cardiovascular system Flashcards
1
Q
atherosclerosis definition
A
pathology of arteries in which there is deposition of lipids in the arterial wall, with surrounding fibrosis and chronic inflammation
2
Q
risk factors for atherosclerosis
A
age tobacco smoking high serum cholesterol obesity diabetes hypertension family history
3
Q
distribution of atherosclerosis
A
found within peripheral and coronary arteries
focal distribution along artery length
4
Q
structure of atherosclerotic plaque
A
contains lipid, necrotic core, connective tissue, fibrous cap
eventually plaque occludes the vessel lumen causing ischaemia or ruptures, forming a thrombus
5
Q
inflammation and atherosclerosis
A
LDL’s pass in and out of arterial endothelial cells
in excess they accumulate in the arterial wall and undergo oxidation and glycation
damage to endothelial cells leads to endothelial dysfunction
6
Q
adhesion of leukocytes in atherosclerosis
A
chemoattractants are released from the endothelium and send signals to leukocytes
7
Q
progression of atherosclerosis
A
fatty streaks intermediate lesions fibrous plaques plaque rupture plaque erosion
8
Q
fatty streaks
A
appear at early age (<10)
consist of aggregations of lipid-laden macrophages and T cells in the intimal layer of the vessel wall
9
Q
intermediate lesions
A
layers:
- lipid laden macrophages (Foam cells)
- vascular smooth muscle cells
- T lymphocytes
- adhesion and aggregation of platelets to vessel wall
- isolated pools of extracellular lipid
10
Q
fibrous plaques
A
impedes blood flow
prone to rupture
covered by dense fibrous cap (collagen and elastin) laid down by smooth muscle cells that overlies lipid core and necrotic debris
may be calcified
smooth muscle cells, macrophages, foam cells, T cells
11
Q
plaque rupture
A
constantly growing and receding
the cap is resorbed and redeposited
if balance is shifted in favour or inflammatory conditions it becomes weak and it ruptures
highly thrombotic plaque constituents are exposed (basement membrane, collagen, necrotic tissue)
thrombus formation
12
Q
plaque erosion
A
fibrous cap does not disrupt
luminal surface under the clot may not have endothelium present but is smooth muscle cell rich
exposed thrombogenic subendothelial basement membrane to blood
13
Q
treatment for coronary artery disease
A
percutaneous coronary intervention- stent implantation
restenosis was a limitation
14
Q
restenosis
A
recurrence of abnormal narrowing of an artery or valve after corrective surgery
15
Q
drug elution
A
anti-proliferative and inhibits healing
works by reducing smooth muscle cell proliferation so reduced the regrowth after placement of a stent
16
Q
other useful drugs in atherosclerosis
A
aspirin- inhibits platelet cyclo-oxygenase but can cause excessive bleeding
statins- reduce cholesterol synthesis
clopidogrel- inhibitor of receptor on platelets
17
Q
ECG
A
electrocardiogram is a representation of the electrical events of the cardiac cycle
18
Q
ECGs can identify:
A
arrhythmias MIs pericarditis chamber hypertrophy electrolyte disturbances drug toxicity
19
Q
pacemakers of the heart
A
SA node
AV node
ventricular cells
20
Q
pacemakers of the heart: SA node
A
dominant pacemaker
intrinsic rate is 60-100 beats/min
21
Q
pacemakers of the heart: AV node
A
back up pacemaker
intrinsic rate of 40-60 beats/min
22
Q
pacemakers of the heart: ventricular cells
A
back up pacemaker
intrinsic rate of 20-45 beats/min
23
Q
ECG: impulse conduction
A
sinoatrial node -> AV node-> bundle of His -> bundle branches -> purkinje fibres
24
Q
ECG: calibration
A
25mm/s
0.1mV/mm
25
ECG: PQRST
p wave= atrial depolarisation
QRS= ventricular depolarisation
T wave= ventricular repolarisation
26
ECG: PR interval
atrial depolarisation and delay in AV junction (AV node to bundle of His)
27
ECG paper
horizontally:
- one small box= 0.04 seconds
- one large box= 0.2 s
vertically:
-one large box= 0.5mV
28
ECG leads
measure difference in electrical potential between two points
29
ECG: bipolar leads
two different points on the body
30
ECG: unipolar leads
one point in the body and a virtual reference point with zero electrical potential, located in the centre of the heart
31
12 lead ECG, type of leads
3 standard limb leads
| 3 augmented limb leads\6 precordial leads
32
ECG: Rule 1 (PR interval length)
PR interval should be 120-200 milliseconds (3-5 small squares)
33
ECG: Rule 2 (QRS width)
width of QRS complex should not exceed 110ms ( or 3 small squares)
34
ECG: Rule 3 (QRS in leads I and II)
QRS complex should be dominantly upright in leads I and II
35
ECG: Rule 4 ( QRS and T)
QRS and T waves tend to have same general direction in the limb leads
36
ECG: Rule 5 (waves in aVR)
all waves are negative in lead aVR
37
ECG: Rule 6 (R and S waves growing)
R wave must grow from v1 to at least V4
| S wave must grow from V1 to at least V3 and disappear in V6
38
ECG: Rule 7 (ST segment)
ST segment should start isoelectric except in V1 and V2, where it may be elevated
39
ECG: Rule 8 (P waves)
P waves should be upright in I,II and V2-V6
40
ECG: Rule 9 (Q waves)
should be no Q wave (or only a small Q , less than 0.04s in I,II and V2-6
41
ECG: Rule 10 ( T waves)
T wave must be upright in I,II and V2-6
42
ECG: P wave
- always positive in I and II but negative in aVR
- <3 small squares in duration
- <2.5 squares in amplitude
- commonly biphasic in V1
- best seen in II
43
ECG: right atrial enlargement
tall (>2.5), pointed P waves
44
ECG: left atrial enlargement
notched, bifid P wave in limb leads
| M for mitrale
45
ECG: short PR interval
wolff-parkinson-white syndrome
| accessory pathway allows early activation of the ventricle
46
ECG: long PR interval
first degree heart block
47
ECG: QRS complex
- non-pathological Q waves present in I,II aVL, V5 and V6
- pathological >25% amplitude of subsequent R wave
- R waves in V6
48
ECG: ST segment
flat- isoelectric
| elevation or depression by 1mm or more is considered normal
49
ECG: T wave
- normal is asymmetrical, first half having a more gradual slope than the second
- should be at least 1/8, but less than 2/3 of the amplitude of R wave
- abnormal= symmetrical, tall, peaked, biphasic or inverted
50
ECG: QT interval
- measured in lead aVL as it doesn't have prominent U waves
- 0.35-0.45s
- decreased when heart rate increases
- HR=70bpm, QT <0.4s
51
ECG: U wave
- related to after depolarisations, which follow repolarisations
- small, round, symmetrical and positive in lead II
- same direction as T wave
52
ECG: rule of 300 or 1500, for determining heart hate
count number of large boxes between QRS complexes and divide this into 300 (smaller boxes with 1500)
e.g. 300/4= 75bpm
53
ECG: 10 second rule for determining heart hate
ECGs record 10 seconds of rhythm per page
count number of beats present on ECG
multiply by 6
better for irregular rhythms
54
ECG: the QRS axis
represents overall direction of the hearts electrical activity
55
ECG: abnormalities in the QRS axis
ventricular enlargement
| conduction blocks
56
ECG: determining the axis
quadrant approach
| equiphasic approach
57
ECG: quadrant approach
QRS complex in leads I and aVF
determine if they are positive or negative
combination should place the axis into one of the 4 quadrants
58
ECG: equiphasic approach
most equiphasic QRS complex
identified lead lies 90 degrees away from the lead
QRS in this second lead is positive or negative
59
ECG: right bundle branch block
- RBB is blocked so septal depolarisation from left to right (what normally occurs)
- left ventricular depolarisation down LBB, no RV depolarisation yet
- RV depolarisation from the LV
60
ECG: left bundle branch block
- LBB is blocked to septal depolarisation from right to left
- RV depolarisation, no LV depolarisation yet
- LV depolarisation from RV
61
angina definition
a symptom which occurs as a consequence of restricted coronary blood flow
almost exclusively secondary to atherosclerosis
62
angina and coronary arteries
epicardial= main exterior arteries e.g. LAD, circumflex etc.
small vessels= microvessels
symptoms occur when diameter falls below 75%
63
angina pathophysiology
Oxygen supply/demand mismatch:
- impairment of blood flow by proximal stenosis
- increased distal resistance
- reduced oxygen carrying capacity of blood- anaemia
64
electro-hydraulic analogy: healthy, rest
resistance of the epicardial arteries is negligible and so the flow through the system is determined by the resistance of the microvascular vessels
flow around 3ml/s
65
electro-hydraulic analogy: healthy, exercise
more flow is needed to meet metabolic demand so microvascular resistance falls so flow increases
flow is increased 5 fold (15ml/s)
66
electro-hydraulic analogy: disease, rest
compensated
epicardial disease causes the resistance of the epicardial vessel to increase
compensation occurs by reduction of microvascular resistance, maintaining flow @ 3ml/s
67
electro-hydraulic analogy: diseased, exercise
decompensated
microvascular resistance falls to try to increase flow, however it will 'max out'
flow can therefore not meet metabolic demand- myocardium is ischaemic
68
types of angina
stable angina
unstable angina
crescendo angina
microvascular angina
69
angina non-modifiable risk factors
gender
family history
personal history
age
70
angina modifiable risk factors
```
smoking
diabetes
hypertension
hypercholesterolaemia
sedentary lifestyle
stress
```
71
angina precipitants (supply)
```
anaemia
hypoxaemia
polycythaemia
hypothermia
hypovolaemia
hypervolaemia
```
72
angina precipitants (demand)
```
hypertension
tachyarrhythmia
hyperthyroidism
hypertrophic cardiomyopathy
cold weather
emotional stress
```
73
angina incidence
```
men= 35/100,00/year
women= 20/100,000/year
```
74
angina prevalence
```
men= 5% (5000/100,000)
women= 4% (4000/100,000)
```
75
angina mortality
annual= 1.2-2.4%
cardiac death= 0.6-1.4%
MI=0.6-2.7%
76
angina history taking
```
chest pain/discomfort:
-heavy, central, tight, radiation to arms/jaw/neck
-precipitated by exertion
-relieved by rest/GTN
(from above):
-3/3= typical angina
-2/3= atypical angina
-1/3 or 0/3= non-anginal pain
```
77
angina differential diagnosis (*=important)
*pericarditis/myocarditis
*pulmonary embolism
chest infection
*aortic dissection
*gastro-oesophageal (reflux/spasm/ulceration)
*MSK
*psychological
MI??
78
angina examination
```
often seem normal or near normal
signs of risk factors:
-smoking
-diabetes
-hypertension
-high cholesterol
signs of complications
```
79
angina basic investigations: 12 lead ECG
often appear normal
| can be signs of ischaemic heart disease
80
angina basic investigations: echo
will seem normal
| can be signs of previous infarcts or give alternative diagnoses
81
angina basic investigations: pre test probability
calculates probabilities of obstructive coronary disease by categorising patients according to their gender, age and typical pain
82
angina diagnosis: treadmill test
induce ischaemia while walking uphill at a fast pace
look for ST segment depression
detects a late stage of ischaemia
unsuitable if:
- can't walk
- unfit
- BBB
- young female
83
angina diagnosis: CT angiogram
- high negative predictive value
- ideal for excluding CAD in younger, low risk individuals
- limited in tachycardia, AF or calcified disease
84
angina diagnosis: invasive angiogram
traditionally purely anatomical
| some modern functional testing techniques such as FFR (pressure gradient across stenosis)
85
angina diagnosis: stress echo
functional test
| dynamic imaging with and without pharmacological stress, looking for regional wall motion abnormalities
86
angina diagnosis: SPECT/myoview
radio-labelled tracer taken up by metabolising tissues
1st scan under stress, if perfusion defect bring back for a 2nd
a rest scan to see if its fixed defect (scar) or reversible (ischaemia)
87
angina diagnosis: cardiac MRI
same principle as stress echo
88
choosing an angina diagnosis test
- pre test probability of CAD
- invasive vs non-invasive
- allergies
- sensitivity/specificity
- radiation
- patient choice
89
angina primary prevention
```
reducing the risk of CAD and it's complications
antihypertensives
statins and lipid modulating therapies
diabetic therapy
smoking cessation
general diet advice
plenty of exercise
```
90
angina secondary prevention
risk factor modification
lifestyle changes similar to primary
pharmacological to reduce symptoms and risk of cardiovascular events
interventional such as surgery and PCI
91
angina treatment: beta blockers
1st line anti-anginal
beta 1 specific
reduce heart rate and contractility by antagonising the sympathetic nervous system
92
angina treatment: beta blocker side effects
bradycardia
tiredness
erectile dysfunction
cold hands and feet
93
angina treatment: beta blocker contraindications
```
excess bradycardia
severe heart block
severe bronchospasm
asthma
coronary spasm
```
94
angina treatment: nitrates
1st line anti-anginal
primary venodilators (systemic veins)
reduce preload of the heart and therefore the work of the heart and O2 demand
95
angina treatment: calcium channel antagonists
1st line anti-anginal
arterodilators (systemic arteries) decreasing BP and afterload of the heart
so reduce energy needed for same CO
dilating coronary arteries antagonises spasm
96
angina treatment: antiplatelets
```
e.g. aspirin
reduce events
cyclo-oxygenase inhibitor:
-decrease prostaglandin synthesis (thromboxane)
-decrease platelet aggregation
```
causes gastric ulceration
97
angina treatment: statins
HMGCoA reductase inhibitors
reduces events
reduces LDL cholesterol
98
revascularisation
restore coronary artery and increase the flow
| performed when medication fails or when risk of disease is high
99
types of revascularisation
percutaneous coronary intervention (PCI- stenting)
coronary artery bypass graft (CABG- surgery)
100
PCI pros
less invasive
convenient
repeatable
acceptable
101
PCI cons
stent thrombosis
restenosis
disease is complex
dual anti-platelet therapy
102
CABG pros
prognosis
| deals with complex disease
103
CABG cons
```
invasive
risk of stroke or bleeding
can't do it if frail
one-time treatment
length of stay
time of recovery
```
104
When to use PCI or CABG
STEMI- PCI
NSTEMI_ mainly PCI but also CABG
stable-PCI or CABG
105
acute coronary syndromes
a spectrum of acute cardiac conditions from unstable angina to MI
all associated with sudden reduced blood flow to the heart
106
acute coronary syndromes: the big five risk factors
```
smoking
hypertension
diabetes mellitus
hypercholesterolaemia
family history
```
107
acute coronary syndromes: other risk factors (not the big five)
```
CKD
peripheral arterial disease (PAD)
inflammatory conditions
ethnicity
stress
```
108
unstable angina clinical classification
cardiac chest pain at rest
cardiac chest pain with crescendo pattern
new onset angina
109
unstable angina diagnosis
history
ECG
troponin (no significant rise)
110
acute MI
supply of blood to the heart is suddenly blocked
| usually causes permanent cardiac muscle damage, although this may not be detectable in small MIs
111
ST elevation MI (STEMI)
sudden complete blockage of a coronary artery
| can usually be diagnosed on ECG at presentation
112
non ST elevation MI (NSTEMI)
severely narrowed coronary artery but it isn't 100% blocked
| retrospective diagnosis made after troponin results are available
113
Q wave MI vs non-Q wave MI
a way of defining MI on the basis of whether pathological Q waves develop on the ECG
114
non-Q wave MI
no new Q waves
poor W wave progression
ST elevation
biphasic T wave
115
Q wave MI
large Q waves
STEMI (or MIs associated with left bundle branch block) are larger infarcts so more likely to lead to pathological Q wave formation
116
MI: symptoms
cardiac chest pain:
- unremitting
- severe (can be mild or absent)
- occurs at rest
- sweating, shortness of breath, nausea/vomiting
- 1/3 occur in bed at night
117
MI: mortality
early:
- 30% outside hospital
- 15% inside hospital
late:
- 5-10% in first year
- 2-5% annually thereafter
118
MI: risk factors
```
higher age
diabetes
renal failure
left ventricular systolic dysfunction
smoking
obesity
high cholesterol
etc.
```
119
acute coronary syndromes: causes
majority= rupture of atherosclerotic plaque and consequent arterial thrombosis
uncommon= coronary vasospasm, drug abuse, artery dissection
120
formation of a thrombus
endothelial injury (exposes subendothelial collagen),
initial adhesion of platelets (GPIb on platelets binds to VWF, assisting binding to collagen),
stable adhesion and aggregation (GPIIb/IIIa, soluble platelet agonists)
121
troponin as an investigation
highly sensitive marker for cardiac muscle injury but not specific as it is a protein released in other forms of muscle injury (regulates actin-myosin contraction)
122
when is troponin also tested positive
```
gram negative sepsis
pulmonary embolism
myocarditis
heart failure
arrhythmias
cytotoxic drugs
```
123
after MI troponin
rises for 4-8 hours, peaking at 12-18 hours
| back to normal in 10-14 days
124
troponin: hsTnT, Rohe assay
make sure one measurement taken at least 6 hours after pain,
if not elevated 6 hours after pain- no MI
if it is elevated, repeat after 3 hours
if significant rise or fall (alongside other diagnostic factors) MI confirmed
125
acute coronary syndromes: initial management
999- to get to hospital fast
paramedics- look for ST elevation (contact primary PCI centre)
take aspirin 300mg immediately
pain relief
126
initial management of an MI
MONA
Morphine
Oxygen
Nitrates
Aspirin
127
acute coronary syndromes: hospital management
```
diagnosis
bed rest
oxygen therapy if hypoxic
pain relief
aspirin
beta blocker
```
128
acute coronary syndromes: pharmacological treatment
P2Y12 inhibitors
GPIIb/IIIa antagonists
anticoagulants
129
acute coronary syndromes: P2Y12 inhibitors
P2Y12 causes amplification of platelet activation
| so inhibitors used in combination with aspirin as dual anti-platelet therapy
130
acute coronary syndromes: GPIIb/IIIa antagonists
GPIIb/IIIa causes amplification of platelet activation
| used in combination with aspirin and P2Y12 inhibitors in patients undergoing PCI
131
acute coronary syndromes: anticoagulants
target formation and/or activity of thrombin
| inhibit both fibrin formation and platelet activation
132
acute coronary syndromes: pharmacological secondary prevention
```
lifelong aspirin
P2Y12 inhibitors for one year or longer in high risk patients
lifelong statins
ACE inhibitors
beta blockers
```
133
acute coronary syndromes: complications to treat after
heart failure
diuretics
implantable defibrillator
heart transplant
134
thrombosis
blood coagulation inside a vessel
135
arterial thrombosis
thrombus formed inside an artery
| high pressure system, platelet rich
136
arterial thrombosis: risks in coronary circulation
can cause an MI
137
arterial thrombosis: risks in cerebral circulation
cerebrovascular accident
| stroke
138
arterial thrombosis: risks in peripheral circulation
peripheral vascular disease
| gangrene
139
venous thrombosis
thrombus formed in a vein
| low pressure system, fibrin rich
140
venous thrombosis: DVT
thrombosis in vein lying deep below the skin
141
venous thrombosis: pulmonary embolus
dislodged thrombus occluding pulmonary vasculature
142
venous thrombosis: circumstantial causes
```
surgery
immobilisation
oestrogen (combined pill, HRT)
malignancy
long haul flights
```
143
venous thrombosis: genetic causes
factor V leiden (5%)
PT20210A (3%)
antithrombin deficiency
protein C or S deficiency
144
venous thrombosis: acquired causes
anti-phospholipid syndrome
lupus anticoagulant
hyperhomocysteinaemia
145
venous thrombosis: DVT investigations
compression ultrasound
doppler
d dimer
146
venous thrombosis: pulmonary embolus investigations
CT scan
CT pulmonary angiogram
V/Q perfusion scan
147
venous thrombosis: treatment
initially: low molecular weight heparin
after: oral warfarin for 3-6 months OR DOAC for 3-6 months
148
venous thrombosis: prevention
thromboprophylaxis: any measure taken to prevent thrombosis such as low molecular weight heparin or early mobilisation and good hydration
149
anticoagulant pharmacology
```
heparin
low molecular weight heparin
aspirin
warfarin
new oral anticoagulant drugs
```
150
anticoagulant pharmacology: heparin
glycosaminoglycan
binds directly to antithrombin and increases its activity
indirect thrombin inhibitor
151
anticoagulant pharmacology: low molecular weight heparin
smaller molecule, less variation in dose and renally excreted
once daily, weight adjusted dose given subcutaneously
152
anticoagulant pharmacology: aspirin
inhibits cyclo-oxygenase irreversibly
| inhibits thromboxane formation and hence platelet aggregation
153
anticoagulant pharmacology: warfarin
```
orally active
prevents synthesis of active factors II, VII, IX and X
antagonist of vitamin K
prolongs prothrombin time
long half life (36 hours)
```
154
anticoagulant pharmacology: new oral anticoagulant drugs
```
NOAC/DOAC
orally active like aspirin and warfarin
directly acting on factor II or X
shorter half life
no blood tests or monitoring
```
155
deep vein thrombosis and pulmonary embolism prevalence
25,000 a year die from these in the uk
50% preventable
premature mortality
156
deep vein thrombosis: symptoms
non-specific
| pain and swelling in the leg
157
deep vein thrombosis: signs
tenderness
warmth
discolouration
oedema
158
pulmonary embolism: symptoms
breathlessness
pleuritic chest pain
rapid breathing
hypotension
159
pulmonary embolism: signs
```
tachycardia
tachypnoea
pleural rub
cyanosis
right heart strain
```
160
inherited cardiac conditions: cardiomyopathies
refers to primary heart muscle disease and is often genetic
161
inherited cardiac conditions: hypertrophic cardiomyopathy
constriction of ventricles due to hypertrophy of the cardiac muscle- this can also block small coronary arteries
caused by sarcomere protein gene mutations
1 in 500 people
the fibrosis is non conduction so electrical impulses travel around, causing arrhythmias
162
inherited cardiac conditions: dilated cardiomyopathy
dilated ventricles due to thinner walls
cytoskeletal gene mutation
systole is ineffective
presents with heart failure symptoms
163
inherited cardiac conditions: arrhythmogenic cardiomyopathy
significant rhythm disturbance
desmosome gene mutations
myocardium replaced with fibrous and fatty tissue- causing arrhythmias
164
inherited cardiac conditions: channelopathy
inherited arrhythmia
caused by ion channel protein gene mutations (K+, Na+ or Ca2+)
structurally normal heart
recurrent syncope
165
inherited cardiac conditions: channelopathy ECG
long QT
short QT
brugada (ST elevation)
tachycardia triggered by adrenaline
166
inherited cardiac conditions: sudden arrhythmic death syndrome (SADS)
usually refers to normal heart and arrhythmia
167
inherited cardiac conditions: familial hypercholesterolaemia
inherited abnormality of cholesterol metabolism
| leads to serious premature coronary and other vascular disease
168
inherited cardiac conditions: aortic aneurysm
aortovascular syndromes include marfan, loeys-dietz and vascular ehler danlos
169
inherited cardiac conditions: family testing
ICCs are usually dominantly inherited- 50% risk of inheritance
risk needs to be assessed for each individual
170
tamponade
compression of the heart by an accumulation of fluid in the pericardial sac
causes hypotension
171
pericardial effusion
too much fluid within the pericardium
172
chronic pericardial effusion
allows adaption of the parietal pericardium
| compliance reduces the effect on diastolic filling of the chambers- rarely causes tamponade
173
acute pericardial effusion
effusion onset is quick and parietal pericardium can't adapt
| volume needed to cause cardiac tamponade is lower
174
acute pericarditis
inflammatory pericardial syndrome with or without effusion
175
acute pericarditis: clinical diagnosis
2/4 at least of the following:
- chest pain (85-90%)
- friction rub(33%)
- ECG changes(60%)
- pericardial effusion (up to 60%)
176
pericarditis: epidemiology
80-90% is idiopathic
| 5% of A&E attendances with chest pain
177
pericarditis: aetiology
```
viral
bacterial
autoimmune
neoplastic
metabolic
traumatic and iatrogenic
other
```
178
pericarditis: viral cause
most common cause in developed world
| enterovirus, herpes virus, adenovirus
179
pericarditis: caused by TB
90% HIV +ve in developed countries
| 17-40% constrictive pericarditis
180
pericarditis: clinical presentation
severe, sharp pleuritic chest pain, with rapid onset- relieved by sitting forward, exacerbated by lying down
dyspnoea
cough
181
pericarditis: differential diagnosis
```
pneumonia
pulmonary embolus
gastro-oesophageal reflux
MI
aortic dissection
pneumothorax
```
182
pericarditis: investigations
```
clinical examination
ECG
bloods
chest xray
echo
```
183
pericarditis: clinical examination
pericardial rub
sinus tachycardia
fever
beck's triad: hypotension, muffled heart sounds, raised jugular venous pressure
184
pericarditis: ECG
diffuse ST segment
concave ST segment
no reciprocal ST depression
PR depression
185
pericarditis: bloods
FBC- modest WBC increase
ESR
troponin
186
pericarditis: chest xray
often normal in idiopathic
pneumonia
modest enlargement of cardiac silhouette
187
pericarditis: management
sedentary activity until resolution of symptoms
NSAIDs
aspirin
colchicine
188
pericarditis: prognosis
have good long term prognosis
15-30% develop recurrence
colchicine reduced recurrence rate by 50%
189
pericarditis: major complications
```
fever >38 degrees
subacute onset
large pericardial effusion
cardiac tamponade
lack of response to aspirin or NSAIDs after a week of therapy
```
190
pericarditis: minor complications
myopericarditis
immunosuppression
trauma
oral anticoagulant therapy
191
heart failure
- a state where the heart is unable to pump enough blood to satisfy the needs of metabolising tissues
- a syndrome and not a diagnosis on its own
192
heart failure incidence/prevalence
incidence= 63,000 cases/year (29,000 females, 34,000 males)
prevalence= 878,000 total ( 405,000 female, 473,000 male)
mean age= 71-76 years
193
heart failure aetiology
most common cause= myocardial dysfunction
| others= hypertension, cardiomyopathy, valvular
194
heart failure risk factors
```
old age
african decent
men before women reach menopause
obesity
people who previously have had an MI
```
195
heart failure pathophysiology
when the heart begins to fail RAAS and sympathetic nervous system try to compensate to maintain cardiac output
However when heart failure progresses these mechanisms are overwhelmed- decompensation
196
heart failure pathophysiology mechanisms
venous return- preload
outflow resistance- afterload
sympathetic system activation
RAAS
197
systolic failure
reduced ejection fraction
inability of the left ventricle to contract normally, resulting in a decrease in cardiac output
caused by ischaemic heart disease, MI and cardiomyopathy
198
diastolic failure
preserved ejection fraction
inability of the ventricles to relax and fill fully, decreasing stroke volume and so decreasing CO
caused by chronic hypertension which increases afterload so heart pumps against more resistance
199
acute heart failure
new onset or decompensation of chronic heart failure
characterised by pulmonary and/or peripheral oedema
w/ or w/o signs of peripheral hypotension
200
chronic heart failure
develops slowly
venous congestion is common
arterial pressure well maintained until quite late
201
heart failure symptoms
three cardinal symptoms= shortness of breath, fatigue ankle oedema
cold peripheries
increased weight
dyspnoea especially when lying flat
202
heart failure signs
```
tachycardia
displaced apex beat
added heart sounds and murmurs
cyanosis
hypertension
```
203
new york heart association classification for heart failure
```
class I: no limitation, asymptomatic
class II: slight limitation, mild heart failure
class III: marked limitation, moderate HF
class IV: inability to carry out physical activity without discomfort, severe HF
```
204
heart failure treatment
```
lifestyle changes
diuretics
ACE inhibitors
beta blockers
digoxin
revascularisation
surgery
heart transplant
```
205
causes of acute decompression of chronic heart failure
```
uncorrected hypertension
obesity
infection
arrhythmias
excess alcohol
NSAIDS
```
206
heart failure complications
```
renal dysfunction
rhythm disturbances
DVT/PE
LBBB and bradycardia
hepatic dysfunction
```
207
heart failure investigations:
blood tests
chest xray
ECG
echo
208
heart failure investigations: blood tests
brain natriuretic peptide- secreted by myocardium in stress
FBC
U&E
epinephrine, vasopressin and renin= high
209
heart failure investigations: chest xray
alveolar oedema
cardiomegaly
dilated upper lobe vessels of lungs
pleural effusions
210
heart failure investigations: ECG
shows underlying causes
if ECG and BNP are normal then heart failure is unlikely
if both abnormal then do an echo
211
heart failure investigations: echo
assess cardiac chamber dimension
| look for wall motion abnormalities
212
infective endocarditis
infection of heart valves or other endocardial lined structures w/i the heart (septal defects, pacemaker leads)
213
infective endocarditis: types
left sided native (mitral, aortic)
left sided prosthetic
Right sided, rarely prosthetic as rare to have those valves replaced
214
infective endocarditis: pathogenesis
have an abnormal valve
regurgitant or prosthetic valves are more likely to get infected
introduce infectious material into blood stream
215
infective endocarditis: epidemiology
```
young= rheumatic heart disease or drug abusers
elderly= weakened immune system
congenital heart disease
anyone with prosthetic heart valves
M:F= 2:1-9:1
```
216
infective endocarditis: incidence
0.6-6/100,000 people/year
| 10 year survival= 60-90%
217
infective endocarditis: presentation
signs of systemic infection (fever, sweats)
embolisation (stroke,pulmonary embolus, bone infections, MI)
valve dysfunction (heart failure)
218
infective endocarditis: diagnosing criteria
definite IE= 2 major, 1 major+3minor or 5 minor
possible IE= 1 major, 1 major+3minor or 5 minor
```
major= bugs grown from culture, evidence of endocarditis on echo
minor= predisposing factors, fever, vascular or immune phenomena and equivocal blood cultures
```
219
infective endocarditis: echos
TTE= transthoracic echo, safe, non invasive, no discomfort, but poor images so lower sensitivity
TOE=transoesophageal echo, excellent pictures, uncomfortable, risk of perforation or aspiration
220
infective endocarditis: peripheral signs of spread and embolism
bruises, infarcts (10-15%)
splinter haemorrhages
osler's nodes (small, tender, purple nodules on the pulp of digits)
roth spots on fundoscopy
221
infective endocarditis: diagnosis
bloods
ECG
TTE/TOE
222
infective endocarditis: blood tests
cultures can be negative in 2-5% of patients
certain organisms require longer incubation
WBC rarely helpful
C-reactive protein (inflammation marker) is almost always present
223
infective endocarditis: diagnosis with TTE/TOE
TTE is crucial for detecting vegetation but sensitivity is still only 60%
TOE sensitivity is 90-95%
224
infective endocarditis: treatment
antimicrobials for 6 weeks depending on the culture
treat complications such as heart failure, abscess drainage, stroke rehab
surgery
225
infective endocarditis: surgery
- when the infection cannot be cured with antimicrobials
- to fix complications such as aortic root abscess or valve damage
- remove infected devices
- remove large vegetations before they embolise
226
infective endocarditis: prevention
NICE recommends not to give prophylaxis
ESC consider prophylaxis in high risk patients
talk to patient and dentist
227
tetralogy of Fallot
ventricular septal defect
pulmonary stenosis
hypertrophy of right ventricle
overriding aorta
228
tetralogy of Fallot: physiology
the stenosis of RV outflow leads to RV being higher pressure than the left
blue blood passes from RV to LV so patients are blue
229
tetralogy of Fallot: epidemiology
10% of all congenital heart defects
1/1000 live births
15% have associated genetic abnormality
230
tetralogy of Fallot: treatment
surgical repair
a shunt between R subclavian artery and R pulmonary artery to increase pulmonary blood flow
often get pulmonary valve regurgitation in adult life so redo surgery required
231
ventricular septal defects
abnormal connection between the two ventricles
common- 20% of all congenital heart defects
1-4/1000 of live births
232
large ventricular septal defects: physiology
very high pulmonary blood flow in infancy
breathless, poor feeding, failure to thrive
require fixing in infancy
can lead to eisenmengers syndrome
233
small ventricular septal defects: physiology
small increase in pulmonary blood flow only
asymptomatic
endocarditis risk
need no intervention
234
large ventricular septal defects: clinical signs
```
small breathless skinny baby
increased respiratory rate
tachycardia
big heart on chest xray
murmur varies in intensity
```
235
small ventricular septal defects: clinical signs
```
loud systolic murmur
thrill
well grown
normal heart rate
normal heart size
```
236
eisenmenger's syndrome
pathophysiology:
- high pressure pulmonary blood flow
- damages delicate pulmonary vasculature
- RV pressure increases
- shunt direction reverses and patient becomes blue
high mortality rate
237
atrial septal defects
abnormal connection between the two atria
common
often present in adulthood
238
atrial septal defects: physiology
slightly higher pressure in LA than RA
shunt left to right
therefore not blue
increase flow into right heart and lungs
239
large atrial septal defects: physiology
significant increased flow through the right heart and lungs in childhood
right heart dilation
SOB on exertion
increased chest infections
240
small atrial septal defects: physiology
small increase in flow
no right heart dilation
no symptoms
leave alone
241
atrial septal defects: clinical signs
pulmonary flow murmur
fixed split-second heart sound
big pulmonary arteries big heart on chest xray
242
atrial septal defects: treatment
surgical closure
| percutaneous (key hole) closure
243
atrioventricular septal defects
2/10,000 live births
common in Down's syndrome
hole in the centre of the heart
interatrial and/or interventricular
244
complete atrioventricular septal defects: physiology
```
breathless neonate
poor weight gain
poor feeding
torrential pulmonary blood flow
needs repair or PA band in infancy
repair is surgically challenging
```
245
partial atrioventricular septal defects: physiology
can present in late adulthood
presents like a small VSD/ ASD
may be left alone if there is no right heart dilation
246
patent ductus arteriosus: signs
continuous machinery murmur
if large, big heart breathless
eisenmenger's syndrome
247
large patent ductus arteriosus: physiology
torrential flow from aorta to pulmonary arteries in infancy
breathless, poor feeding, failure to thrive
common in prem babies
need surgical closure
248
small patent ductus arteriosus: physiology
little flow from the aorta to Pas
usually asymptomatic
murmur found incidentally
endocarditis risk
249
patent ductus arteriosus: treatment
surgical or percutaneous
local anaesthetic
venous approach
low risk of complications
250
coarctation of the aorta
narrowing of the aorta at the site of insertion of the ductus arteriosus
perfusion to lower body is reduced
251
severe coarctation of the aorta
complete or almost complete obstruction to aortic flow
collapse with heart failure
needs urgent repair
252
mild coarctation of the aorta
presents with hypertension
incidental murmur
should be repaired to prevent problems long term
253
coarctation of the aorta: clinical signs
right arm hypertension
bruits over scapulae and back from collateral vessels
murmur
254
coarctation of the aorta: long term problems
hypertension
re-corarctation requiring repeat intervention
aneurysm formation
255
coarctation of the aorta: treatment
surgical vs. percutaneous repair
256
bicuspid AV
```
has 2 cusps instead of the typical 3
1-2% of population
M>F
severely stenotic in infancy or childhood
degenerate quicker than normal valves
```
257
pulmonary stenosis
narrowing of the outflow of the right ventricle
8-12% of all congenital heart defects
valvar, sub valvar, supra valvar, branch
258
severe pulmonary stenosis
```
right ventricular failure as neonate
collapse
poor pulmonary blood flow
RV hypertrophy
tricuspid regurgitation
```
259
mild pulmonary stenosis
well tolerated for many years
| right ventricular hypertrophy
260
pulmonary stenosis: treatment
balloon valvuloplasty
open valvotomy
open trans-annular patch
shunt
261
atrial septal defects: primum
defect level of tricuspid and mitral valves
262
atrial septal defects: secundum
enlarged foramen ovale, inadequate growth of septum secundum, or excessive absorption of septum primum
263
atrial septal defects: sinus venosus
defect involves venous inflow of either SVC or IVC
264
hypertension: prevalence
>75 year olds have 50% risk of hypertension
middle age have 10-30% risk
young have 5% risk
265
hypertension: main causes
85% of cases caused by genetics and lifestyle (obesity, excessive salt, alcohol)
266
hypertension: Conn's syndrome
overproduction of aldosterone due to unilateral adrenal adenoma
results in sodium and water retention which increases BP
267
drugs causing hypertension
```
NSAIDS
combined oral contraceptive
corticosteroids
ciclosporin
cold cures
SNRI antidepressants
```
268
other causes of hypertension
```
renal parenchymal disease
renovascular disease
endocrine
coarctation or aorta
pregnancy
sleep apnoea
```
269
hypertension: investigation
eye exam- only area where blood vessels visible so can see damage caused by hypertension
270
hypertension: calcium channel blockers
inhibit the opening of voltage-gated calcium channels in vascular smooth muscle, reducing calcium entry and thereby calcium available for muscle contraction
271
hypertension: ACE inhibitors
prevents the generation of angiotensin II from angiotensin I
| angiotensin II is vasoconstrictor that stimulates aldosterone release enhancing reabsorption of sodium
272
hypertension: angiotensin receptor blockers
blocks the action of angiotensin II at peripheral receptors
273
hypertension: thiazide diuretics
inhibit sodium reabsorption at distal tubule, reducing extracellular fluid volume which is elevated in hypertension
274
hypertension: beta-blockers
resistant hypertension may also be treated using alpha or beta adrenoceptor antagonists
275
BP response expected from 50mg atenolol
decrease in systolic or 10mmHg
276
white coat hypertension
anxiety when seeing a doctor so BP increases
| 95% of population BP is higher when in a clinical setting
277
how to measure BP at home
ambulatory BP monitoring: patient wears for 24 hours and measure every 20 mins
semi-automated device:
patients measures twice in morning and evening for a week
278
hypertension thresholds
clinical= 140/90
| home=135/85
279
stages of hypertension
stage 1= low risk
clinical=140-160/90-100
home=135-150/85-95
stage 2=high risk
clinical >160/100
home= >150/95
280
illnesses caused by hypertension
```
heart failure
stroke
MI
renal failure
retinopathy
```
281
lifestyle changes to lower blood pressure
```
weight loss
alcohol intake reduction
salt intake reduction
smoking cessation
medication review
stress reduction
```
282
aortic stenosis
normal valve area= 3-4cm2
| symptoms occur when valve area is 1/4 of normal
283
congenital aortic stenosis
occur with unicuspid, bicuspid or tricuspid valves
284
acquired aortic stenosis
degenerative calcification
| rheumatic heart disease
285
aortic stenosis: pathology
pressure gradient develops between the left ventricle and the aorta
LV function initially maintained by compensation but when these mechanisms are exhausted the function declines
286
aortic stenosis: presentation
syncope
angina
dyspnoea on exertion
287
aortic stenosis: signs
slow rising carotid pulse
soft or absent second heart sound
ejection systolic murmur
288
aortic stenosis: natural history
```
onset of symptoms is poor prognostic indicator
mild to sever:
8% in 10 years
22% in 22 years
38% in 25 years
```
289
aortic stenosis: prognosis
angina and AS= 50% survive 5 years
syncope+AS= 50% survive 3 years
HF+AS mean survival <2 years
290
aortic stenosis: investigations
echo- measures left ventricular size and function and valve area
291
mild aortic stenosis: area and velocity
area >1.5cm2
| velocity= 2.6-3 m/s
292
moderate aortic stenosis: area and velocity
1-1.5cm2
| 3-4m/s
293
severe aortic stenosis: area and velocity
<1cm2
| >4m/s
294
aortic stenosis: management
dental hygiene
IE prophylaxis
surgical replacement
transcatheter aortic valve implantation
295
aortic stenosis: indications for intervention
symptomatic patients
any patient with decreasing EF
patients undergoing CABG with severe AS
296
mitral regurgitation
back flow from LV to LA during systole
297
mitral regurgitation: aetiology
myxomatous degeneration
ischaemic MR
rheumatic heart disease
infective endocarditis
298
mitral regurgitation: pathophysiology
pure volume overloads
compensation= left atrial enlargement, increased contractility
RV dysfunction due to pulmonary hypertension
299
mitral regurgitation: signs and symptoms
soft s1 and pan-systolic murmur (auscultation)
exertion dyspnoea
heart failure
300
mitral regurgitation: natural history
compensatory phase= 10-15 years
| patients with asymptomatic sever MR have 5%/year mortality rate
301
mitral regurgitation: investigations
ECG
CXR
ECHO
302
mitral regurgitation: management
medication
serial echo
IE prophylaxis
surgery
303
aortic regurgitation
leakage of blood from aorta into LV during diastole
304
aortic regurgitation: aetiology
bicuspid aortic valve
rheumatic
infective endocarditis
305
aortic regurgitation: pathophysiology
combined pressure and volume overload
| compensatory mechanisms
306
aortic regurgitation: physical examination
wide pulse pressure
| hyperdynamic and displaced apical pulse
307
aortic regurgitation: natural history
asymptomatic until 4th/5th decade
| rate of progression= 4-6% a year
308
aortic regurgitation: investigations
CXR
| echo
309
aortic regurgitation: management
IE prophylaxis
vasodilators
serial echos
surgical treatment
310
mitral stenosis
obstruction of LV inflow that prevents proper filling during diastole
normal area=4.6cm2
symptoms begin at areas <2cm2
311
aetiology
rheumatic heart disease=77-99% of all cases
IE=3.3%
mitral annular calcification =2.7%
312
mitral stenosis: pathophysiology
progressive dyspnoea (70%)
increased transmitral pressures
right heart failure symptoms
313
mitral stenosis: natural history
disease of plateaus:
mild= 10 years after initial RHD
moderate= 10 years later
severe= 10 years later
314
mitral stenosis: signs
right sided heart failure
| pinkish-purple patches on cheeks due to vasoconstriction- mitral facies
315
mitral stenosis: heart sounds
diastolic murmur
| loud opening S1 snap
316
mitral stenosis: investigations
ecg
cxr
echo
317
mild mitral stenosis: valve area
>1.5cm2
318
moderate mitral stenosis: valve area
1-1.5cm2
319
severe mitral stenosis: valve area
<1cm2
320
mitral stenosis: management
serial echos
beta-blockers and diuretics
IE prophylaxis
surgery
