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Phase 2a > Cardiology > Flashcards

Cardiology Flashcards

1
Q

What is pericarditis?

A

inflammation of the pericardium which is the protective covering of the heart

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2
Q

What are the two layers of the pericardium?

A

outer fibrous and inner serous

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3
Q

What are the causes of pericarditis?

A

idiopathic, virus e.g. Coxsackie B or echovirus, trauma, post MI, TB, fungal, malignant, uraemic from accumulating toxins, pericardial effusion

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4
Q

What are the 3 types of pericarditis?

A

acute and relapsing
pericardial effusion and cardiac tamponade
constrictive pericarditis

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5
Q

What is the pain like in pericarditis?

A

sharp central pleuritic chest pain, can spread to neck or shoulders

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6
Q

What exacerbates the pain in pericarditis?

A

movement, coughing, breathing, lying down

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7
Q

What is pericarditis relieved by?

A

sitting up and leaning forward

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8
Q

What other symptoms are associated with pericarditis?

A

fever, chills, dyspnoea, pericardial friction rub, cardiac tamponade

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9
Q

What is a pericarditis friction rub?

A

a cardiac rub or leathery sound that is heard on examination

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10
Q

What does an ECG show in pericarditis?

A

ST elevation
PR depression
IN ALL LEADS BUT aVR WHICH WILL BE OPPOSITE
(different to MI elevation which is limited to infarcted area)

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11
Q

What will a CXR show in pericarditis?

A

cardiomegaly

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12
Q

What will an ECHO show in pericarditis?

A

may show effusion

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13
Q

What will a CT and MRI show is pericarditis?

A

inflamed pericardium

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14
Q

What is the treatment of pericarditis?

A

NSAIDs
aspirin if recent MI
colchicine (before steroids to reduce recurrence)
corticosteroids if resistant or immune cause

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15
Q

How common is relapsing in pericarditis?

A

20% of acute cases relapse

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16
Q

What is a pericardial effusion?

A

a collection of fluid with space of the serous pericardial which accompanies acute

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17
Q

What does pericardial effusion cause?

A

cardiac tamponade, poor ventricular filling and reduced cardiac output, pericarditis

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18
Q

What is the treatment of pericardial effusion?

A

pericardial drainage

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19
Q

What are the symptoms of pericardial effusion?

A

soft distant, dysponea

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20
Q

What happens in chronic pericarditis?

A

the subepicardial layers of myocardium may undergo fibrosis, atrophy and calcification causing a rigid pericardium

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21
Q

What will a CXR show in chronic pericarditis?

A

small heart with pericardial calcification

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22
Q

What will an ECG show in chronic pericarditis?

A

low QRS, flattened T wave

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23
Q

What will an ECHO show in chronic pericarditis?

A

thickened calcification pericardium, small ventricle cavities with thickened walls

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24
Q

Why would you do an endomyocardial biopsy in chronic pericarditis?

A

to distinguish it from restrictive myopathy

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25
Q

What is the treatment of chronic pericarditis?

A

complete resection
pericardectomy if no TB
if TB, antiTB drugs then pericardectomy

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26
Q

What is a true aneurysm?

A

Where all the layers of the vessel dilate together

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27
Q

What is the difference between a fusiform and berry (saccular) aneurysm?

A

A fusiform is symmetrical in its dilation but a berry is asymmetrical

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28
Q

What causes an asymmetrical aneurysm?

A

one side of the blood vessel has had a higher pressure, or one side of the wall was weaker?

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29
Q

What are the two types of true aneurysm?

A

fusiform and saccular

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30
Q

What is a false aneurysm?

A

caused by a hole in vessel causing it to leak forming a pool due to the surrounding tissue keeping it in place so it looks like an aneursym

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31
Q

How big does a vessel have to be to be classed as an aneurysm?

A

1.5-2x the size of the original vessel

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32
Q

Where do arterial aneurysms most commonly occur?

A

in the aorta

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33
Q

What percentage of aortic aneurysms are in the abdominal?

A

60%

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34
Q

Why are most arterial aneurysms in the abdominal?

A

Due to there being less collagen

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35
Q

What does Laplaces law mean in aneurysms?

A

That as the diameter of the blood vessel gets bigger, the pressure gets bigger, it is a positive feedback loop

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36
Q

What can cause blood vessel walls to weaken?

A

high blood pressure

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37
Q

What are risk factors of aneurysm?

A

male, age, smokers, obese, alcohol, high bp

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38
Q

How can hypertension affect arterial muscle wall?

A

Can cause atrophy of the smooth muscle, weakening its wall

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39
Q

What are vasa vosorum?

A

the blood vessels that supply the outer muscle in the abdominal aorta?

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40
Q

What happens to the vasa vosorum in hypertension and how does that lead to aneurysms?

A

they undergo arteriosclerosis, causing their lumen to narrow so they have ischaemia, causing the muscle of the aorta to atrophy and weaken

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41
Q

How does syphilis cause an aneurysm?

A

causes inflammation of the vasa vasorum so the lumen narrows, restricting blood supply to the thoracic aorta causing atrophy

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42
Q

What is a mycotic aneurysm?

A

Where an embolic infection elsewhere in the body can travel in the blood and get stuck in intracranial, visceral or peripheral arteries (also a complication of infective endocarditis)

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43
Q

What common bacteria cause embolic mycotic aneurysm?

A

bacteroides fragilis, pseudomas aeurginosa, all salmonella

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44
Q

Why can some genetic disorders cause aneurysm?

A

because they can affect the connective tissue:fibrillin and collagen

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45
Q

What genetic disroders can cause aneurysm?

A

Marfan sydrome and ehlers danlos

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46
Q

How can Marfan syndrome cause an aneurysm?

A

impaired elastic properties in fibrillin so weakened blood vessels

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47
Q

How can Ehlers Danlos syndrome cause an aneurysm?

A

disrupted ability to make collagen proteins causing weakened vessel walls

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48
Q

What are two main complications of an aneurysm?

A

They can rupture or put pressure on another organ

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49
Q

What does rupture of an aneurysm cause?

A

Decreased blood flow to that tissue, causing ischaemia

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50
Q

What is a complication of a thoracic aneurysm if it is just above the aorta?

A

Can lead to aortic insufficiency when the aortic valve cannot close, so blood flows back into the ventricle, this also puts pressure on the left recurrent laryngeal nerve from the stretch aorta, leading to a high pitch cough

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51
Q

What happens if a aneurysm in the brain ruptures?

A

Bleeds into the subarachnoid space, increasing pressure on brain tissue and causing irritation on meninges, so causes a severe headache and unable to flex neck forward

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52
Q

How can an aneurysm cause a blood clot?

A

It can pull the blood over into the extra lumen space, so is not moving along and clots, which can lead to tissue ischemia and an embolism.

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53
Q

What are the signs of AAA?

A

severe pain in left flank, pulsating mass with heartbeat in that area, hypotension

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54
Q

What are the symptoms of a thoracic aortic aneurysm?

A

usually no symptoms, severe back and abdominal pain

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55
Q

When should you do surgery for an aneurysm?

A

if diameter is >5.5cm, it is expanding >1cm a year and if it is symptomatic

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56
Q

What is the treatment for an aneurysm?

A

stop smoking, control hypertension, lipid lowering medication, US surveillance

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57
Q

What is an aortic dissection?

A

part of the tunica intima of the aorta is teared off causing a tear so blood leaks between the tunica intima and tunica media separating the two layers, causes an increased diameter of the blood vessel and blood collects there

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58
Q

What is the difference between a false and true lumen in an aortic dissection?

A

a false lumen is the new lumen made betweeen the tunica intima and the tunica media, the true lumen is the original lumen

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59
Q

What is the cause of an aortic dissection?

A

chronic hypertenion from stress, increased blood volume, or coarctation (narrowing) of the aorta, weakened aortic wall, decreased blood flow to vasa vasroum, aneurysms

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60
Q

Where does the aortic dissection usually occur?

A

In the first 10cm of the aorta

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61
Q

What complications can an aortic dissection lead to’?

A

blood can back up into pericardial space causing pericardial tamponade, could bleed into a mediastinum causing death, could continue to disect until renal artery, reducing blood flow to kidneys

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62
Q

What are the symptoms of an aortic dissection?

A

sudden, severe, chest pain that feels like tearing, radiates to back and down arms

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63
Q

What is the treatment of an aortic dissection?

A

antihypertensive drugs, IV BB, vasodialators, surgery, stents

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64
Q

What is a type A aortic dissection?

A

involves the aortic arch and aortic valve, proximal to the left subclavian artery origin - DeBakey type 1 and 2

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65
Q

What is a type B aortic aneurysm?

A

involves descending thoracic aorta, distal to the left subclavian artery origin - DeBakey type 3

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66
Q

What is cardiac tamponade?

A

compression of the heart leading to acute cardiac failure following bleeding into the pericardial space

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67
Q

What is atherosclerosis?

A

hardening and narrowing of the arteries due to plaque leading to thrombus formation

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68
Q

What is arteriosclerosis?

A

hardening of arteries

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69
Q

What are risk factors for atherosclerosis?

A

age, smoking, cholesterol, obesity, hypertension, diabetes

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70
Q

Where is atherosclerosis commonly seen?

A

in peripheral and coronary arteries

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71
Q

Whats the distribution of atherosclerosis like along the artery?

A

it is focal

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72
Q

What are the symptoms of atherosclerosis in the coronary arteries?

A

vomiting, anxiety, angina, coughing, feeling faint

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73
Q

What is a complication of atherosclerosis in coronary arteries?

A

leads to reduced blood and oxygen flow to the heart muscles, causing ischemia, and a heart attack

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74
Q

What symptoms of atherosclerosis in the carotid cause?

A

weakness dysphea, headache, facial numbness, paralysis, leading to stroke

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75
Q

What is peripheral vascular disease?

A

reduced blood flow to other parts of the body, not the brain

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76
Q

What symptoms does atherosclerosis in the renal arteries cause?

A

reduced appetite, smaller hands and feet, increased renin release and increased blood pressure

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77
Q

What happens when a atherosclerotic plaque ruptures?

A

Forms a thrombus and a clot

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78
Q

What are LDLs?

A

low density lipoproteins

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79
Q

What does a CXR show in an MI?

A

cardiomegaly, pulmonary oedema, widening of mediastinum

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80
Q

What does a large amount of circulating LDLs cause?

A

they can deposit in the tunica intima and oxidase to activate endothelial cells causing endothelial dysfunction so they express receptors for WBCs

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81
Q

What does the accumulation of WBC to damaged endothelial cells lead to?

A

This allows monocytes and T helper cells to move into the tunica intima part of the vessel, to become macro-phages which take up the LDLs to become foam cells

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82
Q

What are foam cells?

A

macrophages, bound to LDLs, causing fatty streaks

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83
Q

What does the formation of foam cells cause?

A

promote migration of smooth muscle cells from tunica media into tunica intima and causes smooth muscle cell proliferation to increase collagen synthesis, so the plaque hardens

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84
Q

Once collagen is formed in the plaque, foam cells die, what does this cause?

A

causes the foam cells to release their LDL contents, causing plaque growth and increased pressure and release DNA which attracts neutrophils causing inflammation, also release proinflammatory cytokines, so plaque grows

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85
Q

What does growth of the plaque cause?

A

plaque rupture and thrombus formation from blood coagulation

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86
Q

How are LDLs oxidised in the tunica intima layer?

A

dysfunctional endothelial cells release ROS mediated proteases to oxidise them so that the LDL is trapped in the intima

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87
Q

What happens to monocytes when they move into the tunica initima?

A

they become macrophages

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88
Q

What happens to T cells in the tunica intima of an artherosclerotic plaque?

A

bind to adhesion molecules and form IFN-y which activates more WBCs and leucocytes to increase inflammation and cause the plaque to grow

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89
Q

What is ischemic heart disease?

A

coronary artery disease caused by poor or no blood flow to the heart tissue

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90
Q

What causes ischemic heart disease?

A

myocardial necrosis caused by an atherosclerotic plaque rupture causing an occlusion of a coronary artery causing a mycardial infarction

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91
Q

What is angina?

A

a temporary loss of blood supply to heart causing an mismatch of 02 supply and demand causing chest pain, due to impaired blood flow, increased distal resistance or reduced 02 carrying capacity

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92
Q

What are the main 2 types of angina?

A

stable, unstable

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93
Q

What is stable angina?

A

The plaque is a fixed size, so pain is only caused by exertion and relieved by rest

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94
Q

What is unstable angina?

A

Is caused by a haemodynamically unstable plaque causing thrombosis so pain still occurs at rest

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95
Q

What are risk factors for ischemic heart disease?

A

smoking, age, diabetes, hyperlipidaemia, obesity, genetic factors, oral contraceptive pill

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96
Q

What are the symptoms of a myocardial infarction?

A

nausea, sweating, palpatations, breathless, crushing chest pain for more than 20 mins, increase JVP, increased pulse, pallor, anxiety

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97
Q

What are the two types of infarction?

A

transmural and subendocardial

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98
Q

What can a venous blockage cause?

A

oedema

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99
Q

What are the 3 types of myocardial infarction?

A

ST elevation (STEMI), non ST elevation (NSTEMI) and unstable angina

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100
Q

Which of the 3 MIs is a retrospective diagnosis?

A

NSTEMI - made after troponin results

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101
Q

What does an ECG show in an MI?

A

either ST elevation or depression
inverted t waves
can be a Q wave present retrospectively

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102
Q

What is troponin?

A

a protein complex which regulates actin:myosin contraction

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103
Q

When is troponin used?

A

It is a sensitive marker for cardiac injury , but may not represent permanent damage

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104
Q

When does troponin appear positive?

A

in acute coronary syndrome, gram negative sepsis, pulonary embolism and myocarditis

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105
Q

What is a transmural infarct and how does this show on an ECG?

A

affects all of the myocardial wall - leading to ST elevation and Q wave

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106
Q

What is a subendocardial infarct and how does this appear on an ECG?

A

necrosis of a small area in the subendocardial wall of the left ventricle, ventricular septum, or papillary muscles
ST depression

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107
Q

What methods can be used for MI treatment?

A

stop smoking, reduce alcohol, educate, exercise, morphine, oxygen, nitrates, anticoagulants, BBs, ACE-I, aspirin, statins, PCI, LMW heparin, clopidrogrel, GPIIb/IIIa antagonist

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108
Q

What are the complications of an MI?

A

cardiogenic shock, cardic arrhythmia, pericarditis, emoboli, aneurysm formation, rupture of ventricle, dresslers syndrome, rupture of free wall, papillary muscle rupture

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109
Q

What does alpha granule secretion cause?

A

coagulation and inflammation

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110
Q

What does dense granule secretion cause?

A

platelet aggregation

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111
Q

How does clopidrogrel treat MI?

A

it inhibits ADP dependent activation of GPIIb/IIIa complex. Requires hepatic cytochrome p450 enzymes to irreversibly bind to P2Y12 receptors on platelet membranes - used as dual platelet therapy with aspirin

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112
Q

How does percutaneous coronoary intervention treat MI?

A

uses a stent implantation, which is highly effective, placed in with a coronary angiography, need full dose of anticoagulation and high dose heparin

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113
Q

What is a risk of using PCI and how do you prevent this?

A

restenosis, prevent with toxol or slrolimus, drug eluting stents

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114
Q

How does GPIIb/IIIa anatgonist treat MI?

A

used with aspirin of P2Y12 inhibitors to cover P2Y12 delay e.g. Tirofiban, Abciximab

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115
Q

How does aspirin work?

A

causes irreversible inactivation of cyclo oxygenase 1 causing platelet aggregation inhibition also reduces PG synthesis

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116
Q

What factors can exacerbate angina?

A

the cold, exercise, heavy meals, increased demand (hypertension, hyperthyroidism), reduced supply (anaemia, hypoxaemia, hypothermia)

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117
Q

What are the symptoms of angina?

A

chest pain, breathlessness, oedema, palpitations, syncope, 4th heart sound

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118
Q

Who is most likely to get angina?

A

older men

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119
Q

what investigations should you do for angina?

A

ecg, ct scan, coronary calcium score, coronary angiography, thallium scan, cardiac catheter, myoview scan, exercise testing

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120
Q

What is ohms law and what does this mean in terms of pressure?

A

V=IR meaning change in pressure = QR

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121
Q

What is Poisuelles law and what does this mean?

A

change in P=8uLQ/pier4
meaning that nothing in the vessel is really affected until 70% of the diameter of stenosis is reached and then there is a rapid decline.

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122
Q

What is decubitus angina and how does it appear on an ECG?

A

caused by lying down, ST depression

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123
Q

What is a prinzmetal angina and how does it appear on an ECG?

A

caused by coronary artery spasm, ST elevation

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124
Q

What is the treatment of angina?

A

modify risk factors, nitrates, aspirin, Ca blockers, BBs, statins, PCI, coronary bypass, K channel activator, opiates

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125
Q

How is nitrates given for treatment and how does it work?

A

isosorbide mononitrate GTN spray causes vascular dilation to decrease preload / afterload and decrease BP

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126
Q

What are the side effects of nitrates?

A

headache and hypotension

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127
Q

What is a side effect of aspirin?

A

gastric ulceration

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128
Q

What is a side effect of Ca blockers?

A

ankle oedema and flushing

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129
Q

How to statins treat angina?

A

HMG coA reduce inhibitor, reduces cholesterol and is a lipid lowering therapy

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130
Q

What is heart failure?

A

the inability of cardiac output to meet the physiological demands of the body

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131
Q

What are the symptoms of heart failure?

A

exertional dyspnoea, orthopnoea, fatiguem tachycardia, hypotension, pleural effusion, s3 gallop, neck vein dialation

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132
Q

What are the complications of heart failure?

A

renal failure, valve dysfunction, stroke, death

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133
Q

What causes left ventricular heart failure?

A

coronary artery syndrome, hypertension, aortic/mitral valve disease and myocardial disease

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134
Q

What causes right ventricular heart failure?

A

left sided heart failure, tricuspid/pulmonary valve disease and pulmonary vascular disease

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135
Q

What is a consequence of right sided heart failure?

A

blood can be backed up into the liver and abdomen causing congestion, leading to hepatomegaly and ascites

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136
Q

What is a consequence of left sided heart failure?

A

blood can accumulate in the pulmonary veins, causing fluid accumulation in the lungs leading to SOB and oedema

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137
Q

What is congestive heart failure caused by?

A

a mix of left and right heart failure

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138
Q

What is LVSD?

A

heart failure due to left ventricle systolic dysfunction

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139
Q

What is HFPEF?

A

Heart failure due to preserved ejection fraction, diastolic failure

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140
Q

At what age are you most likely to get heart failure?

A

60-90years

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141
Q

What detects myocyte size?

A

brain natireutic peptide (BNP) shows how much they have stretched

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142
Q

What is the treatment of heart failure?

A

smoking cessation, weight loss, healthy diet, exercise, loop diuretics (e.g. furosemide which inhibits Na/K/2cl transporter), heart transplant, neurohumoral blockade inhibiting RAAS and SNS, ACE-I, BBs, aldosterone antagonist, ARBs (candersartan), hydralazine/nitrate combination, digoxin (direct inotropic effect to increase force of heart contraction)

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143
Q

What is the classification called for heart failure?

A

The New York Association Diagnosis

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144
Q

What are the 4 stages of the NYAD?

A

1- no limitation of physical activity (asymptomatic)
2- slight limitation (mild)
3- marked limitation (symptomatic)
4- inability to carry out physical activity

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145
Q

What does a CXR show in heart failure? (ABCDE)

A 
alveolar oedema
kerley B lines
cardiomegaly
dilated upper lobe vessels
pleural effusion
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146
Q

What tests should you do in heart failure?

A

CXR, ECG, ECHO

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147
Q

Would the pre load and after load decrease or increase in heart failure?

A

increase

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148
Q

What is cardiomyopathy?

A

primary heart muscle disease, mainly genetic (autosomal dominant)

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149
Q

What are the 3 main types of cardiomyopathy?

A

dilated, hypertrophic and restrictive (arrhythmogenic)

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150
Q

What is dilated cardiomyopathy?

A

When less blood is pumped from the heart because ventricles are enlarged and weakened

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151
Q

What mutation causes dilated cardiomyopathy?

A

mutation in the genes of the cytoskeleton proteins

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152
Q

What can dilated cardiomyopathy lead to?

A

systolic heart failure with decrease ejection fraction, causing breathlessness and fatigue and conduction defect thromboembolism

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153
Q

What causes dilated cardiomyopathy?

A

left ventricular nonconpaction, myocarditis, toxins, autoimmune, endocrine and neuromuscular

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154
Q

How does a dilated cardiomyopathy appear?

A

dilated ventricles with thin walls

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155
Q

What is the treatment of dilated cardiomyopathy?

A

cardiac reconstruction and as you would for heart failure

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156
Q

What is hypertrophic cardiomyopathy?

A

Less blood pumped from the heart due to the ventricles not being able to relax

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157
Q

What mutation causes hypertrophic cardiomyopathy?

A

mutations of genes encoding sarcomeric proteins leading to disorganization of the cardio myocytes e.g. B myosin heavy chain MYH7 or myosin binding C MYBPC3

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158
Q

What can hypertrophic cardiomyopathy lead to?

A

diastolic heart failure, angina, dyspnoea, palpatations, syncope, chest pain,

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159
Q

How does a hypertrophic cardiomyopathy appear?

A

thick ventricle wall and thick interventriculer septum and small ventricles so ventricles cannot fill properly with blood

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160
Q

What is the most common cause of cardiac death in young people?

A

hypertrophic cardiomyopathy

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161
Q

How does hypertrophic cardiomyopathy appear on an ECG?

A

abnormal, with ventricular arrhythmia

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162
Q

What does a troponin T mutation cause?

A

death

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163
Q

What is a primary restrictive disease?

A

decreased volume of both ventricles and impaired ventricular and impaired ventricular filling

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164
Q

What is sudden arrhythmic death syndrome?

A

an inherited condition in young people

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165
Q

What is the appearance in restrictive cardiomyopathy?

A

Left ventricle maintains normal dimensions but left atrial hypertrophy and dilation and right ventricular hypertrophy due to back flow from left atria.

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166
Q

What is the mutation seen in restrictive cardiomyopathy?

A

mutations of the genes encoding desmosome proteins

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167
Q

What some restrictive cardiomyopathy cause?

A

arrhythmia

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168
Q

What is naxos disease?

A

fibrous fatty replacement of RV causing small hands and feet and woolly hair

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169
Q

What is an ion channelopathy?

A

a mutation in ion channels e.g. K, Cl, Na

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170
Q

What does an ion channelopathy cause?

A

inherited arrhythmia

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171
Q

What is the structure like in ion channelopathy?

A

normal

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172
Q

How is an ion channelopathy diagnosed?

A

on ECG

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173
Q

What does the ECG show in ion channelopathy?

A

long QT
short QT
Brugade and CPVT

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174
Q

What is CPVT?

A

abnormal heat of adrenergic drive arrhythmia problem

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175
Q

Who are the target groups for a cardiomyopathy screening?

A

close relative and athletes to allow early identification

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176
Q

What is the treatment of cardiomyopathy?

A

ICD, BBs, statins, vascular surgery, low sodium diet to remove backed up fluid, diuretics, ACE-1, digoxin, pacemaker

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177
Q

what are the symptoms of ion channelopathy?

A

recurrent syncope

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178
Q

What causes peripheral vascular disease?

A

atherosclerosis in the peripheral arteries, blocking blood flow

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179
Q

What can peripheral vascular disease lead to?

A

MI or losing a leg

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180
Q

Where does acute peripheral vascular disease affect?

A

Parts furthest way from the heart, e.g. the lower limbs

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181
Q

What are the symptoms of peripheral vascular disease? (6Ps)

A

pain, pallor, perishing cold, pulseless, paraesthesia, paralysis

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182
Q

What causes acute peripheral vascular disease?

A

embolic disease from thrombus or arrhythmia or thrombotic disease from arthertosclerosis

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183
Q

What is the treatment of acute peripheral vascular disease?

A

LMW heparin, treat underlying cause, long term warfarin in MI or AF

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184
Q

What complications can acute peripheral vascular disease lead to?

A

embolism, stenosis, occlusion, aneurysm, progression, haemorrhage, plaque rupture, overlying thrombosis

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185
Q

What are the risk factors for chronic peripheral vascular disease?

A

smoking, diabetes, hypochloesterolaemia, hypertension,

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186
Q

What are the symptoms of chronic peripheral vascular disease?

A

cold and dry lower limbs, poor peripheral pulses, ulceration, dark discoloration of toes

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187
Q

What does an ABPI show in intermittent claudication?

A

0.5-0.9

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188
Q

What does an ABPI show in critical ischemia?

A
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189
Q

What does an ABPI show in heavily calcified arteries?

A

falsely elevated

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190
Q

What is the treatment for chronic peripheral vascular disease?

A

manage risk factors, revascularisation if critical, low dose aspirin, exercise, control diabetes

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191
Q

What are the four stages in chronic peripheral vascular disease?

A

asymptomatic, intermittent claudication, rest pain/nocturnal pain, necrosis/ulceration

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192
Q

What does intermittent claudication mean in chronic peripheral vascular disease?

A

calf pain on exertion but relieved on rest

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193
Q

What is nocturnal pain so bad in chronic peripheral vascular disease?

A

means severe unremitting pain in the foot, preventing sleep and poor blood supply even at rest so definitely no blood reserve for increased demand

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194
Q

What is circulatory shock?

A

when the CV system has inadequate organ perfusion for aerobic cellular respiration

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195
Q

What causes circulatory shock?

A

low BP, low systolic, MAP

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196
Q

How is MAP calculated?

A

MAP = CO x systemic vascular resistance

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197
Q

What is CO calculated?

A

CO = SV x HR

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198
Q

What are the 3 main types of shock?

A

hypovolemic (non hemorrhagic and hemorrhagic),

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199
Q

How can you get non hemorrhagic hypovolemic shock?

A

from loss of fluid volume from high dehydration, vomiting, diarrhea etc

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200
Q

How can you get hemorrhagic hypovolemic shock?

A

Through blood vessels bleeding so that volume of blood decreases, decreasing EDV, SV, CO and BP

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201
Q

What happens to hormones when CO is decreased?

A

Catecholamines like adrenaline and noradrenaline, ADH and angiotensin II are released to cause vasoconstriction of blood vessels to increase resistance to blood flow and increase HR to increase CO.

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202
Q

What is MVO2?

A

The amount of O2 bound to Hb in the blood entering the right ventricle (so the amount of O2 left over not used)

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203
Q

What happens to MVO2 in hypovolemic shock?

A

It decreases due to less blood volume and less O2

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204
Q

What symptoms are seen in hypovolemic shock?

A

pale, cold, sweaty, vascoconstricted skin, weak rapid pulse, low pulse pressure, low urine output, confusion, weakness, collapse, coma, tachycardia, dehydration, skin turgor

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205
Q

What is cardiogenic shock?

A

The heart can’t pump enough blood to tissue e.g. secondary to MI and ischemia, due to reduced muscle cells, leading to weaker contractions so decreased in SV and BP

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206
Q

What happens if there is an obstruction to the heart so it cannot fill properly e.g. fluid in chest, stab wound ?

A

This fluid physically constricts the heart from expanding and contracting so reduces SV (obstructive shock)

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207
Q

What is distributive shock?

A

A leakiness of blood vessels with lots of vasodilation, reducing resistance to blood flow and decreased blood pressure.

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208
Q

What is the most common type of distributive shock?

A

Septic shock

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209
Q

What is sepsis?

A

a systemic inflammatory response associated with an infection

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210
Q

What is septic shock?

A

sepsis with persistent hypo-tension, unresponsive fluid resuscitation causing vasodilation from inflammatory cytokines, causing warmth

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211
Q

Which shock is considered a warm shock not a cold shock?

A

septic

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212
Q

What kind of pathogen normally causes septic shock?

A

gram negative endotoxins

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213
Q

How do endotoxins causes septic shock?

A

they damage endothelial cells, causing them to release vasodilators like NO, and they activate the complement pathway to stimulate histamine release, activate macro-phages and pro inflammatory cytokines, this then damages the endothelial cells, increasing their vascular permeability, making the blood vessels leaky. Also produce tissue factor to increase clotting, which reduces perfusion and low vascular resistance so the blood returns to the heart with a high MVO2

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214
Q

Which shock increases MVO2?

A

septic

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215
Q

What is anaphylactic shock?

A

a type 1 hypersensitivity allergic reaction causing low BP

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216
Q

What is neruogenic shock?

A

When the nervous system is damaged causing low BP

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217
Q

What are the 3 types of distributive shock?

A

septic, anaphylactic, neurogenic

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218
Q

How does an anaphylactic allergic reaction cause shock?

A

releases histamine and vasoactive mediators without involving antibodies causing haemodynamic collapse, leading to capillary leak, wheeze, cyanosis, oedema, breathlessness, skin, mucosal uritcana and erythema

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219
Q

What is the blood loss, pulse, PP, BP, RR, urine output and mood in class 1 haemorrhagic shock?

A

15% blood loss, pulse 30ml/hr, slightly anxious

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220
Q

What is the blood loss, pulse, PP, BP, RR, urine output and mood in class 2 haemorrhagic shock?

A

15-30% blood loss, pulse >100bpm, normal BP, reduced PP, 20-30RR, urine output 20-30ml/hr, mild anxious

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221
Q

What is the blood loss, pulse, PP, BP, RR, urine output and mood in class 3 haemorrhagic shock?

A

30-40% blood loss, pulse >120bpm, decreased PP and BP, 30-40RR, urine output 5-15ml/hr, confused

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222
Q

What is the treatment of shock?

A

ensure adequate O2, fluids, maintain organ perfusion, treat cause with specific therapy, ABC, ECG, antibiotics, fluid bolus, low dose steroids

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223
Q

What is a complication of shock?

A

ARDS

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224
Q

What is ARDS?

A

acute respiratory distress syndrome

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225
Q

What is ARDS caused by?

A

direct lung injury or secondary to severe systemic illness

226
Q

What happens in ARDS when there is lung damage?

A

releases inflammatory mediators causing increased capillary permeability, non cardiogenic pulmonary oedeme and multiorgan

227
Q

What are some extrapulmonary causes of ARDS?

A

shock, septicaemia, multiple transfusion, drug reaction, head injury

228
Q

What are some pulmonary cuases of ARDS?

A

pneumonia, gastric aspiration, smoke inhalation, chemical pneumonitis, near drowning

229
Q

What are the symptoms of ARDS?

A

cyanosis, tachypnoea, tachycardia, peripheral vasodilation

230
Q

What is the diagnostic criteria of ARDS?

A

bilateral fine inspiratory crackles, pulmonary capillary wedge pressure

231
Q

what is the treatment of ARDS?

A

ITU, supportive therapy, treat underlying cause, mechanical ventilation, circulatory support to maintain CO, invasive haemodynamic monitoring, sepsis organism identification, broad spectrum antibiotics, nutritional support, high fat and antioxidant formulants

232
Q

What is the mortality of ARDS?

A

50-70%, based on age and cause and no. of organisms

233
Q

What are the 3 stages of lung injury in ARDS?

A

exudative stage, proliferative phase, fibrotic phase

234
Q

Why does shock reduce urine output?

A

reduced BP, reduces GFR

235
Q

What is valvulitis and what is its most common cause?

A

inflammation of the valve, mainly cause by rheumatic heart disease

236
Q

What is rheumatic heart disease?

A

Permanent damage to the heart muscle, mainly caused by rheumatic fever

237
Q

What is rheumatic fever?

A

an inflammatory disease in children and young adults due to a group A streptococcus infection causing and autoimmune reaction

238
Q

What causes rheumatic fever?

A

group A streptococcus infection, leading to pharyngitis causing rheumatic fever and rheumatic heart disease

239
Q

How long after a group A streptococcus infection does rheumatic fever occur?

A

2-3 weeks

240
Q

How common is rheumatic fever?

A

incidence has decreased due to improved sanitation, a change or virulence of the organism and the use of antibiotics

241
Q

What are the clinical features of rheumatic fever?

A

fever, joint pains, loss of appetite, changing heart murmurs, mitral and aortic regurgitation, heart failure, chest pain, pericardial effusion, polyarthritis, erythema marginatum and small non tender subcutaneous nodules over the tendons and bony prominences, Sydenhams chorea

242
Q

What will investigations show in rhuematic fever?

A

leucocytosis, raised ESR, high antistreptolysin O titre, and antiDNAase B

243
Q

What is the diagnosis criteria for Rheumatic fever called?

A

Duckett Jones criteria

244
Q

What is the treatment of rheumatic fever?

A

bed rest, high dose aspirin, penicillin to eradicate streptococcol infections, NSAIDs

245
Q

At what age are you most likely to get rheumatic fever?

A

5-15 years

246
Q

What is a normal cholesterol value?

A

5

247
Q

What is familia hypercholestrolaemia?

A

gene abnormality so unable to uptake cholesterol so have a high cholesterol of 10

248
Q

What does LVNC look like?

A

sponge like appearance of LV

249
Q

What is the difference between a cardiac amyloid and an amyloidosis cardiomyopathy?

A

cardiac amyloid is related to the heart and amyloidosis is part of a systemic disorder

250
Q

What is a sarcoid?

A

a chronic granulomatous disease with numerous granulomas of non caseating giant cell type, can produce widespread fibrosis and compensatory hypertrophy, produce a restrictive cardiomyopathy

251
Q

How many types of glycogen storage disease are there?

A

4

252
Q

What is mucopolysaccharosis?

A

where excess glycosaminoglycans are deposited in cells (Hurler syndrome)

253
Q

In who is endomyocardial disease commonly seen?

A

African settings as a temperature region disorder

254
Q

How does endomyocardial disease present?

A

endomyocardial fibrosis, high grade eosinophilia, rash and progressive endocarditis, cardiac failure

255
Q

What are the ventricles like in endomyocardial disease?

A

stiff and poor compliant, there is grey/white layer of fibrous tissue extending onto the endocardial surfaces of ventricular cavities

256
Q

What is myocarditis?

A

reflects inflammation of the myocardium, associated with muscle cell necrosis and degeneration

257
Q

What are the potential causes of myocarditis?

A

virus, bacteria, metazoa, fungi, protazoa, rickettsia, hypersensitivity/immune related, radiation, sarcoid, uraemia

258
Q

How does myocarditis appear macroscopically?

A

dilated

259
Q

What happens in the cell in acute myocarditis?

A

lymphocyte infiltration cutting through the myocardium and destroying muscle fibres, healed by patchy fibrosis

260
Q

What are the symptoms of myocarditis?

A

palpatations, latitude, upper resp tract infection, chest pain, breathlessness

261
Q

What is giant cell myocarditis?

A

area of muscle cell death due to macrophage giant cells

262
Q

What percentage of births have a cardiac deficit?

A

1%

263
Q

What percentage of those with a cardiac deficit at birth have a poor prognosis?

A

20-25%

264
Q

At how many weeks is the foetal echo?

A

18-22 weeks

265
Q

What causes a congenital heart defect?

A

maternal alcohol, drugs, radiation and disease, or chromosome or genetic abnormalities

266
Q

What is the most common congenital heart defect?

A

Tetrology of Fallot

267
Q

What are the 4 main features of Tetrology of Fallot?

A

ventricular septal defect, overiding aorta, pulmonary stenosis and right ventricular hpertrophy

268
Q

What is a ventricular septal defect?

A

A hole between the two ventricles

269
Q

What does a ventricular septal defect lead to?

A

causes an abnormal blood flow of deoxygenated blood into the left ventricle, can limit blood flow to the lungs leading to pulmonary stenosis.

270
Q

What investigations are used to detect a ventricular spetal defect?

A

ECG, ECHO, CXR

271
Q

Why does a ventricular septal defect affect aorta size?

A

Causes increased blood flow through the left side of the heart, so aortic valve is enlarged to override the VSD so blood still enters the systemic system

272
Q

How does a VSD affect right ventricular size?

A

The RV wall thickens and hypertrophies due to outflow obstruction

273
Q

What is VSD blood shunting?

A

where oxygenated and deoxygenated blood becomes mixed leading to decreased oxygen in systemic system

274
Q

How do patients with Tetrology of Fallot and VSD appear?

A

Bluish appearance

275
Q

How does the heart appear in Tetrology of Fallot?

A

boot shaped

276
Q

What happens to the blood flow in Eisenmegers?

A

there is decreased blood flow through the lungs, damaging the pulmonary vasculature, and resistance to blood flow in lungs increases, RV pressure increases, shunts from right to left causing blue appearance

277
Q

What are the clinical signs in a small VSD?

A

asymptomatic, normal heart rate and size, loud systolic murmur

278
Q

What are the clinical signs in a large VSD?

A

breathless, poor feeding, failure to thrive so must fix in infancy, small baby, increase RR, big heart, tachycardia, murmurs

279
Q

What does a VSD lead to?

A

pulmonary hypertension and Eisenmengers complex

280
Q

How do you treat Tetrology of Fallot and what could this lead to in adults?

A

surgical repair before 2y/o , good prognosis, but some adults then develop pulmonary regurgitation so must redo the surgery to relieve ventricular outflow tract

281
Q

What is an atrial septal defect?

A

an abnormal connection between the two atria

282
Q

Where is the usual place to get an atrial septal defect?

A

in the ostium secundum

283
Q

What is an atrial septal defect which is closer from the bottom, and in who in this normally seen?

A

ostium prinium

Downs syndrome

284
Q

What is an atrial septal defect which comes from the top?

A

Sinus venosus

285
Q

What the clinical signs in an atrial septal defect?

A

asymptomatic, paradoxical embolus, pulmonary flow murmur, fix split second heart sound, large pulmonary arteries and big heart

286
Q

what causes a second heart sound in an atrial septal defect?

A

delayed closure of the pulmonary vein as more blood has to get out form right to left shunt

287
Q

What does an CXR in an atrial septal defect?

A

big pulmonary arteries and big heart

288
Q

What is the treatment of atrial septal defect?

A

surgical or percutaenous key hole to close the hole

289
Q

What causes the shunt in atrial septal defect?

A

higher pressure in left atrium so shunts to right so more blood flows through the lungs

290
Q

Do patients appear blue in atrial septal defect?

A

no, due to no decreased blood flow through the lungs

291
Q

What are the symptoms of a large defect in an atrial septal defect?

A

SOB on exertion, increased chest infections, right heart dilation

292
Q

What are the symptoms of a small atrial septal defect?

A

no dilations so no symptoms

293
Q

What is the ductus arteriosus?

A

persistent communication between the proximal left pulmonary artery and the descending aorta

294
Q

What happens to the ductus artiosus at birth?

A

will close due to increase in o2 from breathing and due to prostagladin production decreases

295
Q

What would the ductus arterious remain open at birth?

A

a premature birth causing undeveloped lungs, increased sensitivity to prostagladins, large amount of prostagladins, mother infected with Rubella

296
Q

What can you hear in a patent ductus arteriosus?

A

the sound of the blood flowing back in the pulmonary artery

297
Q

What clinical features are seen in a patent ductus arteriosus?

A

widening pulse pressure (difference between systolic and diastolic pressure)

298
Q

What is the treatment of a patent ductus arteriosus?

A

PG inhibitors, local anaesthetic, venous approach with AV loop, idomethacin, surgery or percutaneous, NSAIDs, coil occlusion

299
Q

What can a patent ductus arteriosus lead to?

A

pulmonary hypertension, enlarged heart

300
Q

What is a risk in small patent ductus arteriosus?

A

endocarditis

301
Q

What are the symptoms in a large patent ductus arteriosus?

A

breathless, poor feeding, failure to thrive

302
Q

What is an atrioventricular septal defect?

A

hole in the centre of the heart, so 1 big valve instead of 2 separate AV valves

303
Q

In who is an atrioventricular septal defect common in?

A

Downs syndrome

304
Q

When does a partial atrioventricular septal defect present?

A

in late adulthood

305
Q

When does a complete atrioventricular septal defect present?

A

as a neonate

306
Q

How does a complete atrioventricular septal defect present?

A

breathless neonate, poor feeding and poor weight gain,

307
Q

What is the foramen ovale?

A

the septum and hole between the two atrias in the foetus

308
Q

What happens in the patent foramen ovale?

A

when the forman ovale doesn’t close after birth

309
Q

Where is the patent foramen ovale usually occur?

A

in the osteum secundum

310
Q

What is a paradoxical emboli?

A

an emboli that can get lodged in the hole in the heart and cause a CNS infarction

311
Q

What can a patent foramen ovale lead to if not treated?

A

arrhythmias, pulmonary hypertension, right ventricle hypertrophy, cardiac failure, infective endocarditis risk

312
Q

What is complete transportation of the great arteries?

A

when the aorta breaks off the left ventricle and comes to the right ventricle

313
Q

What do people with complete transportation of the heart also have?

A

an atrial septal defect to allow communication of blood, to allow blood mixing

314
Q

Who is most likely to get complete transportation of the heart?

A

males, with diabetes, diabetic mothers, Di George

315
Q

What is the treatment of a complete transportation of the heart?

A

arterial switch, leading to less than 10% mortality

316
Q

What is endocardial fibroetastosis?

A

profound dense collagen and elastic tissues deposited on endocardium of LV causing stiffening of the heart and heart failure

317
Q

What causes endocardial fibroetastosis?

A

genetic, or complication of congenital aortic stenosis and coarction

318
Q

What is dextocardia?

A

abnormal positioning of visceral organs, associated with organ isomerism

319
Q

What is coarctation of the heart?

A

narrowing of the aorta at the insertion of the ductus arteriosis causing excessive blood flow being diverted through the carotid and subclavian vessels into the systemic vascular shunts to supply the rest of the body

320
Q

In who is coarctation of the heart most commonly seen?

A

men are twice as likely , associated with Turner’s, Berry aneurysms,

321
Q

In coarctation of the heart is the aorta normally tricuspid of bicuspid?

A

bicuspid

322
Q

What clinical features are seen in coarctation of the heart?

A

systemic (right arm) hypertension, bruits (buzzes) over the scapula and back, murmur, poor peripheral pulses, cold legs, headaches, nose bleeds

323
Q

What can coarctation of the heart lead to in the long term?

A

hypertension, CAD, stroke, re coarctation, aneurysm at site of rupture, infective endocarditis, cerebral haemorrhage,

324
Q

What is the appearance of coarctation of the heart on investigations?

A

ECHO, CXR, 3 sign and rib notching

325
Q

What is the treatment of coarctation of the heart?

A

PGE1, surgical correction or balloon angioplasty

326
Q

What are the complications of treatment of coarctation of the heart?

A

restenosis, dissection of aneurysm

327
Q

What murmur is heard on coarctation of the heart?

A

systolic murmur in L axilla

328
Q

What murmur is heard in ASD?

A

wide fixed split S2, systolic ejection at upper left SB

329
Q

What murmur is heard in tetrology of Fallot?

A

systolic ejection at upper left SB

330
Q

In who is a bicuspid AV seen more in?

A

males

331
Q

Why is a biscupid AV worse?

A

has 2 cusps not 3 so does not last as long as can become severely stenotic, become regurgitate, coarct and degenerate

332
Q

What is pulmonary stenosis?

A

narrrowing of the outflow of right ventricle (can be valvar, subvalvar, supra valvar or branch)

333
Q

what is the treatment of a pulmonary stenosis?

A

balloon valvuloplasty, open valvotomy, open transannula patch, shunt to bypass the blockage

334
Q

What are the complications in mild pulmonary stenosis?

A

right ventricular hypertrophy

335
Q

What are the complications in severe pulmonary stenosis?

A

RV failure, poor pulmonary blood flow, RV hypertrophy, tricuspid regurgitation

336
Q

What is mitral stenosis?

A

narrowing of the mitral valve of the heart, causing obsturction of LV inflow, preventing proper filling during diastole

337
Q

How does mitral stenosis affect the atria and pulmonary vein?

A

causes increased pressure in the left atria and the pulmonary vein

338
Q

In who is mitral stenosis most common?

A

females

339
Q

What is the cause of mitral stenosis?

A

rheumatic heart disease, calcification of the valave, congenital, rheumatic arthritis, ankylosing spndylitis, SLE, malignant carcinoid

340
Q

What is the main cause of mitral stenosis?

A

rheumatic heart disease

341
Q

How does rheumatic heart disease cause mitral stenosis?

A

it is an inflammatory disease caused by streptococcus group A pyogenes, causing inflammation of the valves with fibrinous repair, thickening the mitral valve

342
Q

What are the symptoms of mitral stenosis?

A

progressive dyspnea, AF palpatations, orthopnea, paraxysaml nocturnal dyspnoea, palpitations, chest pain, hemoptysis, ascites.

343
Q

At what size of the mitral valve is mitral stenosis causing symptoms?

A

a 2cm2

344
Q

What is the difference in area of the mitral valve in mild, moderate and severe mitral stenosis?

A

mild = >1.5cm2
moderate = 1-1.5cm2
severe =

345
Q

What signs are seen in mitral stenosis?

A

malar flush, irregularly irregular pulse, distension of jugular veins, tapping pulse on left side/parasternal impulse due to RV hypertrophy, loud S1, rumbling midiastolic murmur, short S2 indicates more severe

346
Q

What is the pathophysiology behind mitral stenosis?

A

raised LA pressure, causes LA hypertrophy and dilation, causes referred pressure to lungs, causing pulmonary hypertension, leading to RV pressure overload, RV hypertrophy and right sided heart failure

347
Q

What will invetsigations show in mitral stenosis?

A

AF, LA enlargement, RV hypertrophy, prominent pulmonary arteries, Kerley B lines, TTECHO measure mitral area, cardiac catheterisation

348
Q

What is the treatment of mitral stenosis?

A

diuretics for fluid overload, rate control and anticoagulants it AF, valvotomy, valve replacement, prophylaxis against IE and rheumatic fever

349
Q

What do you use to confirm the diagnosis in mitral stenosis?

A

ECHO

350
Q

What is a malar flush?

A

red cheeks from mitral stenosis due to CO2 retention and vasodilation

351
Q

What is mitral regurgitation?

A

the backflow of blood from the LV to the LA during systole

352
Q

What are the causes of mitral regurgitation?

A

infective endocarditis, rheumatic fever, mitral valve prolapse, papillary muscle rupture, myxomatous degeneration, ischemic heart disease, SLE, Marfans syndrome, Ehlers and Danlos syndrome, cariomyopathy

353
Q

What is the pathophysiology behind mitral regurgitation?

A

regurgitation of blood into the LA causing LA dilation from a small increase in pressure, this causes pulmonary hypertension leading to pulmonary oedema so there is LV hypertrophy to maintain SV, leads to heart failure

354
Q

What are the symptoms of mitral regurgitation?

A

dysponoea, orthopnoea, fatigue, lethargy, ascites, ankle oedema, palpitations, weight loss (cardiac cachexia)

355
Q

What signs are heard/seen from mitral regurgitation?

A

deviated apex beat, systolic thrill, harsh pansystolic murmur radiating to axilla, soft S1, prominent 3rd heart sound, AF, pulmonary hypertension, heart failure, IE symptoms,

356
Q

Is it in mitral regurgitation or mitral stenosis that intensity of sound of heart that correlates to the severity?

A

mitral regurgitation

357
Q

What do investigations show in mitral regurgitation?

A

LA and LV enlargement, increase in CTR, valve calcification, P mitrale, AF, TOEECHO, colour doppler, cardiac catheterisation, pulmonary oedema, cardiomegaly, see valve structure

358
Q

What is the treatment of mitral regurgitation?

A

conservative managment, serial ECHO, IE prophylaxis (amoxcillin), control rate and anticoagulants if AF, diuretics , surgery if deteriorating with valve repair/replacement, vasodialators,

359
Q

At what EF would you consider surgery for mitral regurgitation treatment?

A

if

360
Q

What is mitral valve prolapse?

A

degeneration of mitral valve so inner fibrosa layer becomes loose and fragmenty with mucopolysaccharide material accumulation

361
Q

What happens in mitral valve prolapse?

A

valve cusp bows upwards so may not close properly, causing regurgitation

362
Q

What percentage of the female population have mitral valve prolapse?

A

6% - but not all are symptomatic

363
Q

What sounds are heard in mitral valve prolapse?

A

S3 sound on ausculation due to the snap of redundant leaflets as it proplapses in to the LA

364
Q

How many valves does the aortic valve have?

A

3

365
Q

What is aortic stenosis

A

outflow obstruction during systole, when the valve is 1/4 of the original size

366
Q

Causes of aortic stenosis?

A

age related calcification, bicuspid aortic valve which causes local destruction and stenosis, degenerative calcification, rheumatic heart disease, dissection, aneurysm and coarctation, Williams, infected vegetations

367
Q

When does congenital aortic stenosis usually occur?

A

in 30-50yrs

368
Q

When does acquired aortic stenosis usually occur?

A

in 70-80 years

369
Q

What kind of stenosis is seen in children?

A

supravalvular stenosis

370
Q

What is the pathophysiology behind an aortic stenosis?

A

obstructed LV outflow causes an increased LV pressure, with compensatory LV hypertrophy leading to LV myocardium ischemia, angina, arrhythmias and LV failure, resulting in a reduced CO

371
Q

What are the 3 main symptoms seen in aortic stenosis?

A

syncope, angina and dyspnoea

372
Q

does infection endocarditis usually cause regurgitation or stenosis?

A

regurgitation

373
Q

What are the sign of an aortic stenosis?

A

carotid pulse, sinus rhythm, small volume, slow rising
systolic thrill in aortic
apex is sustained
ejection click, soft A2, paradoxically split s2, possible s4
ejection systolic murmur radiating to carotids
Heyders syndrome

374
Q

What will investigations show in aortic stenosis?

A

Lv hypertrophy, thickened calcified immobile cusps, CXR, TTECHO, cariac catheterisation, MRI, CT

375
Q

What is the treatment of aortic stenosis?

A

if symptomatic - AV replacement
asymptomatic - regular review and serial echo
dental hygiene, TAVI, control BP, vasodilation meds

376
Q

What is aortic sclerosis?

A

Valve thickening without outflow obstruction

377
Q

What is the area of a normal aorta?

A

3-4 cm2

378
Q

What is the area of a mild, moderate and severe aortic stenosis?

A

mild=>1.5cm2
moderate=1-1.5cm2
severe=

379
Q

What is TAVI??

A

transcutaenous aortic valve implantation which is a non surgical, minimal invasive catheter up the aorta, passing a balloon acorss the narrow valave to damage the valve and cause regurgitation, then another catheter with a metabllic cage is put above the natural valve

380
Q

When is TAVI preferred over surgery?

A

for co morbidities, has a good prognosis and is less invasive

381
Q

What is aortic regurgitation?

A

an incompetence of the aortic valve causing blood to flow back into the left ventricle during diastole

382
Q

What are the acute causes of aortic regurgitation?

A

cusp rupture, infective endocarditis, connective tissue disease, aortic dissection, perforation secondary to infection, rheumatic fever

383
Q

What are the chronic causes of aortic regurgitation?

A

connective tissue disease, autoimmune diseases (RA, SLE, takayau arteritis), ankylosing spondylitis, sphylis

384
Q

What is the pathophysiology behind aortic regurgitation?

A

reflux of blood into LV leads to LV hypertrophy to maintain CO, then leads to reduced diastolic blood pressure causing reduced coronary perfusion, and increased myocardium metabolic demand leading to cardiac ischemia

385
Q

What are the main symptoms of aortic regurgitation?

A

palpitations, angina, dyspnoea, fatigue, sudden cardiac death

386
Q

What signs are seen in aortic regurgitation?

A

collapsing or bounding pulse, wide pulse pressure, deviated apex beat, high pitched early diastolic murmur at left sternal edge in 4th intercostal space with patient leaning forward and breath held in expiration

387
Q

What will investigations show in aortic regurgitation?

A

LV hypertrophy, ECHO, CXR

388
Q

What is the treatment of aortic regurgitation?

A

treat underlying cause, antibiotics, vasodilators, inotropes, aortic valve replacement, surgery

389
Q

What causes a low pitched mid diastolic murmur with opening snap?

A

mitral stenosis

390
Q

What causes a harsh pansystolic murmur radiating to axilla?

A

mitral regurgitation

391
Q

What causes a decrescendo early diastolic murmur?

A

aortic regurgitation

392
Q

What causes a crescendo-decrescendo ejection systolic murmur that radiates to the carotids?

A

aortic stenosis

393
Q

What causes a waterhammer pulse and a wide pressure pulse?

A

aortic regurgitation

394
Q

What causes a slow rising pulse and a narrow pulse pressure?

A

aortic stenosis

395
Q

What causes a displaced apex beat?

A

Mitral regurgitation

396
Q

What causes an irregular irregular pulse if in AF?

A

mitral regurgitation

397
Q

What causes a malar flush with a tapping apex beat , a hoarse voice and an irregularly irregular pulse if in AF?

A

mitral stenosis

398
Q

What percentage of the world have hypertension?

A

25%

399
Q

What is stage 1 hypertension?

A

140-159/90-99mmHg

400
Q

What is classed as pre hypertension?

A

120-139/80-89mmHG

401
Q

What is a normal BP?

A

90-119/60-79mmHg

402
Q

What is stage 2 hypertension?

A

160-179/100-109mmHg

403
Q

What is stage 3 hypertension?

A

> 180/>110mmHg

404
Q

What is isolated systolic hypertension?

A

When systolic BP is hypertensive but diastolic isnt. and vice versa for isolated diastolic

405
Q

What effect does hypertension have on blood vessels?

A

causes damage to the endothelial cells, leading to tears, MI, aneuryms etc

406
Q

What percent of hypertension are primary?

A

90%

407
Q

What are the risk factors for hypertension?

A

old age, obesity, high salt diets, lack of exercise

408
Q

What causes secondary hypertension?

A

atherosclerosis, vasculitis, aortic dissections, fibromuscular dysplasia, tumour that secrets aldosterone

409
Q

What happens when BF is lowered to the kidneys?

A

the kidneys secrete renin so the kidneys can retain more water in the arteries so they are more full, so there is increased hypertension

410
Q

How does fibromuscular dysplasia cause hypertension?

A

in young women, causing the artery walls to thicken

411
Q

What is classed at benign hypertension?

A

stage 1 and 2 which causes no immediate symptoms

412
Q

What is classed at malignant hypertension?

A

stage 3 which can cause organ failure

413
Q

What can untreated hypertension lead to?

A

eye problems, MI, stroke, renal failure

414
Q

What antihypertenisve drugs are available?

A

ACE-I, angiotensin receptor blockers, B blockers, calcium channel blockers, a-1-adrenoreceptor blockers, centrally acting antihypertensives and direct renin inhibito, diuretics, endothelin antagonists

415
Q

How do alpha-1-antagonists treat hypertension?

A

prevent function of alpha 1 and alpha 2 receptors in the post synpatic cells like on the smooth muscle e.g.doxazosn blocks binding site of neuroadrenaline so no contraction so lowers blood pressure

416
Q

How do ACE-I treat hypertension?

A

blocks the conversion of angiotensin 1 to angiotensin 2 in the lung, but by doing this increases bradykinin

417
Q

What is the function of angiotensin 2?

A

cause aldosterone release to increase salt reabsorption and retention, and causes vascular hypertrophy and hyperplasia and increased peripheral resistance via vasoconstriction

418
Q

Examples of ACE-I?

A

ramipril, enalapril, trandolapril, lisinopril, inudapril, catotopril

419
Q

How do angiotensin receptor blockers treat hypertension?

A

Block angiotensin 2 receptors, preventing angiotensin 2 function

420
Q

Side effects of ARBs?

A

renal failure, first dose hypotension, hyperkalaemia, rash, angiooedema

421
Q

When are ARBs contraindicated?

A

in renal artery stenosis, concurrent NSAIDs and pregnancy

422
Q

Examples of ARBs?

A

candesartan, valsartan, telmisartan, eposartan

423
Q

When are ACE-I contraindicated?

A

renal artery stenosis, concurrent NSAIDs, pregnancy

424
Q

What are the side effects of ACE-I?

A

due to decreased angiotensin 2 = hypotension, acute renal failure, hyperkalaemia, tetratogenic effects in pregnancy
due to increased angiotensin 1 = cough, rash, anaphylactoid reaction

425
Q

How do Beta Blocks treat hypertension?

A

block the action of the receptors that cause contraction, and the selectivity is relative non absolute

426
Q

Examples of B1 selective BBs?

A

metranolol, bisoprol

427
Q

Examples of B2 selective BBs?

A

propanolol, nadalol, carvedilol

428
Q

Examples of non selective BBs?

A

atenolol

429
Q

side effects of BBs?

A

HF, heart block, cold peripheries, fatigue, headaches, sleep disturbance, bradycardia, hypotension, erectile dysfunction

430
Q

When are BBs contraindicated?

A

unstable HF, heart block, asthma, concurrent verapamil, COPD, pulmonary complications (due to B2 receptors in the lungs that normally cause bronchodialation)

431
Q

When are BBs preferred for hypertension?

A

good in the young or those who are contraindicated or intolerant to ACE-I

432
Q

How do calcium channel blockers treat hypertension?

A

inhibit contraction of vascular smooth muscle, myocytes and conduction of the heart leading to a decrease in blood pressure.

433
Q

What are the 3 main types of CCBs and how do each work??

A

dihydropyridines - vasodialtors
phenylakyamines - negatively chonotrophic and negatively inotropic
benzothiazipines - intermediate heart/vascular effects

434
Q

Examples of CCBs?

A

amiodipine, nifedipine, diltvazen

435
Q

Examples of dihydropyridine CCBs?

A

nifedipine, amlodipine

436
Q

Examples of phenylakyamine CCBs?

A

verapamil

437
Q

Lifestyle change to treat hypertension?

A

diet, physical exercise, biofeedback, relaxation, meditation, low sodium,

438
Q

When are CCBs the preferred treatment for hypertension?

A

When over 55 or in Afro Caribbean, they are the 1st stage treatment

439
Q

What is the first stage treatment for hypertension if under 55 or not afro caribbean?

A

ace-i or arbs

440
Q

What is the treatment for stage 2 hypertension?

A

ace-1/arb with ccb

441
Q

What is the treatment for stage 3 hypertension?

A

add a thiazide diuretic to the meds

442
Q

What is the treatment for stage 4 hypertension?

A

potenially add a spironolactone, or a high dose thiazine diuretic

443
Q

What are the 4 types of diuretics?

A

thiazides, loop, aldosterone angiotensins or potassium

444
Q

Example of thiazide diuretic?

A

bendrofluemethiazide

445
Q

Example of loop diuretics?

A

frusemide

446
Q

Example of potassium diuretic?

A

spironolactone

447
Q

How do thiazide diuretics treat hypertension?

A

block sodium reabsorption at the distal convoluted tubule, given at loss dose, decreases potassium

448
Q

Side effects of thiazide diuretics?

A

renal failure, hypovalemic

449
Q

Contraindications of thiazide diuretics

A

kidney stones?, pre existing gout

450
Q

How do centrally acting medications treat hypertension?

A

act directly on the sympathetic nervous system to reduce peripheral reisistance and reduce cardiac output

451
Q

What is malignant hypertension?

A

fibrinoid necrosis of the vessel with local inflammation and focal smooth muscle proliferation

452
Q

What is Monckeberg medial sclerosis?

A

degenerative calcification of large and medium sized arteries

453
Q

What is fibromuscular dysplasia?

A

abnormal architecture for the arteries producing variable lumen narrowing and distal poverty of circulation. Occurs in the renal arteries, producing renal vascular insufficiency and progressive hypertension due to RAAS.

454
Q

What is phaeochromocytoma?

A

rare tumour of the SNS, that secretes catecholamines, noradrenaline, adrenaline and their metabolites

455
Q

In how man cases of hypertension does phaeochromocytoma occur?

A

1/1000

456
Q

What is phaechromocytoma called if not in the adrenal medulla?

A

paragangliomas

457
Q

symptoms of phaechromocytoma?

A

pallor, palpatations, panic, pain

458
Q

in large phaechromocytoma tumours, what is mainly produced?

A

noradrenaline

459
Q

What causes phaechromocytoma?

A

genetics, bilateral adrenal, malignant, extra adrenal

460
Q

What is Conn’s syndrome?

A

cuases 60% of primary hyperaldosterone cases, which causes increased in aldosterone which account for 5-10% of all hypertenisve cases

461
Q

What is Cushings syndrome?

A

increased cortisol from ACTH

462
Q

What are the main causes of Cushings syndome?

A

cushings disease (increased ACTH from pituitary), ectopic tumour producing AcTH, adrenal tumour, nodular hyperplasia

463
Q

What are the clinical features of Cushings syndrome?

A

pigmentation of skin, cushingoid appearance, hypertension

464
Q

What is the treatment of cushings syndrome?

A

BBs

465
Q

What causes renal artery stenosis?

A

fibromuscular disease of renal arteries and atherosclerotic renovascular disease

466
Q

what is tachycardia?

A

fast heart rate >100bpm

467
Q

What is sinus tachycarida?

A

a raised heart beat which is expected e.g. from exercise - caused by the bodys requirement for more o2

468
Q

What is a premature ventricular contraction?

A

a single beat originating from the ventricles

469
Q

What is defined as a ventricular tachycardia?

A

3 beats in a row that are PVC

470
Q

What can ventricular tachycardia lead to?

A

sudden death

471
Q

symptoms of ventricular tachycardia?

A

chest pain, fainting, dizziness, shortness of breath

472
Q

What are the two types of ventricular tachycardia?

A

focal or reentrant

473
Q

What is focal ventricular tachycardia?

A

part of the ventricle has abnormally fast automaticity rate which is faster than the sino atrial rate so the heartbeat is being driven by the ventricles

474
Q

What is automaticity rate?

A

the frequency at which a cell sends out a signal

475
Q

What can cause ventricular tachycardia?

A

medications, illicit drugs, electroylyte imbalance, ischaemia to ventricular muscle

476
Q

What is reentrant ventricular tachycardia?

A

caused by mismatch of refractory periods and conduction times in cariomyocytes

477
Q

What is a monomorphic ventricular tachycardia?

A

when all the QRS complexes are the same duration

478
Q

What kind of ventricular tachycardia has a monomorphic pattern?

A

reentrant or focal if one group of cells is responsible

479
Q

What is a polymorphic ventricular tachycardia?

A

the shape of the QRS complex changes because the signal is originating from different points in the venticles

480
Q

When is a polymorphic ventricular tachycardia seen?

A

in focal ventricular tachycardia when multiple parts are affected e.g. in severe hypoxia

481
Q

What is a complication of ventricular tachycardia?

A

ventricular fibrillation

482
Q

What is the treatment of ventricular tachycardia?

A

drug or electrical cardioversion

483
Q

What is electrical cardioversion?

A

Where it pulse is set to be delievered to the heart on the R wave to avoid it being delievered during a vunerable period in the T wave which could cause fibrillation

484
Q

What is a radiofrequency catheter ablation?

A

Radio frequency waves are used to heat up and destroy the tissue causing the irregular heartbeat

485
Q

What is an implantable cardioverter defibrillator?

A

delivers electrical cardioversion

486
Q

What happens in supraventricular tachycardia?

A

the SA node is overriden by another part of the heart which controls the pulse

487
Q

What kind of heart beat occurs in supraventricular tachycardia?

A

a fast regular heart beat, constant PR interval, narrow QRS

488
Q

What are the 3 types of supraventricular tachycardia?

A

atrioventricular nodal reentry, atrial and Wolff Parkinson White syndrome

489
Q

Which is the most commmon supraventricular tachycardia?

A

Atrioventricular nodal reentry - there is a short circuit in the centre of the heart

490
Q

At what age are you most likely to get Atrioventricular nodal reentry?

A

20-30years

491
Q

Where does atrial tachycardia arise from?

A

the atria - no underlying cause

492
Q

What causes Wolff Parkinson syndrome?

A

congenital abnormality

493
Q

What are the symptoms of Wolff Parkison syndrome?

A

palpitations, severe dizziness or syncope

494
Q

In which supraventricular tachycardia is there an accessory pathway between atria and ventricles?

A

the wolff parkinson syndrom

495
Q

What are the symptoms of supraventricular tachycardia?

A

tachycardia, palpitations, dizziness, breathlessness, chest discomfort, asymptomatic

496
Q

What are the features of atrial fibrillation?

A

absent p wave, narrow QRS complex, irregular rhythm, varying rate

497
Q

What is the most important kind of atrial fibrillation?

A

the permanent one which is long standing over a year and not terminated by cardioversion

498
Q

What are the causes of atrial fibrillation?

A

hypertension, coronoary artery disease, valve disease, hyperthyroidism,

499
Q

What investigations should be done for atrial fibrillation?

A

ECG, ECHO, CXR, routine bloods

500
Q

what is the treatment of atrial fibrillation?

A

BB or CCB, electrical cardioversion, rhythm control pharmacology, thromboprophylaxis, digoxin, maintain sinus rhythm with flecainide, amiodarome, sotalol and dronedarone

501
Q

What score can be used for thromboprophylaxis in atrial fibrillation?

A

CHA2DS2-VASc score

502
Q

What can be used as thromboprophylaxis?

A

warfarin

503
Q

How many types of heart block are there?

A

3

504
Q

What is seen in a first degree heart block

A

a prolonged P-R interval (>200ms)

505
Q

How long is a p wave and pr interval?

A

120-200ms

506
Q

What are the 2 types of 2nd degree heart block?

A

Mobitz 1 (Wenckeback) and Mobitz 2

507
Q

What is seen in a Wenckeback heart block?

A

gradual progressive P-R prolongation before a QRS is dropped

508
Q

What is seen in a Mobitz 2 heart block?

A

the same P-R interval followed by an absent QRS complex

509
Q

What is seen in a 3rd degree heart block?

A

There is no association between P wave and QRS complex

510
Q

What are the causes of first degree heart block?

A

athletes, myocarditis, hypokalaemia, hypomagnesaemia, medications

511
Q

What are the causes of second degree heart block?

A

athletes, post MI, lyme disease, medications

512
Q

What are the causes of 3rd degree heart block?

A

complication of heart surgery, coronary heart disease, radiotherapy, injection, hypertension, medications

513
Q

What are the symptoms of first degree heart block?

A

asymptomatic

514
Q

What are the symptoms in a Wenckebach heart block?

A

light headedness, dizziness, syncope

515
Q

What are the symptoms in a Mobitz 2 heart block?

A

chest pain, shortness of breath, tiring on exertion, postural hypotension

516
Q

What are the symptoms of a third degree heart block?

A

light headedness, dizziness, fainting, fatigue, chest pain, slow heart beat (bradycardia)

517
Q

What is the management of a heart block?

A

a pacemaker

518
Q

What is an ectopic beat?

A

an arrhythmia which is not sustained arising from the atira or ventricles, normally benign, symptoms of skipped or missed beats

519
Q

In what pattern do ectopic beats occur?

A

in couplets/triplets or in bigeminy/trigeminy

520
Q

What type of tachyarrhythmia is associated with a narrow QRS complex?

A

supraventricular

521
Q

What is the most commmon sustained arrhythmia?

A

atrial fibrillation

522
Q

What are the two types of atrial fibrillation?

A

paroxysmal (self terminates) or persistant

523
Q

What are the symptoms of atrial fibrillation?

A

palpitations, breathlessness, chest pain, fatigue, stroke risk

524
Q

What new types of oral agents are there to treat atrial fibrillation?

A

Direct Xa inhibitors and Direct thrombin inhibiotrs

525
Q

Examples of direct Xa inhibitors?

A

Rivaroxaban and apixaban

526
Q

Examples of direct thrombin inhibitors?

A

Dabigatran

527
Q

What is an atrial flutter?

A

often coexists with atrial fibrillation, can be paroxysmal or persistent

528
Q

What are the 3 types of narrow complex tachycardias?

A

atrioventricular nodal reentry, atrioventricular reentry, focal atrial tachycardia

529
Q

In who is atrioventricular nodal reentry tachycarida most common?

A

females in their 20s

530
Q

What is an accessory pathway?

A

a congenital remnant muscle strand between the ventricle and the atria, can be manifest or concealed

531
Q

What kind of complex is in atrioventricular reentry tachycardia?

A

narrow or broad

532
Q

What are the two types of broad complex tachycardias?

A

ventricular tachycardia or supraventricular tachycardia with bundle branch block or pre excitation

533
Q

Which is more dangerous VT or SVT?

A

VT so treat this if in doubt and the patient is unstable , if stable, then work it out

534
Q

What causes a diseased ventricle?

A

MI, cardiomyopathy

535
Q

What is the difference between william and marrow?

A

left bundle branch block and right bundle branch block

536
Q

What is the diagnosis if atrial activity can be seen or looks less typical looking?

A

ventricular tachycardia

537
Q

When can a normal heart VT be seen?

A

younger patients with a structurally normal heart, have a better prognosis

538
Q

What are the typical patterns seen in a normal heart VT?

A

outflow tract Vt or fascicular VT

539
Q

What is long QT syndrome?

A

rare condition where delayed repolarization of the heart following a heartbeat increases the risk of torsades de pointes

540
Q

What can trigger long QT syndrome?

A

stress, sudden noise, strenuous exercise, slow heart rate during sleep

541
Q

What causes long QT syndrome?

A

delayed flow of potassium ions out the hearts muscle, so each heart beat takes longer to rest itself, can be inherited or drug induced

542
Q

What is the treatment of long QT syndrome?

A

BBs, pacenaker, ICD, potassium rich foods

543
Q

What is infective endocarditis?

A

infection of the endocardium involving the heart valves and vegetation of infectious agents, causing holes in the heart valves mainly in the mitral valve

544
Q

what organisms cause infective endocarditis?

A 
streptococcus viridans
staphylococcus aureus
staphylococcus epidermidis
diphtheroids
microaerophilic streptococci
haemophilius actinobacillus cardiobacterium eikenella kingela (HACEK)
545
Q

What criteria is used for infective endocarditis?

A

Dukes criteria

546
Q

What is classed as infective endocarditis in the dukes criteria?

A

2 major, 1 major and 3 minor or 5 minor

547
Q

What are major factors in dukes criteria?

A

2 separate positive blood cultures

endocardial involvement

548
Q

What are the minor factors in dukes criteria?

A 
fever >38
IV drug user/predisposing heart condition
immunological phenomena
vascular phenomena
echocardiograph findings
549
Q

What are the 5 types of infective endocarditis?

A 
L native IE
L prosthetic IE
R IE (right is rarely prosthetic)
Device IE
Prosthetic IE
550
Q

What investigations should be done for infective endocarditis?

A

blood cultures - 3 separate cultures from 3 peripheral sites
bloods for anaemia
urinalysis, shoes microscopic haematuria
CXR
ECHO - for vegetations (TOE is better than TTE for looking for vegatations and if the patient is ventilated
ECG
raised ESR, Ig and cryoglobins

551
Q

What symptoms will infective endocarditis show?

A

fever, roth spots, osler nodes, new murmur, janeway lesions, anemia, nail splinters and haemorrhages, emboli

552
Q

What are janeway lesions?

A

painless papules on palms and plantars

553
Q

What are osler nodes?

A

painful nodules on fingers and toes

554
Q

What complications can infective endocarditis lead to?

A

heart fialure, arrhythmias, abscess formation incardiac muscle, emboli formation, stroke, vision loss, infection spread

555
Q

What are the main sites of vegetations in infective endocarditis??

A

atrial surface of AV valves
ventricular surfaces of semilunar valves
jet lesion in a shunt including venous or pulmonary side of AV fistula

556
Q

What is non bacterial thrombotic endocarditis?

A

sterile thrombotic deposit on valves with variable valve dysfunction in patients, neoplastic conditions and degenerative valve disease

557
Q

In who is infective endocarditis more common?

A

females

558
Q

What is the 10year survival for infective endocarditis?

A

60-90%

559
Q

What are risk factors for infective endocarditis?

A

elderly, young IV drug abusers, young with congenital heart disease, prosthetic heart valves, rheumatic heart disease, dental treatment, poor dental hygiene

560
Q

What is the mortality for infective endocarditis?

A

30-40%

Phase 2a (15 decks)

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