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Medicine Year 2 2 > Cardiology > Flashcards

Cardiology Flashcards

1
Q

CARDIAC PHARMACOLOGY

What is the main aim when treating hypertension

A

Control peripheral resistance! This involves controlling the RAAS and SNS

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2
Q

CARDIAC PHARMACOLOGY

what are the functions of Angiotensin II?

A
  • Vasoconstrictor
  • Increase peripheral resistance
  • increase CO
  • encourage release of noradrenaline- increased sympathetic activity
  • water retention through encouragement of aldosterone release
  • tubular Na+, Cl- reabsorption, K+ excretion
  • ADH secretion so increase water absorption
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3
Q

CARDIAC PHARMACOLOGY

Name some examples of ACE inhibitors

A
  • Ramipril
  • enalapril
  • Perindopril
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4
Q

CARDIAC PHARMACOLOGY

Name some side effects of ACE inhibitors

A
  • Hypotension
  • Chronic cough
  • Acute renal failure
  • Hyperkalaemia
  • foetus abnormalities
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5
Q

CARDIAC PHARMACOLOGY

Angiotensin II receptor blockers (ARB’s) act on what receptor?

A

AT-1 receptor

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6
Q

CARDIAC PHARMACOLOGY

Name some examples of ARB’s

A
  • Candesartan
  • Losartan
  • Valsartan
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7
Q

CARDIAC PHARMACOLOGY

Name some examples of calcium channel blockers (CCB’s)

A
  • Amlodipine
  • Nifedipine
  • Verapamil
  • Diltiazem
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8
Q

CARDIAC PHARMACOLOGY

Amlodipine and nifedipine are Dihydropyridines, what is their function

A

Peripheral arterial vasodilators

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9
Q

CARDIAC PHARMACOLOGY

Verapamil is a phenylalkylamine, what is its function

A

Negatively chronotropic/ Inotropic

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10
Q

CARDIAC PHARMACOLOGY

Diltiazem is a benzothiazepine, what is its function

A

intermediate heart and peripheral effects, ( bit of both)

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11
Q

CARDIAC PHARMACOLOGY

Common side of effect Verapamil?

A
  • constipation
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12
Q

CARDIAC PHARMACOLOGY

Negatively chronotropic and inotropic effects can cause what?

A
  • ve chronotropic= Bradycardia and AV block

- ve inotropic= worsening of HF

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13
Q

CARDIAC PHARMACOLOGY

Name examples of Beta- adrenoceptor blockers (BB’s)

A
  • Bisoprolol (B1 selective)
  • Metoprolol
  • Atenolol
  • Propranolol (B1/B2 non selective)

in order of selectivity

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14
Q

CARDIAC PHARMACOLOGY

Name the types of Diuretics

A
  • Thiazides ( work on DCT and are long acting)
  • Loop diuretics ( work on Loop of Henle and are POWERFUL)
  • aldosterone antagonists (K+ sparing diuretics)
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15
Q

CARDIAC PHARMACOLOGY

Name some examples of Thiazides

A
  • Bendroflumethiazide

- Hydrochlorothiazide

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16
Q

CARDIAC PHARMACOLOGY

Name some examples of loop diuretics

A
  • Furosemide

- Bumetanide

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17
Q

CARDIAC PHARMACOLOGY

Name some examples of K+ sparing diuretics

A
  • Spironolactone

- Eplerenone

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18
Q

CARDIAC PHARMACOLOGY

What is a common side effect of spironolactone

A

It has oestrogenic effects so can increase breast tissue

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19
Q

CARDIAC PHARMACOLOGY

1st line treatment for HTN for an under 55?

A
  • ACE-I or ARB
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20
Q

CARDIAC PHARMACOLOGY

1st line treatment for HTN for an over 55 or afro-Caribbean?

A

CCB

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21
Q

CARDIAC PHARMACOLOGY

2nd line treatment for HTN?

A

Both ACE-1/ARB and CCB

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22
Q

CARDIAC PHARMACOLOGY

What is the 3rd line treatment for HTN?

A

Add a Thiazide

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23
Q

CARDIAC PHARMACOLOGY

what is the 4th line treatment for HTN?

A

add spironolactone/ alpha/ beta- blocker

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24
Q

CARDIAC PHARMACOLOGY

1st line treatment for heart failure?

A

ACE-I and beta blocker ( low dose and slow uptitration)

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25
Q

CARDIAC PHARMACOLOGY

2nd line treatment for HF?

A

aldosterone antagonist

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26
Q

CARDIAC PHARMACOLOGY

if a patient has an intolerance for ACE-I what do you give them instead?

A

If ACE-I intolerant use ARB

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27
Q

CARDIAC PHARMACOLOGY

If a patient is ACE-1 and ARB intolerant what do you give them?

A

Hydralazine/ nitrate combo

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28
Q

CARDIAC PHARMACOLOGY

What do you try as a 4th option if all HF treatments fail?

A

consider digoxin

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29
Q

CARDIAC PHARMACOLOGY

What peptides do the atria and ventricles naturally release?

A

atria- atrial natriuretic peptide (ANP)

ventricle- brain natriuretic peptide (BNP)

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30
Q

CARDIAC PHARMACOLOGY

In what circumstances are ANP and BNP released?

A
  • Increased atrial/ ventricle pressure
  • stretch of heart tissue
  • volume overload
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31
Q

CARDIAC PHARMACOLOGY

What is the function of ANP ands BNP?

A

1) increase renal excretion of sodium and water (natriuresis and diuresis)
2) relax vascular smooth muscle
3) increase vascular permeability

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32
Q

CARDIAC PHARMACOLOGY

What does ANP and BNP inhibit the release of?

A

1) Aldosterone
2) AG-II
3) Endothelin
4) ADH

(vasoconstrictors!)

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33
Q

CARDIAC PHARMACOLOGY

Neutral Endopeptidases metabolise what?

A

ANP/BNP

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34
Q

CARDIAC PHARMACOLOGY

Name a nitrate and say its functions

A
  • Isosorbide mononitrate, GTN spray

1) reduction of preload/afterload
2) Lower BP
3) Arterial/ venous dilator

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35
Q

ANGINA

What is Angina?

A

Angina is the descriptive pain caused by myocardial ischaemia

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36
Q

ANGINA

What are the different types of angina and when do they occur?

A
  • Stable (effort)
  • Unstable (random)
  • Nocturnal (night)
  • Decubitis (lying down)
  • Variant (no provocation)
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37
Q

ANGINA

What is Levine’s Sign?

A

Clenched fist over chest to deal with pain

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38
Q

ANGINA

Why does angina happen?

A

There is a rupture of a fibrous cap of a plaque due to inflammation. Constant rupture and healing over time occludes more of the artery each time which causes ANGINA.

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39
Q

ANGINA

Main cause of angina?

A

ATHEROMA

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40
Q

ANGINA

What is the diagnostic criteria?

A
  • Central crushing chest pain radiating to arm/jaw
  • Exacerbated by exercise
  • Relieved by rest/ GTN spray
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41
Q

ANGINA

What is the differential diagnosis of Angina? (also has central chest pain)

A
  • ACS
  • Pericarditis
  • Myocarditis
  • PE
  • GORD
  • Aortic Dissection
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42
Q

ANGINA

What would you investigate if a patient is suspected to have Angina?

A
  • ECG and stress ECG (ST segment depression and inverted T wave)
  • Cardiac MRI
  • CT coronary Angiogram
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43
Q

ANGINA

What is the first line treatment?

A
  • GTN spray
  • Beta Blocker ( atenolol, metoprolol)
  • Calcium Channel Blocker ( Diltiazem, Amlodipine)
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44
Q

ANGINA

What is the secondary prevention for Angina?

A

Aspirin/ clopidogrel and statin

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45
Q

ANGINA

If 1st line treatment is not enough, what are the next stages?

A

2nd- Add nitrate (isosorbide mononitrate), to reduce pressure and dilate, or K+ channel activator (Nicorandil)

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46
Q

ANGINA

what surgical interventions can be done?

A
  • Percutaneous coronary intervention (PCI)

- Coronary artery bypass graft (CABG)

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47
Q

ACUTE CORONARY SYNDROMES

What are the different types of ACS?

A
  • Unstable Angina
  • Non ST elevation MI (NSTEMI)
  • ST elevation MI (STEMI)
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48
Q

ACUTE CORONARY SYNDROMES

What are the blood markers for an NSTEMI?

A
  • Raised troponin and creatine kinase ( this shows myocardial damage)

(STEMI is the same but also there is ST elevation)

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49
Q

ACUTE CORONARY SYNDROMES

Symptoms of an ACS?

A
  • same as angina ( central crushing pain)
  • Not relieved by GTN
  • 4th heart sound- Sweats and Palpitations
  • Dyspnoea ( difficulty breathing)
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50
Q

ACUTE CORONARY SYNDROMES

What tests would you do?

A
  • Bloods ( raised troponin)

- ECG ( LBBB, tall T-waves, ST elevation/ depression)

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51
Q

ACUTE CORONARY SYNDROMES

Treatment?

A 
M- Morphine
O- Oxygen
N- Nitrate
A- Aspirin
T- Clopidogrel/ Ticragelor

(A and T are both antiplatelet)

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52
Q

ACUTE CORONARY SYNDROMES

How would you assess someone with Angina?

A
  • Assess using the GRACE score
  • If high, start GPIIb/IIIa infusion and do angiography
  • If low repeat troponin and investigate for ischaemia with angiography
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53
Q

ATHEROGENESIS

Name some non modifiable and modifiable risk factors of atherogenesis

A

Non Modifiable

  • Age
  • Gender
  • Family History

Modifiable

  • smoking
  • HTN
  • Obesity
  • Hyperlipidaemia (high LDL’s)
  • Sedentary lifestyle
  • High alcohol intake
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54
Q

ATHEROGENESIS

Name the cause of atherogenesis

A
  • Injury to endothelium means lymphocytes migrate into vessel migrate into the vessel walls and the vessel begins to narrow.
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55
Q

ATHEROGENESIS

What are the stages of atherogenesis?

A

1) Fatty Streaks (the beginning, T cells and macrophages)
2) Intermediate Lesions
3) Fibrous Plaques
4) Rupture of fibrous cap
5) Erosion

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56
Q

ATHEROGENESIS

What happens after the lymphocytes enter the vessel walls?

A
  • Foam cell production
  • Smooth muscle and T- lymphocyte proliferation
  • platelet adhesion
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57
Q

ATHEROGENESIS

What is myocardial Ischaemia?

A

Imbalance between myocardial oxygen demand and supply

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58
Q

ATHEROGENESIS

What is the QRISK2?

A

QRISK2 is a prediction algorithm for cardiovascular disease (CVD).

If there is >10% risk over 10 years, then this is an indication for primary prevention. e.g- lifestyle changes and begin statin.

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59
Q

ACUTE STEMI

What are the ECG changes of an acute STEMI

A

mins-hrs: Hyperacute T waves and ST elevation

hrs: T waves invert and broad deep Q waves
weeks: T returns. Q remains. STEMI can present with a new LBBB.

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60
Q

ACUTE STEMI

What is the treatment?

A

1) Primary PCl in under 120 mins and Thrombolysis
2) Start GPIIb/IIIa antagonist (abciximab)

Long-Term: statin, aspirin, clopidogrel, B blocker, ACE-I, (for 12 months)

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61
Q

HEART FAILURE

What is the definition of heart failure?

A

When the cardiac output is inadequate for the bodies requirements

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62
Q

HEART FAILURE

Causes?

A
  • IHD
  • Valvular HD
  • Congenital HD
  • Pericardial disease
  • Cardiomyopathies
  • Hyperthyroidism, pregnancy, obesity
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63
Q

HEART FAILURE

In detail, describe the pathology of HF?

A

1) HF= Compensatory mechanisms (maintain CO)
2) HF progresses = Overwhelmed mechanisms
3) Activation of SNS, increased HR, contractility, vasoconstriction
4) SNS stimulation leads to arteriolar constriction, increased after load, fall in renal perfusion activates RAAS- water and salt retention - oedema. AG-II- more arteriolar constriction/ work of heart

5) Myocardial failure -> increase in ESV
o Increased volume =stretch of myocardium
o Eventually leads to pulmonary and peripheral oedema, and increased oxygen requirements of the myocardium

6) Ventricular remodelling
o	Hypertrophy
o	Loss of myocytes
o	Increased interstitial fibrosis
= irreversible contractile failure
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64
Q

HEART FAILURE

What is systolic failure?

A
  • Inability to contract normally
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65
Q

HEART FAILURE

What is diastolic failure?

A
  • Inability to fill normally
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66
Q

HEART FAILURE

Symptoms of left ventricular failure?

A
  • Exertional dyspnoea
  • Fatigue
  • Cyanosis
  • Paroxysmal nocturnal dyspnoea
  • Tired, wheeze, weight loss
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67
Q

HEART FAILURE

Symptoms of right ventricular failure?

A
  • Peripheral Oedema
  • Dyspnoea and Fatigue
  • Increased weight
  • Ascites
  • Nausea
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68
Q

HEART FAILURE

What do you call it if someone has left and right ventricular failure?

A

Congestive Cardiac Failure (CCF)

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69
Q

HEART FAILURE

What are the signs and symptoms of CCF?

A
  • Ascites
  • 3rd and 4th heart sounds
  • Cardiomegaly
  • Displaced apex beat
  • Hepatomegaly
  • Tachycardia
  • Elevated JVP
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70
Q

HEART FAILURE

What are pleural effusions?

A
  • Bibisal coarse crackles (crackles at base of both lungs)

- Bibisal decreased breath sounds (both lungs)

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71
Q

HEART FAILURE

What are the different classes of HF?

A

Class 1- No dyspnoea at rest

Class 2- Comfortable at rest but fatigue/ palpitations/ dyspnoea after regular exercise

Class 3- Mild exercise causes fatigue/ palpitations/ dyspnoea

Class 4- Fatigue/ palpitations/ dyspnoea at rest

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72
Q

HEART FAILURE

Name the major criteria for HF

A 
S- S3 heart sound (gallop)
A- Acute pulmonary oedema
W- Weight loss >4.5kg in 5 days
P- Paroxysmal nocturnal dyspnoea
A- Abdominojugular reflex (hepatojugular)
N- Neck vein distension
I- Increased cardiac shadow on XR (cardiomegaly)
C- Crackles in lungs
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73
Q

HEART FAILURE

Name the minor criteria for HF?

A 
H- Hepatomegaly
E- Effusions (pleural)
A- Ankle Oedema
exeR- tional dyspnoea
T- Tachycardia
V- Vital capacity decreased by 1/3
N- Nocturnal cough
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74
Q

HEART FAILURE

What tests would be carried out to check for HF?

A
  • Bloods (anaemia, high BNP)
  • Echo (systolic/diastolic function)
  • Calculate eject fraction <35% is severe
  • Chest X-ray
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75
Q

HEART FAILURE

What do we look for on a chest X-ray when looking for heart failure?

A 
A- alveolar oedema
B- kerley B lines
C- Cardiomegaly
D Dilated upper lobe vessels
E - pleural effusions
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76
Q

HEART FAILURE

When would you give a patient O2?

A

Only give patient oxygen if they’re hypoxic.

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77
Q

HYPERTENSION

Causes?

A

(90%)- Obesity, genetics, high salt, diabetes, alcohol
(8%)- Kidney Disease
rare- endocrine, the pill

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78
Q

HYPERTENSION

To measure hypertension we carry out 24 hour ambulatory blood pressure monitoring. At what BP would this be offered?

A

over 140/90

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79
Q

HYPERTENSION

What is End Organ Damage?

A
  • Retinopathy
  • Renal Failure
  • Stroke/ TIA
  • MI/Angina
  • LV Hypertrophy
  • HF
  • Peripheral vascular disease
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80
Q

HYPERTENSION

Treatment of hypertension

A

1st- <55= ACE-I
>55 or afro-Caribbean= CCB

2nd- Both

3rd- Add thiazide

4th- Add extra diuretic/alpha/ beta blocker

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81
Q

ARRHYTHMIAS

Symptoms?

A
  • Palpitations
  • Syncope
  • Dyspnoea
  • Dizziness

OR asymptomatic

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82
Q

ARRHYTHMIAS

How are cardiac arrhythmias diagnosed?

A

24 hour ambulatory ECG -> Loop recorder

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83
Q

ARRHYTHMIAS

Causes of heart block?

A
  • CAD
  • Cardiomyopathies
  • Fibrosis of conducting pathways (in the elderly)
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84
Q

ARRHYTHMIAS

Name the different types of AV block

A

1) First degree AV Block
2) Second degree AV Block
3) Third degree AV Block

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85
Q

ARRHYTHMIAS

Name the different types of second degree AV Block

A
  • Mobitz Type 1
  • Mobitz Type 2
  • 2:1 or 3:1 Block
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86
Q

ARRHYTHMIAS

What is 1st degree AV Block and what does it look like on an ECG?

A
  • 1st degree AV Block is delayed AV conduction and on an ECG it has:

A prolonged PR interval >0.22s

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87
Q

ARRHYTHMIAS

What happens in 2nd degree AV block?

A

Some impulses fail to reach the ventricles

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88
Q

ARRHYTHMIAS

What does an ECG look like for a patient with Mobitz Type 1 AV block?

A
  • Progressively longer PR interval until the P wave fails to conduct. It then resets and occurs again
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89
Q

ARRHYTHMIAS

What does an ECG look like for a patient with Mobitz Type 2 AV block?

A

Random dropping of QRS complexes due to failed conduction of P. On an ECG there is:

-Wide QRS complexes

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90
Q

ARRHYTHMIAS

What does an ECG look like for a patient with 2:1 or 3:1 AV Block and what is it?

A

It is when there are 2 or 3 P waves for every QRS complex due to failed conductions.
(e.g- 3:1 AV block has 3 P waves for every QRS.)

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91
Q

ARRHYTHMIAS

What is the treatment for each of the different types of AV block?

A

1st: No Rx
2nd- Mobitz 1- Monitor
Mobitz 2, 2:1/3:1, 3rd: Pacemaker

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92
Q

ARRHYTHMIAS

What is 3rd degree AV block and what does an ECG look like?

A
  • Complete heart block
  • No association between atrial and ventricular activity.
  • Contractions occur due to an escape rhythm.

ECG: P and QRS occur independently

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93
Q

ARRHYTHMIAS

What are the causes of an Right Bundle Branch Block? (RBBB)

A
  • IHD
  • PE
  • Cardiomyopathies
  • Congenital heart disease
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94
Q

ARRHYTHMIAS

What are the ECG changes for someone with a RBBB?

A
  • wide QRS
  • secondary R wave in V1 (RSR)
  • QRS in V6- slurred S

(MARRoW)

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95
Q

ARRHYTHMIAS

Pathologically, what occurs if someone has an LBBB?

A
  • LBB fails to conduct
  • Depolarisation spreads across LV via cell to cell
  • Therefore, RV contracts BEFORE LV
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96
Q

ARRHYTHMIAS

Pathologically, what occurs if someone has an RBBB?

A
  • RBB fails to conduct
  • Depolarisation spreads across RV via cell to cell
  • Therefore, LV contracts BEFORE RV
97
Q

ARRHYTHMIAS

What are the causes of a Left Bundle Branch Block? (LBBB)

A
  • IHD
  • HTN
  • LVH
  • aortic valve disease
  • Fibrosis of conducting pathways
98
Q

ARRHYTHMIAS

What ECG changes can be found for someone with an LBBB?

A
  • Wide QRS
  • Secondary R wave in LV leads ( 1, aVL, V4-V6)
  • QRS in V1 (W)
  • RSR in V6 (M)

(WiLLiaM)

99
Q

ARRHYTHMIAS

In a normal ECG in leads 1 and 2, QRS is positive, what changes in:

  • Left Axis Deviation?
  • Right Axis Deviation?
A

LAD: Lead 1- positive Lead 2- negative
RAD: Lead 1- negative Lead 2- positive

100
Q

ARRHYTHMIAS

What is Sinus Tachycardia?

A

Physiological response to exercise and excitement

101
Q

ARRHYTHMIAS

what happens to someone’s ECG if they have Supraventricular Tachycardia?

A
  • P wave is absent or inverted after QRS
102
Q

ARRHYTHMIAS

What are the signs of a supraventricular tachycardia?

A
  • Rapid palpitations
  • Dizziness
  • Dyspnoea
  • Central chest pain
103
Q

ARRHYTHMIAS

How are supraventricular tachycardias managed?

A

1) Vagal Manoeuvres (carotid massage)
2) Adenosine

If fails Verapamil or (atenolol/ sotalol)

LONG TERM= ABLATION

104
Q

ARRHYTHMIAS

What is a ventricular tachycardia and how is it treated?

A

It is a rapid ventricular rhythm with broad abnormal QRS complexes

Treatment: Amiodarone IV + Defib

105
Q

ARRHYTHMIAS

What is a Ventricular Ectopic and how is it treated?

A

Premature beats and abnormal P wave.

Ectopic electrical activity is not conducted through normal tissue

Treatment: beta blockers

106
Q

ARRHYTHMIAS

Prolonged QT syndrome is when what is prolonged?

A

Ventricular repolarisation

107
Q

ARRHYTHMIAS

What are the causes of prolonged QT syndrome?

A
  • Congenital ( mutation to Na/ Mg channel genes)
  • Electrolyte disturbances (hyper/hypo)
  • Drugs ( TCA’s, phenothiazines)
108
Q

ARRHYTHMIAS

What are the symptoms of prolonged QT syndrome?

A
  • Palpitations
  • Syncope
  • Torsade de pointes (polymorphic VT)
    (rapid irregular QRS, changing from upright to inverted)
109
Q

ARRHYTHMIAS

Treatment for prolonged QT syndrome?

A
  • IV isoprenaline and treat underlying causes
110
Q

ARRHYTHMIAS

What is Wolff- Parkinson White?

A

Congenital accessory conduction pathway between the atria and ventricles (Bundle of Kent)

Patient presents with Supraventricular Tachycardia

111
Q

ARRHYTHMIAS

WPW is a type of Atrioventricular re-entry Tachycardia (AVRT), but what is an AVRT?

A

It is when an impulse can travel down 1 route but back up another.

112
Q

ARRHYTHMIAS

What are the ECG changes for someone with an AVRT

A
  • Short PR due to speed of accessory pathway

- Slurred QRS, ‘pre-excitation’

113
Q

ARRHYTHMIAS

How is AVRT and AVNRT managed?

A

1st- Electrical cardioversion or carotid massage
2nd- Adenosine
3rd- Verapamil

Long Term- Ablation

114
Q

ARRHYTHMIAS

What is AF?

A

Atrial Fibrillation is chaotic atrial rhythm at a rate of 300-600bpm

115
Q

ARRHYTHMIAS

What are some causes of AF?

A
  • HF
  • HTN
  • Mitral Valve Disease
  • Hyperthyroidism
  • Alcohol
  • MI
  • PE
116
Q

ARRHYTHMIAS

Symptoms of AF?

A
  • Asymptomatic, palpitations, fatigue

It is IRREGULARLY IRREGULAR

117
Q

ARRHYTHMIAS

Investigations for AF?

A

ECG and bloods (U+E, thyroid function, cardiac enzymes)

Absent P waves

118
Q

ARRHYTHMIAS

Management of acute AF?

A

1st- Cardioversion or IV amiodarone
02 and U+E’s
Verapamil or bisoprolol

119
Q

ARRHYTHMIAS

Management of chronic AF?

A
  • Beta blocker (rate control)
  • Warfarin
  • Add digoxin then amiodarone
120
Q

ARRHYTHMIAS

How is an atrial flutter found on an ECG?

A
  • Sawtooth baseline
121
Q

ARRHYTHMIAS

What is an atrial flutter?

A

Atrial Tachycardia, atria beats at 300bpm and ventricles only conduct every second beat/ e.g it is regular so 150bpm

122
Q

ARRHYTHMIAS

How is an atrial flutter treated?

A
  • Anticoagulate and cardioversion

- Amiodarone (restore sinus rhythm)

123
Q

ARRHYTHMIAS

What is a sinus arrest?

A

When the SAN fails to discharge on time, P wave stops

124
Q

ARRHYTHMIAS

What is a SA block?

A

When an impulse doesn’t reach the atria

125
Q

There are 10 basic ECG rules. Try name a few

A

1) PR interval- 120-200ms
2) QRS < 110ms
3) Leads I and II predominantly upright
4) QRS and T same direction
5) All negative in aVR!
6) R grows V1-V4
7) S grows V1-V3 and goes at V6
8) P wave is upright in leads (I, II, V2-V6)
9) no/small Q <0.04ms in leads ( I, II V2-V6)
10) T wave upright in leads ( I, II, V2-V6)

126
Q

What does a statin do?

A

statins inhibit HMG-CoA reductase and reduce cholesterol synthesis

127
Q

what does clopidogrel/ ticagrelor do?

A

inhibitors of P2Y12 ADP receptor

128
Q

What does aspirin do?

A

unlike other NSAIDs, aspirin action is IRREVERSIBLE inhibitor of COX enzyme. (cyclo- oxygenase)

129
Q

What is a foam cell?

A

macrophage that localises to fatty deposits in BV walls (ingest LDL’s).

130
Q

What is electrocardiography?

A

summation of the hearts electrical activity

131
Q

At what rate does the dominant SAN beat?

A

60-100bpm

132
Q

what are the two back-up pacemakers of the heart?

A

AVN- 40-60bpm

Ventricular cells- 20-45bpm

133
Q

On an ECG what does a small box represent horizontally?

A

0.2 seconds

134
Q

On an ECG what does a small box represent vertically?

A

0.5mV

135
Q

Lead I is said to be at 0 degrees. At what angles are the other leads in relation to lead I

A 
Lead II  +60
aVF +90
Lead III +120
aVR -150
aVL -30
136
Q

What is Einthoven’s triangle?

A

Einthoven’s triangle is an imaginary formation of three limb leads in a triangle used in electrocardiography, formed by the two shoulders and the pubis.

RA - + LA
- -

         \+  LL +
137
Q

AORTIC STENOSIS

Causes?

A
  • Degeneration and calcification of a normal valve (elderly)
  • Calcification of congenital bicuspid valve (middle-aged)
  • Rheumatic heart disease
138
Q

AORTIC STENOSIS

Pathology?

A

1) obstruction to LV emptying (LV Hypertrophy)
2) increased myocardial demand = ischaemia of myocardium
3) This leads to Angina, arrhythmias and left heart failure

139
Q

AORTIC STENOSIS

Symptoms?

A

Classic Triad

1) angina
2) syncope
3) heart failure and congestive HF

also, dyspnoea, dizzy, fatigue

140
Q

AORTIC STENOSIS

Tests?

A
  • CXR (dilated aorta and enlarged heart)
  • ECG Tall R waves in aVL and V4-V6
  • Doppler Ultrasound - assess pressure gradient across valve
    Echo- Would find LVH
141
Q

AORTIC STENOSIS

Treatment?

A

Valve replacement/ repair

142
Q

AORTIC STENOSIS

Signs?

A

1) systolic ejection murmur
2) ejection click- sudden opening
3) soft S2 heart sound
4) Slow rising pulse with narrow pulse pressure
5) LVH signs- heaving, displaced apex beat
6) pulsus parvus et tardos

143
Q

MITRAL REGURGITATION

Cause?

A

Prolapsing mitral valve
Rheumatic HD
Infective Endocarditis

144
Q

MITRAL REGURGITATION

What happens in chronic MR?

A

LA and LV dilation (time to adjust)= exertional dyspnoea

145
Q

MITRAL REGURGITATION

What happens in acute MR?

A

1) LA pressure increases

2) backs up into lungs = Pulmonary Oedema + exertional dyspnoea

146
Q

MITRAL REGURGITATION

Signs?

A
  • AF
  • pansystolic murmur (heart murmur that occurs over the entire systole, from the 1st to the 2nd heart sounds)
  • displaced apex beat
  • weak S1
    5) RV heave
147
Q

AORTIC REGURGITATION

Causes?

A
  • Infective Endocarditis
  • Rheumatic Heart disease
  • Bicuspid Aortic Valve
148
Q

AORTIC REGURGITATION

What happens in chronic AR?

A

1) Blood backs up into LV= LV hypertrophy and dilation
2) Stroke volume and pulse pressure increased
3) results in LV failure and dyspnoea

149
Q

AORTIC REGURGITATION

What happens in acute AR?

A

there is no adaptations as there is not enough time therefore:

Pulmonary oedema and decreased stroke volume

150
Q

AORTIC REGURGITATION

Signs?

A
  • High pitched early diastolic murmur
  • wide pulse pressure
  • collapsing pulse
  • displaced apex
  • Breathless when lying down
151
Q

AORTIC REGURGITATION

Tests and treatment?

A

ALL VERY SIMILAR

1) beta blockers (control rate)
2) ACE-I (reduce LV hypertension)
3) Surgery- valve replacement
4) anticoagulants

152
Q

MITRAL STENOSIS

Tests?

A

CXR- enlarged LV, dilation of AA

ECG- LVH, P Mitrale (bifid P waves, bit like a curly M)

153
Q

MITRAL STENOSIS

Causes?

A

1) Thickening of valves leads to obstruction between LA and LV, thus, increasing LA pressure
2) this leads to pulmonary oedema, HTN and right heart dysfunction

also, rheumatic HD

154
Q

MITRAL STENOSIS

very simply, describe the pathology

A
  • increased LA pressure and dilation= LA dysfunction= AF= dyspnoea
155
Q

MITRAL STENOSIS

Signs?

A
  • mitral facies (pink/ purple patches on cheeks due to low CO)
  • Mid diastolic murmur
  • Loud S1
  • Opening snap when mitral valve opens

more severe: longer murmur and snap is closer to S2

156
Q

MITRAL STENOSIS

Treatment?

A

ALL VERY SIMILAR

1) beta blockers (control rate)
2) ACE-I (reduce LV hypertension)
3) Surgery- valve replacement
4) anticoagulants

also diuretics

157
Q

AORTIC ANEURYSM

Causes?

A
  • Atheroma

- Marfan’s Syndrome

158
Q

AORTIC ANEURYSM

Symtpoms?

A
  • Epigastric pain radiating to back
  • Expansible abdominal mass
  • Unruptured may be asymptomatic
159
Q

AORTIC ANEURYSM

Tests?

A

Ultrasound + CT

160
Q

AORTIC ANEURYSM

Treatment?

A
  • Immediate surgery if symptomatic or >5.5cm
161
Q

AORTIC DISSECTION

What is it?

A
  • Tear in the intima of the aorta, leading to blood flowing in and creating a false lumen in the diseased media
162
Q

AORTIC DISSECTION

Symptoms?

A
  • Sudden severe tearing chest pain- radiating through back
163
Q

AORTIC DISSECTION

Tests?

A
  • CXR
  • CT
  • TOE
  • MRI
164
Q

AORTIC DISSECTION

Treatment?

A
  • BP control- (IV Labetalol and immediate surgery)

- Hypotensive to keep systolic BP at 100-110mmHg

165
Q

ENDOCARDITIS

what is it?

A

Destruction of valve due to fibrin, platelets and infective organisms forming vegetation on the valve

166
Q

ENDOCARDITIS

Risk Groups?

A
  • Intravenous Drug Users
  • Prosthetics
  • Structural Heart Defects
167
Q

ENDOCARDITIS

Causes?

A
  • S. viridans
  • S. aureus
  • coliforms
  • enterococci
  • s. epidermis
168
Q

ENDOCARDITIS

Features?

A
  • Fever
  • Night sweats
  • Weight loss
  • Malaise
  • Anaemia
  • NEW HEART MURMURS
  • Haematoma occurs in 70%
169
Q

ENDOCARDITIS

Signs of Left Emboli?

A

Brain - Stroke
Kidney- Haematuria
Bone- Osteomyelitis
Skin- Janeway’s Lesions

170
Q

ENDOCARDITIS

Signs of Right Emboli?

A
  • Pulmonary Infraction

- Pneumonia

171
Q

ENDOCARDITIS

Signs of causation by immune complex deposition?

A
  • Osler’s Nodes (painful lesions on hand/feet)
  • Splinter haemorrhages under nails
  • Roth spots on retina
  • Joints = arthralgia
172
Q

ENDOCARDITIS

Tests?

A
  • Transoesophageal echocardiography (TOE)

- Blood cultures ( 3 from different sites over 24hrs)

173
Q

ENDOCARDITIS

Major Criteria for Endocarditis?

A

1) Positive blood cultures (typical organisms in 2/3)
2) Endocardial involvement
3) Positive echo
4) New regurgitation murmur

174
Q

ENDOCARDITIS

Minor criteria for Endocarditis?

A

1) fever >38C
2) vascular phenomena
3) Immunological phenomena
4) Cardiac lesion

175
Q

ENDOCARDITIS

Treatment?

A
  • IV benzylpenicillin & gentamycin for 6 weeks

- If staph suspected- vancomycin instead of penicillin

176
Q

PERICARDITIS

Viral Causes?

A
  • Coxsackie B
  • HIV
  • Varicella
  • Mumps
  • Influenza
  • Echovirus
177
Q

PERICARDITIS

Bacterial Causes?

A
  • Staphs/ Streps
178
Q

PERICARDITIS

Symptoms?

A
  • Sharp retrosternal chest pain
  • Pain worse on inspiration, lying flat
  • Leaning forward relieves!!!!!!!!
179
Q

PERICARDITIS

Cardinal Signs?

A

Pericardial Rub

180
Q

PERICARDITIS

ECG changes?

A
  • Concave ST elevation in ALL leads
181
Q

PERICARDITIS

Bloods?

A

increased CRP, WCC, troponin

182
Q

PERICARDITIS

Treatment?

A
  • treat underlying causes + NSAIDs
183
Q

CONSTRICTIVE PERICARDITIS

What is it?

A

when the heart is enclosed in a rigid, fibrotic pericardium, preventing diastolic filling of ventricles

184
Q

CONSTRICTIVE PERICARDITIS

Symptoms?

A

Symptoms of right HF:

  • Ascites
  • Lower limb oedema
  • increased JVP
185
Q

CONSTRICTIVE PERICARDITIS?

Tests and treatment?

A

CXR shows calcification

Treated with pericardiectomy

186
Q

PERIPHERAL ARTERIAL DISEASE

Risk Groups?

A
  • CAD
  • Atherosclerosis
  • General CVS problems
187
Q

PERIPHERAL ARTERIAL DISEASE

Symptoms?

A
  • Intermittent Claudication

(cramp felt in calf, buttock or thigh after walking a certain distances- relieved by rest)

  • burning or numbness
  • Differences between limbs in relation to colour and/or warmth
  • Decreased rate of hair and nail growth on the impacted limb
188
Q

PERIPHERAL ARTERIAL DISEASE

Stages of PAD?

A

1) Asymptomatic
2) Intermittent Claudication
3) Ischaemia rest pain
4) 3+ gangrene/ ulceration (critical ischaemia)

189
Q

PERIPHERAL ARTERIAL DISEASE

A normal Ankle Brachial Pressure Index is 1-1.2, what would somebody’s ABPI be if they had PAD?

A

0.5-0.9

190
Q

PERIPHERAL ARTERIAL DISEASE

Signs?

A
  • Absent lower limb pulses
  • cold, white legs
  • ulcers
  • atrophic skin
  • slow growth of nails and hair
191
Q

PERIPHERAL ARTERIAL DISEASE

Investigations?

A
  • Colour duplex ultrasound
  • FBC- anaemia
  • ABPI
192
Q

PERIPHERAL ARTERIAL DISEASE

Treatment?

A

1) risk factor modification (e.g. smoking, control BP/cholesterol, antoiplatelet- clopidogrel)

2) Manage claudication
- exercise programmes- increase collateral blood flow
- exercise to point of maximum pain

3) Revascularisation
- percutaneous transluminal angioplasty (PTA)- balloon in narrowed segment

4) Surgical Reconstruction - arterial bypass graft

193
Q

CARDIOMYOPATHY

What is it?

A

Disease of the myocardium

194
Q

HYPERTROPHIC CARDIOMYOPATHY

Causes?

A

Autosomal dominant Mutations

Hypertrophic non-compliant ventricles impair diastolic filling and reduce SV so results in HEART FAILURE

195
Q

HYPERTROPHIC CARDIOMYOPATHY

Symptoms?

A
  • Asymptomatic
  • Breathless, angina, syncope
  • jerky carotid pulse
  • ejection systolic murmur
  • pansystolic murmur
196
Q

HYPERTROPHIC CARDIOMYOPATHY

Investigations?

A

ECG- LVH and progressive T wave inversion
Cardiac Imaging:

  • Ventricular Hypertrophy (echo and MRI)
  • fibrosis (MRI)
197
Q

HYPERTROPHIC CARDIOMYOPATHY

Treatment?

A
  • b- blockers or verapamil (CCB)
  • amiodarone for arrhythmias
  • anticoagulate to avoid emboli
  • consider implantable defib if HIGH RISK
198
Q

DILATED CARDIOMYOPATHY

Features? (same as HF)

A
  • Dyspnoea
  • Emboli or arrhythmia
  • Progressive HF
  • increased JVP, HTN
199
Q

DILATED CARDIOMYOPATHY

Investigations

A
  • CXR
  • ECG
  • Echo
200
Q

DILATED CARDIOMYOPATHY

treatment?

A
  • bed rest
  • diuretics
  • digoxin
  • ACE inhibitors
  • anti- coagulate

implantable defib

201
Q

ATRIAL SEPTAL DEFECT

What is it?

A

a hole that connects the atria

202
Q

Which cardiac drugs:

Control rate?
Restore sinus rhythm?
Reduce Hypertrophy?

A

beta blockers (control rate)
Amiodarone (restore sinus rhythm)
ACE-I (reduce LV hypertension)

203
Q

ATRIAL SEPTAL DEFECT

Investigations?

A
  • ECG ( RBBB with LAD and prolonged PR interval)

- CXR- small aortic knuckle and pulmonary plethora

204
Q

ATRIAL SEPTAL DEFECT

Treatment?

A

transcatheter closure> surgery

205
Q

What is an Atrioventricular Septal Defect (AVSD) and what disease often causes AVSD?

A

A hole in the centre of the heart seen often in Down’s syndrome.

206
Q

What is a Patent ductus Arteriosus and what does it require?

A

Persistent communication between proximal left PA and descending aorta- continuous left to right shunt that requires a heart transplant

207
Q

What is restrictive cardiomyopathy identical to clinically?

A

Restrictive pericarditis (R sided failure)

208
Q

How is diagnosis of restrictive cardiomyopathy made, and what is the treatment?

A

Diagnosis by cardiac catheterisation showing characteristic pressure changes. No treatment.

209
Q

SHOCK

What is it?

A

Circulatory failure resulting from inadequate organ perfusion

210
Q

SHOCK

Give 6 signs

A 
anuria, 
low GCS, 
tachycardia, 
tachypnoea, 
agitation,
confusion, 
pallor (unhealthy, pale appearance)
211
Q

SHOCK

What are the types of shock?

A

Hypovolaemic: bleeding, trauma, burns, dehydration.

Cardiogenic: acute coronary syndromes, arryhthmias, cardiac tamponade, PE.

Septic: systemic inflammatory response syndrome 

sepsis: SIRS occurring with an infection. 

Septic shock: sepsis with organ hypoperfusion.

Anaphylactic: mast cell degranulation.

Neurogenic: attributed to the autonomic pathways in spinal cord. Surgery, trauma.

212
Q

SHOCK

What is the definition of SIRS, and when does this become sepsis? How is sepsis managed?

A

SIRS: systemic inflammatory response syndrome

(Temp <36 or >38, tachypnoea>20, tachycardia>90, white cells > 12,000/L, hyperglycaemia. I like my TTT white with sugar.).

Sepsis is SIRS + Infection.

BUFALO: blood cultures, urine output, fluids, antibiotics (don’t delay past 1 hour. Good cover is IV co-amoxiclav + IV gentamicin + IV metronidazole), lactate, oxygen.

213
Q

SHOCK

How is sepsis managed?

A 
BUFALO: 
blood cultures, 
urine output, 
fluids, 
antibiotics (don’t delay past 1 hour. Good cover is IV co-amoxiclav + IV gentamicin + IV metronidazole), 
lactate, 
oxygen.
214
Q

SHOCK

Management of anaphylaxis?

A

Secure airway. Remove cause. 0.5ml of 1/1000 adrenaline IM, repeating every 5 mins, IV hydrocortisone, chlorphenamine.

anti-histamines

215
Q

SHOCK

What cells are involved in anaphylaxis?

A

It is a Type 1 IgE- mediated hypersensitivity and involves the degranulation of MAST CELLS that release histamine

216
Q

SHOCK

What are the stages (in terms of blood loss) of hypovolaemic shock, and how is it managed?

A

1: 0-15%.
2: 15-30%.
3: 30-40%.
4: >40%.
Treat by identifying the cause and stopping it and giving fluids.

217
Q

When are congenital heart defects particularly dangerous?

A

During pregnancy

218
Q

What are the 4 things in tetralogy of Fallot?

A

1) Ventricular septal defect,
2) overriding of the aorta of the VSD into LV and RV,
3) pulmonary stenosis,
4) right ventricular hypertrophy.

219
Q

Tetralogy of Fallot

What pressure differences are there between the R and L and what does this cause?

A

Pulmonary stenosis causes RV pressure to be higher than LV pressure, so blood goes right to left. Causes cyanosis of patient.

220
Q

Tetralogy of Fallot

What does CXR show and how is it managed?

A

Boot shaped heart. Managed with surgery before age of 1.

221
Q

What pressure changes occur in Ventricular Septal Defect?

A

LV higher than RV, so blood flows from left to right.

222
Q

What can a large Ventricular Septal Defect cause? Why is this bad?

A

High pressure into pulmonary vasculature = damage. This resists flow and RV pressure increases, becoming higher than the left and the shunt is reversed – Eisenmenger’s syndrome.

Bad as there is a really poor prognosis.

223
Q

ATRIAL SEPTAL DEFECTS

What causes atrial septal defects?

A

Ostium secundum defects.

224
Q

ATRIAL SEPTAL DEFECTS

Which way is blood shunted?

A

LA to RA

225
Q

ATRIAL SEPTAL DEFECTS

Give 2 clinical features.

A

Dyspnoea at 40-60, pulmonary flow murmur.

226
Q

What 3 shunts can there be?

A

Intra-atrial, intra-ventricular, or both combined

227
Q

When is a patent ductus arteriosus more likely, and what does it cause in terms of blood flow?

A

In premature babies. Causes torrential bloodflow to lungs in infancy causing dyspnoea.

228
Q

At what point are most cases of coarctation of the aorta?

A

Just distal to L subclavian artery

229
Q

What murmur is heard in patent ductus arteriosus?

A

A continuous machinery murmur (throughout the whole cycle)

230
Q

What will a mild coarctation present with, and what is the classic sign?

A

Hypertension in the 20’s. sign is radiofemoral delay.

231
Q

What murmur would be heard in a mild coarctation?

A

Systolic murmur over scapulae due to collaterals being formed.

232
Q

How is mild coarctation diagnosed and treated?

A

Diagnosed with CT, treated with surgery.

233
Q

What is the inevitable fate of a bicuspid aortic valve?

A

Aortic stenosis

234
Q

Give 3 things that severe pulmonary stenosis causes.

A

Pulmonary hypertension, dyspnoea, RV failure, collapsing

235
Q

How is pulmonary stenosis treated?

A

Balloon valvuloplasty

236
Q

What is arryhthmogenic cardiomyopathy caused by?

A

Desmosome mutations affecting gap junctions

237
Q

What does arrhythmogenic cardiomyopathy present with on ECG?

A

epsilon waves after QRS

238
Q

What is Eisenmenger’s syndrome?

A

1) Ventricular septal defect causes increased blood flow to pulmonary arteries.
2) Eisenmenger syndrome occurs when the pressure in the pulmonary arteries becomes so high that it causes oxygen-poor (blue) blood to flow from the right to left ventricle (shunt reversal)
3) This goes to the body, causing cyanosis. The high pressure also causes the wall of your heart’s right ventricle to thicken (hypertrophy).

Medicine Year 2 2 (15 decks)

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