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(SG) Phase 2A lectures > cardio > Flashcards

cardio Flashcards

1
Q

atherosclerosis is the principal cause of what?

A

heart attack
stroke
gangrene of the extremities

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2
Q

what are the major cell types involved in atherogenesis?

A

endothelium
macrophages
smooth muscle cells
platelets

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3
Q

what is the critical bit of atherosclerotic plaque life?

A

inflammation

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4
Q

what is the most successful treatment for atherosclerotic plaques?

A

stents + medical therapies

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5
Q

what kinda consistency do plaques have?

A

oatmeal like at first - then gets really hard (like drainpipes)

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6
Q

when does atherosclerosis become a problem?

A

when the plaque ruptures, leading to thrombus formation and ultimately death

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7
Q

list some risk factors for atherosclerosis

A 
FH (v strong predictor)
age
tobacco smoking
high serum cholesterol
obesity
diabetes
hypertension
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8
Q

where are atherosclerotic plaques found?

A

within peripheral and coronary arteries

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9
Q

distribution of atherosclerotic plaques is governed by what?

A

haemodynamic factors

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10
Q

what are the haemodynamic factors that govern plaque distribution? (3)

A
  1. changes in flow/turbulence (eg at bifurcations) cause artery to alter endothelial cell function
  2. wall thickness also changes leading to neointima
  3. altered gene expression in key cell types is vital
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11
Q

changes in flow/turbulence can cause arteries to alter endothelial cell function - possibly leading to plaques. where is this most likely to happen?

A

at bifurcations

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12
Q

an atherosclerotic plaque is a complex lesion consisting of: (4)

A

lipid
nectrotic core
connective tissue
fibrous “cap”

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13
Q

define angina

A

chest pain or pressure, usually due to not enough blood flow to the heart

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14
Q

what are the 2 consequences of plaques?

A
  1. occlusion - of vessel lumen resulting in angina
    OR
  2. rupture - thrombus formation - death
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15
Q

name some examples of good inflammation

A

pathogens
parasites
tumours
wound healing

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16
Q

name some examples of bad inflammation

A 
myocardial repercussion injury
atherosclerosis
ischaemic heart disease
rheumatoid arthiritis
asthma
inflammatory bowel disease
shock
excessive wound healing
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17
Q

neutrophils have an important role in cleaning up dead/injured cells in wound healing but can also what?

A

extend area of injury beyond that originally cut off blood supply (this is known as ischaemia-reperfusion injury)

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18
Q

in septic/traumatic shock, large number of _______ are mobilised from bone marrow n recruited to tissues to fight potential infection

A

neutrophils

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19
Q

what helps ignite inflammation in arterial wall?

A

modified/oxidated LDL (normal too big to enter)

endothelial dysfunction

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20
Q

what is the stimulant for adhesion of leukocytes?

A

chemoattractants (chemicals that attract leukocytes)

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21
Q

how do chemoattractants work?

A

once inflammation is initiated, chemoattractants are released from endothelium and send signals to leukocytes

chemoattractants are released from site of injury and a conc gradient is produced

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22
Q

what is a non-specific indicator of inflammation?

A

CRP

c reactive protein

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23
Q

list some inflammatory cytokines found in plaques?

A 
IL-1
IL-6
IL-6
IFN-gamma
TGF-ß
MCP-1
CRP
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24
Q

leukocyte recruitment to vessel walls is mediated by what?

A

selectins

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25
Q

transmigration in inflammation is controlled by what?

A

interns n chemoattractants

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26
Q

what are the 5 steps in progression of atherosclerosis

A
  1. fatty streaks
  2. intermediate lesions
  3. fibrous plaques/advanced lesions
  4. plaque rupture
  5. plaque erosion
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27
Q

describe (1) fatty streaks (in the progression of atherosclerosis)

A

plaque constantly grows and recedes

fibrous cap has to be resorbed and redeposited in order to be maintained

if balance shifts eg in favour of inflammatory conditions, cap becomes weak n plaque ruptures

basement membrane, collagen n nectrotic tissue exposure

  • thrombus (clot) formation and vessel occlusion
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28
Q

what is a thrombus aka

A

clot

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29
Q

how can we detect plaque rupture

A

by ECG

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30
Q

describe (5) plaque erosion (in the progression of atherosclerosis)

A

2nd most prevalent cause of coronary thrombosis
lesions tend to be small ‘early lesions’
fibrous cap does not disrupt
luminal surface underneath clot may not have endothelium but is smooth muscle rich
v difficult to detect w imaging

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31
Q

describe (2) intermediate lesions (in the progression of atherosclerosis)

A

composed of layers of:

  • foam cells (lipid laden macrophages)
  • vascular smooth muscle cells
  • t lymphocytes
  • adhesion n aggregation of platelets to vessel wall
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32
Q

describe (3) fibrous plaques/advanced lesions (in the progression of atherosclerosis)

A

implodes blood flow
prone to rupture
covered by dense fibrous cap made of collagen, elastin etc
may be calcified
contains: smooth muscle cells, macrophages, foam cells, t lymphocytes

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33
Q

describe (4) plaque rupture (in the progression of atherosclerosis)

A

plaque constantly growing receding
fibrous cap has to resorbed and redeposited in order to be maintained
if balance shifted eg in favour of inflammatory conditions, the cap becomes weak and plaque ruptures
clot formation and vessel occlusion

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34
Q

how do u treat CAD

A

PCI

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35
Q

what does PCI stand for?

A

percutaneous coronary intervention aka a stent

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36
Q

5-10y ago, restenosis was a MAJOR limitation but no longer is. why?

A

drug eluting stents!

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37
Q

how do drug eluting stents work?

A

by reducing smooth cell proliferation and this in turn reduces regrowth after placement of the stent

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38
Q

what is a major adverse reaction of aspirin/clopidogrel/ticagrelor?

A

excessive bleeding

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39
Q

what is myocarditis aka

A

inflammatory cardiomyopathy (inflammation of the heart muscle)

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40
Q

what is inflammatory cardiomyopathy aka

A

myocarditis (inflammation of the heart muscle)

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41
Q

what is the normal weight of the heart

A

230-280g for females

280-340g for males

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42
Q

what is contraction of the heart initiated by?

A

depolarisation

changes to Ca concentration

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43
Q

what is normal systolic EF (ejection fraction)?

A

60-65%

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44
Q

failure to transport blood out of the heart is WHAT?

A

cardiac failure

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45
Q

cariogenic shock = what?

A

severe failure

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46
Q

myocardial hypertrophy can be an adaptive/physiological response when?

A

athletes

pregnancy

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47
Q

if u exceed stretch capability of sarcomeres, what happens to cardiac contraction force?

A

it diminishes

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48
Q

hypertrophic response can be triggered by what?

A 
angiotensin 2
ET-1
insulin like growth factor 1
TGF-ß
(these activate mitogen-activated protein kinase)
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49
Q

what happens w left sided cardiac failure?

A

pulmonary congestion

then overload of right side

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50
Q

what happens w right sided cardiac failure?

A

venous hypertension n congestion

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51
Q

diastolic cardiac failure results in what?

A

a stiffer heart

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52
Q

the heart comprises a single chamber until which week of gestation?

A

5th

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53
Q

congenital heart disease results from what?

A

faulty embryonic development

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54
Q

what are some single genes associated with heart disease?

A

trisomy 21 (downs)
turners (XO)
di-George syndrome

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55
Q

which drugs can influence heart disease?

A 
thalidomide
alcohol
phenytoin
amphetamines
lithium
oestrogenic steroids
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56
Q

what is PDA?

A

patent ductus arteriosus

- persistent opening between the 2 major blood vessels leading from the heart

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57
Q

what is VSD?

A

ventricular septal defect

- hole in the wall separating the two ventricles of the heart

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58
Q

what is ASD?

A

atrial septal defect

- hole in the septum of the 2 atria

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59
Q

what is truncus arteriosus?

A

rare type of heart disease

in which a single blood vessel (truncus arteriosus)

comes out of the R&L ventricles, instead of pulmonary artery & aorta

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60
Q

what is total anomalous pulmonary venous return (TAPVR)?

A

heart disease in which the 4 veins that take blood from the lungs to the heart do not attach normally to the left atrium

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61
Q

what is hypo plastic left heart syndrome (HLHS)?

A

birth defect that affects normal blood flow through the heart.
as the baby develops during pregnancy, the left side of the heart does not form correctly

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62
Q

what does tetralogy of fallot result in?

A

low oxygenation of blood

due to the mixing of oxygenated and deoxygenated blood in the LV via the VSD

and preferential flow of the mixed blood from both ventricles through the aorta

bc of the obstruction to flow through the pulmonary valve

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63
Q

what are the 4 components of tetralogy of fallout?

A

1) large VSD
2) pulmonary stenosis
3) overriding of the aorta above VSD
4) bc of these, RV becomes hypertrophied (thickened)

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64
Q

what is tricuspid atresia?

A

when tricuspid valve is missing or abnormally developed.

the defect blocks blood flow from RA to RV

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65
Q

what are some examples of left-right shunts?

A 
VSD
ASD
PDA
truncus arteriosus
TAPVR
hypoplastic left heart syndrome
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66
Q

what are some examples of right-left shunts?

A

tetralogy of fallot

tricuspid atresia

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67
Q

which heart conditions result in no shunts?

A 
complete transposition of great vessels
coarctation
pulmonary stenosis
aortic stenosis
coronary artery origin from pulmonary artery
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68
Q

what is Eisenmenger’s syndrome?

A

process in which a long-standing L-R cardiac shunt caused by a congenital heart defect

causes pulmonary hypertension & eventual reversal of the shunt into a cyanotic R-L shunt

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69
Q

how can a PDA be solveD?

A

can be closed:

  • surgically
  • by catheters
  • or by prostaglandin inhibitors (indomethacin)
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70
Q

what is the characteristic shape of tetralogy of Fallot on radiology?

A

boot-shape

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71
Q

what is complete transposition of the great arteries?

A

aorta coming off RV and pulmonary trunk off LV

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72
Q

what are some risk factors of complete transposition of great arteries (when aorta comes off RV and pulmonary trunk off LV)

A

male bias

associated w diabetes

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73
Q

coarctation of the aorta usually happens where?

A

just after the arch
with excessive blood flow being diverted through carotid/subclavian vessels into systemic vascular shunts to supply the rest of the body

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74
Q

coarctation of the aorta is particularly associated with which syndrome?

A

turner’s

also an association w berry aneurysms of the brain

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75
Q

what is endocardial fibroelastosis?

A

thickening within the muscular lining of the heart chambers

due to an increase in the amount of supporting connective tissue (inelastic collagen) and elastic fibers.

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76
Q

what is a frequent complication of congenital aortic stenosis and coarctation?

A

secondary endocardial fibroelastosis (thickening within muscular lining of heart)

can lead to stiffening of heart n cardiac failure

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77
Q

primary endocardial fibroelastosis follows what kinda pattern?

A

familiar

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78
Q

what is dextrocardia?

A

when ur heart points to right side rather than left

usually associated w CV abnormalities but can be normal

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79
Q

name 4 risk factors for ischaemic heart disease

A
  1. systemic hypertension
  2. cigarettes
  3. DM
  4. elevated cholesterol

(also obesity, age, male, FH, sedentary lifestyle habit)

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80
Q

remember: coronary heart disease = ischaemic heart disease

A

IHD is what it used to be called

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81
Q

list some reasons for imperfect blood supply to heart

A

atherosclerosis
thrombosis
thromboembolism
artery spasm

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82
Q

healthy individual has coronary reserve ___ of resting blood flow

A

4-8x

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83
Q

what is an aneurysm

A

dilation of part of the myocardial wall (usually associated w fibrosis and myocyte atrophy)

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84
Q

what is pericarditis?

A

a delayed pericarditic reaction following infarction (2-10w)

inflammation of the pericardium

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85
Q

whats the WHO classification for hypertension?

A

> 140/90 mmHg

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86
Q

what is hypertensive heart disease?

A

reflects cardiac enlargement due to hypertension and in absence of other cause

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87
Q

compensatory hypertrophy of the heart initially starts with what….

A

increased myocyte size
squaring of nuclei
slight increase of interstitial fibrous tissue

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88
Q

what is cor pulmonale?

A

condition that most commonly arises out of complications from pulmonary hypertension

aka right-sided heart failure (RV)

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89
Q

what happens in cor pulmonale?

A

RV hypertrophy

dilation due to pulmonary hypertension

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90
Q

what is acute rheumatic fever? and why is in the cardio flashcards?

A

group A ß-haemolytic streptococcus infection
usually upper RI

remains a major factor with regard to heart disease in developing world

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91
Q

what are some clinical features of acute rheumatic fever

A

carditis (cardiomegaly, murmurs, pericarditis, cardiac failure)

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92
Q

what is cardiomegaly?

A

abnormal enlargement of the heart

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93
Q

what is infective endocarditis?

A

an infective process involving cardiac valves. usually caused by bacteria

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94
Q

what are some consequences of (rheumatic) infection?

A

rapidly increasing cardiac valve distortion and disruption with acute cardiac dysfunction

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95
Q

calcific aortic stenosis may reflect what?

A

rheumatic aortic valve disease or degenerative processes

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96
Q

calcific aortic stenosis is accelerated where?

A

in bicuspid aortic valves

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97
Q

calcification of the mitral valve results is usually what?

A

asymptomatic and of no significance

only of significance following rheumatic valvular disease/previous vulvitis

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98
Q

what is mitral valve prolapse?

A

when the 2 flaps do not close evenly

degeneration of the mitral valves such that

the inner fibrous layer becomes more loose and fragmentary with accumulation of mucopolysaccharide material

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99
Q

what are the main problems that affect mitral valve?

A

prolapse
regurgitation
stenosis

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100
Q

what sound do u get on auscultation when the mitral valve prolapses?

A

S3

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101
Q

what is the most common form of myocarditis?

A

viral

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102
Q

list some infectious causes of myocarditis

A 
viruses (coxsackie, echo, influenza)
rickettsia
bacteria (diphtheria, streptococcal)
fungi and protozoa parasites
metazoa
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103
Q

what are some non-infectious causes of myocarditis?

A

hypersensitivity/immune related diseases (rheumatic fever, rheumatoid arthritis)
radiation
miscellaneous - sarcoid, uraemia

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104
Q

myocarditis can often have an association with what?

A

an upper RI preceding

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105
Q

how can drug reactions influence myocarditis?

A

causes inflammatory infiltrate particularly around blood vessels within the myocardium - predominance of eosinophils

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106
Q

what is DCM?

A

dilated cardiomyopathy - heart becomes enlarged, can’t pump blood effectively

(poorly generated contractile force leads to dilation of heart)

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107
Q

is DCM (dilated cardiomyopathy) genetic?

A

one third familiar

mostly autosomal dominant

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108
Q

what is secondary dilated cardiomyopathy?

A

enlargement of the heart caused by a med cond

eg alcohol, catecholamines, cocaine, pregnancy

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109
Q

what is HCM?

A

hypertrophic cardiomyopathy - thickened heart

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110
Q

what is the diff btwn dilated and hypertrophic cardiomyopathy?

A

dilated - swollen, enlarged
hypertrophic - thickened

therefore, harder for the heart to pump blood

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111
Q

mutations associated with troponin T are associated with what?

A

risk of sudden death

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112
Q

what is an amyloid?

A

a protein that is deposited in the liver, kidney, spleen or other tissues in certain diseases

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113
Q

what is a cardiac myxoma?

A

noncancerous tumour in the upper LHS/RHS

mostly grows in the septum

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114
Q

what are blood vessels lined by to maintain vascular integrity?

A

endothelial cells

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115
Q

blood coagulation occurs when fibrinogen is converted to what?

A

fibrin

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116
Q

clot lysis involves what?

A

plasminogen being converted to plasmin which then acts on fibrin to produce fibrin degradation products

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117
Q

what is the racial bias for hypertensive vascular disease?

A

afro-caribbean

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118
Q

what is the main function of ANP?

A

to lower BP

balances RAAS system

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119
Q

what is vasculitis?

A

group of disorders that destroy blood vessels by inflammation (primarily caused by leukocyte damage)

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120
Q

what is abdominal aortic aneurysm?

A

localised enlargement of the abdominal aorta such that the diameter is greater than 3 cm or more than 50% larger than normal diameter

usually cause no symptoms except when ruptured

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121
Q

what is a berry aneurysm?

A

small aneurysm that looks like a berry and classically occurs at the point at which a cerebral artery departs from the circular artery (the circle of Willis) at the base of the brain

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122
Q

what is syphilis?

A

an STI - inflammatory disease affecting vasa vasorum

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123
Q

what’s vasa vasorum?

A

network of small blood vessels that supply the walls of large blood vessels, such as elastic arteries and large veins

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124
Q

what is a varicose vein?

A

enlarged and torturous vein, mostly affecting superficial leg veins

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125
Q

what is angiosarcoma?

A

highly aggressive malignant neoplasm of endothelial cells

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126
Q

what is kaposi’s sarcoma linked to?

A

HIV and AIDS

cancer that causes patches of cancer to grow under the skin

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127
Q

what are some risk factors for DVT

A 
venous flow stasis from any cause eg cardiac falure
injury 
hypercoagulability
advanced age
sickle cell disease
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128
Q

what is hypercoagulability?

A

thrombophilia/prothrombotic stage - abnormality of blood coagulation that increases thrombosis risk

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129
Q

what is type A behaviour pattern characterised by?

A

competitiveness, impatience and hostility

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130
Q

what are some unmodifiable risk factors for CHD?

A

age
sex
ethnicity
genetic

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131
Q

what are some lifestyle risk factors for CHD?

A

smoking
diet
physical inactivity

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132
Q

what are some clinical risk factors for CHD?

A

hypertension
lipids
diabetes

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133
Q

what are some psychosocial risk factors for CHD?

A 
modifiable:
behaviour traits
depression/anxiety
work
social support
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134
Q

what is type A?

A

coronary prone behaviour pattern

competitive, hostile, impatient

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135
Q

how can u assess behaviour?

A

questionnaires eg self-report (poor), Minnesota multiphase personality index (MMPI)
structured clinical interview eg speech, answer content

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136
Q

what are the 3 aspects of recurrent coronary prevention?

A

cognitive - reconstructing thoughts to positive
behavioural - relaxation, walk at a steady pace
emotional - learn to relax in response to early signs of anxiety or anger

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137
Q

discuss psychosocial work characteristics

A

there are sig associates btwn psychosocial job characteristics and MI
those working 11h+ a day, 67% more likely to have an MI

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138
Q

how is social support linked to CHD?

A

both quality and quantity of social relationships are related to morbidity/mortality

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139
Q

what are epicardial vessels?

A

L & R CA’s lie on the surface of the heart - distribute blood to diff regions of the heart

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140
Q

what is angina?

A

a symptom which occurs as a consequence of restricted coronary blood flow

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141
Q

what is angina always almost exclusively secondary to?

A

atherosclerosis

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142
Q

why does angina happen?

A

bc there’s a mismatch btwn oxygen demand and supply

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143
Q

remember: atherosclerosis develops over time….

A

stable angina tends to be at approx a 4 (on a scale of 1-7 where 1 is a normal blood vessel)

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144
Q

what is SCAD?

A

spontaneous coronary artery dissection - uncommon emergency condition that occurs when a tear forms in 1 of the BV in the heart

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145
Q

what does myogenic control ensure?

A

insert graph

that flow (Q) remains constant in a physiological range of BP (P)

so for any given BP, heart is able to maintain blood flow!

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146
Q

when can there be a oxygen supply and demand mismatch? (3)

A
  1. impairment of blood flow by proximal arterial stenosis
  2. increased distal resistance eg LVH
  3. reduced oxygen-carrying capacity of blood eg anaemia
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147
Q

remember pouiselle’s law, why?

A

diameter of ?arteries has to fall below 75% before symptoms occur

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148
Q

in the healthy system, the resistance of the epicardial artery is negligible and so the flow through the system is determined by what?

A

the resistance (tone) of the microvascular vessels

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149
Q

discuss healthy rest (in the electro-hydraulic analogy)

A

in the health system, the resistance of the epicardial artery is negligible and so the flow through the system is determined by the resistance (tone) of the microvascular vessels

total flow is 3ML/S

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150
Q

discuss healthy exercise (in the electro-hydraulic analogy)

A

under exercise conditions, more flow is needed to meet metabolic demand
the microvascular resistance falls so that flow can increase

total flow can increase up to around 5x (15ml/s)

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151
Q

discuss diseased rest (in the electro-hydraulic analogy)

A

epicardial disease causes the resistance of the epicardial vessel to increase
to compensate, the microvascular resistance falls

so that flow can be maintained at 3ml/s

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152
Q

discuss diseased exercise (in the electro-hydraulic analogy)

A

epicardial resistance is high due to the stenosis
during exercise, the microvascular resistance falls to try and increase flow
but there comes a point where minimising microvascular resistance is ‘maxed out’ and can fall no more
at this pt, flow cannot meat metabolic demand

myocardium becomes ischaemic and pain is typically experienced
only way to reverse this is to rest, thus reducing demand for flow

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153
Q

name some other anginas

A 
printzmetal's angina (coronary spasm)
microvascular angina (syndrome x)
crescendo angina and unstable angina... ACS
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154
Q

what are some non-modifiable risk factors for angina?

A

gender
FH
personal history
age

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155
Q

what are some modifiable risk factors for angina?

A

smoking
diabetes
hypertension
sedentary lifestyle

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156
Q

what are some signs of ischaemic heart disease?

A 
male
middle aged
transverse ear cases
midline sternotomy
tar stained fingers
corneal arcus
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157
Q

what is the presentation of angina like? (3)

A
  1. heavy, central, tight, radiation to arms, jaw, neck
  2. precipitated by exertion
    3, relieved by rest/SL GTN
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158
Q

what does GTN do?

A

dilate arteries

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159
Q

what is the presentation of chest pain like?

A

v subjective

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160
Q

the scale of 3 for NICE diagnostic pathways

A 
3/3 = typical angina
2/3 = atypical pain
≤1/3 = non-anginas pain
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161
Q

what is OPQRRRSTT?

A 
O - onset
P - position (site)
Q - quality (nature/character)
R - relationship (with exertion, posture, meals, breathing and with other symptoms)
R - radiation
R - relieving or aggravating factors
S - severity
T - timing
T - treatment
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162
Q

what is the presentation of angina like?

A 
differential diagnosis 
pericarditis
pulmonary embolism/pleurisy
chest infection
dissection of the aorta
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163
Q

what is a differential diagnosis?

A 
the process of differentiating between 2+ conditions which share similar signs or symptoms
pericarditis/myocarditis
pulmonary embolism/pleurisy
dissection of the aorta
MSK
psychological
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164
Q

what is the presentation of angina on examination?

A

often normal or near normal

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165
Q

what is Htn short for?

A

hypertension

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166
Q

does ECG have direct markers of angina?

A

no, it is often normal

but Q waves, T-wave inversion, BBB are some sign of IHD

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167
Q

why might u do an echo for angina?

A

to check for LV function

there are no direct markers of angina
but there may be signs of:
previous infarcts (Q waves, T wave inversion, BBB)

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168
Q

list some anatomical investigations for angina

A 
CT angiography (non-invasive)
invasive angiography
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169
Q

what are some physiological investigations of angina?

A 
all non-invasive:
what is
exercise stress treadmill 
stress echo 
SPECT (nuclear perfusion) 
perfusion
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170
Q

what is the treadmill test?

A

induces ischaemia while walking uphill, incrementally fast
look for ST segment depression
detects a ‘later’ stage of ischaemia so not used that much anymore (also bc so many patients are unsuitable - can’t walk, v unfit, BBB)

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171
Q

whats the diff btwn sensitivity and specificity

A

sensitivity - if u have it, how likely is the measurement to pick it up
specificity - looking at PPV, so if u have a positive result, how likely is it that u have the disease?

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172
Q

what does the invasive angiogram involve?

A

its purely anatomical

for a long time was the “gold standard” for CAD patients
u pass wire, n measure the pressure before n after the clot

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173
Q

what is the main primary prevention of CAD?

A 
reducing risk and complications!!
eg hypertension - antihypertensives
hypercholesterolaemia - statins n lipid modulating therapies
T2DM - diabetic therapy
smoking - smoking cessation
diet - general advice
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174
Q

what are the 3 major arms of therapy?

A
  1. lifestyle changes
  2. pharmacological
  3. interventional (PCI and sometimes surgery)
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175
Q

what is the are some 1st line antianginals?

A

beta blockers
nitrates
calcium channel antagonists

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176
Q

what are some ß1 specific beta blockers?

A

bisoprolol and atenolol

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177
Q

what do beta blockers do?

A

antagonise sympathetic nervous activation
- reduce HR (negative chronotrope)
- reduce contractility (negative inotrope)
so, reduce work of heart. oxygen demand

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178
Q

why is coronary blood flow unique?

A

it occurs in diastole. if u lower HR, u naturally spend more time in diastole thus increasing time to fill arteries

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179
Q

do patients tolerate beta blockers well?

A

a lot don’t

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180
Q

what are some side effects of beta blockers?

A

tiredness, nightmares
bradycardia
erectile dysfunction
cold hands n feet

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181
Q

what are some contraindications for beta blockers?

A

severe bronchospasm; asthma

prinzmetal’s angina

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182
Q

what are nitrates?

A

1st line antagonists
primary VENOdilators
diates systemic veins (reduces venous return to RHS of the heart)
SO reduces preload
therefore (via F-S mechanism) reduces work of heart and oxygen demand
(also dilate coronary arteries - antagonise spasm)

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183
Q

what are calcium channel antagonists?

A 
1st line antagonists
primary ARTEROdilators
dilate systemic arteries (lower BP)
reduce afterload on the heart
lower energy required to prod same CO
tf reduce work of heart n oxygen demand
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184
Q

what are some 2nd line antianginals?

A

nicorandil

ivbridine

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185
Q

what does nicorandil do?

A

2nd line antianginal

mixed veno and artero-dilatory properties

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186
Q

what does ivbridine do?

A

2nd line abtianginal

only useful in sinus rhythm

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187
Q

what do anti platelets do? and whats an example?

A

reduce cardiovascular events
decrease prostaglandin synthesis
decrease platelet aggregation
aspirin

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188
Q

what is a caution for anti platelets?

A

gastric ulceration

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189
Q

what are some alternatives instead of anti platelets?

A

includes p2y12 inhibitors

eg clopidogrel, prasugrel, ticagrelor

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190
Q

what are statins

A

hmgcoa reductase inhibitors

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191
Q

what do statins do?

A

reduce CV events
reduce LDL cholesterol
anti-atherosclerotic

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192
Q

why is a stent inserted?

A

to restore patent (open/unobstructed) coronary artery and increase flow reserve

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193
Q

when is a stent inserted?

A

either when med fails (mostly)

when high risk disease identified (fewer)

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194
Q

how is a stent inserted?

A

PCI - percutaneous coronary intervention - stenting

CABG - coronary artery bypass graft - surgery

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195
Q

what are the pros of PCI

A

less invasive than CABG
convenient
repeatable
acceptable

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196
Q

what are the pros of CABG

A

prognosis

deals with complex disease

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197
Q

what are the cons of PCI

A

risk of stent thrombosis
risk of restenosis
can’t deal w complex disease
dual anti platelet therapy

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198
Q

what are the cons of CABG

A 
invasive
stroke risk, bleeding
can't do if frail, comorbid
1 time treatment
length of stay
time for recovery
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199
Q

do we tend to do more or less CABG?

A

less, more PCI done

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200
Q

*LOOK AT TABLE OF +++++S AND —–S OF PCI/CABG

A

*WB 7TH JAN

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201
Q

define ACS

A

acute coronary syndrome - includes unstable angina, NSTEMI, and STEMI

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202
Q

what does unstable angina and NSTEMI constitute?

A

NSTE-ACS

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203
Q

how is MI generally diagnosed

A

on the basis of symptoms of myocardial ischaemia associated with characteristic elevation in serum cardiac troponin levels and/or characteristic ECG changes

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204
Q

how can the extent of MI be classified

A

non-Q-wave
or Q-wave
depending on whether or not there is development of pathological Q waves on ECG, which is associated with transmural infarction

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205
Q

list risk factors for atherosclerosis

A 
smoking
high plasma cholesterol level
hypertension
DM 
old age
renal failure
FH
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206
Q

what is diagnosis of ACS based on

A

firstly, the recognition of symptoms of myocardial ischaemia (inc chest pain)
secondly, on investigations that support diagnosis

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207
Q

what does the likelihood of the diagnosis be determined by

A

assessment of clinical risk factors for CAD

using a risk score eg GRACE, TIMI risk scores

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208
Q

what does anti platelet therapy usually involve

A

dual:
aspirin
platelet p2y12 receptor antagonist (ticagrelor,clopidogrel, prasugrel)

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209
Q

list some beta blockers

A

bisoprolol
metoprolol
atenolol

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210
Q

when are beta blockers used

A

following STEMI orphan indicated in NSTE-ACS

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211
Q

what is the clinical classification for ppl with unstable angina

A

cardiac chest pain at rest
cardiac chest pain with crescendo pattern (eg unstable angina)
new onset angina

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212
Q

what is crescendo angina aka

A

unstable angina

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213
Q

how does troponin change w unstable angina

A

no significant rise

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214
Q

how is a STEMI diagnosed

A

on ECG at presentation

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215
Q

how is a NSTEMI diagnosed

A

retrospectively, after troponin results n sometimes other investigation results are available

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216
Q

what proportion of MI’s happen in bed?

A

a third

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217
Q

what symptoms is MI associated with?

A

sweating
breathlessness
nausea
vomiting

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218
Q

what is a higher risk of MI associated with?

A

higher age
diabetes
renal failure
left ventricular systolic dysfunction

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219
Q

what is the initial management for an MI?

A

get to hosp ASAP
for paramedics: if ST elevation, contact primary PCI centre for transfer
take 300mg aspirin immediately
pain relief

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220
Q

what is hosp management for MI?

A 
make diagnosis
bed rest
oxygen therapy if hypoxic
pain relief - narcotics/nitrates
aspirin +/- P2y12 inhibitor
consider beta blockers
consider other abtianginal therapy
consider urgent coronary angiography
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221
Q

what is the cause of majority of ACS cases?

A

rupture uf atherosclerotic plaque

and consequent arterial thrombosis

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222
Q

what are some minor causes of ACS?

A

coronary vasospasm without plaque rupture

drug use eg amphetamines, cocaien

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223
Q

what is troponin?

A

protein complex that regulates actin:myosin contraction

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224
Q

what is troponin a highly sensitive marker for, and is it specific to ACS?

A

cardiac muscle injury

no

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225
Q

when is troponin also positive, if not ACS?

A

gram neg sepsis
pulmonary embolism
heart failure
arrhythmias

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226
Q

when are p2y12 inhibitors used?

A

in combo w aspirin in management of ACS (dual anti platelet therapy)

227
Q

what are oral p2y12 inhibitors?

A

clopidogrel
prasugrel
ticagrelor

228
Q

what is a short-acting IV p2y12 inhibitor

A

cangrelor

229
Q

what is the caution with p2y12 inhibitors in dual anti platelet therapy?

A

increased bleeding risk

exclude serious bleeding prior to admin

230
Q

what are GpIIb/IIIa antagonists?

A

only IV drugs available

used in convo with aspirin/oral p2y12 inhibitors - for management of patients undergoing PCI for ACS

231
Q

what are anticoagulants used in addition to?

A

antiplatelets

232
Q

what do anticoagulants do?

A

inhibit fibrin formation and platelet activation

233
Q

what is PCI?

A

percutaneous coronary intervention

234
Q

what is PCI aka

A

angioplasty w stent

235
Q

list 2 anticoagulants

A

fondaparinux

heparin

236
Q

what is the treatment of choice for STEMI?

A

primary PCI

237
Q

what are some adverse effects of P2y12 inhibitors?

A

bleeding eg GI bleeds
rash
GI disturbance

238
Q

summarise secondary prevention of MI

A

DAPT; high dose statin eg atorvastatin 40-80mg; ACEI; beta blocker; aldosterone antagonist if heart failure and K+ not high

239
Q

what are symptoms/signs of DVT like?

A

non-specific

clinical diagnosis unreliable

240
Q

list 2 symptoms of DVT

A

pain

swelling

241
Q

list 4 signs of DVT

A

tenderness
swelling
warmth
discolouration

242
Q

how can u investigate DVT?

A

d-dimer: pos doesn’t confirm diagnosis, but normal excludes

US compression test proximal veins

243
Q

what is DVT treatment

A

LMW heparin SC OD for min 5d
oral warfarin, INR 2-3, for 6m
compression stockings
treat/seek underlying cause

244
Q

list some risk factors for DVT

A

surgery, immobility, leg fracture
OC pill, HRT, pregnancy
long haul flights/travel

245
Q

what are some mechanical prevention measures for DVT

A

hydration
early mobilisation
compression stockings
foot pumps

246
Q

what is a chemical prevention of DVT?

A

LMW heparin

247
Q

why is LMW heparin used for DVT prevention?

A

low molecular weight
prods a more predictable anticoagulant response
frequent monitoring not needed to adjust dose

248
Q

what can cause pulmonary embolism?

A

hypotension
cyanois
severe dyspnoea
right heart strain/failure

249
Q

what is a common presentation of PE?

A

differential diagnosis of chest pain n sob

consider also MSK, infection, malignancy, cardia, gastro causes

250
Q

what are some symptoms of PE?

A

breathlessness
pleuritic chest pain
may have signs/symptoms of DVT
no other diagnosis more likely

251
Q

what are some signs of PE?

A

tachycardia
tachypnoea
pleural rub

252
Q

what is the initial CXR of PE like?

A

usually normal

253
Q

what is the ECG of PE patient like

A

tachy

254
Q

what do blood gases of a patient w PE look like

A

t1 resp failure

decreased o2 and co2

255
Q

what are some further investigations of PE?

A

d-dimer

v/q scan

256
Q

what is the treatment of PE the same as?

A

DVT

ensure normal Hb, platelets, renal function, baseline clotting

257
Q

what is DOAC

A

direct oral anticoagulant

258
Q

what is INR

A

intl normalised ratio AKA prothrombin time

259
Q

what is the prevention of PE same as?

A

DVT

260
Q

what is thrombosis?

A

blood coagulation inside a vessel

261
Q

what is appropriate coagulation?

A

when blood escapes a vessel

failure of coagulation here leads to bleeding

262
Q

what is the diff btwn arterial/venous thrombosis?

A

arterial: high pressure so PLATELET RICH
venous: low pressure so FIBRIN RICH

263
Q

an arterial thrombus in coronary circulation is called WHAT?

A

MI

264
Q

an arterial thrombus in the cerebral circulation is called WHAT?

A

CVA (stroke)

265
Q

what is CVA?

A

cerebrovascular incident aka stroke

266
Q

what is an arterial thrombus in the peripheral circulation called?

A

peripheral vascular disease

267
Q

how can an MI be diagnosed>?

A

history
ECG
cardiac enzyme

268
Q

how can a stroke/cva be diagnosed?

A

history
exam
CT/MRI

269
Q

how can PVD be diagnosed?

A

history
exam
ultrasound
angiogram

270
Q

what are some risk factors for atherosclerosis

A 
smoking
hypertension
diabetes
hyperlipidaemia
obesity/sedentary lifestyle
stress/type A personality
271
Q

what is the major enzyme responsible for clot breakdown?

A

TPA - tissue plasminogen activator
found on endothelial cells
catalyses conversion of plasminogen to plasmin

272
Q

what is plasmin?

A

important enzyme present in blood - degrades many blood plasma proteins, including fibrin clots. it ‘dissolves’ already formed clots by degrading fibrin.

273
Q

what is the degradation of plasmin termed?

A

fibrinolysis

274
Q

what is the major enzyme of the fibrinolytic system?

A

plasmin

275
Q

what does it feel like to have DVT?

A

swollen, warm, tender leg

276
Q

what does a PE feel like?

A

pleuritic chest pain, breathlessness, cyanosis, death

277
Q

how would u treat venous thrombosis?

A

initially: LMW heparin SC OD
then: oral warfarin 3-6m
or DOAC for 2-6m

278
Q

what does heparin do?

A

binds to antithrombin and increases its activity

indirect thrombin inhibitor

279
Q

what does aspirin do?

A

inhibits cyclo-oxygenase irreversibly (COX)

so stops clotting

280
Q

what are the enzymes that prod prostaglandins called?

A

COX1/2

281
Q

what do cox1 n cox2 do? and what does cox1 specifically prod?????

A

produce prostaglandins that promote inflammation, pain, and fever;

however, only COX-1 produces prostaglandins that activate platelets and protect the stomach and intestinal lining

282
Q

waaaait, what are prostaglandins?

A

a group of physiologically active lipid compounds that have diverse hormone-like effects in animals.

they are derived enzymatically from the fatty acid arachidonic acid

283
Q

how does warfarin reduce clotting?

A

blocs the formation of vitamin K–dependent clotting factors (10, 9, 7, 2) think 1972

prolongs prothrombin time

284
Q

what are the vit K dependent clotting factors?

A

10
9
7
2

285
Q

what is warfarin an antagonist for?

A

vit K

286
Q

which vit is involved in coagulant?

A

k

(german - koagulation) !!!

287
Q

what is PT?

A

Prothrombin time - blood test that measures how long it takes blood to clot

288
Q

when is PT looked @?

A
  • to check for bleeding problems.

- also to check whether anticoagulants are working

289
Q

what can a PT test aka?

A

INR - international normalised ratio, standardised measurement of the time it takes for blood to clot

290
Q

what is hypertension a major risk factor for? (6)

A 
stroke
MI
heart failure
chronic renal disease
cog decline
premature death
291
Q

how is hypertension diagnosed?

A

clinical BP of 140/90 mmHg or higher

292
Q

ppl w suspected hypertension are offered whaT?

A

ambulatory BP monitoring (ABPM) to confirm diagnosis

293
Q

what are the main targets for BP control?

A

cardiac output n peripheral resistance
interplay between RAAS n SNS
local vascular vasoconstrictor/vasodilator mediators

294
Q

what are some drug types that affect RAAS for BP control?

A 
renin inhibitor (stops angiotensinogen --> angiotensin I)
ace inhibitor (stops angiotensin I --> angiotensin II)
295
Q

what are some drug types that affect SNS (noradrenaline) for BP control?

A

alpha blocker
beta blocker
calcium channel blocker?

296
Q

what are ACE inhibitors good for?

A

hypertension
heart failure
diabetic nephropathy

297
Q

name some ace inhibitors

A

ramipril
trandolapril
perindopril

298
Q

what are the main adverse effects of ace inhibitors?

A
  • related to red. ang II formation (hypotension, acute renal failure, hyperkalaemia)
  • related to incr. kinin prod (cough, rash)
299
Q

how are ace inhibitors generally tolerateD?

A

pretty well!

300
Q

what are the main reasons why calcium channel blockers (CCB) might be used?

A

hypertension
IHD - angina
arrhythmia (tachycarida, fast)

301
Q

name some CCB’s

A

amldipine
nifedipine
felodipine
verapamil

302
Q

what are L type calcium channel blockers?

A

drugs used as cardiac antiarrhythmics or antihypertensives

depending on whether the drugs have higher affinity for the heart (the phenylalkylamines, like verapamil), or for the vessels (the dihydropyridines, like nifedipine).

303
Q

what can L type calcium channel blockers be used as?

A

cardiac antiarrhythmics
or
cardiac antihypertensives

304
Q

which type of L type CCB’s have a high affinity for the heart? n an example?

A

phenylalkamines
eg verapamil

so used as an antiarrhythmic

305
Q

which type of L type CCB’s have a high affinity for the vessels? n an example?

A

dihydropyridines
eg nifedipine

so used as an antihypertensive

306
Q

what are some adverse effects of CCB’s?

A

mainly dihydropyridines/antihypertensives
- flushing, headache, oedema, palpitations

mainly phenylalkamines/antiarrhythmics
- bradycardia, AV block

307
Q

when are beta-adrenoceptor blockers used?

A

IHD - angina
heart failure
arrhythmia
hypertension

308
Q

list some beta-adrenoceptor blockers (BB)

A

bisoprolol
propranolol
metoprolol
atenolol

309
Q

what are the main adverse effects of BB?

A 
fatigue
headache
sleep disturbances/nightmares
bradycardia
hypotension
worsening of: asthma, PVD
310
Q

when are diuretics used?

A

to treat several conditions in medicine including heart failure, high blood pressure, liver disease and some types of kidney disease.

311
Q

what is a diuretic?

A

any substance that promotes diuresis

312
Q

what is a BB (beta-adrenoceptor blocker)?

A

prevent stimulation of adrenergic receptors

predominantly used to manage abnormal heart rhythms, and to protect the heart from a second heart attack after a first heart attack

313
Q

what are diuretics aka

A

water pills

314
Q

what is diuresis?

A

increased(/excessive) urine prod

315
Q

name the 4 classes of diuretics

A

thiazides n related drugs (distal tubule)
loop diuretics (LoH)
k-sparing diuretics
aldosterone antagonists

316
Q

name a thiazide and related diuretics

A

bendroflumethiazide

317
Q

name a loop diuretic

A

furosemide

318
Q

name a k-sparing diuretic?

A

spironolactone

eplerenone

319
Q

what are the main adverse effects of diuretics?

A 
hypovolaemia
hypotension
low serum K, Na, Mg, Ca
raised uric acid (gout?)
impaired gluc tolerance
320
Q

what is hypovolaemia?

A

state of decreased blood volume; more specifically, decrease in volume of blood plasma

321
Q

how do the treatment steps for hypertension differ if u are under vs over 55 yrs (or A-C of any age)?

A

under: ACE inhibitor/ang II blocker
over: calcium channel blocker

322
Q

what is the next step if ace-inhibitors/CCB don’t work in hypertension?

A

combine both
then add a diuretic
etccccc

323
Q

what is the diff btwn ANP and BNP?

A

atrial natriuretic peptide

british national p-…… brain natriuretic peptide *

324
Q

where is ANP found?

A

atria

325
Q

where is BNP found?

A

ventricles

326
Q

what does ANP do?

A

hormone - causes a reduction in expanded ECF vol by increasing renal sodium excretion

327
Q

what does BNP do?

A

hormone - secreted by cardiomyctes in response to stretching caused by increased ventricular blood volume

328
Q

when are ANP/BNP released?

A

stretching of atrial/ventricular muscle cells

329
Q

what are the main effects of the cardiac natriuretic peptides (ANP/BNP)

A

increase renal Na/water excretion
relax vascular smooth muscle
increased vascular permeability
inhibit release of : aldosterone, ang II, endothelia, ADH

330
Q

the cardiac natriuretic peptide system is counter regulatory to whattttt??????

A

RAAS

331
Q

what are the symptoms of chronic stable angina?

A 
anginas chest pain
predictable
exertional
infrequent 
stable
332
Q

what are the symptoms of unstable angina/acute coronarysyndrome (NSTEMI)

A

unpredictable
may be at rest
frequent
unstable

333
Q

what are the symptoms of STEMI ??

A

unpredictable;e
resp pain
persistent
unstable

334
Q

what are the treatment options for chronic stable angina?

A

anti platelet therapy (aspirin, clopidogrel if aspirin intolerant)
lipid lowering therapy eg statins
short acting nitrate eg GTN

335
Q

what are the treatment options for ACS (nstemi/stemi)

A 
pain relief (GTN, opiates)
DAPT (aspirin+ticagrelor/prasugrel/clopidogrel)
antithrombin therapy
lipid lowering therapy (statins)
etc
336
Q

how is ABPM (ambulatory BP monitoring) used to confirm high BP diagnosis?

A

at least 2 measurements per hour during person’s usual waking hours
avg at least 14 measurements to confirm diagnosis

337
Q

how is HBPM (home BP monitoring) used to confirm high BP diagnosis?

A

2 consecutive seated measurements, min 1min apart
BP recorded 2x a day for at least 4d and preferably for 1w
measurements on d1 discarded - avg value for remaining used

338
Q

if u suspect a patient is hypertensive, wwyd?

A

measure BP in both arms …. if diff is 20 mmHg+ repeat. use arm w higher BP as measurement!

339
Q

what are the 3 main antihypertensive effects of ACE inhibitors?

A
  1. reduced vascular resistance
  2. reduced ECF volume
  3. bradykinin elevated NO
340
Q

what is bradykinin?

A

an inflammatory mediator.

a peptide that causes blood vessels to dilate so decr BP

ACE inhibitors increase bradykinin (by inhibiting its degradation), further lowering BP

341
Q

what are some advantages of ACE inhibitors?

A

good with diuretics
no effect on insulin or glucose
increased quality of life

342
Q

do CCB’s inhibit calcium?

A

no

they prevent opening of voltage gated calcium channels

343
Q

what can fibrosis lead to?

A

arrhythmias

344
Q

what is dilated cardiomyopathy?

A

when the muscle of the heart is abnormal (can be too thick or thin)

345
Q

what is dilated cardiomyopathy often mistaken for?

A

asthma

346
Q

what is SADS?

A

sudden arrhythmic death syndrome

347
Q

what are u predisposed to with Marfan syndrome?

A

aneurysm of ascending aorta

348
Q

males or females w familiar hypercholesterolaemia have 100x risk of MI compared to normal?

A

females

349
Q

what does cardiomyopathy refer to?

A

primary heart muscle disease

350
Q

unexplained primary cardiac hypertrophy is referred to as what?

A

HCM

351
Q

what does DCM stand for?

A

dilated cardiomyopathy

352
Q

what happens with DCM?

A

LV/RV or 4 chamber dilatation/dysfunction

353
Q

what is the main feature of arrhythmogenic cardiomyopathy

A

arrhythmia

354
Q

all cardiomyopathies carry an _______ risk

A

arrhythmogenic

355
Q

what is channelopathy

A

inherited arrhythmia

356
Q

what is inherited arrhythmia (channelopathy) caused by?

A

ion channel protein gene mutations (usually K, Na, Ca)

357
Q

how may channelopathies present?

A

recurrent syncope

358
Q

sudden cardiac death in young ppl is often due to what?

A

an inherited condition

359
Q

an inherited abnormality of cholesterol is referred to as what?

A

familiar hypercholesterolaemia

360
Q

ICCs are usually inherited how?

A

dominantly

361
Q

how thick is the fibrous parietal layer

A

2mm

362
Q

parietal layer has WHAT to fix the heart in the thorax?

A

fibrous attachments

363
Q

LA is mainly outside what

A

pericardium

364
Q

pericardium has similar properties to what? n how

A

rubber - initially stretchy but becomes stiff at higher tension

365
Q

pericardial sac has big/small reserve vol?

A

small

366
Q

what is tamponade physiology?

A

small amt of vol added to space has dramatic effects on filling but so does removal of a small amt

367
Q

what is cardiac tamponade?

A

aka pericardial tamponade

when fluid in the pericardium builds up, resulting in compression of the heart - reduces CO

368
Q

define acute pericarditis

A

an inflammatory pericardial syndrome with or without effusion

369
Q

define effusion

A

accumulation of fluid in an anatomic space

370
Q

what are some infectious causes of pericarditis?

A

viral (common)
bacterial
fungal (v rare)
parasitic (v rare)

371
Q

what are some non-infectious causes of pericarditis?

A 
autoimmune (common)
neoplastic
metabolic
traumatic and iatrogenic
drug-related (rare)
372
Q

describe some features of chest pain in pericarditis

A

severe
sharp and pleuritic
rapid onset
radiates to arm or more specifically trapezius ridge
relieved by sitting forward, exacerbated by lying down

373
Q

what is pleuritic chest pain

A

characterised by sudden and intense sharp, stabbing, or burning pain in the chest when inhaling and exhaling

374
Q

what are some other symptoms of pericarditis?

A

dyspnoea (difficulty breathing)
cough
hiccups

375
Q

what does qds mean?

A

once a day

376
Q

what does qid mean?

A

4x a day

377
Q

what is differential diagnosis?

A

differentiating between 2+ conditions which share similar signs or symptoms

378
Q

what are some differential diagnoses compared to pericarditis?

A 
pneumonia
pulmonary embolus
GORD
MI/ischaemia
pneumothorax
peritonitis
pancreatitis
379
Q

how can u diagnose pericarditis?

A 
pericardial rub
sinus tachycardia
fever
signs of effusion
beck's triad
ecg 
bloods
car
380
Q

what does beck’s triad consist of?

A

hypotension
elevated JVP
quiet heart sounds

381
Q

what is pericardial friction rub?

A

audible medical sign used in the diagnosis of pericarditis.

on auscultation, this sign is an extra heart sound of to-and-fro character

resembles the sound of squeaky leather and often is described as grating, scratching, or rasping

382
Q

what is tamponade

A

when fluid in pericardium builds up

resulting in compression of the heart

383
Q

what is pulsus paradoxus

A

abnormally large decrease in stroke volume, systolic blood pressure and pulse wave amplitude during inspiration.

fall in systolic BP > 10mmHg

384
Q

what are blood tests like if u have pericarditis

A

fbc: modest WCC incr, mild lypmphocytosis
high ESR
high troponin
cxr often normal in idiopathic

385
Q

what is the management of pericarditis usually like?

A

sedentary activity until resolution of symptoms

NSAIDs or aspirin

386
Q

patients w acute pericarditis, what is their LT prognosis like?

A

good

387
Q

what is the commonest cause of pericarditis in developed world

A

viral

388
Q

define heart failure

A

inability of the heart to deliver blood (and oxygen) at a rate commensurate with the requirements of metabolising tissues

despite normal/increased cardiac filling pressures

389
Q

what is the commonest cause of myocardial dysfunction

A

heart failure

390
Q

what is HFREF

A

heart failure w reduced ejection fraction

391
Q

what is ejection fraction eyes emoji

A

% of blood u empty out of LW w/ each beat

392
Q

what are the 3 cardinal symptoms of heart failure

A

SOB
fatigue
ankle swelling

393
Q

what are some signs of HF

A

tachycardia
displaced apex beat
added heart sounds
ascites

394
Q

what is the NYHA classification like

A 
class I - asymptomatic (no limitation)
class II - mild HF (slight limitation)
class III - moderate HF (marked limitation)
class IV - severe HF (inability to carry out physical activity w/o discomfort)
395
Q

what are some complications of heart failure

A

renal dysfunction
rhythm disturbances
DVT, PE’s
neurologica and psych complications

396
Q

ACEI are less effective in who?

A

black ppl

397
Q

with aldosterone antagonists in HF, beware of what?

A

renal impairment

hyperkalaemia

398
Q

what % of all live births have some form of cardiac defect?

A

1%

399
Q

what involves tetralogy of Fallot?

A
  1. VSD
  2. pulmonary stenosis
  3. hypertrophy of RV
  4. overriding aorta
400
Q

what are some severe pregnancy risks in CVS?

A

pulmonary hypertension
marfan’s
systemic ventricular impairment

401
Q

what are some moderate pregnancy risks in CVS?

A

coarctation
moderate to severe aortic stenosis
mechanical heart valves

402
Q

what is the physiology of tetralogy of Fallot like

A

stenosis of RV outflow –> RV at higher pressure than LV
blue blood passes from RV to LV
so patients are BLUE

403
Q

what is VSD?

A

ventricular septal defects
abnormal connection btwn 2 ventricles
many close spontaneously during childhood

404
Q

what % of all congenital heart defects is VSD?

A

20%

405
Q

what is the physiology of VSD like?

A

high pressure LV
low pressure RV
blood flows from high pressure to low
therefore NOT BLUE

406
Q

what are some clinical signs of VSD (large hole)

A

small, breathless, thin baby
increased response rate
big heart on CXR
murmur varies in intensity

407
Q

what are some clinical signs of VSD (small hole)

A

loud systolic murmur
well grown
normal HR, heart size

408
Q

discuss what happens in Eisenmenger’s syndrome

A 
high pressure pulmonary blood flow
damage to delicate pulmonary vasculature
RV pressure increases
shunt direction reverses
patient becomes BLUE
409
Q

what is ASD?

A

atrial septal defect
abnormal connection btwn atria
often presents in adulthood

410
Q

discuss what happens in ASD

A

slightly higher pressure in LA vs RA
shunt L–>R
patient NOT BLUE

411
Q

what happens if u have a large hole in ASD

A

sig increased flow through RH/lungs during childhood
right heart dilatation
increased chest infections

412
Q

what happens if u have a small hole in ASD

A

small increase in flow
no RH dilatation
no symptoms

413
Q

what are some clinical signs of ASD

A

pulmonary flow murmur

CXR: big pulmonary arteries/heart

414
Q

how can ASDs be closed

A

surgical

percutaneous (key hole)

415
Q

AVSD (atrio-ventricular septal defects) tend to happen w what?

A

downs syndrome

416
Q

what does AVSD involve

A

ventricular septum
atrial septum
mitral and tricuspid valves

417
Q

what is the physiology of AVSD like (complete defect)

A 
breathlessness as neonate
poor weight gain
poor feeding
torrential pulmonary blood flow
surgically challenging repair
418
Q

what is the physiology of AVSD like (partial defect)

A

can present in late adulthood
presents like small VSD/ASD
may be left alone - there’s no RH dilatation

419
Q

what is PDA?

A

patent ductus arteriosus

when ductus arteriosus fails to close after

420
Q

in the foetus, what is the ductus arteriosus?

A

BV connecting main pulmonary artery to the proximal descending aorta.

allows most of the blood from the right ventricle to bypass the foetus’s fluid-filled non-functioning lungs.

421
Q

what is the physiology of PDA like

A 
large
torrential flow from aorta to pulmonary arteries
breathless
poor feeding
failure to thrive
more common in prem babies
422
Q

what is the risk of complications from PDA like

A

low

423
Q

define coarctation of the aorta

A

narrowing of the aorta at the site of insertion of ductus arteriosus

424
Q

what is severe coarctation of the aorta like

A

complete/almost complete obstruction to aortic flow
collapse w heart failure
needs urgent repair

425
Q

what is mild coarctation of the aorta like

A

presents w hypertension
incidental murmur
should be repaired to prevent LT problems

426
Q

what are some clinical signs of coarctation of the aorta

A

right arm hypertension

murmur

427
Q

what are some LT problems of coarctation of the aorta

A

hypertension (early CAD/strokes)
re-coarctation - requires repeat intervention
aneurysm at site of repair

428
Q

normal AV has how many cusps?

A

3

429
Q

why is a bicuspid AV an issue?

A

degenerates quicker than normal valves
become regurgitant earlier than normal valves
associated with coarctation and dilatation of ascending aorta

430
Q

what is pulmonary stenosis

A

narrowing of RV outflow (to pulmonary artery)

431
Q

what happens w severe pulmonary tenosis

A

RV failure as neonate
collapse
poor pulmonary blood flow

432
Q

list common structural heart defects

A 
VSD
ASD
AVSD
PDA
coarctation of aorta
bicuspid aortic valve
pulmonary stenosis
tetralogy off allot
Eisenmenger syndrome
433
Q

NICE guidelines say that the use of _____ may reduce misdiagnosis of hypertension

A

ABPM

434
Q

list some drugs that cause hypertension (≈8)

A 
NSAIDs
comb oral contraceptive
corticosteroids
ciclosporin
cold cures eg phenlephedrine
SNRI antidepressants
some recreational drugs etc cocaine n amphetamines
435
Q

list some lifestyle causes of hypertension (3)

A

obesity
excessive salt
excessive alcohol

436
Q

majority of calcium antagonists used for hypertension are what classed?

A

I - dihydropyridines

437
Q

how do calcium antagonists work? (CCB)

A

inhibit opening of voltage-gated (L type) Ca channels in vascular smooth muscle this reduces calcium entry
so reduces calcium available for muscle contraction
this reduction in peripheral resistance reduces systemic BP

438
Q

beta blockers reduce what?

A

plasma renin

439
Q

what does angiotensin II do

A

vasoconstricts
stimulates aldosterone release
enhances reabsorption of sodium

440
Q

ACE inhibitors may induce a persistent what?

A

dry cough

441
Q

how do thiazide diuretics help hypertension

A

inhibit Na reabsorption by DCT

reduce ECF which is elevated in hypertension

442
Q

what is one of the most common SPECIFIC causes of BP?

A

hyperaldosteronism

too much aldosterone - incr BP - bc too much salt in body (high K)

443
Q

if a patient has vvvv high BP - what would u examine?

A

eyes

can have damage to BV at back of eyes, haemorrhage, swelling of optic nerve

444
Q

what is the clinical threshold to consider drug treatment for hypertension?

A

140/90

445
Q

what is the home threshold to consider drug treatment for hypertension?

A

135/85

446
Q

what is s1 hypertension

A

above 140/90
lower than 160/100

lifestyle changes. if high risk, treatment

447
Q

what is s2 hypertension

A

above 160/100

448
Q

what are the symptoms of high BP

A

NONE

449
Q

treatment of high BP can reduce what?

A

headaches

450
Q

why prevent high BP?

A

stroke
ischaemic heart disease
heart failure

451
Q

what is NNT for paracetamol

A

5

452
Q

what is NNT for lifelong antihypertensives

A

NNT 3/4

453
Q

losing how much weight has same effect as taking a BP lowering tablet?

A

5-10kg

454
Q

what is the most common valvular heart disease?

A

aortic stenosis

455
Q

in aortic stenosis, symptoms occur when valve area is ___ of normal?

A

1/4th

456
Q

what is the main type of aortic stenosis

A

valvular

457
Q

what is the pathophysiology of aortic stenosis?

A

a pressure gradient develops btwn LV and aorta (incr after load)
LV function initially maintained by compensatory pressure hypertrophy
when comp. mechanisms exhausted, LV function declines

458
Q

what are some presentations of aortic stenosis

A

syncope
angina
dyspnoea
sudden death

459
Q

what are some indications for intervention in aortic stenosis?

A

any symptomatic patient with severe AS
any patient with decreasing EF
any patient undergoing CABG with moderate/severe AS

460
Q

AS is a disease of whaT?

A

ageing

461
Q

to assess severity of AS, wwyd?

A

echocardiogram

462
Q

asymptomatic AS: wwyd?

A

medical management

surveillenace

463
Q

symptomatic AS: wwyd?

A

AoV replacement

even in elderly/CHF

464
Q

what is AoV

A

aortic valve

465
Q

what is chronic mitral regurgitation?

A

back flow of blood from LV –> LA during systole

466
Q

mild MR is seen in what % of normal individuals?

A

80%

467
Q

what are some compensatory mechanisms of MR (mitral regurgitation)

A

LA enlargement
LVH
increased contractility

468
Q

what does an ECG of MR show

A

LA enlargement
AF
LV hypertrophy
(With severe MR)

469
Q

what does a CXR of MR show

A

LA enlargement

central pulmonary artery enlargement

470
Q

how can MR be managed?

A

medications - vasodilators (ACEi), rate control for AF (beta blockers, CCB)
anticoagulation in AF/fkutter
diuretics for fluid overload

471
Q

define aortic regurgitation (AR)

A

leakage of blood into LV during diastole due to ineffective coaptation of aortic cusps

472
Q

what are some causes of AR

A

bicuspid AoV

infective nedocarditis

473
Q

what are some compensatory mechanisms of AR?

A

LV dilation
LVH
progressive dilation leads to HF

474
Q

AR tends to be asymptomatic until when?

A

4th/5th decade

475
Q

what will CXR show if pt has AR

A

enlarged cardiac silhouette

aortic root enlargement

476
Q

define mitral stenosis

A

obstruction of LV inflow that prevents proper filling during diastole

477
Q

what Is the predominant cause of mitral stenosis

A

rheumatic carditis

478
Q

define carditis….

A

inflammation of the heart or its surroundings

479
Q

what is HTN

A

hypertension

480
Q

what is haemoptysis

A

coughing up blood that comes from lungs/bronchial tubes

can be small flecks to a lot of bleeding

481
Q

management of mitral stenosis is dictated by what?

A

symptoms

state of ventricular function

482
Q

what is infective endocarditis?

A

infection of heart valve(s) or other endocardial linked structures within the heart

serious n largely preventable complication of bacteraemia, usually in a patient w structurally abnormal heart valve

483
Q

what are some endocardial linked structures in the heart that aren’t valves

A

septal defects
pacemaker leads
surgical patches
etc

484
Q

which patients are predisposed to developing infective endocarditis?

A

abnormal, regurgitant or prosthetic valves

485
Q

which type of patients are most commonly affected by infective endocarditis

A

elderly
IV drug users
young w/ congenital heart disease

486
Q

a pt with infective endocarditis presents with signs of what?

A 
systemic infection (fever, sweating, etc)
may also have signs of embolisation of infected material eg stroke, PE, etc
487
Q

when is surgery required for infective endocarditis?

A

if infection cannot be cured with ABs ie recurs after treatment/CRP doesn’t fall
to treat complications eg aortic root abscess, severe valve damage
to remove infected devices
to replace valve after infection hw
to remove large vegetations before they embolism

488
Q

what is dukes criteria for infective endocarditis?

A

2 major criteria:

  • bugs grown from blood cultures
  • evidence of endocarditis on echo, or new valve leak

5 minor criteria:

  • predisposing factors
  • fever
  • vascular phenomena
  • immune phenomena
  • equivocal blood cultures
489
Q

raised ___ is almost always present in IE

A

CRP

490
Q

how can IE be treated

A

antimicrobials
treat complications eg arrhythmia, HF etc
surgery

491
Q

as an F1, if a pt has suspected IE what should u do?

A

do lots of blood cultures
always write ?IE on diff of its with sepsis, request an echo
do it even more in high risk patients

beware of pt whose INR has shot up; sometimes 1st sign of IE!

492
Q

what is an ECG aka

A

EKG

493
Q

define ecg

A

representation of the electrical events of the cardiac cycle

494
Q

what can we identify with ecgs? (6)

A

arrhythmias
myocardial Ischaemia/infarction
pericarditis
chamber hypertrophy
electrolyte disturbances ie hyper/hypokalaemia
drug toxicity (ie digoxin/drugs which prolong QT interval)

495
Q

contraction of any muscle is associated with electrical changes called what?

A

depolarisation

496
Q

what is the dominant pacemaker in the heart? n what’s its intrinsic rate?

A

SA node

60-100 bpm

497
Q

what is a back-up pacemaker and what is its rate?

A

AV node

40-60 bpm

498
Q

what is the standard calibration of an ECG?

A

25 mm/s

499
Q

electrical impulse that travels TOWARDS the electrode produces a what?

A

upright/positive deflection

500
Q

what is the path of an impulse conduction from SA node to purkinje fibres?

A

SA node > AV node > bundle of His > bundle branches > Purkinje fibres

501
Q

P wave is WHAT

A

atrial depolarisation

502
Q

QRS wave is WHAT

A

ventricular depolarisation

503
Q

T wave is WHAT

A

ventricular repolarisation

504
Q

what is the PR interval ?

A

atrial depolarisation and delay in AV junction

delay allows time for atria to contract before ventricles contract

505
Q

on ecg paper, 1 small box horizontally is how many seconds

A

0.04s

506
Q

on ecg paper, 1 large box horizontally is how many seconds

A

0.20s

507
Q

on ecg paper, 1 large box vertically is how many mV?

A

0.5mV

508
Q

standard ecg has how many leads?

A

12

509
Q

what are the 12 leads for ecg?

A

3 standard limb leads
3 augmented limb leads
6 precordial leads

510
Q

PR interval should be 120-200ms, how many lil squares?

A

3-5

511
Q

width of QRS complex should not exceed 110ms, less than how many lil squares?

A

3

512
Q

QRS complex should be dominantly upload in which leads?

A

I and II

513
Q

QRS and T waves tend to have what in the limb leads?

A

same general direction

514
Q

all waves are what in lead aVR?

A

negative

515
Q

R wave must grow from V1-?

A

V4

516
Q

S wave must grow from V1-? and then disappear in V6

A

V1-3

517
Q

ST segment should start isoelectric, except where, where it may be elevated?

A

V1/V2

518
Q

P waves should be upright where?

A

I
II
V2-6

519
Q

should be no Q wave/small Q wave (less than 0.04s in width) where?

A

I
II
V2-6

520
Q

T wave must be upright in which leads?

A

I
II
V2-6

521
Q

P wave is always negative where?

A

lead aVR

522
Q

P wave should be less than how many small squares in duration (across)?

A

3

523
Q

P wave should be less than how many small squares in amplitude (up)?

A

2.5

524
Q

where is P wave best seen

A

lead II

525
Q

how does right atrial enlargement impact P wave?

A

tall

526
Q

how does left atrial enlargement impact p wave?

A

notched (‘m’) shaped

527
Q

short PR interval happens in which syndrome?

A

wolff-parkinson-white syndrome

528
Q

long PR interval occurs when?

A

1st degree heart block

529
Q

what does isoelectric mean?

A

flat

530
Q

normal T wave is what?

A

asymmetrical (1st half having gradual slope than 2nd)

531
Q

what are abnormal t waves like

A 
symmetrical
tall
peaked
biphasic
inverted
532
Q

what is the QT interval

A

total duration of depolarisation and repolarisation

533
Q

QT interval does WHAT when HR increases?

A

decreases

534
Q

QT interval should be btwn what (time)

A

0.35-0.45s

535
Q

U waves are related to what?

A

afterdepolarisations

536
Q

U waves are more prominent in ppl w what?

A

slow heart rates

537
Q

what is the rule of 300 for HR? (regular rhythm)

A

counter number of “big boxes” btwn 2 QRS complexes, and divide 300 by this (smaller boxes w 1500)

538
Q

if there are 1 big boxes btwn 2 QRS complexes, what is the HR?

A

300 by 300/1

539
Q

if there are 3 big boxes btwn 2 QRS complexes, what is the HR?

A

100 bc 300/3

540
Q

if there are 4 big boxes btwn 2 QRS complexes, what is the HR?

A

75 bc 300/4

541
Q

what rule is it for irregular rhythm?

A

10 second rule

542
Q

what is the 10second rule

A

for irrregular rhythm

so, ecgs record 10secs of rhythm per page
COUNT no. of beats present on the ECG
multiply by 6

543
Q

QRS axis represents what?

A

overall direction of the heart’s electrical activity

544
Q

what do abnormalities of QRS axis hint at?

A

ventricular enlargement

conduction blocks

545
Q

normal QRS axis is from what?

A

-30degrees to +90degrees

546
Q

-30degree to +90degree QRS axis is referred to as what?

A

left axis deviation

547
Q

what is right axis deviation on QRS axis range?

A

+90degrees to +180degrees

548
Q

amplitude of ECG deflection is related to what?

A

mass of the myocardium

549
Q

width of ECG deflection reflects what?

A

spread of conduction

550
Q

low amplitude p wave can be linked to which conditions?

A

atrial fibrosis
obesity
hyperkalaemia

551
Q

high amplitude (tall) p wave can be linked to what?

A

right atrial enlargement

552
Q

broad noticed “bifid” p wave is linked to what?

A

left atrial enlargement

553
Q

broad QRS complex is linked to what?

A

ventricular conduction delay/BBB

554
Q

small QRS complex is linked to what?

A

obese patient
pericardial effusion
infiltrative cardiac disease

555
Q

tall QRS complexes are linked to what?

A

LVH

thin patient

556
Q

when can ST segment be elevateD?

A

in early repolarisation
MI
pericarditis
myocarditis

557
Q

excessively rapid/slow depolarisation can be arrhythmogenic. why may this be

A

congenital
drugs
electrolyte disturbances

558
Q

list some causes of bradycardia

A

conduction tissue fibrosis
ischaemia
inflammation/infiltrative disease

559
Q

in ischaemia/infarction what happens to ST segment?

A

depression

560
Q

how does Hyperkalaemia affect ecg

A

tall T waves
flattened P wave
broadening of QRS

eventually sine pattern

561
Q

how does hypokalaemia affect ECG

A

flattening of T wave

QT prolongation

562
Q

how does hypercalcaemia affect QT?

A

shortens

563
Q

how does hypocalcaemia affect QT?

A

prolongation

564
Q

when does rheumatic fever usually present?

A

2-3w after a pharyngitis episode from strep. pyogenes

(SG) Phase 2A lectures (14 decks)

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