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Heart (HLB) Flashcards

1
Q

Which syndromes come under the heading of IHD?

A

Angina
MI
HF (ischaemic cardiomyopathy)
Arrythmias
Mitral valve dysfunction

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2
Q

What is IHD caused by?

A

Atherosclerosis of the coronary arteries

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3
Q

What is the difference between incidence and prevalence?

A
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4
Q

What are the S&S of angina?

A
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5
Q

What is the difference between stable and unstable angina?

A

Stable = pain on exertion
Unstable = pain at rest but no MI

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6
Q

What is the difference between MI and angina?

A

Angina is exertion, MI the pain is there, even at rest.

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7
Q

Why do you get pain with angina?

A

Is a form of demand ischaemia - usually due to fixed obstruction / narrowing of the coronary arteries. Is inadequate when BF demands increases (e.g. exertion, other demands for blood or tachyarrythmia).

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8
Q

What makes angina worse?

A

Exertion
Cold
Large meal

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9
Q

What type of pain is cardiac pain?

A

A referred pain - heart does not have own nerve supply – uses thoracic (T1-5 chest) and cervical (C5-6 shoulder) spinal nerves. Tends to spare C7-8 (distal arm).

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10
Q

How does myocardial infarction present?

A
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11
Q

Why do Ps look grey when having an MI?

A

Vasculature gets shut down by the ANS = grey pallor

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12
Q

What is a myocardial infarction?

A

Form of supply ischaemia – acute coronary artery occlusion -> inadequate blood flow even for basal requirements

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13
Q

How does a coronary thrombosis occur?

A
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14
Q

How long after initial blockage of a coronary artery do you have before myocyte necrosis begins?

A

15 minutes

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15
Q

Describe what happens in the ischaemic cascade

A

Hypoperfusion = reduced amount of blood flow.
Lack O2 = Na pumps stop working à metabolic processes.
Accumulate K outside the myocytes à rhythm abnormalities. Low K and High K = v dangerous because of the rhythm abnormalities that they cause. Some Ps die here.
Heart muscle starts to malfunction – initially it becomes stiff = diastolic dysfunction. Then it becomes weak = systolic dysfunction à acute HF – fluid on chest and BP can be very low – some Ps die here.
If damage not too great – see changes on ECG recording = ST seg elevation MI. Chest pain = large MI. Occurs relatively late in the cascade.
15 mins after complete occlusion of coronary artery - myocyte necrosis starts

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16
Q

What are the S&S of HF?

A

Fatigue (low CO)
Leg swelling
SOB - cough
Orthopnoea
Paroxysmal Nocturnal Dyspnoea

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17
Q

What are most cases of IHD caused by?

A

Previous MI
Chronic ischaemia

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18
Q

What is silent ischaemia?

A

That there are no clinical signs of abnormality of IHD until sudden death.

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19
Q

How is ischaemic heart disease managed?

A
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20
Q

What RF for IHD should be managed medically?

A

HT
Hyperlipidaemia
Diabetes

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21
Q

Is IHD more prevalent in M or F?

A

M

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22
Q

Which anti platelet drugs can be given for IHD?

A

Aspirin
Clopidogrel
Tirofiban

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23
Q

What is the mode of action of aspirin?

A

COX1 Inhibitor -
COX1 converts arachidonic acid to thromboxane A2. TA2 binds to thromboxane receptors on platelets and activates them = this causes activation, adhesion and aggregation. Thus aspirin stops this from happening.

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24
Q

What is the mode of action of clopidogrel?

A

P2Y12 receptor antagonist - activated platelets released ADP which binds to other platelets via P2Y12 receptors - causing activation, adhesion and aggregation.

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25
Q

What is the mode of action of tirofiban?

A

GP2b3a antagonist - stops platelets binding to fibrinogen and therefore each other by this receptor - prevents activation, adhesion and aggregation.

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26
Q

What is the difference between anti platelet drugs and anti coagulant drugs?

A

Antiplatelet agents inhibit clot formation by preventing platelet activation and aggregation, while anticoagulants primarily inhibit the coagulation cascade and fibrin formation.

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27
Q

What drugs are used in the case of acute MI?

A

Need drugs that work quickly - IV heparin is unpredictable so we use LMWH instead (Fondaparinux)

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28
Q

What drug treatment is given to prevent angina?

A

Β blockers
Calcium channel antagonists
Nitrates

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29
Q

Why are β blockers used for angina?

A

They block cardiac β 1 receptors = reduced force of contraction and reduced response to exercise

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30
Q

What β blocker drugs can you name?

A

Bisoprolol
Atenolol
Metoprolol

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31
Q

Why are calcium channel antagonists used for angina?

A

Reduce calcium entry to myocyte & vascular muscle contraction = REDUCED force of heart contraction + DILATION of coronary arteries & peripheral arteries = REDUCED after load

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32
Q

What Calcium channel antagonist drugs can you name?

A

Amlodipine
Dilitiazem
Verapamil

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33
Q

Why are nitrates used for angina?

A

Mimics the effects of NO - dilates coronary partiers and dilates veins = reduced preload.
Reduced preload = reduces how hard the heart has to work

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34
Q

Which nitrate drugs can you name?

A

GTN spray (short acting)
Isosorbide mononitrate (long acting)

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35
Q

Which artery is bigger - the right or left coronary artery?

A

Left coronary artery

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36
Q

What will a blockage in the right coronary artery cause on ECG?

A

Elevation in leads II, III & aVF

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37
Q

What are the two branches of the left coronary artery?
Where do these branches show on ECG?

A

Left anterior descending - supplies 45% of heart muscle (V1-4)
Circumflex coronary artery - predominantly back and lateral wall of the heart - V5,6 & aVL

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38
Q

Blockage in which artery is known as the widow maker?

A

Blockage in the left mainstream coronary artery - survival rates are very low.

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39
Q

What percentage of the heart muscle is supplied by the following arteries?
- LAD
- Cx
- RCA

A

LAD = 45%
Cx = 20-30%
RCA = 25-35%

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40
Q

How can you revascularise the heart?

A

CABG - Coronary artery bypass graft - uses conduits to bypass coronary stenoses

Percutaneous Coronary Intervention (Angioplasty) - dilate with a balloon and stent.

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41
Q

With an MI necrosis is detectable to heart muscle after 15 minutes - but is not uniform - which area is more sensitive to the ischaemia, and why?

A

Sub-endocardial myocardium is more sensitive - this is because collateral blood vessels provide partial protection to other areas.

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42
Q

How long after coronary occlusion can myocardium be salvaged?

A

Up to 12 hours after

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43
Q

How is mean blood pressure calculated?

A

(SBP + 2xDBP) / 3

Spend x2 as long in diastole as you do in systole

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44
Q

What is blood flow like in
- arteries
- veins and capillaries

A

Pulsatile

Laminar

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45
Q

What determines blood pressure?

A

BP = CO x SVR

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46
Q

How does blood viscosity affect BP?

What things can make blood more viscous?

A

Viscous blood = more resistant to flow - ins SVR - inc BP.

Made more viscous by inc protein / cell numbers or dehydration

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47
Q

How is Cardiac Output calculated?

A

CO = SV x HR

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48
Q

What factors affect stroke volume?

A

Starling mechanism
- Preload
- Contractility of heart

Higher preload and contractility = inc Stroke volume

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49
Q

What factors can affect preload?

A

Blood volume
Compliance of veins (venous tone) - affected by ANS, vasoconstrictors (ADR) and local vasoactive substances (NO, Prostacyclin, endothelin)

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50
Q

What are ionotropes?

A

Medicines that change the force of your heart’s contractions. There are 2 kinds of inotropes: positive inotropes and negative inotropes. Positive inotropes strengthen the force of the heartbeat. Negative inotropes weaken the force of the heartbeat.

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51
Q

What is stroke volume normally?

A

5L per minute (80ml per beat)

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52
Q

What factors affect systemic vascular resistance?

A

Structure of vasculature
Endothelium
NO
Prostacyclins
SS
RAAS

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53
Q

What affects contractility?

A

Adrenaline - increases contractility

Decreased by
HF
Acidosis
Drugs

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54
Q

What is heart fibre length affected by?

A

End diastolic volume (in turn determined by venous return).

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55
Q

How do NO and prostacyclin affect the venous system?

A

Cause vasodilation

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56
Q

How does endothelin affect the venous system?

A

Causes vasoconstriction

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57
Q

How does aldosterone affect BV?

A

Released by adrenal cortex

Causes Na retention (reabsorption inc in DCT) -> inc BV

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58
Q

How does ADH affect BV?

A

Released by posterior pituitary

Causes reabsorption of water in the DCT and CD (inc the amount of aquaporin channels = more H20 reabsorption)

Released when plasma osmolarity increases

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59
Q

What is the heart rate set by?

A

The sinus node in the right atrium

Intrinsic due to If channel in SAN – spontaneously depolarises – intrinsic = 70-80bpm. Controlled by ANS – SS = b1 receptors, inc HR. PSS = vagus nerve – M2 receptors – slows HR.

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60
Q

Which receptors in the heart are responsive to the ANS?

A

β 1 receptors = respond to SS = inc HR

M2 receptors (via vagus nerve) = respond to PSS = slow HR

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61
Q

Which part of the vasculature primarily determines systemic vascular resistance?

A

The arterioles (85%)

Arteries (15%)

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62
Q

Tissue perfusion is auto regulated in response to need - by what mechanism?

A

Arteriole constriction and dilation

Dilation occurs in response to Low O2, high CO2, acidosis, NO, prostacyclin

Constriction occurs in response to endothelin release

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63
Q

What do alpha receptors in the arterioles do?

A

Cause vasoconstriction when activated

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64
Q

What doe β receptors do?

A

Cause vasodilation and inc HR and force

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65
Q

What receptors do the following work as agonists against?
- Noradrenaline
- Adrenaline

A

Noradrenaline = α agonist

Adrenaline = α and β agonist

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66
Q

Where are baroreceptors found?

A

Aortic arch
Carotid body at the bifurcation

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67
Q

Which control centres of the brainstem are responsible for controlling HR and BP?

A
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68
Q

Which pathologies can cause high BP?

A

CKD
Renal artery stenosis
Aortic coarctation
Conn’s syndrome (high aldosterone)
Cushing’s syndrome (cortisol = Na retention)
Phaeochromocytoma (too much Adr / NOR)
Acromegaly
Pregnancy
Pre-Eclampsia

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69
Q

What are the effects of chronic HT?

A

HF

Large Vessel Damage (AA, stroke, angina, MI, claudication, amputations)

Small Vessel Damage (CKD, multi-infarct dementia, retinopathy, peripheral nerve damage)

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70
Q

What can acute malignant hypertension cause?

A
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71
Q

What causes vasovagal episodes?

A

Disproportional PSS activation to a stimulus = arteriolar dilation & slowed HR = drop in BP

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72
Q

When does blood flow in the coronary arteries?

A

In diastole

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73
Q

How much of the blood volume is contained in the pulmonary system?

A

20%

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74
Q

How do pulmonary arteries respond differently to systemic arteries?

A

They constrict in areas of low O2 or high CO2 to minimise perfusion of non-functional lung tissue.

In the rest of the body they would dilate.

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75
Q

What does stimulation of the following receptors cause?
- α 1
- α 2
- β 1
- β 2

A
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76
Q

What effects do β blockers have?

What side effects do they have?

A

Dec force and rate of heart contraction = dec BP
+ bronchoconstriction, dec blood to muscles, skin and penis

SE = fatigue, bradycardia, breathlessness (can exacerbate asthma), claudication, cold hands/feet, erectile dysfunction

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77
Q

What do you need to beware of if Ps are diabetic and given β blockers?

A

Β blockers can mask the SS effects of hypos. Therefore they are CI in diabetic Ps who have recurrent hypoglycaemia

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78
Q

What thiazide BP drug can you think of?

A

Bendroflumethazide

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79
Q

What is the MOA of thiazides?

A

Block the Na/Cl symporter in the DCT = less Na reabsorption = decreased BP due to less BV

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80
Q

Name a thiazide-like BP drug?
What is its MOA?

A

Indapamide

MOA = Also blocks Na/Cl symporter in DCT ( diuretic effect) AND activates K+ATP channels - ­ Ca2+ into vascular smooth muscle = vasodilation

Therefore dec BP and vasodilates

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81
Q

What are the side effects of thiazides?

A

Hyponatremia
Hypokalaemia
Hypomagnesaemia
Alkalosis
(I.e. Low Na, K, Mg and H)

Hypercalcaemia
Inc in urate

Insulin resistance => DM

Inc in lipids = arterial disease

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82
Q

What are thiazides used for in addition to BP control?

A

Oedema
Urinary tract stones
Nephrogenic Diabetes Insipidus

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83
Q

Name an α blocker for BP.

What is its MOA?

A

Doxazosin

Blocks alpha 1 receptors (Gq pathway) = decreased Ca+ in arteriole smooth muscle = vasodilation

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84
Q

What is Doxazosin also used for?

A

Prostatic hypertrophy causing obstruction - used to relax the bladder outflow sphincter

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85
Q

What are the side effects of Doxazosin?

A

Palpitations (reflex tachycardia - body tries to compensate for dec BP by inc levels of adrenaline = tachycardia)

First dose - can get hypotension
Postural hypotension with older Ps

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86
Q

Name a Ca channel blocker.

How do they reduce BP?

A

Amlodipine
Dilitiazem
Verapamil

Block Ca channels = dec intracellular Ca =>
- Vasodilation (all 3)
- Dec ionotropy of heart (D & V)
- Dec heart rate (due to relaxation of SA and AV node) (D& V)

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87
Q

Which Ca channel blocker causes the most vasodilation?

A

Amlodipine

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88
Q

Apart from BP control, what else are Ca channel blockers used for?

A

Angina
Raynaud’s syndrome
Arrythmias

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89
Q

What are the side effects of ACEIs?

A

Dry cough (bradykinin accumulates in the lungs)
Renal impairment - esp if renal artery stenosis
Hyperkalaemia

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90
Q

What are possible SEs from Ca Channel blockers?

A

Ankle swelling - due to preferential dilatation of the pre-capillary arteriole

Palpitations (reflex tachycardia)
Constipation
Flushing
Headache
Exacerbation of HF (D&V)

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91
Q

What is the MOA of ACEIs?

A

Inhibits ACE – which cleaves ATI into ATII AND breaks down bradykinins. AT II needed for vasoconstriction, bradykinins cause inflammation.

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92
Q

Name a AR2B for BP control.

What is their method of action?

A

Losartan

Block action of Angiontension II at its receptor - similar effects to ACEIs except no inflammation due to bradykinins = no cough.

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93
Q

Name a Aldosterone antagonist for BP control.

What is their MOA?

A

Spironalactone
Eplerenone (fewer SEs)

Aldosterone acts on nucleus of cells in DCT - stops upregulation of Na channels to epithelium = more Na is excreted = more diuretic effect

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94
Q

What are the SE of spironalactone?

A
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95
Q

What should be done with Ps for the following readings?

SBP > 180mmHg

BP > 160/100

BP > 140 / 90

A
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96
Q

What Tx should be given for a P with HT younger than 55?

A

ACEI or AR2B

Then add in Ca CB or TD

Then add the other one in.

Finally - add in more diuretic or α blocker or β blocker

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97
Q

What Tx should be given for a P with HT who is older than 55 or black P of any age?

A

Start on CCB or TD

Then add ACEI or AR2B

Then add CCB or TD

Finally - add in more diuretic or α blocker or β blocker

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98
Q

What is the NICE targets for BP for the following Ps?

<80

> 80

DM

A

<80 = <140/90

> 80 = <150/90

DM = <135/85

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99
Q

In which Ps are the following drugs CI?
- β blockers

  • Thiazide-like drugs
  • Amlodipine
  • Diltiazem / Verapamil
  • Ramipril
  • Losartan
A

β blockers = diabetic Ps with hypoglycaemia

TLD = diabetes, high cholesterol (they inc lipids and arterial disease + insulin resistance)

Amlodipine = Ps with angina - due to reflex tachycardia

Dilitiazem / Verapamil = Ps with heart failure - can exacerbate

Ramipril = renally impaired Ps; pregnancy - is teratogenic

Losartan = Teratogenic

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100
Q

When should you be concerned about corneal arcus?

A

In Ps under 45 - can be a sign of dyslipidemia

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101
Q

What is cholesterol important form?

A

Is an integral part of cell membranes

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102
Q

What are the two forms of lipids in the blood?

A

Cholesterol (lipid steroid)
Triglycerides (Glycerol + 3FAs) (is an Ester)

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103
Q

Which lipids are linked to arterial disease?

A

Cholesterols

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104
Q

What are lipoproteins?

A

How fats are carried - attached to proteins as fats are immiscible with water.

Made of proteins + cholesterol, 3Gs and apolioproteins

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105
Q

What are the types of lipoproteins? Which are the smallest?

A

HDL (smallest)
LDL
IDL
VLDL
Chylomicrons

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106
Q

Which lipoproteins are thought to be protective against arterial disease?

Which are thought to be at higher risk of atherosclerotic disease?

A

Protective = HDL (healthy DL)

Risky = LDL esp. Lp(a) subgroup = highly atherogenic (lardy DL)

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107
Q

What is the function of the following?
- Chylomicrons
- VLDL
- LDL
- HDL

A

Chylomicrons = Transport fats from gut to liver
VLDL = 3Gs from liver to tissues
LDL = cholesterol from liver to tissues
HDL = cholesterol from tissue to liver

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108
Q

What is the difference between the exogenous and endogenous pathway of cholesterol?

A

Exogenous = cholesterol obtained from food ingested when it is broken down

Endogenous = cholesterol that is made in the liver (most of blood cholesterol is made this way)

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109
Q

What is cholesterol made from in the liver and which enzyme facilitates the formation of this to cholesterol?

A

Made from HMG-CoA

Enzyme = HMG-CoA Reductase

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110
Q

What do statins target to reduce the blood levels of cholesterol?

A

HMG-CoA Reductase - if this enzyme is inhibited = less cholesterol is made

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111
Q

What is the ideal lipid profile for a P?

A

Low cholesterol (<5), LDL (<3), 3Gs (0.5-2) and total:HDL ratio (<3.5)

High HDL (>1.5)

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112
Q

What is secondary dyslipidemia?

A

High cholesterol due to other pathology in the body - e.g.
- DM
- Hypothyroid
- CKD
- Chronic liver disease
- Obesity
- Smoking
- Meds (thazide diuretics)
- Alcohol excess (inc TGs)

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113
Q

What is primary dyslipidemia?

A

High cholesterol levels caused by a genetic predisposition - not due to high intake or synthesis. Instead due to abnormal lipoprotein structures / receptors

114
Q

Which classification system is used for genetic dyslipidemias?

A

Fredrickson classification system

115
Q

What are the fredrickson classifications of primary dyslipidemia?

What are the common and which are the rare ones?

A

Type 1 = Hyperchylomicronaemia

Type II (a) = Hypercholesterolaemia

Type II (b) = Combined hyperlipidemia

Type III = Dysbetalipoproteinemia

Type IV = Hypertriglycerimeia

RARE = 1 & 3

116
Q

What is the cause of Type I dyslipidemia (Hyperchylomicronemia)

What do you need to remember about this form?

A

Deficiency of lipoprotein lipase

Causes high 3Gs, normal cholesterol
Spun blood appears creamy
Causes pancreatitis not IHD

117
Q

What is the cause of
Type II(a) - familial hypercholesterolaemia?

What do you need to remember about this one?

A

Cause mutations that lead to none or very few LDL receptors.

Ps have very high cholesterol (>7.5) - can cause severe atherosclerosis and IHD in young Ps.

118
Q

What is the cause of Type II(b) combined hyperlipidemia?

What do you need to remember about this one?

A

Genetic defects = overproduction of apolipoprotein B-100.

Causes high levels of all bad lipids (LDL, VLDL, 3Gs).
Causes 20% of premature IHD, also causes insulin resistance and obesity

119
Q

What is the cause of Type III familial dysbetalipoproteinemia?

What do you need to remember about this one?

A

Caused by deficiency of Apolipolipoprotein E.

Chylomicrons and IDL remain in the blood, is modest elevations of cholesterol and 3Gs.

Inc risk of IHD
Get palmar xanthomas!

120
Q

What are fatty deposits around the eye called?

What do they consist of?

A

Xanthlasmata

Lipid-laden macrophages

121
Q

What is the cause of Type IV - Familial hypertriglyceridaemia?

What do you need to remember about this one?

A

Multiple genetic defects = elevated 3Gs >5mmol

Can cause insulin resistance and obestity.

Often will have normal cholesterol, HDL often low.

122
Q

How can excess fats occur on tendons?

A

They can attach to extensor surface tendons = tendon xanthomas

123
Q

What are palmar xanthomas? What are they specific to?

A
124
Q

What skin condition can be seen in severe hypertrigyleridaeima?

A

Eruptive xanthomas

125
Q

What lifestyle factors can be adopted to manage hyperlipidaemia?

A
126
Q

What medication can be given for hyperlipidaemia?

A

Statins - target HMG-CoA reductase

Atorvastatin
Simvastatin

127
Q

Why are statins extra special drugs?

A

Proven to reduce all cause mortality - inc MI, stoke, CABG and PCI Ps.

128
Q

What are potential side effects of statins?

A

Myalgia
Rhabdomyolysis
Arthralgia
Liver dysfunction

129
Q

Which risk score determines whether Ps should be treated with statins?

What does it calculate?

A

The Framingham Risk Score

The risk of a patient having a cardiovascular event in the next 10 years.

130
Q

When does NICE recommend that statins should be started?

A
131
Q

What drug can be used for Ps with very high 3Gs?

A

Bezafibrate

132
Q

Which drug can be given to inhibit absorption of cholesterol by the small intestine?

A

Ezetimibe

133
Q

What are the possible side effects of Ezetimibe?

A

GI disturbance

134
Q

Why is omega-3 good for cholesterol?

A

Reduces VLDL synthesis by the liver and reduces the amount of 3Gs converted to cholesterol

135
Q

What is the cause of HF?

A

Myriad of causes - results in the heart being unable to deliver sufficient blood to the body.

136
Q

What is the life expectancy with HF?

A

5 - year mortality = 50%
<1 year if advanced HF

137
Q

What is the main symptom of:
- chronic HF?
- acute HF?
- cardiogenic shock?

A
  • Chronic HF = peripheral oedema
  • Acute HF = pulmonary oedema (e.g. MI)
    Cardiogenic shock = low BP (<90mmHg)
138
Q

What is LV systolic HF?

A

Left ventricular weakness, dilation & thinning

Aka dilated cardiomyopathy

139
Q

What causes LV systolic HF?

A

70% = IHD (i.e. acute MI or chronic ischaemia)

Also - HT, genetic AD, ETOH Xs, viral, toxins (chemo), metabolic (hypothyroid, iron Xs, thiamine deficiency), idiopathic

140
Q

What is LV function dependant upon?

A

Preload and afterload.

Starling = heart beats harder with a bigger preload.

141
Q

How is HF measured?

A

By LV ejection fraction

142
Q

How is ejection fraction calculated?

A

EF = SV / End Diastolic Volume

143
Q

What is normal LV ejection fraction?
When is it classified as HF?

A

Normal LVEF = 55-70%

Systolic HF = <40%

144
Q

What are the consequences of decreased LV contractility?

A

Decreased CO -> SS activation -> RAAS activation = inc Na and H20 retention = inc preload = inc contractility and inc CO (aka Forwards mechanism)

Increased LA / Pul vein pressures (causes pul oedema) -> can push back into pul a.; RV and RA -> peripheral oedema. (aka Backwards mechanism)

145
Q

What are the symptoms of HF?

A

SOB - exertion, orthopnoea and PND
Fatigue
Oedema of legs

146
Q

How is HF classified?

A

New York Heart Association Severity Classification
Class 1 = asymptomatic
Class 2 = mild sx (exertion)
Class 3 = mod sx (minor exertion)
Class 4 = sx at rest

147
Q

What are the signs of HF?

A

Elevated JVP
Oedema
Lung crackles
Low vol pulse, low BP (this -> release of adrenaline = inc HR and RR)
Tachycardia and tachypnoea
Displaced apex beat (beyond 5th IC space)
Murmur (as heart stretches you can get leakage from the mitral valve = MR)
Liver enlargement

148
Q

What investigations can be done for HF?

A

ECG - rarely normal if HF!
BNP levels (sensitive for HF)
Echo
Cardiac MRI
Cardiac catheterisation

149
Q

How does HF present on ECG?

A

Tall complexes = LV hypertrophy
Broad complexes (LBBB)
T wave inversion

150
Q

Why is BNP a test for HF?

A

Is released by the left atrium in response to increased LA pressure - not specific but if >2000, chronic HF is likely.

If <400 - HF is v unlikely

151
Q

What is the main investigation for valve and heart muscle disease?

A

Echocardiogram
- can measure the EF and estimate intra-cardiac pressures

152
Q

How can you get a direct measurement of intra-cardiac pressures?

A

Cardiac catheterisation

153
Q

How does pulmonary oedema appear on CXR?

A

Batwing appearance - bases and apices are spared

154
Q

When does pulmonary oedema occur?

A

When pulmonary capillary pressure is > 25mmHg (haemodynamic pressure exceeds the oncotic pressure)

155
Q

Why does pulmonary oedema occur?

A

Acute left-sided heart failure (e.g. MI) = elevated pressures are transmitted back to the pulmonary capillaries

156
Q

What blood pressure can indicate cardiogenic shock?

A

<90mmHg systolic

157
Q

Is peripheral oedema a sign of acute HF?

A

No - is not a sign of acute HF - is chronic HF sign.

158
Q

What is the most common cause of peripheral oedema?

A

Left heart disease
LA dilates = inc pressures = transmits backwards into SVC and IVC

Causes elevated JVP, leg oedema, pleural effusions and ascites

159
Q

What is Cor Pulmonale?

A

Right-sided HF not due to problem with LH heart.

Caused by chronic lung disease = blood pressure in lung arteries becomes high = transmits backwards into RV and RA then SVC and IVC. Causes elevated JVP, leg oedema, pleural effusions and ascites.

160
Q

How does low CO activate the RAAS system?

A

Low Co = impaired renal perfusion. Baroreceptors can detect BP in kidney arteries. Low BP ->
Kidney secrete renin

Low NaCl delivery to kidney in DCT can also activate production of renin.

Renin = converts angiotensinogen (from liver) to AGT1.

ACE is produced by lungs and kidneys - converts AGT1 to AGT2.

AGT2 = vasoconstriction in BV and efferent arteriole, inc reabsorption of Na in PCT, inc production of aldosterone and prediction of ADH (inc aquaporins)

161
Q

How does the SS activation affect the RAAS system and the heart itself?

A

Inc ADR and NOR act on β 1 receptors = make heart beat harder.

Also activate RAAS = inc after load (vasoconstriction) - heart has to work harder (short term maintains BP but long term = inc workload for weaker heart)

NOR and ADR are cardiotoxic - cause remodelling of the heart (stretching and dilatation) => LV dilation and systolic dysfunction

162
Q

What is diastolic HF?

A

HFpEF

Problem is not weakness of heart muscle RATHER is stiffness of the heart (reduced compliance)

Restrictive cardiomyopathy

Is HF but the LV systolic function is good

163
Q

Can you get pul oedema and peripheral oedema with HFpEF?

A

Unusual to get pulmonary oedema
V common to get peripheral oedema

164
Q

What are the RF for HFpEF?

What diseases cause HFpEF?

A

RF = Age (elderly)
HT
Diabetes
AF

Causes = amyloid heart disease, sarcoidosis, severe LV hypertrophy

165
Q

What drug Rx can we give for chronic HF?

A

Diruetics = Furosemide
ACEIs = Ramipril
ARBs = Losartan, Candesartan
Aldosterone antagonists = Spironalatone
β Blockers = Bisoproplol

Can also give
- Dapagliflozin if fluid retention remains on furosemide (SGLT2 inhibitor)
- Valsartan (angiotensin antagonist)
- Ivabradine (If inhibitor)

166
Q

When do we NOT give β blockers?

A

They can decrease the ionotropy of the heart = and therefore make acute HF worse if the heart is not beating properly

167
Q

PODMAN is used for acute HF management. What do these stand for?

A

Position = sit upright
Oxygen
Diuretics (IV furosemide)
Morphine
Anti-emetic
Nitrates (GTN or IV Isosorbide mononitrate)

168
Q

How do the heart walls appear in
- Diastolic HF
- Systolic HF

A

Diastolic = thick heart walls

Systolic = thin heart walls

169
Q

What happens to the heart to cause reduced ejection fraction in systolic HF?

A

Contractility of the heart is reduced - doesn’t empty properly = ventricle becomes dilated as a result

Therefore weak and dilated heart that can’t empty properly = reduced EF

170
Q

Why do coronary thrombi form?

A
171
Q

What is troponin?
What subtypes are there?
Which are specific to cardiac muscle?

A

Involved in the cross-bridging in muscle between thick and thin filaments.

Subtypes = Tn-C (all muscle),
Tn-T and Tn-I (cardiac specific)

172
Q

What blood markers of myocardial damage are there?

A

Troponin T or I
Creatinine kinase MB
Myoglobin
AST (non specific)
LDH (non specific)

173
Q

What is the difference between creatine and creatinine?

A

Creatinine is a chemical waste product formed by skeletal muscles in the process of creatine phosphate metabolism.

174
Q

What is creatine kinase used for?

A

Moves P from ATP in mitochondria to ADP in the cytoplasm (forming ATP again)

175
Q

Creatine kinase is common to all muscle. Which form of CK is specific to cardiac muscle?

A

Creatine kinase MB

176
Q

What heart disease can cause false-positive troponin?

A
177
Q

What are the acute coronary syndromes?

How can you differentiate between them?

A

Unstable angina
NSTEMI (partially occluded artery)
STEMI (completely occluded artery)

Differentiate by cardiac pain, ECG and cardiac markers.

  • Unstable angina – pain +/- ECG changes + normal troponin
  • Non-ST elevation MI (NSTEMI) – pain +/- ECG changes + elevated troponin
  • ST-Elevation MI (STEMI) – pain + Ischaemic ST elevation
178
Q

How do we define MI?

A

Elevated troponin - 2 measurements must show a rise or fall

plus clinical signs - chest pain +/- ECG changes

179
Q

What things do we look for on ECG for ACS?

A

ST elevation
ST depression (widespread ischaemia)
T wave inversion

180
Q

How can an anterior STEMI appear on ECG?

A

V2-4 = anterior leads - can show ST elevation (tombstone pattern)

Can also get ST depression in inferior leads (II, III and aVF)

181
Q

What can cause ST depression on an ECG?

A

Widespread ischaemia
Also = hypokalaemia and LBBB

182
Q

How can an anterior NSTEMI appear on ECG?

A

Marked T-wave inversion, especially in the anterior leads

183
Q

How do we manage the ACSs?

A

Anti-platlets (Aspirin, tirofiban or clopidogrel)
Anti-coagulants - LMWH (enoxaparin)
Anti-anginal Rx (GTN)

If possible - can do revascularisation dependant on timings

184
Q

ST elevation in leads II, III and aVF indicate what?

A

Inferior STEMI

185
Q

For how long following occlusion can the myocardium be salvaged?

A

Up to 12 hours

186
Q

What is the best way to revascularise the heart?

A

Catheterisation, stents and angioplasty - less mortality than thrombolysis.

187
Q

How long after ischaemia do you start to get myocyte necrosis?

A

15 minutes

188
Q

Is ischaemia of the myocardium uniform?

A

No - sub-endocardium is more sensitive to ischaemia as collateral blood vessels can provide partial protection to other areas

189
Q

How does Tx of NSTEMI an unstable angina differ from a STEMI?

A

STEMI - need PCI asap, within 12 hours

NSTEMI & unstable angina - need PCI within 72 hours

190
Q

What is the usual discharge cocktail for Ps with ACS?

A

Dual platelet Tx = aspirin and clopidogrel (12m)
Atorvastatin
Ramipril
Bisoprolol

191
Q

What complications can arise from an MI?

A

Acute pul oedema
Shock
Arrythmias
Cardiac rupture (e.g. ruptured papillary muscle)
VSD
Mitral valve dysfunction
Stent thrombosis

192
Q

What does this ECG show?

A

Ventricular fibrillation

In VFib, there is a rapid irregular tracing but p waves and the QRS signal are unidentifiable.

No blood goes anywhere - so there are no QRS complexes on the ECG.

193
Q

What is sudden cardiac death?

A

Unexpected death due to cardiac cause within 1 hour of onset (normally within seconds).

194
Q

What are the causes of SCD?

A
195
Q

What is a rare disruption of heart rhythm that occurs as a result of a blow to the area directly over the heart (the precordial region) at a critical instant during the cycle of a heartbeat called? The condition is 97% fatal if not treated within three minutes.

A

Commotio cordis

196
Q

What is the commonest cause of SCD?

A

IHD if >30 yo

Hypertrophic cardiomyopathy if <30 yo

197
Q

What is the epidemiology of SCD?

A

50% of cardiac deaths

M:F = 3:1

Age = 45-75 yo

80% caused by acute MI or chronic IHD

198
Q

What is hypertrophic cardiomyopathy?

A

AD genetic => inappropriate LV hypertrophy (no other cause)

Can get so thick it causes outflow tract obstruction or mitral regurgitation = systolic murmur

199
Q

How does hypertrophic cardiomyopathy present?

A

Anginal type Chest pain
SOB
Palpitations
Dizziness
Syncope
May have murmur from LV outflow tract obstruction or mitral regurgitation

200
Q

How can you tell hypertrophic cardiomyopathy on ECG?

A

Big complexes
Very deep T wave inversion

Often confused with NSTEMI - BUT age is good distinguisher. If young and out running - think HTCM. If old think NSTEMI.

201
Q

What must you do if you diagnose hypertrophic cardiomyopathy?

A

Screen all relatives
- can show abnormalities in β myosin heavy chain and troponin-T in some cases

202
Q

What is arrhythmogenic RV cardiomyopathy?

A

Fatty infiltration of the RV free wall -> hypertrophy and dilatation

Can have genetic cause

S&S = exertion dizziness and loss of consciousness

2% annual risk of SCD

203
Q

How does arrhythmogenic RV cardiomyopathy appear on ECG?

What is the best investigation to diagnose?

A

Subtle changes on ECG = epsilon waves

Best investigation = cardiac MR scan

204
Q

What causes Long QT syndrome?

A

Na+ or K+ channel abnormalities = results in long interval between Q and T on ECG

205
Q

What may be associated with long QT syndrome?

A

Deafness (1/3 have neuronal deafness)

206
Q

Why is long QT syndrome important?

A

Because it is linked to SCD from sudden shock - e.g. cold water swimming, alarm clocks

207
Q

What is Brugada syndrome?

How can it present on ECG?

A

Brugada syndrome is characterized by ventricular arrhythmias and sudden cardiac death (SCD), more frequent during nighttime. Autonomic cardiovascular control during sleep has been implicated in triggering the ventricular arrhythmias.

Involves Na+ channel abnormalities.

May present with high ST on V1-2

208
Q

What is Catecholamiergic Polymorphic VT? (CPVT)

A

Is characterized by episodic syncope occurring during exercise or acute emotion. The underlying cause of these episodes is the onset of fast ventricular tachycardia (bidirectional or polymorphic). Spontaneous recovery may occur when these arrhythmias self-terminate. In other instances, ventricular tachycardia may degenerate into ventricular fibrillation and cause sudden death if cardiopulmonary resuscitation is not readily available.

Due to abnormal intracellular handling of Ca2+.

Will have normal resting ECG. Linked to exercise / extreme emotion.

209
Q

If a person has an inherited cardiac condition, who should be screened?

A
210
Q

What is the most common mechanism of arrhythmia in the heart?

A

Re-entry mechanism

There are 2 pathways in the heart (can be from a scar e.g. from previous MI) - one conducts faster than the other. The fast pathway often dominates and removes the slower signal.

Occasionally an ectopic beat will occur, which annihilates the fast signal and allows the slow signal to set off the short circuit.

211
Q

Why does an acute MI cause inhomonogenity of conduction?

A

Because the zone of injury surrounding the MI will not conduct electricity as fast as the rest of the heart = potential for shortcuts.

212
Q

What does this ECG show?

A

Ventricular tachycardia

Can tell by fast, regular and broad complexes

213
Q

How does SVT differ from VT?

A

SVT - there is a short circuit in the atrium rather than the ventricle (as in VT). This leads to fast, regular and narrow complexes.

214
Q

What can cause VT?

A

Often established MI
Also = hypertrophic cardiomyopathy, dilated cardiomyopathies, RV cardiomyopathy (anything that causes a fat heart)

215
Q

What can VT degenerate into?

A

VF

216
Q

What does this ECG show?

A

SVT

217
Q

What is WPW syndrome?

A

A disorder due to a specific type of problem with the electrical system of the heart involving an accessory pathway able to conduct electrical current between the atria and the ventricles, thus bypassing the atrioventricular node.

60% of people with the electrical problem developed symptoms, which may include an abnormally fast heartbeat (SVT), palpitations, shortness of breath, lightheadedness, or syncope. Rarely, cardiac arrest may occur.

218
Q

How does WPW appear on ECG?

A

The ECG will show a short PR interval (<120 ms), prolonged QRS complex (>120 ms), and a QRS morphology consisting of a slurred delta wave.

219
Q

How do anti-arrhythmic drugs work?

A

Generally reduce arrhythmia frequency and reduce symptoms

Do not improve prognosis (except β blockers in long QT syndrome)

220
Q

Which anti-arrhythmic drugs may be pro-arrhythmic?

A

Class I and III drugs - may prolong the QT interval

221
Q

Which rhythm is seen in this ECG?

What causes this?

A

Torsade de Pointes

Can be caused by = Drug-induced QT prolongation and less often diarrhea, low serum magnesium, and low serum potassium or congenital long QT syndrome. It can be seen in malnourished individuals and chronic alcoholics, due to a deficiency in potassium and/or magnesium.

222
Q

How can you identify syncope?

A
  • Transient LOC
  • Caused by cerebral hypoperfusion
  • Rapid onset
  • Short duration
  • Spontaneous complete recovery
223
Q

What are the red flags for syncope?

A
  • sudden onset – benign comes on within a few mins – so less than 10s = red flag
  • exertional – red flag, or supine – very unusual as well – red flag
  • associated chest pain or SOB
  • known cardiac disease – indicator of rhythm abnormality
  • loud murmur - AS
  • sig injury – vaso-vagal often retain some muscular tone preventing sig injury – whereas blackout due to low CO dont
  • abnormal ECG
224
Q
A
225
Q

How does complete atrio-ventricular block present on ECG?

A

Lots of P waves without QRS complexes

226
Q

What is on this ECG?

A
227
Q

What can be used for Ps with fast rhythm abnormalities?

A

An implantable cardioverter defibrillator (ICD) - shocks P when in V fib.

228
Q

What is used to calculate the risk of SCD for patients with hypertrophic cardiomyopathy?

A

The HCM Risk-SCD Calculator

229
Q

How can you differentiate between SVT, VT and AF on ECG?

A

SVT = rapid, regular, narrow complexes

VT = rapid, regular, broad complexes

AF = rapid and irregular complexes

230
Q
A
231
Q
A
232
Q
A
233
Q
A
234
Q
A
235
Q
A
236
Q

Which part of the mediastinum is the heart found?

A

Middle mediastinum

237
Q

The pericardium consists of fibrous and serous layers. What is the function of the fibrous layer?

A

To prevent overfilling of the heart

238
Q

What are the three layers of the serous layer of the pericardium?

A

Parietal layer
Pericardium cavity
Visceral layer (epicardium)

239
Q

What are the three layers of the heart wall?

A

Endocardium - endothelium and CT
Myocardium - myocytes
Epicardium - viscous serous pericardium

240
Q

Which valves are atrioventricular and which are semilunar?

A

Atrioventricular = Tricuspid and Mitral

Semilunar = Pulmonary and Aortic

241
Q

What happens in diastole?

A

Blood fills the ventricles

242
Q

What causes the first heart sound?

A

Atrioventricular valves closing (tricuspid and mitral)

243
Q

What causes the second heart sound?

A

Semilunar valves (pulmonary and aortic) closing

244
Q

Where does blood arrive from in the right and left atria?

A

Right = SVC, IVC and coronary sinus

Left = 4 x pulmonary veins

245
Q

What are the following and what are they known as after birth?

Foramen ovale
Ductus arteriosus
Ductus venosus
Umbilical vein and arteries

A

Foramen oval = shunt between RA and LA

Ductus arteriosus = shunt between pulmonary trunk and arch of aorta

Ductus venosus = shunts blood from the umbilical vein to the IVC bypassing the liver

Umbilical vein and arterties = used for blood supply in the neonate

246
Q

What type of muscle is found in the atria?

A

Pectinate muscle

247
Q

Where do the coronary arteries arise from?

A

The right and left aortic sinuses in the ascending aorta

247
Q

What muscle is found in the ventricles? What does this attach to?

A

Trabeculae carnae = attaches to papillary muscle - in turn attacks to cordae tendinae which attaches to the leaflets of the valves.

248
Q

Which coronary artery does the posterior interventricular branch a. most commonly arise from?

A

67% = RCA
Otherwise LCA

249
Q

Which coronary artery gives off the circumflex a.?

A

The LCA

250
Q

What do the coronary veins drain into?

A

The coronary sinus

251
Q

Where is the SAN located?

A

At the entrance of the SVC to the RA.

252
Q

Where does the AVN bundle split into R and L bundles?

A

In the interventricular septum

253
Q

Which nerve (and dermatome) innervates the pericardium?

A

Phrenic nerve (C3-5)

254
Q

What provides the myocardium with autonomic SS and PSS innervation?

A

SNS = Sympathetic trunk - T1-5/6

PNS = Vagus nerve

255
Q

What gives rise to somatic pain?

A

Skeletal muscle, bones, connective tissue

Is a sharp, localised pain.

256
Q

Why do you get visceral pain?

A

Often due to stretch, ischaemia or chemical irritation

257
Q

In which dermatomes can heart pain be felt?

A

T1-5/6

258
Q

What is stroke volume?

A

The volume of blood pumped by the left ventricle

259
Q

What is cardiac output?

A

The volume of blood pumped in a minute (L/min)

260
Q

What is the equation for cardiac output?

A

CO (Q) = SV x HR

261
Q

What is preload?

A

The amount of blood in the ventricle at the end of diastole

262
Q

What is contractility?

A

The strength of squeeze - the more the heart is filled, the greater the contractility will be

263
Q

What is afterload?

A

The resistance against ejection into vessels (comes mostly from capillaries)

264
Q

What is compliance?

A

The ability of the BV to expand & contract (stretchiness)

265
Q

What can sensitise the atria (atrial reflex) - what happens when this occurs?

A

ANS or ADR/NOR can sensitise.

Increases heart rate

Called the atrial reflex

266
Q

What is stroke volume affected by?

A

Preload, contractility and afterload

267
Q

What is contractility affected by?

A

ANS (SS)
ADR & NOR
Inc by high Ca+
Dec by high K+, low Ca+

268
Q

What type of innervation do blood vessels have from the ANS?

A

Most have SS - can control constriction and some dilatation.

However not many have PSS innervation. Rather is the lack of SS stimulation that allows BVs to vasodilate.

269
Q

How does adrenaline affect receptors in the body for the SS? (α 1, α 2, β 1 & β 2)

A
270
Q

What cells produce renin?

A

Juxtaglomerular cells in the glomerulus

271
Q

What stimuli stimulates the juxtaglomerular cells to produce renin?

A

1). SS (β 1 receptors)

2) Renal a. hypotension

3). Decreases Na+ levels in the DCT - this is sensed by macula densa cells

272
Q

What effects does angiotensin II have on the body?

A

1) Vasoconstriction of BVs = inc SVR

2). Inc Na reabsorption in kidney

3). Pokes adrenal cortex to produce aldosterone

4). Stimulates release of ADH from the posterior pituitary

5). Inc thirst

273
Q

What affect does aldosterone have?

A

Inc absorption of Na+ from the DCT and CD

274
Q

What cells in the body produce adrenaline?

A

The chromaffin cells of the adrenal medulla

275
Q

What effect does adrenaline have on the CVS?

A

At low levels - it is β 2 selective and causes vasodilation.

At high levels - causes widespread vasoconstriction, inc HR and contractility.

Also causes vasoconstriction of the renal arterioles

276
Q

Where is antidiuretic hormone made and released?

What stimulates its release?

A

Made in the hypothalamus

Released from the posterior pituitary gland

Release is stimulated by:
1). decreased plasma volume
2). increased plasma osmolality

277
Q

What is the effect of ADH when released?

A

Causes arteriolar vasoconstriction of BVs (V1 receptors)

Incs amt of water reabsorbed by the kidney (V2 receptors)

278
Q

What are the two types of natriuretic peptides released by the heart? Where are they made and released?

A

ANP (atrial natriuretic peptide) - made by the atrial myocytes and released when they are stretched

BNP (brain natriuretic peptide) - made by the ventricular myocytes and released when the ventricles are stretched

279
Q

What effect does release of ANP or BNP have?

A

Incs Na excretion in the kidneys (because stretch is caused by inc BV - therefore want to reduce BV)

280
Q
A

MLA Revision (9 decks)

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