBB)
Ischaemia (e.g. inferior infarct)
digoxin
hypokalaemia

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19
Q

LBBB (WiLLiaM) causes

A

ALWAYS pathological
Ishcaemia: Ischaemic heart disease, MI (Sgarbossa criteria helps diagnose)
Aortic stenosis
Cardiomyopathy

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20
Q

RBBB (MaRRoW) causes

A

Can be normal variant seen with age

RVH e.g due to corpulmonale/PE

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21
Q

Hypokalaemia ECG

A 
U waves
small/absent T-waves
Prolonged PR
Long QT
ST depression
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22
Q

Hyperkalaemia ECG

A

Widened QRS
ST depression
Tall Tented T-waves
p-wave depression

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23
Q

Hypothermia ECG

A

Brady - 1st degree heart block
Long QT
Arrhythmia

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24
Q

Degrees of Heart Block

A

1st - PR over 0.2 (benign)

2nd type 1 Wenkebeck

  • Inc PR until dropped beat
  • AV nodal failure

2nd type 2
- PR constant until dropped beat (bundle branch conduction failure - can progress to complete block)

3rd

  • Complete.
  • P not assoc with QRS
  • Broad complex QRS
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25
Q

Which 2nd degree heart block is higher risk?

A

Type II - due to bundle branch failure

More commonly progress to complete failure

Pacing might be required

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26
Q

What is Bradycardia?

Physiological and pathological causes.

A

Under 60bpm
Phys = young (increased Nodal tone), fit

Pathological = acute MI, drugs (BB, digoxin, amiodarone), hypothyroid, hypothermia, inc ICP

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27
Q

Bradycardia symptoms & Tx

A 
Syncope
Fatigue
Dizzyness
Ischeamic chest pain
Palpitations

Tx: only if less than 40 bpm

  • IV atropine: anti-cholinergic. reduces vagal tone
  • Temp pacing wire
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28
Q

Sick sinus pathophys, ECG changes and Tx.

A

Cause = fibrosis of AV node (idopathic, ischemis, digoxin, toxicity, sarcoid/amyloid)

ECG = sinus block/arrest with escape rhythms. Bursts of atrial tacky interspersed with Brady

Brady: dual chamber pacing
Tachy: Digoxin or Verapamil (CCB)

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29
Q

Investigating Bradycardia

A

ECG, U&E, Glucose, Ca, Mg, TFT, drugs, FBC

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30
Q

Tx in Bradycardia

A 
Treat any underlying (remove negative chronotrope, tx electrolyte disturbances)
IV atropine (if poor response e.g. heart block do transcutaneous pacing
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31
Q

Tachycardia Presentation

A 
Palpitations
Fatigue
Dizzyness
Chest discomfort
Syncope
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32
Q

Tx of tachycardia (Acute pres)

Tx if unstable (high HR, low BO)

Tx if irregular tachy

Tx if regular tachy

A 
O2 and IV access
If HR over 200, BP under 90, MI or HF then GA + IV amiodorone (class III - K+ channel block)

If irregular tachycardia (usually AF) control with IV BB or Diltiazem. If onset less than 48 hours amiodarone cardioversion

If regular IV adenosine

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33
Q

Tachy Precipitating factors

A

MI/Ischamia
Thyrotoxicosis
Electrolyte disturbances
Drug/Caffeine/Alcohol

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34
Q

SVT - What is it, possible site or origin and what is the main concern

A

HR over 100bpm
Narrow complexes
Can be from Atria (AF and flutter)
Can be from AV node (nodal re-entry tachycardia)

Increased HR means decreased coronary filling time (angina type symptoms, chest pain, faintness, SOB)

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35
Q

Causes and Tx of sinus tachycardia (100-200bpm, regular with P-waves)

A

Physiological - pain, anxiety, exertion

Pathological - fever, anaemia, hypovolaemia, thyrotoxicosis, phaeo

Pharmacological - sympathomimetics, adrenaline, alcohol, caffeine, salbutamol

Tx: treat underlying (e.g. hypovolaemia), vagal manoeuvres (carotid massage, valsalva).
If ongoing sinus SVT give BB or non-dihydropyridine CCB (diltiazem, verapamil-

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36
Q

AV node re-entry pathophysiology.

A
  • Two pathways in AV node one fast with slow refractory and one slow with fast refractory
  • usually slow pathway is blocked as common pathway is in refractory when impulse arrives
  • if an impulse goes down the slow pathway when not in refractory then impulse can travel up fast pathway giving a re-entry circuit
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37
Q

AV node re-entry ECG

A

Narrow QRS
Rate 130-250
retrograde conduction = inverted P=waves in II, III and aVF

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38
Q

AV node re-entry Tx

A

Vagal manoeuvres 1st line
Adenosine 2nd line (transient AV block fees like death)

Long term: Beta block or digoxin, diltiazem, verapamil, flecanide (class 1c Na channel blocker – increases QRS time)

Cure: Radiofrequency ablation

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39
Q

AVRT ?

A

WPW

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40
Q

WPW pathophys

A

Bundle of Kent usually light sided. formed due to developmental failure.

Accessory pathway allows re-entry circuit formation (critical timing needed when pathways not in refractory)

Broad complex (anterograde)

Narrow (Orthodromic 90% - retrograde up accessory path used to get impulse back to atria)

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41
Q

WPW Tx

  • Acute
  • Prophylaxis
  • Cure
A

Vagal manoeuvres ± adenosine

Prophylaxis Flecainide (1c- inc refractory period) or sotalol (3)

Cure: RFA

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42
Q

What is AF

A

Chaotic firing of ectopics in atria.

Leads to irregularly irregular ventricular rhythm on ECG

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43
Q

AF complications

A

Stagnation of blood in atria can cause thrombus and inc risk stroke.

Reduced cardiac output may lead to HF

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44
Q

Types of AF

A

Paroxysmal: spontaneous termination in less than 7 days (usually 48hr)

Recurrent: 2+ episodes

Persistent: lasts over 7 days (may become permanent)

Permanent: long-standing (over 1 year) not terminated by cardioversion

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45
Q

AF

Symptoms & Signs

ECG

Other Presentations

A

Symptoms: Palpitations, Dyspnoea, Chest pain

Signs: Irregularly irregular heart beat

ECG: No P-waves, Oscillating baseline

Other: Syncope, TIA, stroke

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46
Q

AF Investigations

A

24 hour ECG
TFT, FBC (anaemia can cause), U&E (Potassium), LFT/Coag
Imaging - trans thoracic echo

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47
Q

AF management: Three areas to address

A

Rate
Rhythm
Anticoagulation

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48
Q

Rate control in AF

A

Beta blocker or CCB (Diltiazem) 1st line

Combination therapy 2nd line (NOT Verapamil - risk heart block) adding the above two OR adding in Digoxin

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49
Q

Rhythm control in AF

  • What should be considered
  • Who should get this
  • What is used
A
  • Thromboembolism
  • Only those with short term symptoms (less than 48 hours) or anticoagulant for over 3W
  • DC cardioversion or Amiodarone
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50
Q

Risk Control score in AF

A 
Chronic heart failure (1)
HTN over 140/90 (1)
Age of 75 (2)
DM (1)
Prior Stroke/TIA (2)
Vasc disease (PVD, MI)(1)
Age over 65 (1)
Sex: Female (1)
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51
Q

When to offer anticoagulant in AF

A

CHA2DS2VASc
Consider Warfarin or NOAC in males with 1 and anyone over 2 points
INR 2-3 (n.b prostetic heart valves/post MI = 2.5-3.5)
If poor warfarin control switch to NOAC

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52
Q

Bleeding Risk score

A 
Hypertension
Abnormal Liver/Renal
Stroke
Bleeding
Labile INRs
Elderly (over 65 years)
Drugs or alcohol (1 point each)

in those with score one 3 use Warfarin with care

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53
Q

What is atrial flutter, causes and ECG

A

This is due to re-entry circuits in the atria

Causes: HTN, CAD, hyperthyroid, Obesity, alcohol

ECG: sawtooth appearance

Tx: anticoagulation then DC cardioversion / Amiodarone / sotalol / flecainide
Recurrent = RFA

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54
Q

What causes broad complex tachycardia?

A

Ventricular origin.

Either ventricular conduction (BBB) problem OR not using AV node.

Note any SVT with poor conduction can present as broad complex too

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55
Q

Causes of:

Regular VT
Irregular VT

A

Reg - monomorphic VT (all QRS look the same) most commonly due to MI

Irregular - Torsades de Points (Plyomorphic VT), VF

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56
Q

Pathophysiology of Monomorphic VT

A

Re-entry circuits in zones of fibrosis/ischaemia

e.g. iscahmia/damaged myocardium post MI

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57
Q

Pathophysiology of Torsades

A

Commonly due to electrolyte disturbance.

Treated by giving Magnesium sulphate

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58
Q

ECG in VT - P waves and capture beats

A

Broad complex (ventricular)

  • VT: regular
  • VF: irregular

P wave dissociation: AV node continues independently of ventricle

Capture beats are when some P-waves translate into normal QRS complexes intermittently

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59
Q

Broad complex Tachy symptoms

A

Dizziness, palpitations, syncope, chest pain, HF

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60
Q

Broad complex Tachy Tx

A

ABC, O2 and venous access

in unstable DC cardioversion (3 shocks) may be needed

Amiodarona IV

In Plyomorphic VT give magnesium 2g for non-Torsades, IV Mg sulphate for TdP

VT is usually due to damage so BB/CCB and consider Implantable cardioversion defibrillator

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61
Q

Torsades de Points

Causes
Morphology
Tx

A

Hypokalaemia, hypomagnesia,
Class III antiarrhythmics (amiodarone/sotalol)
Antibacterials (erythromycin, trimethoprim)

Varied axis and amplitude of QRS

Tx: Magnesium sulphate IV

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62
Q

VF

  • Causes
  • Morphology
  • Acute/Long term Tx
A

Cause of cardiac arrest and sudden death.
Random contracting of ventricular fibres giving failed ventricular function.

  • Antiarrhythmic drugs, AF, hypoxia, ischaemia, heart disease
  • Chaotic (varying amplitudes, no identifiable P, QRS, T
    -Acute: Defibrillation
    Long term: BB, implantable cardioverter defibrillates
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63
Q

What are shockable rhythms?

A

VF and Pulseless VT

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64
Q

Non-shockable rhythms?

A

Asystole and PEA (Pulseless electrical activity)

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65
Q

Brugada

What is?
ECG?
Tx?

A
  • Geneticalli inherited condition affecting sodium channels. Family history of sudden death less than 45 yrs
  • Risk of sudden death
  • Coved ST segment elevation followed by negative T
  • ICD (implantable defibrillator)
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66
Q

PE ECG

A

S1Q3T3

Deep S in I, Deep Q in III Deep T in III

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67
Q

Class 1
Class 2
Class 3
Class 4

A 
1 = Na channel blocker
2 = CCB
3 =  Potassium channel blocker
4 = Beta blocker
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68
Q

Amiodarone

  • Use
  • Mech
  • Adverse
A

For irregular tachycardia (AF, SVT)

Block/Na/K/Ca, antagonist alpha and beta adrenergic
Reduces automaticity/conduction in atria

Hypotension, Pneumonitis (upper lobe fibrosis), AV block, grey skin, hypothyroidism

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69
Q

Adenosine

  • Use
  • Mech
  • Adverse
A
  • Used in certain SVT that don’t respond to Vagal maneouvers
  • Causes trainsient block in the AV node by causing hyperpolarization through inc potassium flux
  • Short term: Feeling of impending doom
  • Long term: Chest pain, Bronchospasm (caution in asthmatics), can cause increased conduction down accessory pathways - caution here
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70
Q

Digoxin (cardiac glycoside)

  • Use
  • Mech
  • SE
A

Reduces ventricular rate after CCB and BB
3rd line in HF

Negative chronotropic(reduced AV node conduction), positive inotropic (Ca accumulation intracellular)

Toxicity - arrhythmias, low therapeutic index

  • GI upset
  • nausea
  • Hypokalaemia (competes with K+ and Na/K pump
  • visual disturbance (yellow)
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71
Q

Types of CCB

A

Dihydropyridine (More smooth muscle relax)
- Amlodipine
Non-dihydropyridine (more cardiac depression - SA and AV node block)
- Verapamil, Diltizem

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72
Q

Mechanism of CCB

A

Decrease Calcium entry to vascular and cardiac cells

  • induce relaxation and vasodilation in arterial smooth muscle
  • suppress cardiac conduction esp at the AV node
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73
Q

CCB effect in HF/IHD

A

Reduced rate and after load, decreases oxygen demand preventing angina

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74
Q

Amlodipine SE

A

ankle swelling, flushing

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75
Q

Verapamil facts

A

ONLY CCB which can be given IV in SVT

DONT give with BB (both negatively chronotropic and inotropic so = Heart block

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76
Q

Beta blockers use

A

IHD - reduces angina

Congestive HF - improves prognosis

AF - reduces rate and maintain rhythm

SVT - restore sinus rhythm

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77
Q

Receptors and action of BB

A

B1 (heart) - reduces force and rate of conduction in heart (prolonged AV refractory period).
= reduced cardiac work and oxygen demand. increased myocardial perfusion

B2 (vasc smooth muscle) - lower peripheral vasc resistance and also lowers BP through reducing renin secretion.

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78
Q

SE of BB

A

Fatigue, cold extremities, headache, impotence

Asthma - causes bronchospasm so contraindicated (choose B1 specific e.g. atenolol not non-specific e.g. Bisoprolol)

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79
Q

Where to listen for mitral area?

A

Mid clavicular

5th intercostal space

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80
Q

Where to listen for Tricuspid?

A

inferior right sternal

4th intercostal space

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81
Q

Where to listen for Pulmonary valve?

A

Left 2nd intercostal

Next to sternum

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82
Q

Where to listen for Aortic valve?

A

Right 2nd intercostal next to sternum

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83
Q

S1 and S2?

A

S1 = closure of mitral and tricuspid

S2 = closure of aortic and pulmonary

there may be delayed P2 (pulm part of S2) in inspiration. Third heart sound in diastole (aka after s2 is pathological)

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84
Q

Mitral regurgitation

A

Pansystolic blowing murmur at apex radiating to axilla

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85
Q

Mitral stenosis

A

Loud opening snap in S1 and mid-diastolic murmur

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86
Q

Aortic stenosis

A

Radiates to carotids
Soft S2
crescendo decrescendo murmur between S1 and S2

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87
Q

Aortic Regurg

A

Diastolic murmur
Collapsing pulse
not well transmitted to carotids

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88
Q

PDA murmur

A

Late systolic best heard across back

Continusous machinery murmur

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89
Q

VSD murmur

A

Harsh systolic murmur best a left sternal edge

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90
Q

Starlings Law

A

Preload or degree fo stretch is critical factor for stroke volume.

Thus increased end-diastolic volume increases stretch and also contractility giving a lower end systolic volume (after load)

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91
Q

Aortic stenosis

  • Triad
  • other features
  • Cause
  • Investigations
A
  • Chest pain, HF (LV hypertrophy due to obstruction), syncope (insufficient blood)
  • slow rising pulse, narrow pulse pressure (higher pressure needed to eject), transmitted to carotids
  • calcification of aortic ring
  • ECG (LV strain), Transthoracic echo, CXR (Calcifications)
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92
Q

Aortic valve anatomy

A

Tricuspid valve

Coronary sinus sits behind

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93
Q

Aortic stenosis Tx and complications of Tx

A

1st line is valve replacement

2nd line saloon valvuloplasty

SE of infection (need Abx prophylaxis) and risk emboli (esp metal valves) needing anticoagulant aiming for 2.5-3.5 INR

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94
Q

Aortic regurgitation

  • Causes
  • Associated diseases
  • Presentation
A
  • Bicuspid aorta, thematic fever (autoimmune), infective endocarditis, collagen disease, age (degenerative)
  • SLE, Marfans, Ehlers-Danlos, Turner’s, Ank spond
  • Shortness of breath, orthostatic/nocturnal dyspnoea
  • Wide pulse pressure and collapsing water hammer pulse
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95
Q

Aortic regurgitation

  • Investigations
  • Tx
  • screening
A
  • ECG (may have LVH), CXR (HF due to fluid overload), Transthoracic echo
  • acute surgery (valve replace) is symptomatic, give ace inhibitor if chronic

screen those with assoc diseases e.g. marfans

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96
Q

Mitral stenosis

- complications

A
  • Inc LA and pulmonary artery pressure.
  • May progress to cause RV failure and subsequent raised JVP, liver congestion, ascites and peripheral oedema
  • Thromboembolic risk due to blood stasis in atria
97
Q

Mitral stenosis

  • Causes
  • Pres
  • Signs
A
  • congenital, rheumatic fever, degenerative calcification in elderly
  • progressive breathlessness, palpitations due to AF, systemic emboli effects, hoarseness (LA hypertrophy)
  • Malar flush (CO2 retention), raised JVP, Laterally displaced apex, RV heave, signs of RHF (hepatomegaly, ascites etc)
98
Q

Mitral Stenosis

  • Investigation
  • Tx
  • Prevention
A
  • ECG (P- mitrale = bifid), CXR - LA enlargement & interstitial oedema (Kerly B lines) & prominent pulmonary vessels
  • diuretics and nitrates fo SOB, BB or CCB for exercise tolerance, valve balloon if symptomatic
  • Prophylaxis for rheumatic fever and infective endocarditis is penicillin
99
Q

Mitral regurgitation

  • Causes
  • Presentation
  • Complications
  • Investigations
  • Tx
A
  • advancing age, rheumatic fever (less commonly), MI, IHD, post surgical, ehlers-Danlos, SLE
  • Acute forms lead to rapid pulmonary oedema (e.g. papillary muscle rupture).
  • Chronic forms give HF, Breathlessness, can cause pulmonary HTN
  • ECG P-mitrale, CXR left heart hypertrophy, Echo
  • Surgery (valve repair), ACEi, nitrates, diuretics
100
Q

Rheumatic fever

A
  • Antigen mimicry to strep pyoges (Group A beta haemolytic)
  • affects joint skin heart and nervous system 2-4 weeks post infection (sore throat)
  • IV Benzylpenicillin for strep, NSAIDs suppress inflammation
  • long term MR due to papillary muscle fibrosis and shortening
101
Q

Why is Rhematic fever less common

A

Group A - Strep Pyogenes infection is less common

102
Q

infective endocarditis

  • Pathogenesis
  • presentation
  • complications
  • RF
A
  • strep viridian’s (dental procedures), Staph aureus (invasive procedures IVDUs). Poor blood supply to valves (hard for WBC and drugs to reach), fibrin-platelet/organisms vegetation formed –> destroys valve leaflets
  • Fever + New Murmur = endocarditis until proven otherwise
  • valvular insufficiency, systemic emboli (can have embolic or infective effect (block or make abscess), immune complexes (cutaneous, kidney, arthritis)
  • structural heart defect, IVDU, previous IE
103
Q

Infective endocarditis features

A

Fever + new murmur (usually MR, tricusp with Staph aureus)

Roth’s spots - eyes, retinal haemorrhage with pale centre

Osler’s nodes - painful red blisters @ terminal phalanges and toes

Janeway lesions - painless red maculae on thenar eminence

Nail haemorrhage - splinter - red and linear

Embolic phenomena e.g. stroke
Subacute: clubbing

104
Q

Infective endocarditis Tx

A

Amoxicillin + Gentomycin IV

Surgery may be needed if damaged heart valves

105
Q

What is cardiomyopathy

A

Functional/Structural abnormality of heart muscle WITHOUT Coronary/valvular/congenital disease HTN

106
Q

Classification of cardiomyopathy

A

Dilated - most common. imparted contraction, most common need for transplant

Hypertrophic - (HOCM) L/R ventricular hypertrophy. usually familial due to data-myosin dysfunction

Restrictive - rare. reduced diastolic filling

107
Q

Causes of cardiomyopathy

A

Dilated - Ischaemic, Alcohol, Thiamine deficiency (Beri Beri), SLE

Hypertrophic = familial

Restrictive - amyloidosis, sarcoidosis, radiation, haemochromatosis

108
Q

Presentation, Investigation and Tx of dilated cardiomyopathy

A
  • congestive HF, Right sided HF, cardiomegaly, AF or VT, thromboembolism by stasis
  • CXR ABCDE (Alveolar oedema, Batwing, kersey B, interstitial Cardiomegaly, Dilated upper lobe vessels, pleural Effusion
    Bloods - BNP (b-type natriuretic peptide)
  • Loop diuretics / thiazide, ACEi (Digoxin if doesn’t respond)
    Nitrates, Warfarin, pacing

Most common cause for heart transplant

109
Q

Most common cause of sudden cardiac death in young people

A

Hypertrophic cardiomyopathy.

Genetic inheritance
gene coding for Beta myosin

Mitral regurgitation may be present giving atrial enlargement

110
Q

Management of Restrictive cardiomyopathy

A

Amiodarone if ventricular arrhythmia, anticoagulant, BB and CCB if AF

Transplant sometimes indicated

111
Q

What is Myocarditis and how does it occur?

A

acute/chronic inflammation of myocardium (fatigue, chest pain, fever)

might be due to viral (Coxsakie), immune mediated (SLE, Sarcoid, scleroderma), Alcohol, Heavy metals, Electric shock

112
Q

Heart failure features

A 
Dyspnoea
Cough - worse at night (pink frothy sputum)
Orthopnoea/nocturnal dyspnoea
Wheeze
Weight loss
Bibasal crackles 
Peripheral oedema/ascites
113
Q

HF acute management

A 
O2
diuretics (furosemide)
Opiates (for SOB)
Vasodilators
Inotropes
CPAP
114
Q

HF - Drug management

A

1st - ACei and BB
2nd - Aldosterone agonist or hydralazine in combo with nitrates
Diuretics for fluid overload
Annual influenza vaccine and pneumococcal vaccine

3rd line is digoxin

115
Q

HF classification

A

NYHA
I = no sympt

II = mild symptoms, slight limitation

III = moderate symptoms, unable to carry our physical activity without discomfort

IV = severe, symptoms of HF at rest

116
Q

HF investigations

A

BNP (released my myocardium stretched)
ECG for aetiology at Tx

Gallop murmur due to S3

117
Q

Causes of HF

A

Mostly IHD and HTN, 10% valvular (AS causing LVH)

Myocardial disease - ischaemia, cardiomyopathy, HTN, drugs (bb, cbb, doxorubicin), alcohol and cocaine, infiltrative (haemochromatosis, sarcoidosis)

high output: anaemia, pregame’s, hyperthyroidism, pagers disease of bone

118
Q

Atherosclerosis

4 stages

A

1) Fatty streak formation - this is due to endothelial dysfunction causing lipid and monocyte infiltration.monocytes engulf fat to become foam cells = fatty streak
2) Intimal hyperplasia - platelet derived growth factor, TGF-B from macrophages and SMC causes hyperplasia
3) Fibrous cap formation - SMC produce collagen
4) Plaque formation or Rupture - may have a fatty necrotic core. Plaque might continue growing to narrow lumen or become unstable and rupture

119
Q

What can be found within intimal plaques in Atherosclerosis?

A

Lipid
Macrophages
Smooth Muscle cells

120
Q

Two type of Cholesterol

A

HLD - Carries fat away from arteries to Liver for synthesis of bile salts and steroids

LDL - Carry fat towards arteries causing plaque formation

121
Q

What carries fat from intestine to muscle

A

Chylomicrons

122
Q

Statins:

  • Mechanism
  • When NICE recommend
  • SE
  • Which statin
  • Monitoring
A
  • HMG-CoA reductase inhibitor
  • QRISK2 over 10%, Hx of CVD, familial hypercholesterolaemia, over 65
  • Myalgia, stiffness, weakness, cramping
  • Atorvastatin 20mg (primary prev), 80mg for secondary prev
  • LFTs
123
Q

HTN complications

A

Stroke, IHD, MI, CKD

124
Q

HTN modifiable RF

A

Smoking, weight, alcohol, stress, exercise, salt

125
Q

HTN non-modifiable RF

A

AGe, Fam Hx, Ethnicity, Gender

126
Q

HTN stages and when to Tx

A

Stage 1: over 140/90 (135/85 ABPM/HBPM)
Stage 2: over 160/100 (150/95ABPM/HBPM)
Stage 3: over 180/110

Intervene at stage 2

127
Q

Symptoms of HTN and screening

A

Often no symptoms (unless 200 systolic then headaches etc)

Screen adults every 5 years up to 80

128
Q

Causes

A

Primary - Essential HTN (95%) env, gene etc

Secondary - Renal disease (inc renin due to dec perfusion), Endocrine (Cushing, Conns, Thyroid, Phaeo), Pre-eclampsia and preg, Drugs (steroids, COCP, decongestant)

129
Q

What is malignant HTN

A

High BP or fast inc in BP

Causes end-organ damage

130
Q

End organ damage in HTN

A 
Brain - Seizure, Vomit, Stroke
Dissection
Pulmonary oedema (HF)
Nephropathy
Retinopathy (grade 1 = tortuous retinal arteries, grade 4 = papilloedema)
131
Q

Investigations for secondary HTN

A

Lipids and FBC

VMA - breakdown prod of adrenaline

Urinary free cortisol

Renin/aldosterone levels

Plasma Ca

MRI renal arteries

132
Q

Treatment of HTN

A

LIFESTYLE!
diet, weight, salt, all, exercise, smoking

Target of under 140/90

A or C (amlodipine - ankle swelling)

  • A for under 55
  • C for afrocarib or over 55

A + C

A + C + D (indapamide )

if still then if K+ low add Spironolactone if high then inc ‘D’

133
Q

IHD Causes

A

Mechanical obstruction of CA (atherosclerosis, thrombosis, spasm-prinzmetals, arteritis)

Decrease blood O2 (anaemia, decreased CO - HF, poor oxygenation in lung)

inc heart demand = more O2 and reduced coronary filling time (HTN, valvular disease, hyperthyroid, fever, exercise)

134
Q

IHD symptom

A

Angina (stable is when exercise induced, unstable is at rest)

135
Q

IHD RF

A

modifiable:
- smoking, poor diet, weight, low exercise, alcohol, stress, HTN, depression, diabetes, hyperlipidaemia

non-modifiable:
- age, male, genetics, FH

136
Q

What is stable angina?

A

Narrow lumen from atherosclerosis decrease blood flow = chest pain on exertion

constricting discomfort front of neck/shoulder/jaw/arms

Brought on by exercise, received by rest/GTN

137
Q

What is Prinzmetals angina?

A

Angina due to coronary spasm

138
Q

Referral of new angina

A

All cases to acute chest pain clinic for confirmation of Dx and severity assess

within 2 week

139
Q

How does unstable angina occur

A

Either progressive luminal narrowing or Plaque rupture.

140
Q

Angina Dx

A 
MI - if pain over 5 mins
Pericarditis - worse on inspiration or lying flat
MSK - worse on moving
PE - pleuritic
GORD
141
Q

Investigation of angina

A 
ECG - S/T or T flattening or inversion
FBC (anaemia), Blood glucose diabetes)
LFT (baseline befor statin)
U&E (renal function)
TFT

Coronary angiography will confirm (this is invasive)

142
Q

Stable angina management:

A

Modify CV RF + educate patient

GTN (if doesn’t relieve then 2nd dose after 5 min and third dose after 5 min then wait 5 min then call 999)

1s line: BB (atenolol - dec HR and BP, brady, cold hands, fatigue) or CCB (diltiazem (ankle swelling flushing)

2nd line dihydroperidine CCB + BB

To reduce RF: Aspirin or Clopidogrel, Statin if indicated

143
Q

Angina not controlled by medications

144
Q

ACS ECG

ST elevation =
No ST elevation =

A

STEMI

NSTEMI (if cardiac markers raised)

Unstable angina if they are not raised

145
Q

ACS investigation

A

ECG - ST elevation (acute infarct) ST depression/T-inverstion (unstable angina or NSTEMI)

Cardiac enzymes: (best 3-6 hours post infarct, max at 12-24hours troponin T, troponin I, Creatine kinase
–> minimal inc may suggest future risk

Bloods (FBC - anaemia, glucose - if high poor prognosis, renal/tyroid function)

Imaging:
CXR - complications like pulmonary oedema, PE, pneumothorax, TAA

146
Q

ACS presentation

A

New onset angina, prolonged anginas pain at rest (over 20 min)

Other: sweating, vomit, fatigue, SOB, palpitations

147
Q

Initial management of ACS

A

MONA

morphine, O2, Nitrates, Aspirin

Monitor with ECG

148
Q

Risk assessments in ACS

A

TIMI - bleeding risk in MI thrombolysis

GRACE - assess Tx of NSTEMI

149
Q

GRACE

A

used in ACS to predict 6 month mortality

Low risk = Clopidogrel 12 months

Medium risk = angiography within 4 days

High risk = PCI or CABG for revascularisation

150
Q

Dressler’s syndrome

A

late pericarditis. Inflammatory reaction to necrotic tissue occurring 2-8 weeks after ACS

151
Q

Discharge management for ACS

A

Cant drive for 4 weeks (1 week if angioplasty)

ACEi, dual platelet (aspirin+clopidogrel), BB, Statin, monitor BP and renal function regularly.

IF HF offer Spironolactone

LIFESTYLE - smoking, weight

152
Q

ACS complications

A

Acute MI
Pericarditis
Dresslers syndrome

153
Q

MI complications

A 
Death
Dresslers
PEricarditis
Rupture of free wall
Aneurysm (persistent ST elevation)
Tamponade (Becks)
HF
Shock (cariogenic)
VT
154
Q

Cardiac arrest management

A

call 999
A+B
C once airway secured (30:2 uninterrupted)
D - automatic defibrillates
2 mins CPR between defibrillates attempts
after 3rd shock adrenaline + Amiodarone
2min CPR.. Adrenaline etcetcetc

155
Q

Pericarditis

  • Anatomy
  • Pathogen
  • Causes
A

Pericardium is outer fibrous layer and inner serous membrane with 5ml fluid. Fixes heart to pericardium and prevent dilation.

inflammation results in exudate/adhesions/effusions (haemorrhage or serous)

viral (Coxsackie, EBV, staph)
Rheum (RA, SLE, Sarcoid)
MI (dresslers)
Other (drugs e.g. hydralazine, fungal)

156
Q

Acute pericarditis

- Presentation, Signs/sympt

A

Chest pain (dull, sharp, burning),

Substernal/precordial radiates to neck or leg trapezius

Aggravated - Cough, lying flat
Relieved - siting up

tachypnoea, tachycardia, fever

If tamponade may have becks

60-85% have pericardial friction rub

157
Q

Acute Pericarditis Investigations

A

ECG - Concave ST elevation (saddle shape)

Bloods - FBC (WCC), ESR/CRP (raised), U+E (uraemia can cause), Cardiac enzymes (point to MI as cause of pericarditis)

Echo - if suspecting fluid or tamponade (over 20mm free fluid)

158
Q

Pericarditis Tx

A

If RA or Ventricular collapse on echo - Pericardiocentesis

Stable Patients:

  • Rest, Treat cause, NSAIDs (naproxen)
  • If uraemia consider dialysis
159
Q

When to admit for Pericarditis

A 
Fever
evidence of tamponade
Large effusion (echo free space over 20mm)
On Warfarin
Trauma
Fail to respond to NSAIDs
160
Q

Complications of Pericarditis

A

Falling BP and shock - suspect tamponade

161
Q

What is Cardiac Tamponade.

Why Important?

A

Blood/Fluid/Pus/Gas in pericardial space.

Large volume = reduced ventricular filling leading to haemodynamic compromise
medical emergency

162
Q

Causes of Tamponade

A

Pericarditis, malignancy, Dressler’s (post MI), infective (HIV, TB), connective tissue disease (SLE, RA, dermatomyositis, systemic sclerosis), Trauma.

163
Q

Presentation of Tamponade

A

Anxiety, Fatigue, Oedema (peripheral, pulmonary), SOB, tachycardia, tachypnoea

164
Q

Becks Triad: when and what

A

Seen in ACUTE Tamponade

1) Muffled Heart sounds
2) Raised JVP
3) Hypotension

165
Q

Tamponade ECG

A

Low voltage QRS

166
Q

Tamponade CXR

A

Water bottle shaped heart

167
Q

Gold standard Investigation in Tamponade

A

Transthoracic Echo

168
Q

Tamponade Tx

A 
O2
Volume Expansion
Increase venous return (legs up)
Inotrope (dobutamine)
Pericardiocentesis
169
Q

What is peripheral artery disease?

A

Narrowing of peripheral vasculature

Most often due to atherosclerosis

170
Q

Peripheral artery disease classification

A

1) Asymptomatic
2) Intermittent Claudication
3) Ischaemic rest pain
4) Critical limb ischaemia (P’s - Pulseless, perishing cold, Painful, Pale, Parasthesia, Paralysed)

171
Q

Intermittent Claudication:

A

Cramping pain in calf/thigh/buttock on walking.

symptoms worse uphill/stairs
relieved by rest

172
Q

Intermittent Claudication - determinants of severity

A

Claudication distance

Rest time

173
Q

Ischaemic rest pain

A

Unremitting pain in limb.

Wakes from sleep, relieved on dangling foot/cold floor

174
Q

Peripheral artery disease other signs

A

Skin changes (atrophic)

Hairless

175
Q

Peripheral artery disease DDx

A

Sciatica
Spinal stenosis
DVT
Nerve entrapment

176
Q

Peripheral artery disease investigations

A 
FBC (anaemia aggravates)
ESR (giant cell arteritis)
Thrombophilia screen (DVT)
ECG (look for coronary disease)
Doppler US to calc ABPI
- Normal = 1
- 0.9 mild, 0.8 mod, below 0.5 ischaemic rest pain.
177
Q

Acute limb ischaemia

  • 6 P’s
  • Cause
  • Investigation
  • Tx
  • Complications
A
  • Pulseless, Paralysed, Parasthesia, Pale, Perishing cold, Pain
  • Thrombus or Embolism giving sudden occlusion
  • Urgent doppler and urgent angiography
  • Revascularisation in 4-6 hours with immediate heparinisation (embolectomy for embolus, thrombolysis/angioplasty/bypass if thrombotic
  • Infection, poor healing, gangrene
178
Q

General management of Peripheral Limb Ischaemia.

A

RF: smoking, weight, statins, ACEi (beware renal artery stenosis), Manage DM/HTN

Antiplatelet - Clopidogrel

179
Q

Management of intermittent claudication

A

Vasodilator therapy - Naftidrofuryl oxalate

Supervised exercise

ABPI (doppler USS) ± CT angio

Revascularisation if tried lifestyle improve (angioplasty + stenting

180
Q

Management of Critical ischaemia

A

Pain: para+opioid
doppler USS ± contrast angio

Revascularisation with angioplasty and stenting

Some cases may need amputation

181
Q

Aortic Dissection what is it?

A

Intimal tearing gives disruption of media

Intramural bleeding separates layers leading to a false lumen creation

182
Q

Aortic Dissection Types

A 
Type A (70%) aortic arch + ascending aorta
Type B (30%) descending aorta
183
Q

Aortic Dissection RF

A

Cardiovascular disease
Aortic disease
Cocaine/amphetamines
Bicuspid aortic valve

184
Q

Aortic Dissection Presentation

  • Acute
  • possible systemic effect
A
  • Sudden tearing/sharp pain. Radiates to back, Pulse loss

- Spinal arteries (paraplegia), Distal aorta (limb ischaemia), Carotids (Neurological deficit), Coronary (angina)

185
Q

Aortic Dissection expansion phase

A
  • Cardiac tamponade

- Pleural Haemothorax

186
Q

Important Dx in Aortic Dissection

A

Differentiate from MI as thrombolysis will be fatal in Aortic Dissection

187
Q

Aortic Dissection investigations

A

CXR - widened mediastinum (if -ve can’t exclude dissection)

TTUS - site and extent of dissection

MRI - good for diagnosis and looking for other vessel involvement

ECG - needed to differentiate if MI suspected

188
Q

Aortic Dissection Tx

A

IV access, analgesia (morphine) and O2 initially

ICU

Aggressive HTN management aim for BP 100-120 systolic

  • IV BB (labetalol) to reduce contraction
  • IV nitropruside (emergency Vasodilation)

Surgical repair

  • Type A gets graft
  • Type B TEVAR
189
Q

TAA

  • True aneurysm
  • Location
  • Pathogenesis
  • RF
A
  • Involves all three layers
  • Ascending aorta (51%), arch, descending
  • Inflammation, proteolysis and reduced SMC survival
  • CTD (marfans etc), genetic, Infective (HIV, syphilis), Aortitis (GCA, RA, Takyasu’s arteritis, Trauma (weight lifting), Cocaine/amphetamines, bicuspid aortic valve, HTN, smoking, age
190
Q

What level is Aortic Hiatus in diaphragm?

191
Q

TAA presentation

A

Pain - chest, neck, upper back, epigastrium. dissection sudden tearing
Compression symptoms - hoarseness, SVC obstruction, stridor

if rupture: acute pain, collapse/shock, haematemesis/haemoptysis, haemothorax/tamponade

192
Q

TAA investigations

A

Acute: FBC, clotting, U&E, LFT, CT contrast, ECG, MR angio

Non-acute: above plus USS, TTE

193
Q

TAA Tx

A

Surgery: TEVAR
smoking cessation, Tx CV RF
6 monthly MRI/CT
Inform DVLA if above certain size

194
Q

TAA surgery complications

A

paraplegia (spinal ischaemia)
Stroke
AKI

195
Q

AAA

  • Location
  • Causes
A
  • Mainly below level of renal arteries
  • Atherosclerotic disease, FH, smoking, male, inc age, cardiovasc disease/RF, Arteritis (Takyasu, Behcets), CTD ( marinas etc), infective (TB, HIV)
196
Q

AAA

  • Presentation
  • Examination findings
A
  • Often incident finding, pain in back/loin (DDX for loin to groin), pulsatile abode swelling, rupture = shock
  • Bimanual palpation, Abdominal bruit, retroperitoneal haemorrhage - Grey Turner sign (flank bruising)
197
Q

AAA investigations

A 
FBC, clotting, U&E (renal), LFTs, Crossmatch, 
USS --> initial assess
ECG
CXR
CT --> more anatomical detail

MRI angio

198
Q

AAA Management

A

USS monitoring

  • 3-4.5cm = yearly
  • 4.5-5.5cm = 3mnthly

Over 5.5 consider surgery

Inform DVLA over 6cm

surgery - over 5.5cm or rapid expansion over 1cm/year or if symptomatic

  • Open repair
  • EVAR
199
Q

AAA rupture

  • Pres
  • Investigation
  • Management
  • Prognosis
A
  • Thoracic chest pain, Haemoptysis ± tamponade, pale, sweaty, weak pulse, hypotension. Triad
    1) flank/back pain
    2) hypotension
    3) pulsatile abdo mass
  • FBC, crosshatch, baseline U&E, CXR, ECG
  • Large bore IV access, Immediate theatre - Prosthetic graft repair and stem bleeding
  • 1 in 3 reach hospital alive
200
Q

Types of shock

A

Cardiogenic - heart can’t supply enough blood (dec CO)

Septic - dec systemic vasc resistance

Anaphylactic - Type I hypersensitivity, mast cell histamine and vasoactive mediators dec systemic vasc resistance

Neurogenic - spinal cord injury, epidural/spinal anaesthesia causes dec vasc resist

201
Q

Triad seen in shock?

A

Triad

1) Coagulopathy
2) hypothermia
3) Metabolic acidosis

202
Q

Shock and Organ systems

A

Kidney - acute tubular necrosis
Lung - ARDS
Heart - MI
Brain - Confusion, Coma

203
Q

Sepsis def

Septic shock def

A
  • Life threatening organ dysfunction from dysreg response to host infection (dec SOFA 2 points or more)
  • Circulatory and metabolic dysfunction as a result of sepsis
204
Q

Hypovolaemic shock

  • Aim of resus
  • Presentation
  • Investigations
A
  • correct hypo perfusion of vital organs e.g. kidneys
  • Pale, sweaty, tachycardia/pnoea, cold periphery, inc cap refill time, hypotension
  • FBC (Hb), U&E (kidney), Group and Crossmatch, ABG+Lactate, urine output
205
Q

Hypovolaemic shock

staging

A 
Like Tennis:
Class I 15% loss
Class II 30%
Class III 40%
Class IV over 40%
206
Q

Compensation mechanisms to hypovolaemia

A

Baroreceptor feedback (via CN IX sensation) causes vagal inc in contractility, tachycardia, vasoconstriction

Release of Vasopressin, Aldosterone, Renin (Kidney compensation)

207
Q

what is occurring in hypovolaemia which is:

  • Uncompensated
  • Irreversible
A
  • Myocardial depression and failure of vasomotor reflex, inc capillary permeability, lactic acidosis
  • End organ failure
208
Q 
Features of:
Class I
Class II
Class III
Class IV

When to transfuse

A

Class I: Physiological compensation

Class II: postural hypotension, dec urine

Class III: Tachycardia over 120 bpm, urine under 20ml/hr, confused

Class IV: marked hypotension, tachycardia

209
Q

Tx Hypovolaemic shock

A
  • Raise legs (venous return)
  • ABCDE
  • Fluid resus: Saline or - Hartmann’s 500ml over 15 min
  • If haemorhhagic give O -ve blood
  • Pain relief (pain inc metabolic rate and inc ischaemia) IV opiates
  • Surgery may need fro stem blood loss
210
Q

Cariogenic shock

  • Cause
  • Presentation
  • Management
A
  • MI mostly, can also be Tamponade/constrictive pericarditis/PE/tension pneumothorax
  • Dyspnoea, sweat, confusion, palpitations, pale, mottled, slow cap refill, hypotension
  • A+B = intubation and ventilation, C = venous access (may need central due to peripheral shut down, IV morphine, cardiac inotropes
211
Q

Anaphylactic shock

  • Definition
  • Presentation
A
  • Type 1 hypersensitivity due to mast cell histamine/other vasomediator release. sudden onset, life threatening airway + circulatory problems
  • breathless/wheeze, profound vasodilation (warm periphery, low BP, tachycardia), angio-oedema/hives, oedema of face/pharynx/larynx
212
Q

Anaphylactic shock Tx

A

A (call help if signs of obstruction), B (treat rest distress - O2), C (assess with colour, pulse, BP), D (responsive?)

Give:

  • high flow O2
  • raise legs (venous return)
  • IM adrenaline (most important) 0.5mg adult
  • Expert intubation
  • IV fluid challenge: 500ml CRYSTALLOID in 5-10 min
  • IV chlorphenamine + hydrocortisone
  • Bronchodilators: IV salbutamol (or nets), ipratropium inhaled, Aminophylline (IV)
213
Q

Sepsis Presentation

A 
Bounding pulse
temperature
Rigors
Rapid cap refill
Vasodilation
warm peripheries
214
Q

Sepsis BUFALO

A
  • Blood cultures
  • Urine output - monitor hourly
  • Fluid resus
  • Abx - Tazocin, Gent (according to local guidelines)
  • Lactate (ABG/VBG)
  • Oxygen to correct hypoxia
215
Q

Sepsis complications

A

DIC
Renal failure
Cardiorespiratory failure

216
Q

ECG Hyperkalaemia

A

Peaking of T waves (occurs first)
Loss of P waves
Broad QRS complexes
Ventricullar fibrillation

217
Q

Hypercalcaemia features

A

Bones, Stones, Groans and Psychic moans.

ShortenedQT interval on ECG

218
Q

DVLA and driving with cardio disease

A 
Angioplasty - 1 week
CABG - 4 week
ACS - 4 week
Pacemaker - 1 week
AA over 6cm - tell DVLA
219
Q

When is BNP released?

Effects on BNP

What can cause a rise in BNP?

A

Hormone prod. mainly in LV in response to strain

Vasodilator, diuretic and natriuretic (suppresses both RAAS and sympathetic tone)

ischaemia, valvular disease, an LV dysfunction

220
Q

What is Buerger’s Disease

A

Small and medium vessel vasculitis assoc with smoking

Causes IgA nephropathy but also Intermittent Claudication, Ischaemic ulcers, Raynauds

221
Q

TOF

A
  • Over-riding aorta
  • VSD
  • LVH
  • Pulmonary stenosis
222
Q

Types of ASD

A 
Ostium Secundum (most common)
Ostium primum
223
Q

Ostium Secundum Aetiology

A

70% due to failed closure of Foramen Ovale

224
Q

Clopidogrel

  • Action
  • When used
  • Names of similar drugs
A
  • Blocks ADP receptor (P2Y12) inhibiting platelet activation
  • 1st line in ischaemic stroke and peripheral artery disease
  • Ticagrelor, Prasugrel
225
Q

Antiplatelet use

  • NSTEMI
  • STEMI
  • TIA
  • Ischaemic stroke
  • Periphreal artery disease
A
  • Aspirin (lifelong), clopidogrel/ticagrelor (12mnth)
  • Aspirin (lifelong), clop 1 month
  • Clopi (lifelong)
  • Clopi (lifelong)
  • Clopi (lifelong)
226
Q

ACEi SE

A

Cough in 15% due to inc bradykinin levels

Small risk angio-oedema

Hyperkalaemia

227
Q

Cautions and contraindications ACEi

A

Pregnancy and BF

Renovascular disease risk renal impairment if bilateral renal artery stenosis

228
Q 
Action of antiarrhythmics 
Class 1 -
Class 2 -
Class 3 -
Class 4 -
A

Class 1 - sodium channel blockers
Class 2 - B-block (Propanolol)
Class 3 - K+channel block (Amiodarone, Sotalol)
Class 4 - Ca channel block (verapamil, diltiazem)

229
Q

Class 1 antiarrhythmics examples

A

1a (moderate): Quinidine
1b (weak): Lidocaine, phenytoin
1c (strong): Flecainide

230
Q

Action potential changes of Antiarrhythmics

A

Class 1: Change slope of phase 0
Class 2: decrease HR and conduction velocity
Class 3: inc AP duration and absolute refractory period, prolong repolarization
Class 4: slow rise of action potential. prolonged depolarisation at AV node

231
Q

When does ductus arterioles close

  • What drug keeps open & what one closes early
A

2-3 days

PG

NSAID

232
Q

Reduced femoral pulse / Radio femoral delay.. what is diagnosis

A

Coarctation (constriction) of the aorta

233
Q

What is 1st management of Pulseless electrical activity

A

Chest compression then

Give 1mg IV adrenaline

234
Q

In VF/VT when is adrenaline given

A

After chest compression started

235
Q

In Asystole what should be done

A

2 mins chest compressions and see if changes

236
Q

CCB used in HTN

A

Dihydroperidones: Amlodipine

237
Q

When is electrical rather than pharmacological cardioversion used in AF?

What should be done prior?

A

Any AF lasting for over 48 hour s= DC cardioversion

Must receive oral anticoagulant for 3 weeks prior if AF symptoms last over 48hr

238
Q

Definition of Pulseless electrical activity

A

Sinus tachy on eCG

No pulse felt

Final (26 decks)

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