CVS Flashcards
(445 cards)
1
Q
What is an ECG?
A
representation of the electrical events of the cardiac cycle
2
Q
What 6 things can you identify with an ECG?
A
- arrhythmias
- myocardial ischaemia and infarction
- pericarditis
- chamber hypertrophy
- electrolyte disturbances
- drug toxicity (digoxin/ drugs which prolong QT interval)
3
Q
What is the SA node?
A
- dominant pacemaker
- intrinsic rate 60-100bpm
- fastest depolarising tissue
4
Q
What is the normal heart rate?
A
60-100bpm
5
Q
What is the AV node?
A
- back up pacemaker
- intrinsic rate 40-60 bpm
6
Q
What are ventricular cells?
A
- back up pacemaker
- intrinsic rate 20-45bpm
7
Q
What is the impulse conduction pathway?
A
sinoatrial node - atrioventricular node - bundle of His - bundle branches - purkinje fibres
8
Q
AV node delay at beginning of a normal ECG trace - how long is it?
A
0.12 - 0.2 s
9
Q
How long is atrial depolarisation (ECG) ?
A
0.08 - 0.1 s
10
Q
How long is ventricular depolarisation (ECG)?
A
0.06 - 0.1 s
11
Q
P wave
A
- atrial depolarisation
- seen in every lead except aVR
12
Q
PR interval
A
- time taken for atria to depolarise and electrical activation to get through AV node
13
Q
QRS complex
A
- ventricular depolarisation
- still called QRS even if Q and/or S missing depending on what lead
14
Q
ST segment
A
interval between depolarisation and repolarisation
15
Q
T wave
A
ventricular repolarisation
16
Q
Tachycardia
A
increased heart rate
17
Q
Bradycardia
A
decreased heart rate
18
Q
Dextrocardia
A
heart on right side of chest instead of left
19
Q
Acute anterolateral myocardial infarction
A
ST segments are raised in anterior (V3-V4) and lateral (V5-V6) leads
20
Q
Acute inferior MI
A
ST segments raised in inferior (II, III, aVF) leads
21
Q
Can atrial repolarisation be seen on an ECG?
A
No- not usually seen, occurs at same time as QRS complex so hidden
22
Q
IMPORTANT - ECG paper, value of one small box horizontally?
A
0.04s / 40ms
23
Q
IMPORTANT - ECG paper, value of one large box horizontally?
A
0.20s
24
Q
IMPORTANT - ECG paper, value of one large box vertically?
A
0.5mV
25
Left ventricle definition?
- Palpated in 5th intercostal space and mid clavicular line
| - Responsible for apex beat
26
Stroke volume definition?
The volume of blood ejected from each ventricle during systole
27
Cardiac output definition?
The volume of blood each ventricle pumps as a function of time eg litres per min
28
IMPORTANT - cardiac output equation
CO (L/min) = stroke volume (L) x heart rate (bpm)
29
Total peripheral resistance definition?
The total resistance to flow in systemic blood vessels from beginning of aorta to vena cava (arterioles provide most resistance)
30
Preload definition?
The end diastolic volume that stretches the right or left ventricle of the heart to its greatest dimensions under variable physiologic demand
31
End diastolic volume definition?
How much blood is in the ventricles before it pumps
32
When veins dilate does this result in an increase or decrease in preload?
Decrease in preload - venous return has decreased
33
Afterload definition
The pressure the left ventricle must overcome to eject blood during contraction (dilate arteries = decrease afterload)
34
Contractility definition
force of contraction and change in fibre length - how hard the heart pumps (when muscle contracts myofibrils stay same length but sarcomere shortens - force of heart contraction that is independent of sarcomere length
35
Elasticity definition
myocardial ability to recover normal shape after systolic stress
36
Diastolic dispensibility definition
the pressure required to fill the ventricle to the same diastolic volume
37
Compliance definition
how easily the heart chamber expands when filled with blood volume
38
Starlings law ?
Force of contraction is proportional to the end diastolic length of cardiac muscle fibre - the more ventricle fills harder it contracts
39
At rest is the cardiac muscle at optimal length?
No, force of contraction decreased, inefficient
40
What happens when there is increased venous return to the heart?
increase venous return - increase end diastolic volume - increase preload - increase sarcomere stretch - increase force of contraction - increase stroke volume
41
What happens to venous return when standing?
Decreases venous return due to gravity - cardiac output decreases - drop in blood pressure - stimulating baroreceptors to increase blood pressure
42
Heart sound S1 ?
mitral and tricuspid valve closure
43
Heart sound S2?
aortic and pulmonary valve closure
44
Heart sound S3?
- in early diastole
- during rapid ventricular filling
- normal in children, pregnant women
- associated with mitral regurgitation and heart failure
45
Heart sound S4?
- 'gallop'
- in late diastole
- produced by blood being forced into a stiff, hypertrophic ventricle
- associated with left ventricular hypertrophy
46
Which coronary arteries commonly develop atheroscleroses?
- right coronary artery
- left anterior descending
- circumflex
47
7 risk factors for atherosclerosis?
- age
- family history
- high serum cholesterol
- tobacco (endothelium erosion)
- obesity (more pericardial fat, thus increase inflammation)
- diabetes (hyperglycaemia damages endothelium)
- hypertension
48
Distribution of atherosclerotic plaques?
- Peripheral and coronary arteries
| - Focal distribution along artery length
49
An atherosclerotic plaque is a complex lesion of what 4 things?
- lipid
- necrotic core
- connective tissue
- fibrous 'cap'
50
2 serious consequences of an atherosclerotic plaque?
- occlude vessel lumen - restriction of blood flow - angina
| - rupture - thrombus formation - death
51
atherosclerosis formation - stage 1
initiated by injury to endothelial cells, leads to endothelial dysfunction
52
Atherosclerosis formation - stage 2
chemoattractants released from endothelium to attract leucocytes which accumulate and migrate into vessel wall
53
What are chemoattractants?
Chemicals which attract leucocytes. They are released from the site of injury and a conc gradient is produced
54
3 inflammatory cytokines found in plaques?
- IL-1 (key one)
- IL-6
- IFN-gamma
55
Atherosclerosis - fatty streaks
- earliest lesion of atherosclerosis
- appear at very early age (less than 10)
- aggregations of lipid laden macrophages and T lymphocytes within intimal layer of vessel wall
56
Atherosclerosis - intermediate lesions
```
layers of
lipid laden macrophages (foam cells)
vascular smooth muscle cells
T lymphocytes
(there is adhesion and aggregation of platelets to vessel wall)
```
57
Atherosclerosis - fibrous plaques/ advanced lesions
- impede blood flow
- prone to rupture
- covered by dense fibrous cap of extracellular matrix proteins - collagen (strength) - elastin (flexibility) laid down by smooth muscle cells that overly lipid core and necrotic debris
- may be calcified
58
Atherosclerosis - fibrous plaques/ advanced lesions contain?
- smooth muscle cells
- macrophages and foam cells
- T lymphocyte
- Red cells
- filled with fibrin
59
What is a foam cell?
lipid laden macrophage
60
Plaque rupture
- plaque constantly growing and receding
- fibrous cap needs to be resorbed and redeposited in order to be maintained
- if balance shifts eg in favour of inflammatory conditions (increase enzyme activity) cap weakens, plaque ruptures
- basement membrane, collagen, necrotic tissue exposure, haemorrhage of vessel within plaque
- thrombus formation, vessel occlusion
61
Angina - definition
- Chest pain or discomfort as a result of reversible myocardial ischaemia
- Usually implies narrowing one/more coronary arteries
- Usually exacerbated by exertion and relieved by rest
62
2 types of angina
- Stable angina - induced by effort, relieved by rest
- Unstable (crescendo) angina - recent (less 24hrs) onset OR deterioration stable angina (symptoms frequently occurring at rest) OR angina increasing frequency or severity, minimal exertion, at rest - form of acute coronary syndrome
63
3rd rare type of angina?
Prinzmetal's angina - caused by coronary artery spasm
64
Angina epidemiology
Myocardial ischaemia resulting in angina occurs when mismatch between blood supply and metabolic demand - due to:
- atheroma/ stenosis coronary arteries
- valvular disease
- aortic stenosis
- arrhythmia
- anaemia
65
Most common cause of angina?
atheroma/ stenosis of coronary arteries thereby impairing blood flow
66
What causes the pain in angina?
Ischaemic metabolites eg adenosine stimulate nerve endings and produce pain
67
Is angina more common in men or women?
Men
68
Angina 9 risk factors?
- smoking
- sedentary lifestyle
- obesity
- hypertension
- diabetes mellitus
- family history
- genetics
- age
- hypercholesterolaemia
69
Pathophysiology of angina
atherosclerosis developing narrowing of coronary arteries that results in ischaemia and thus pain
70
pathophysiology of angina - initiation
- endothelial dysfunction/ injury at sites of sheer/ damage --> lipid accumulation at sites impaired endothelial barrier
- local cellular proliferation, incorporation oxidised lipoproteins
- mural thrombi on surface - subsequent healing, repeat of cycle
71
pathophysiology of angina - adaptation
- as plaque progresses to 50% vascular lumen size, vessel no longer compensate by remodelling, becomes narrowed
- drives variable cell turnover within plaque, new matrix surfaces, degradation matrix
- may progress to unstable plaque
72
pathophysiology of angina - clinical stage
- plaque continues encroach upon lumen, risk of haemorrhage/ exposure tissue to HLA-DR antigens, may stimulate T cell accumulation
- rives inflamm reaction to part of plaque
- complications:ulceration, fissuring, calcification, aneurysm change
73
pathophysiology angina - pathophysiological stages - fatty streak
- foam cells
| - smooth muscle cells filled with fat
74
pathophysiology of angina - pathophysiological stages - intimal cell mass
collections of muscle cells and connective tissue without lipids - 'cushions'
75
pathophysiology of angina - pathophysiological stages - the atheromatous plaque
- distorted endothelial surface with lymphocytes, macrophages, smooth muscle cells, variably complete endothelial surface
- local necrotic and fatty matter, scattered foam cells
- evidence local haemorrhage: iron deposition, calcification
- complicated plaques: calcification, mural thrombus- vulnerable to rupture
76
what is a complicated plaque?
show calcification and mural thrombus (making them vulnerable to rupture)
77
Angina - complications of plaque rupture
- acute occlusion due to thrombus
- chronic narrowing vessel lumen with healing of the local thrombus
- aneurysm change
- embolism of thrombus/ plaque lipid content
78
Angina - clinical presentation
- central chest tightness/heaviness
- provoked by exertion, especially after meal, cold windy weather, anger, excitement
- relieved by rest/ GTN spray
- pain may radiate to one/both arms, neck, jaw, teeth
- dyspnoea (difficult breathing), nausea, sweaty, faintness
79
Angina scoring
1. Central, tight pain, radiating to arms, jaw, neck
2. Precipitated by exertion
3. Relieved by rest, GTN spray
3/3 typical angina
2/3 atypical angina
1/3 non-anginal pain
80
Angina - differential diagnosis
- pericarditis/myocarditis
- pulmonary embolism
- chest infection
- dissection of aorta
- GORD
81
Angina - diagnosis - 5 things
- 12 lead ECG
- treadmill test/ exercise ECG
- CT scan calcium scoring
- SPECT/myoview
- cardiac catheterisation
82
angina diagnosis - 12 lea ECG
- often normal
- may show ST depression
- flat or inverted T waves
- look for signs of past MI
83
angina diagnosis - treadmill test/exercise ECG
- ECG and run on treadmill uphill - trying to induce ischaemia
- monitor how long able to exercise for
- ST segment depression - sign of late stage ischaemia
- unsuitable for many patients cant walk, very unfit, exercise induced bundle branch block in young females
84
angina diagnosis - CT scan Calcium scoring
CT heart, if atherosclerosis calcium will light up white - significant calcium would indicate angina
85
angina diagnosis - SPECT/myoview
- radio labelled tracer injected into patient
- taken up by coronary arteries (good blood supply) so will show up here
- little blood supply - areas will not light up
- no light up after exercise indicative of myocardial ischaemia
86
angina - treatment
- modify risk factors (smoking, exercise, weight loss)
- treat underlying conditions
- pharmacological
- revascularisation
87
What pharmacological interventions can be used to treat angina?
- Aspirin
- Statins
- Beta blockers
- Glyceryl Trinitrate spray
- Calcium ion channel antagonists
88
Angina - aspirin
- antiplatelet - inhibits platelet aggregation in coronary arteries - avoiding platelet thrombus
- to reduce events
- eg salicylate
- COX inhibitor - reduced prostaglandin synthesis inc thromboxane A2
- side effects - gastric ulceration
89
Angina - statins
- HMG- CoA reductase inhibitors - reduces cholesterol produced by liver
- reduces events and LDL-cholesterol
- anti-atherosclerotic
90
Angina - betablockers
```
1st line antianginal
- reduces force of contraction of heart
- BISOPROLOL, ATENOLOL
- act on B1 receptors in heart as part of adrenergic sympathetic pathway
B1 - Gs - cAMP to ATP - contraction
```
91
angina - what 3 things do betablockers reduce?
- heart rate (negatively chronotropic)
- left ventricle contractility (negatively inotropic)
- cardiac output
92
angina - betablockers - side effects
- tiredness
- nightmares
- bradycardia
- erectile dysfunction
- cold hands and feet
DO NOT GIVE in asthma, heart failure/heart block, hypotension, bradyarrhythmias
93
angina - glyceryl trinitrate spray
1st line antianginal
- nitrate that is a venodilator
- dilates systemic veins - reducing venous return to right side of heart
- reduces preload
- thus reduces work of heart and O2 demand
- also dilates coronary arteries
side effect: profuse headache immediately after use
94
angina - calcium ion channel antagonists/ blockers
- primary arterodilators
- dilates systemic arteries (BP drop)
- reduces afterload on heart
- thus less energy required to produce same cardiac output
- thus less work on heart and O2 demand
- VERAPAMIL
95
angina - revascularisation - 2 types
-Percutaneous Coronary Intervention (PCI)
-Coronary artery bypass graft (CABG)
To restore patient coronary artery, increase flow reserve, done mostly when medication fails or when high risk disease identified
96
angina - PCI
- dilating coronary atheromatous obstructions by inflating balloon within it
- insert balloon and stent, inflate balloon and remove it, stent persists, keeps artery patent
- expanding plaque = make artery bigger
97
angina - PCI pros and cons
pros - less invasive, convenient, short recovery, repeatable
| cons - risk of stent thrombosis, not good for complex disease
98
angina - CABG
- left internal mammary artery (LIMA) used to bypass proximal stenosis in LAD artery
- pros: good prognosis, deals with complex disease
- cons: invasive, risk of stroke or bleeding, one time treatment, long recovery period
99
'Acute coronary syndrome' umbrella term for what?
- ST elevation myocardial infarction (STEMI)
- Unstable (crescendo) angina (UA)
- non ST elevation myocardial infarction (NSTEMI)
100
What is an ST elevation myocardial infarction?
- complete occlusion of major coronary artery prev affected by atherosclerosis
- full thickness damage of heart muscle
- usually diagnose on ECG @ presentation
- pathological Q wave some time after MI (so aka Q wave infarction)
101
What is unstable (crescendo) angina (UA) ?
- angina recent onset (less 24hrs) or
- cardiac chest pain w/ crescendo pattern
- deterioration in prev stable angina (symptoms freq. occurring at rest)
- angina increasing frequency or severity, occurs minimal exertion, rest - form of acute coronary syndrome
102
What is a non ST elevation myocardial infarction?
- complete occlusion minor coronary artery OR partial occlusion of major coronary artery prev affected by atherosclerosis
- retrospective diagnosis, made after troponin results and sometimes other investigations
- partial thickness damage of heart muscle
- non Q wave infarction
- ST depression and/or T wave inversion
103
What is the difference between NSTEMI and UA?
NSTEMI = an occluding thrombus leads to myocardial necrosis and rise in serum troponin or creatinine kinase-MB (CK-MB)
104
The 5 types of MI - type 1
spontaneous MI with ischaemia due to a primary coronary event eg plaque erosion/rupture, fissuring, dissection
105
5 types of MI - type 2
MI secondary to ischaemia due to increased O2 demand or decreased supply eg coronary spasm, coronary embolism, anaemia, arrhythmias , hypertension, hypotension
106
5 types of MI - types 3,4,5
MI due to sudden cardiac death related to PCI, CABG
107
How many people per annum have STEMI in UK?
5/1000 per annum
108
Acute coronary syndrome risk factors
```
Age
Gender - male
Family history (IHD/ MI in first degree relative below 55)
Smoking
Hypertension
Diabetes mellitus
Hyperlipidaemia
Obesity and sedentary lifestyle
```
109
Acute coronary syndrome pathophysiology
- rupture/erosion fibrous cap of coronary artery plaque
- causes platelet aggregation/adhesion, localised thrombus, vasoconstriction(platelet release serotonin, thromboxane A2), distal thrombus embolisation
- myocardial ischaemia due to reduction coronary blood flow
110
Acute coronary syndrome- what 2 things mean increased risk plaque rupture?
- rich lipid pool within plaque
| - thin fibrous cap
111
Acute coronary syndrome - stages of plaque development
fatty streak - fibrotic plaque - atherosclerotic plaque - plaque rupture/fissure and thrombosis - MI/ischaemic stroke or critical limb ischaemia or sudden CVS death
112
Unstable angina - what is the plaque like?
- necrotic centre
- ulcerated cap
- thrombus results in PARTIAL occlusion
113
Myocardial infarction - what is the plaque like?
- necrotic centre
| - thrombus results in TOTAL occlusion
114
Acute coronary syndrome - clinical presentation - unstable angina presentation?
- chest pain, new onset, at rest, crescendo pattern
- breathlessness
- pleuritic pain (sharp pain inhale and exhale)
- indigestion
115
Clinical presentation acute coronary syndrome?
Acute central chest pain more than 20mins
- sweating
- nausea and vomiting
- dyspnoea
- fatigue
- shortness of breath
- palpitations
116
Clinical presentation acute coronary syndrome?
- without chest pain (silent infarct) (elderly, diabetics)
- distress, anxiety
- pallor
- increased pulse, reduced BP
- reduced 4th heart sound
- may be heart failure sings (increase jugular venous pressure)
- tachycardia/ bradycardia
- peripheral oedema
117
Acute coronary syndrome - differential diagnosis?
- angina
- pericarditis
- myocarditis
- aortic dissection
- pulmonary embolism
- oesophageal reflux/spasm
118
Acute coronary syndrome diagnosis tools?
- 12 lead ECG
- biochemical markers
- chest X-ray
119
Acute coronary syndrome - 12 lead ECG
- can be normal
- ST depression/ T wave inversion (hours/days after NSTEMI) highly suggestive of acute coronary syndrome, esp if associated with anginal chest pain
- hyperacute (tall) T waves
120
Acute coronary syndrome - an STEMI on an ECG?
- persistant ST elevation
- hyperacute (tall) T waves
- new left BBB pattern
- pathological Q waves few days after MI
121
acute coronary syndrome - 4 biochemical markers?
- troponin T
- troponin I
- creatinine kinase-MB (CK-MB)
- myoglobin
122
acute coronary syndrome - troponin T and I
- T and I most sensitive and specific markers of myocardial necrosis
- serum levels increase 3-12hrs onset of chest pain, peak 24-48hrs
- fall back to normal over 5-14days
- prognostic indicator determine mortality risk define which patients benefit from aggressive medical therapy and early coronary revascularisation
123
acute coronary syndrome - CK-MB
- marker for myocyte death
- low accuracy,can be present in normal state, patients significant skeletal muscle damage
- tests for reinfarction: levels drop back to normal after 36-72hrs
124
acute coronary syndrome - myoglobin
- elevated v early in MI
| - poor specificity: myoglobin present in skeletal muscle
125
acute coronary syndrome - chest X ray
-look for cardiomegaly, pulmonary oedema, widened mediastinum (aortic rupture)
126
acute coronary syndrome - types of treatment
- pain relief
- anti-emetic
- oxygen
- pharmacological (antiplatelets, BBs, statins, ACEi)
- coronary revascularisation
- modify risk factors
127
acute coronary syndrome - pain relief?
- GTN spray
| - IV opioid
128
acute coronary syndrome - oxygen
- aim for 94-98% saturation
| - 88-92% COPD
129
acute coronary syndrome - antiplatelet therapy - how thrombotic clot forms
- atheromatous plaque rupture = platelets exposed ADP/thromboxane A2/adrenaline/thrombin/collagen tissue factor
- causes platelet activation/aggregation via IIb/IIIa glycoproteins binding to fibrinogen
- thrombin enzymatically converts fibrinogen to fibrin(insoluble) forms fibrin mesh over platelet plug, formation thrombotic clot
130
Examples of 3 antiplatelet drugs
- aspirin
- P2Y12 inhibitors (oral)
- glycoprotein IIb/IIIa antagonists (IV)
131
How does aspirin work?
COX-1 inhibitor - blocks formation of thromboxane A2 from thus prevents platelet aggregation
132
acute coronary syndrome - P2Y12 inhibitors (oral)
-inhibit ADP dependant activation IIb/IIIa glycoproteins, preventing amplification response of platelet aggregation
-use if allergic to aspirin
-dual anti-platelet therapy w/ aspirin
-clopidogrel , prasugrel , ticagrelor
side effects:neutropenia, thrombocytopenia, increased risk bleeding
-AVOID if CABG planned
133
acute coronary syndrome - glycoprotein IIb/IIIa antagonists (IV)
- only IV available
- used w/ aspirin AND oral P2Y12 inhibitors patients with ACS undergoing PCI
- increases risk major bleeding
- abciximab , tirofiban , eptifbatide
134
acute coronary syndrome - beta blockers (IV and oral)
- avoid with asthma, heart failure, hypotension, bradyarrhythmias
atenolol (IV then oral)
metoprolol (IV then oral)
135
acute coronary syndrome - statins (oral)
- HMG-CoA reductase inhibitors
| - simvastatin , pravastatin , atorvastatin
136
acute coronary syndrome - ACE inhibitors (oral)
- ramipril , lisonopril
| - monitor renal function
137
acute coronary syndrome - coronary revascularisation
- percutaneous coronary intervention (PCI)
| - coronary artery bypass graft (CABG) - high risk mortality in high risk groups eg recent MI
138
acute coronary syndrome - risk factor modification
- stop smoking
- loose weight , exercise daily
- healthy diet
- treat hypertension + diabetes
- low fat diet with statins
139
Cardiomyopathy - definition
Group of diseases of the myocardium that affect the mechanical or electrical function of the heart
140
Cardiomyopathy - epidemiology
- in general: inherited genetic conditions, although some acquired ones
- all carry arrhythmic risk
- can occur younger ages
- restrictive cardiomyopathy rare in childhood, poor outcome once symptoms develop
141
The 4 types of cardiomyopathy?
- hypertrophic
- dilated
- restrictive
- arrhythmogenic right ventricular
142
cardiomyopathy - 5 risk factors?
- family history
- hypertension
- obesity
- diabetes
- previous MI
143
hypertrophic cardiomyopathy - what is it?
ventricular hypertrophy/ thickening of the muscle
144
hypertrophic cardiomyopathy - epidemiology
- quite common, 2nd most common cardiomyopathy
- 1/500 have it
- autosomal dominant - familial
- may present at any age
- most common cause of sudden cardiac death in the young
- HCM refers to otherwise unexplained primary cardiac hypertrophy
145
hypertrophic cardiomyopathy - pathophysiology
- sarcomeric protein gene mutations eg troponin T, B-myosin
- in absence of hypertension, valvular disease
- hypertrophic, non-compliant ventricles impair DIASTOLIC filling: reduced stroke volume, reduced cardiac output
- myofibrillar disarray = conduction is affected
146
hypertrophic cardiomyopathy - clinical presentation (7)
- hypertrophy of myocardium esp interventricular septum
- sudden death may be first manifestation
- chest pain, angina, dysponea, dizziness, palpitations, syncope
- LV outflow obstruction
- cardiac arrhythmia
- ejection systolic murmur
- jerky carotid pulse
147
hypertrophic cardiomyopathy - 3 diagnosis tools?
- ECG
- echocardiogram
- genetic analysis
148
hypertrophic cardiomyopathy - ECG
ECG: abnormal, LV hypertrophy signs, progressive T wave inversion, deep Q waves
149
hypertrophic cardiomyopathy - echocardiogram
ventricular hypertrophy, small left ventricle cavity
150
hypertrophic cardiomyopathy - genetic analysis
can confirm diagnosis - most cases are autosomal dominant and familial
151
hypertrophic cardiomyopathy - treatment - 3 drugs
AMIODARONE - anti-arrhythmic medication, if at high arrhythmia risk: implantable cardiac defibrillator
CALCIUM CHANNEL BLOCKER- eg verampil
BETA BLOCKER - eg atenolol
152
Dilated cardiomyopathy - definition
Dilated left ventricle (or RV or all 4 chambers) which contracts poorly/ has thin muscle - thus dysfunction
153
dilated cardiomyopathy - epidemiology
- MOST COMMON cardiomyopathy
- autosomal dominant - familial
- caused by: ischaemia, alcohol, thyroid disorder or familial/genetic
154
dilated cardiomyopathy - pathophysiology
- caused by cytoskeletal gene mutations
- LV, RV, all 4 chamber dilatation thus dysfunction
- theory:poorly generated contractile force causes progressive dilatation of heart with some diffuse interstitial fibrosis
155
dilated cardiomyopathy - clinical presentation
- shortness of breath, fatigue
- dysponea
- heart failure (cant contract well)
- arrhythmias
- thromboembolism
- sudden death
- increased jugular venous pressure
156
dilated cardiomyopathy - 3 diagnostic tools and what they will show?
- chest X ray (cardiac enlargement)
- ECG (tachycardia, arrhythmia, non specific T wave changes)
- echocardiogram (dilated ventricles)
157
dilated cardiomyopathy - treatment
heart failure and atrial fibrilation treated in conventional way
158
Restrictive cardiomyopathy - epidemiology
- Rare
| - Causes: amyloidosis, idiopathic, sarcoidosis, end-myocardial fibrosis
159
Arrythmogenic right ventricular cardiomyopathy - definition
-progressive genetic cardiomyopathy characterised by progressive fatty and fibrous replacement of ventricular myocardium
160
arrythmogenic right ventricular cardiomyopathy - epidemiology
- cause unknown
| - familial form usually autosomal dominant w/ incomplete penetrance but can be recessive
161
arrtyhmogenic right ventricular cardiomyopathy - pathophysiology
- desmosome gene mutation (normally hold cardiac cells together-cell junctions)
- RV replaced by fat and fibrous tissue
- muscle dies, replaced by fat as part of inflammatory process
162
arrhythmogenic right ventricular cardiomyopathy - clinical presentation
- impairment of holding together of cardiac cells thus conduction issues
- ARRHYTHMIA most common
- syncope
- late stages - maybe signs right heart failure
163
arrhythmogenic right ventricular cardiomyopathy - diagnosis tools and findings
- ECG: usually normal, may show T wave inversion
- echocardiogram: maybe normal, advanced disease: RV dilatation
- genetic testing: gold standard
164
arrhythmogenic right ventricular cardiomyopathy - treatment
- BETA BLOCKERS eg atenolol for patients non life threatening arrhythmias
- AMIODARONE for symptomatic arrhythmias
- occasional cardiac transplant indicated eg cardiac failure, devastating arrhythmia
165
Structural/ congenital heart defects
- 1% all live births some form cardiac defect
- minor ---- incompatible with life ex utero
- overall male predominance
- atrial septal defect, persistant ductus arteriosus more common females
- usually: misplaced structures, arrest of progression of normal structure development
166
Causes of congenital heart disease?
- 1 child with defect increases likelihood 2nd child having another defect
- drugs eg thalidomide, amphetamines,lithium
- diabetes of mother
- genetic abnormalities eg familial form ASD, congenital heart block
167
Maternal prenatal rubella infection associated with which congenital abnormalities?
- persistant ductus arteriosus
- pulmonary valvular stenosis
- arterial stenosis
168
Maternal alcohol misuse associated with which congenital abnormality?
- septal defects
169
Single genes - what congenital heart defects are associated with Trisomy 21?
- septal valve defects
- mitral valve defects
- tricuspid valve defects
170
Clinical presentation of congenital heart defects
should be recognised early as possible (response better the earlier the treatment)
- central cyanosis
- pulmonary hypertension
- clubbing of fingers
- growth retardation
- syncope
- specific problems in adults/adolescents
171
Clinical presentation congenital heart defects - central cyanosis
- right to left shunting of blood OR
- complete mixing of systemic+pulmonary blood flow=poorly oxygenated blood entering systemic circulation
- skin goes blueish
- Tetralogy of Fallot, Tricuspid atresia
172
clinical presentation congenital heart defects - pulmonary hypertension
- large left to right shunts
- persistant raised pulmonary flow = increased pulmonary artery vascular resistance = pulmonary hypertension
- thickening of pulmonary artery walls in response to high pressure
- resistance causes RV pressure to increase = REVERSAL OF SHUNT = cyanosis
173
Eisenmenger's reaction
- L to R shunt = pulmonary hypertension leading to thickening pulmonary artery walls, increase RV pressure, reversal of initial shunt so now shunt is right to left = cyanosis
- Eisenmenger's complex specifically in relation to VSD
174
Does presence of pulmonary hypertension make prognosis of congenital heart defect better or worse?
Significantly worsens the prognosis
175
congenital heart defects - what leads to clubbing of fingers?
associated with prolonged cyanosis
176
congenital heart defects - what type is associated with growth retardation?
common in children with cyanotic heart disease
177
congenital heart defects - syncope
- presence of severe LV or RV outflow tract obstruction
| - exertional syncope associated with keeping central cyanosis, may occur in Fallot's tetralogy
178
Congenital heart defects presentation 6 specific common problems in adolescents/adults
- endocarditis (small VSD/bicuspid aortic valve)
- calcification and stenosis of congenitally deformed valves (bicuspid aortic valve)
- atrial and ventricular arrhythmias
- sudden cardiac death
- right sided heart failure
- end stage heart failure
179
congenital heart disease - Bicuspid aortic valve (BAV)
- most common cong heart disease (1-2% live births)
- can work well at birth (go undetected) but severely stenotic infancy/childhood
- degenerate quicker and become regurgitant earlier than normal valves
- predisposed to infective endocarditis
- intense exercise may accelerate complications - yearly ECGs on affected athletes
180
congenital heart defects- Bicuspid aortic valve - more common in males or females?
Males
181
congenital heart defects - bicuspid aortic valve - what other malformation is it associated with?
coarctation and dilation of ascending aorta
182
congenital heart defects - atrial septal defects - epidemiology
- often first diagnosed in adulthood
- one third of congen heart defects
- more common in females
- abnormal connection between 2 atria
183
congenital heart defects - atrial septal defects
- probe can be passed through layers of foramen ovale (primum, secundum) so aka probe patent foramen ovale
- higher pressure LA, so shunt left to right - so not blue - ACYANOTIC
184
congenital heart defects - atrial septal defects - physiology
- increased flow into right side of heart/lungs
- untreated=right sided overload, dilatation- RV compliant, easily dilates to accomodate increased pulmonary flow, can cause:
- RV hypertrophy
- pulmonary hypertension, Eisenmenger's
- +risk infective endocarditis
185
congenital heart defects - atrial septal defects clinical presentation
- dysponea
- exercise intolerance
- atrial arrhythmias (artia dilation)
- pulmonary flow murmur
- fixed split 2nd heart sound (delayed closure pulmonary valve-more blood has to get out)
186
congenital heart defects - atrial septal defects - chest X ray findings
- large heart
| - large pulmonary arteries
187
congenital heart defects - atrial septal defects - ECG findings
right bundle branch block (RBBB) due to right ventricle dilatation
188
congenital heart defects - atrial septal defects - echocardiogram findings
hypertrophy and dilation of right side of heart and pulmonary arteries
189
congenital heart defects - atrial septal defects - treatment
- surgical closure
| - percutaneous (key hole technique)
190
Congenital heart defects - Ventricular septal defects
- abnormal connection between 2 ventricles
- many close spontaneously during childhood
- 20% all congen heart defects
- LV higher pressure: L to R shunt, acyanotic
- increased blood flow through lungs
191
Congenital heart defects - Ventricular septal defects - clinical presentation of LARGE defects
- pulmonary hypertension (Eisenmenger's)
- small breathless skinny baby
- increased resp rate
- tachycardia
- murmur that varies in intensity
- big heart on chest X ray
192
Congenital heart defects - Ventricular septal defects - clinical presentation of SMALL defects
- large systolic murmur (audible)
- thrill (buzzing sensation)
- well grown
- normal heart rate
- normal heart size
193
Congenital heart defects - Ventricular septal defects - treatment
- medical initially: many will spontaneously close
- surgical close
- small defect = no intervention required
- prophylactic antibiotics
- moderate sized lesion: furosemide, ACEi (ramipril) , digoxin may suffice
194
Congenital heart defects - Atrio-ventricular septal defects (AVSD)
- associated with Down's syndrome
- hole in very centre of heart
- involves ventricular and atrial septum, mitral and tricuspid valves
- can be complete or partial
- one big malformed AV valve-usually leaks
195
congenital heart defects - AVSD - clinical presentation of complete defect
- neonate breathlessness
- poor feeding and weight gain
- torrential pulmonary flow can result in Eisenmenger's (cyanosis over time)
196
congenital heart defects - AVSD - clinical presentation of partial defect
- can present late adulthood
| - presents similar to septal defect eg dysponea, tachycardia, exercise intolerance
197
congenital heart defects - AVSD - treatment
- pulmonary artery banding (if large defect infancy) reduces blood flow to lungs reducing pulmonary hypertension
- surgical repair challenging
- partial defect can left alone if no right heart dilatation
198
congenital heart defects - patent ductus arteriosus - epidemiology and definition
- females more than males
| - persistant communication proximal left pulmonary artery - descending aorta
199
congenital heart disease - patent ductus arteriosus
- foetal life R heart pressure exceeds left
- blood R to L through foramen ovale, and pulmonary artery to aorta via ductus arteriosus
- abnormal L to R shunt (aorta to P artery)
- pulmonary hypertension
- right side cardiac failure (+ afterload)
200
congenital heart disease - 2 risk factors for having patent ductus arteriosus?
(normally shuts due to decreased pulmonary resistance)
- premature babies
- maternal rubella
(also having it increases risk of infective endocarditis)
201
congenital heart disease - patent ductus arteriosus - clinical presentation
- continuous 'machinery' murmurs
- bounding pulse
- (large defect)large heart and breathlessness
- Eisenmenger's but pink, not clubbed fingers
- tachycardia
202
congenital heart defects - patent ductus arteriosus - chest X ray
-(large shunt) aorta and pumonary arterial system may be prominent
203
congenital heart defects - patent ductus arteriosus - ECG and echocardiogram
- may be left atrial abnormality, left ventricular hypertrophy
- echo: may show dilated left atrium, left ventricle
204
congenital heart defects - patent ductus arteriosus - treatment
- closed surgically or percutaneously
- low risk complications
- venous approach may require AV loop
- INDOMETACIN (prostaglandin inhibitor) given to stimulate duct closure
205
congenital heart defects - coarctation of the aorta
-more males than females
-narrowing of aorta, at or just distal insertion
ductus arteriosus
-net result:narrowing aorta just after arch, excessive blood flow diverted through carotid, subclavian vessels, systemic vascular shunts to supply rest of body (stronger perfusion of upper body)
206
congenital heart defects - coarctation of aorta - what other 4 conditions are associated?
- Turner's syndrome
- Berry aneurysms
- Patent ductus arteriosus
- Systemic hypertension due to decrease renal perfusion (persists after surgical correction)
207
congenital heart defects - coarctation of aorta clinical presentation
- asymptomatic for many years
- right arm hypertension
- bruits (buzzes) over scapulae/back (collateral vessels)
- murmur
- headaches, nosebleeds (hypertension)
- hypertension in upper limbs
- discrepant blood pressure in upper and lower body (radial before femoral pulse)
208
congenital heart defects - coarctation of aorta long term problems
HYPERTENSION
- early coronary artery disease
- early strokes
- sub-arachnoid haemorrhage
209
congenital heart defects - coarctation of aorta - chest X ray, ECG, CT
CXR: dilated aorta, indented at side of coarctation
ECG: left ventricular hypertrophy
CT: accurately demonstrate coarctation, quantify flow
210
congenital heart defects - coarctation of aorta - treatment
- surgery
- balloon dilation (preferred for recoarctation and stenting)
- risk aneurysm at site of repair
211
congenital heart defects - Tetralogy of Fallot
MOST COMMON form cyanotic congenital heart disease
212
congenital heart defects - Tetralogy of Fallot - the 4 things?
- Large MALIGNED ventricular septal defect
- Overriding aorta
- RV outflow obstruction (eg due to pulmonary stenosis)
- RV hypertrophy
213
congenital heart defects - Tetralogy of Fallot - cyanosis
- stenosis of RV outflow (eg pulmonary valve)
- RV higher pressure than LV
- so blue blood from RV to LV
- patients are blue (cyanotic)
214
congenital heart defects - Fallots tetralogy - clinical presentation
- central cyanosis
- low birth weight and growth
- dyspnoea on exertion
- delayed puberty
- systolic ejection murmurs
- boot shaped heart on chest X ray
215
congenital heart defects - Fallots tetralogy - treatment
- full surgical during first 2 years life (progressive cardiac debility and cerebral thrombosis risk)
- often get pulmonary valve regurgitation in adulthood - require redo surgery
216
congenital heart defects - Pulmonary stenosis
- narrowing of outflow of RV
(can be valvular, subvalvar, supravalvar) (99% valvular)
- can be severe or mild
217
congenital heart defects - severe pulmonary stenosis
- RV failure as neonate
- collapse
- poor pulmonary blood flow
- RV hypertrophy
- tricuspid regurgitation
218
congenital heart defects - mild pulmonary stenosis
- well tolerated many years
| - RV hypertrophy
219
congenital heart defects - pulmonary stenosis - treatment
- balloon valvoplasty - catheter with balloon through femoral vein- inflate at stenosis to crush (can result in regurgitation)
- open valvotomy
- shunt to bypass blockage
220
congenital heart defects - complete transposition of great arteries
- aorta off RV and pulmonary trunk off LV !
- 2 closed circulations
- male more common, associated w/ diabetes
- survival only if communication between 2 circuits
- most have an ASD, with blood mixing
221
congenital heart defects - complete transposition of great arteries - treatment
- atrial switch operation with good results
222
congenital heart defects - dextrocardia
- heart points to right side chest, rather than left
| - associated with severe cardiovascular abnormalities
223
Pericarditis
- pericardium=protective covering of heart
- outer fibrous pericardial sac
- inner serous pericardium
224
Pericarditis - layers of pericardium
Inner serous pericardium:
- inner visceral layer - single cell layer adherent to epicardium (myocytes), lines heart and great vessels
- outer parietal layer - mainly collagen and elastin fibres, no cells, lines fibrous sac
225
Pericarditis - around how much fluid is found in the pericardial sac?
50ml serous fluid - lubricant
226
Pericardium - general anatomy
- great vessels lie in pericardium - if proximal/ascending segment aorta ruptures will bleed into pericardial space=tamponade
- LA mainly outside pericardium
- promotes cardiac efficiency - limiting dilation, maintaining ventricular compliance, distributing hydrostatic forces
227
Pericarditis - how does pericardium aid atrial filling?
- creating a closed chamber
- also reduces external friction, barrier against infection + extension of malignancy
- anatomically fixes heart to sternum, diaphragm, costal cartilages
228
Pericarditis - pericardium is similar to an elastic band
- initially stretchy but stiff at higher tension
- low tension - small reserve volume
- volume exceeded-pressure translated to cardiac chambers = pressure on heart
229
Pericarditis - what happens if small amount volume is added into the pericardial space?
- dramatic effects on filling eg cardiac tamponade
| - pressure in pericardium is very low
230
Pericarditis - what happens in a chronic pericardial effusion?
-pericardium adapts slowly
- lays down elastin and collagen
- becomes more elastic, much slower tamponade (no RA collapse)
- pressure equalises
(entrance fluid making up effusion must be slow)
231
Acute pericarditis
Acute inflammation of the pericardium - with or without effusion
232
Acute pericarditis - epidemiology
- most idiopathic
- most common young, prev healthy patient
- males more than females
- adults more than children
233
Acute pericarditis - causes
- infectious (bacterial,viral,fungal)
| - non infectious (autoimmune, neoplastic, Dressler's, traumatic and iatrogenic)
234
Acute pericarditis - infectious causes
- viral (common) : enteroviruses eg echoviruses, adenoviruses
- bacterial: mycobacterium tuberculosis
- fungal (very rare) : Histoplasma spp (most likely seen in immunocompromised pt)
235
acute pericarditis - non infectious causes
- autoimmune (Sjorgren's, rheumatoid arthritis, SLE)
- neoplastic (secondary metastatic tumor)
- Dressler's syndrome - post cardiac injury syndromes
236
acute pericarditis - traumatic and iatrogenic
- early onset (rare) : direct injury/penetrating thoracic injury/ oesophageal perforation or indirect injury/non penetrating thoracic injury/radiation
- delayed onset (common) : pericardial injury syndromes, iatrogenic trauma eg PCI, pacemaker lead insertion
237
acute pericarditis - pathophysiology
- pericardium becomes acutely inflamed
- pericardial vascularisation, infiltration polymorphonuclear leucocytes
- fibrinous reaction freq results in exudate, adhesions within pericardial sac, serous, hemorrhagic effusion may develop
238
acute pericarditis - clinical presentation
- chest pain
- dysponea
- cough
- hiccups (phrenic involvement)
- pericardial friction rub (auscultation)
- fever, lymphocytosis (if virus, bacteria)
- tachycardia
239
acute pericarditis - chest pain
- severe
- sharp and pleuritic (without constricting, crushing character of ischaemic pain)
- rapid onset
- worse on inspiration
- L anterior chest/epigastrium
- radiates to arm/ TRAPEZIUS RIDGE (coinnervation phrenic nerve - differs from STEMI)
240
acute pericarditis - differential diagnosis
- MI (most important to rule out)
- angina
- pleuritic pain
- pulmonary infarction
- pneumonia, GI reflux, peritonitis, aortic dissection
241
acute pericarditis - ECG
- DIAGNOSTIC
- widespread concave upwards SADDLE SHAPED ST ELEVATION
- diffuse ST elevation present all leads (in STEMI would be LIMITED to infarcted area)
- PR depression
242
acute pericarditis - chest X ray
- cardiomegaly in cases of effusion (confirm with echo)
- often normal in idiopathic
- pneumonia common with bacterial pericarditis
243
acute pericarditis - FBC
- slight increase white cell count
- anti neutrophil antibody young females(SLE)
- elevated troponin suggests myopericarditis
244
acute pericarditis - erythrocyte sedimentation rate/ C reactive protein levels
Hight ESR suggests autoimmune
245
acute pericarditis - treatment
- restrict physical activity until resolution of symptoms/ ECG/CRP improvements
- NSAID or ASPIRIN for 2 weeks
- COLCHICINE 3 weeks (nausea, diarrhoea )
246
Recurrent or relapsing pericarditis
- 20% acute go on to develop idiopathic relapsing pericarditis
- 6 weeks weaning off NSAIDs or intermittently
- first line treatment oral NSAIDs (ibuprofen)
- Colchicine more effective than aspirin alone
247
Recurrent or relapsing pericarditis - resistant cases
- oral corticosteroids eg prednisolone
| - pericardiectomy
248
Pericardial effusion/ cardiac tamponade
- pericardial effusion: collection fluid within potential space serous pericardial sac
- commonly accompanies acute pericarditis
- large volume=ventricular filling compromised embarrassment circulation - cardiac tamponade
249
clinical presentation pericardial effusion
- reflect underlying pericarditis
- soft, distant heart sounds
- apex beat obscured
- raised jugular venous pressure
- dysponea
250
clinical presentation cardiac tamponade
- high pulse but low blood pressure
- high jugular venous pressure
- muffled 1st and 2nd heart sounds
- Kussmaul's sign
- pulsus parodoxus
- reduced cardiac output
251
Kussmauls sign definition
| Pulsus parodoxus definition
- rise jugular venous pressure, increased neck vein distention during inspiration
- exaggeration normal variation pulse pressure with inspiration - drop in systolic BP
252
Pericardial effusion diagnosis
CXR: large globular heart
ECG: low voltage QRS complexes, sinus tachycardia
Echo: most useful demonstrating effusion, echo free zone surrounding heart
253
Cardiac tamponade diagnosis
CXR: big globular heart
ECG: low voltage QRS
Echo: DIAGNOSTIC, echo free zone around heart, late diastolic collapse RA, early diastolic collapse RV
254
cardiac tamponade diagnosis - Beck's triad
- falling blood pressure
- rising jugular venous pressure
- muffled heart sounds
255
pericardial effusion - treatment
- underlying cause sought and treated
- most resolve spontaneously
- may re-accumulate due to malignancy: pericardial fenestration(window allows slow release fluid to surrounding tissues)
256
cardiac tamponade - treatment
- seek expert help
- urgent drainage via pericardiocentesis
- fluid sent for Ziehl-Nielsen stain, cytology
257
Constrictive pericarditis
- tuberculosis, bacterial infection, rheumatic heart disease result in pericardium becoming thick, fibrous, calcified
- cause often unknown, can occur after any pericarditis
258
constrictive pericarditis - pathophysiology
- many cases- no symptoms
- constrictive pericarditis if so inelastic to interfere w/ diastolic filling
- changes are chronic - allows time for body to compensate - not as life threatening
259
Constrictive pericarditis vs restrictive cardiomyopathy
- very similar presentation
| - constrictive pericarditis treatable - restrictive cardiomyopathy not
260
Constrictive pericarditis - myocardium changes
- later stages of condition
| - sub endocardial layers of myocardium may undergo fibrosis, atrophy, calcification
261
constrictive pericarditis - clinical presentation
- Kussmaul's sign
- pulsus parodoxus
- diffuse heart sounds
- ascites
- oedema
- right heart failure signs
- atrial dilatation
262
constrictive pericarditis - diagnosis
CXR: small heart with/without pericardial effusion
ECG: low voltage QRS
Echo: thickened, calcified pericardium, small ventricular cavities w/ normal wall thickness
263
constrictive pericarditis - treatment
-complete resection of pericardium (risky, high complication rate)
264
Cardiac failure
'The inability of the heart to deliver blood and thus O2 at a rate commensurate with the requirement of metabolising tissue of the body'
- syndrome, not diagnosis on own
- result from any structural/functional cardiac disorder impairs hearts ability to function, meet O2 demands metabolising body
265
Cardiac failure - epidemiology
25-50% die within 5yrs diagnosis
- 1-3% general population
- 10% among elderly
266
cardiac failure - main causes
- IHD - main cause
- cardiomyopathy
- valvular heart disease
- cor pulmonae
- hypertension
- alcohol excess
- anything increases myocardial work (anaemia,arrhythmias,obesity,hyperthyroidism)
267
cardiac failure - risk factors
- 65 and older
- african descent
- men (oestrogen protects IHD)
- obesity
- prev had MI
268
Cardiac failure - pathophysiology
- physiological compensatory changes to try maintain CO and peripheral perfusion
- these mechanisms become overwhelmed as progresses - become pathophysiological = decompensation
- venous return
- outflow resistance
- sympathetic system activation
- RAAS
269
cardiac failure - pathophysiology - venous return (preload)
- reduction blood volume ejected
- increase volume left in ventricles
- increased preload stretched myocardial fibres - Starlings law - contraction force +
- heart failure, myocardium cannot contract harder in response, CO not maintained
270
cardiac failure - pathophysiology - outflow resistance (afterload) definition
- load/resistance against which ventricles must contract, made up of:
- pulmonary and systemic resistance
- physical characteristics vessel walls
- volume of blood ejected
271
cardiac failure - pathophysiology - outflow resistance (afterload)
- increase afterload, increase end-diastolic volume
- decrease stroke volume, decrease CO
- results in increase end diastolic volume, dilatation ventricle, further exacerbates problem of afterload
272
cardiac failure - pathophysiology - sympathetic system activation
- baroreceptors (drop arterial pressure) stimulate sympathetic activation
- increases SV and HR, increasing CO
- cardiac failure - chronic symp activation
- less receptor to act on - effect of symp activation diminished, CO stops increasing in response
273
cardiac failure - pathophysiology - RAAS
- reduced CO, diminished renal perfusion
- RAAS activated (increase blood volume)
- so increased preload, stretching of heart, force contraction, SV, CO
- cardiac myocytes require more energy, more blood - heart failure (IHD) - no increase blood, myocytes die, decrease CO
274
cardiac failure - classification - classes
- systolic vs diastolic
| - acute vs chronic
275
cardiac failure - classification - systolic
- inability ventricle contract normally (so decreased CO)
| - caused by IHD, MI, cardiomyopathy
276
cardiac failure - classification - diastolic
- inability ventricles relax, fill fully, decrease SV, decrease CO
- caused by ventricle hypertrophy - less space for blood - decreased CO
- aortic stenosis increases afterload, decreases CO
277
cardiac failure - classification - acute
- new onset or decompensation chronic heart failure
- pulmonary and/or peripheral oedema
- may be signs peripheral hypotension
278
cardiac failure - classification - chronic
- develops slowly
| - venous congestion common, arterial pressure well maintained until v late
279
cardiac failure - clinical presentation
3 cardinal symptoms: shortness breath, fatigue, ankle swelling (non specific)
- dyspnoea - esp when lying flat
- cold peripheries
- raised jugular venous pressure (JVP)
- murmurs, displaced apex beat
- cyanosis
- hypotension
- peripheral/pulmonary oedema
- tachycardia and 3rd and 4th heart sounds
- ascites and bi-basal crackles
280
cardiac failure - clinical presentation - use of New York Heart Association (NYHA) classification for severity of symptoms:
- Class I: no limitation/asymptomatic, exercise= no dyspnoea, fatigue, palpitation
- Class II: slight limitation/mild heart failure, comfortable at rest, normal activity= D, F, P Class III: marked limitation/moderate heart failure, comfy at rest, gentle activity=D, F, P
- Class IV: inability carry out any physical activity without discomfort/ severe heart failure - symptoms at rest
281
cardiac failure - diagnosis
- blood tests
- chest X ray
- ECG
- echo
282
cardiac failure - diagnosis - blood tests
Brain natriuretic peptide (BNP)
- secreted by ventricles response increase myocardial wall stress
- increased in patients heart failure
- levels correlate ventricular wall distress, severity heart failure
- FBC, U+Es, liver biochemistry
283
cardiac failure - diagnosis - chest X ray
ACDE
- Alveolar oedema
- Cardiomegaly
- Dilated upper lobe vessels lungs
- Effusions (pleural)
284
cardiac failure - diagnosis - ECG
- shows underlying cause eg IHD, LVH
- if ECG and BNP normal,heart failure unlikely
- if both abnormal, do echocardiogram
285
cardiac failure - diagnosis - echocardiogram
- assess cardiac chamber dimension
- regional wall motion abnormalities , valvular disease, cardiomyopathies
- sign of MI
286
cardiac failure - treatment
- lifestyle changes
- diuretics, ACE inhibitors, beta blockers
- digoxin, inotropes
- revascularisation, surgery to repair
- heart transplant (young people)
- cardiac resynchronisation
287
cardiac failure treatment - lifestyle changes
- avoid large meals
- loose weight
- stop smoking
- exercise
- vaccination
288
cardiac failure treatment - diuretics
- reduce preload, decreasing systemic and pulmonary congestion
- symptomatic relief
- loop diuretic - furosemide
- thiazides eg bendroflumethiazide
- aldosterone antagonsit eg spirolactone
289
cardiac failure treatments - ACE inhibitors
- ramipril, enalipril, captopril
- cough,hypotension,hyperkalemia,renal dysfunc
- cough problem - angiotensin receptor blockers
290
cardiac failure treatment - beta blockers
- bisoprolol, nebivolol, carvedilol
- start low dose, titrate upwards
- DO NOT GIVE TO ASTHMATICS
291
cardiac failure treatment - revascularisation
- when some viable myocardium remains
| - illicit PCI stenting
292
cardiac failure treatment - surgery to repair
-mitral valve repair, aortic or mitral valve replacement
293
cardiac failure treatment - resynchronisation
-improve coordination of atria and ventricles
294
Clinical example cardiac failure treatment - biventricular failure
Shortness of breath = due to right ventricular failure
| Leg oedema = due to left ventricular failure
295
Valvular heart diseases - mitral stenosis
obstruction of left ventricle inflow - prevents proper filling during diastole
(mitral valve has 2 cusps)
296
valvular heart disease - mitral stenosis epidemiology
- normal 4-6cm2, symptoms less than 2cm2
- most common cause rheumatic heart disease secondary rheumatic fever from group A beta haemolytic streptococcus infection eg Streptococcus pyogenes
- more common men
- prev and inc reducing, reduc rheum heart disease
297
valvular heart disease - mitral stenosis - rheumatic heart disease
- inflammation from rheumatic fever = commissural fusion
- reduction orifice area (causes characteristic doming seen on echo)
- years: valve thickening,cusp fusion,calcium deposition,severely narrowed orifice,progressive immobility valve cusps
298
valvular heart disease - mitral stenosis - other causes
- infective endocarditis
| - mitral annular calcification
299
valvular heart disease - mitral stenosis - risk factors
- history rheumatic fever
| - untreated streptococcus infections
300
valvular heart disease - mitral stenosis - pathophysiology
-obstruction flow LA->LV
-maintain CO=LA pressure +, LA hypertrophy, dilatation
-pulmonary venous, pulmonary arterial, right heart pressure increase
+pulmonary cap pressure=pulmonary oedem (particularly when atrial fib occurs)
-alveolar, capillary thickening, reactive pulmonary hypertension ->RV hypertrophy,dilatation, tricuspid regurg
301
valvular heart disease - mitral stenosis - clinical presentation
- symptoms at 2cm2 area
- several decades after first rheumatic fever
- progressive dyspnoea (LA dilatation) worse with exercise, fever, tachycardia, pregnancy
- haemoptysis
- right heart failure (weakness,fatigue, abdo/lower limb swelling)
302
valvular heart disease - mitral stenosis - clinical presentation -
- atrial fibrillation (LA dilatation) - palpitations
- systemic emboli(atrial fib)(common cerebral)
- prominent 'a' wave jugular ven pulsations
- mitral facies/malar flush - bilateral, cyanotic, dusky pink discolouration upper cheeks
303
valvular heart disease - mitral stenosis - heart sounds - what is the murmur like?
- low pitched diastolic (when blood flows over a valve) rumble most prominent at apex
- patient lying L side, held inspiration
304
valvular heart disease - mitral stenosis - loud opening S1 snap
- at apex when leaflets still mobile
- abrupt halt leaflet motion early in diastole after rapid initial opening due to fusion leaflet tips
- MORE immobile, sound decreases
- more severe stenosis = longer diastolic murmur, closer opening snap to S2
305
valvular heart disease - mitral stenosis - diagnosis
CXR: LA enlargement, pulmonary oedema, maybe calcified mitral valve
ECG: atrial fibrillation, left atrial enlargement
Echo: GOLD standard for diagnosis, asses valve mobility, gradient, valve area
306
valvular heart disease - mitral stenosis - 5 treatment options
mechanical problem, medical therapy not prevent progression
- beta blockers
- digoxin
- diuretics
- percutaneous mitral balloon valvotomy
- mitral valve replacement
307
valvular heart disease - mitral stenosis - pharmacological treatment
- Digoxin and beta blockers eg atenolol - control heart rate, prolong diastole, improved diastolic filling
- Diuretics for fluid overload eg furosemide
308
valvular heart disease - mitral stenosis purcutaneous balloon valvotomy
- local anaesthetic, catheter to RA via femoral vein
- puncture interatrial septum, RA to LA
- balloon inflated across mitral valve, pressure, opens leaflets, increases area
309
valvular heart disease - mitral regurgitation
- backflow blood LV->LA during systole
| - mild physiological mitral regurg seen 80% normal individuals
310
valvular heart disease - mitral regurgitation - what is it
-abnorms of valve leaflets, chordae tendinae, papillary muscles, LV
311
valvular disease - mitral regurgitation - 6 causes
- myxomatous degeneration (MVP) (weakening chordae tendinae) causing floppy mitral valve that prolapses
- ischaemic mitral valve
- rheumatic heart disease
- infective endocarditis
- papillary muscle dysfunction/rupture
- dilated cardiomyopathy
312
valvular disease - mitral regurg - risk factors
- females
- lower BMI
- older age
- renal dysfunction
- prior MI
313
valvular disease - mitral regurg - pathophysiology
- LA dilatation
- pure volume overload (leakage blood into LA during systole)
- compensatory mechanisms: LA enlarge, LV hypertrophy, increased contractility
- pulmonary hypertension so progressive LA dilatation, RV dysfunction
- LV volume overload, dilatation, progressive heart failure
314
valvular disease - mitral regurg - clinical presentation
- auscultation (eg pan systolic murmur)
- exertion dysponea
- dysponea (pul ven hypertension, LV failure)
- fatigue and lethargy (CO reduced)
- palpitations due to increased stroke volume
- R heart failure symptoms (congestive cardiac failure)
- heart failure w/ + haemodynamic burden eg pregnancy, infection, atrial fib
315
valvular disease - mitral regurg - natural history
- 10-15yrs compensatory phase
- once ejection fraction less 60% and/or symptomatic - mortality sharp increase
- severe has 5% year mortality rate
316
valvular disease - mitral regurg - diagnosis
ECG: maybe LA enlargement, atrial fib, LV hypertrophy (severe) but not diagnostic
CXR: LA enlargement, central pulmonary artery enlargement
Echo: estimate LA,LV size and function, valve structure assessment, transoesophageal very helpful
317
valvular disease - mitral regurg - treatment options
- medications
- serial echocardiography
- surgery
318
valvular disease - mitral regurg - treatment - medications
- vasodilators eg ACE inhibitors (Ramipril, Hydralazine - smooth muscle relaxer)
- BBs (atenolol) , Ca channel blockers, digoxin (HR control for atrial fib)
- anticoagulation (atrial fib, flutter)
- diuretics - fluid overload - Furosemide
319
valvular disease - mitral regurg - treatment - serial echo
mild: 2-3 years
moderate: 1-2 years
severe: 6-12 months
320
valvular disease - mitral regurg - treatment - indications for surgery
- ANY SYMPTOMS at rest or exercise - initiate repair if feasible
- Asymptomatic: if ejection fraction less than 60%, if new onset atrial fib
321
valvular disease - aortic stenosis
narrowing aortic valve resulting in obstruction LV SV leading to symptoms breathlessness, syncope, fatigue, chest pain
322
valvular disease - aortic stenosis - epidemiology
- normal valve area 3-4cm2
- symptoms: valve area 1/4 normal
- primarily disease of ageing
- congenital 2nd most common cause
- most common valve disease western world
323
valvular disease - aortic stenosis - types
- supravalvular (above valve) eg congen fibrous diaphragm above aortic valve
- subvalvular (below valve) eg congen fibrous ridge/diaphragm immediatley below aortic valve
- valvular - MOST COMMONE
324
valvular disease - aortic stenosis - 3 main causes
- calcific aortic valvular disease (CAVD) calcification aortic valve resulting in stenosis- most commonly seen in eldery
- calcification of congen bicuspid aortic valve (BAV) resulting in stenosis
- rheumatic heart disease (rare-eradication)
325
valvular disease - aortic stenosis - risk factor
-congen bicuspid aortic valve (BAV) (occurs mainly in males) predisposes to stenosis, regurgitation
326
valvular disease - aortic stenosis - pathophysiology
- narrowing=obstructed LV emptying, pressure gradient develops (LV-aorta) = increased afterload
- so increased LV pressure=LV hypertrophy
- relative ischaemia LV myocardium=anginas, arrhythmias, LV failure
- severe on exercise-requires increase CO. BP falls, coronary ischaemia worsens, myocardium fails, arrhythmias develop
327
valvular disease - aortic stenosis - clinical presentation
suspect in ANY elderly person with chest pain, exertional dysponea, syncope
- classic triad
- sudden death
- slow rising carotid pulse
- heart sounds/ murmurs
328
valvular disease - aortic stenosis - clinical presentation - classic triad
- chest pain / angina
- heart failure (usually after 60) (dysponea on exertion)
- syncope - usually exertional
329
valvular disease - aortic stenosis - clinical presentation - pulsus tardus and pulsus parvus
- pulsus tardus - slow rising carotid pulse
| - pulsus parvus - decreased pulse amplitude
330
valvular disease - aortic stenosis - clinical presentation - heart sounds
- soft or absent 2nd heart sound
- prominent S4 : LV hypertrophy
- ejection systolic murmur: crescendo-decrescendo character
- loudness is not associated with severity
331
valvular disease - aortic stenosis - differential diagnosis
- aortic regurgitation
| - subacute bacterial endocarditis
332
valvular disease - aortic stenosis - diagnosis - ECG
- LV hypertrophy
- LA delay
- LV 'strain pattern' due to 'pressure overload' : depressed ST segments, T wave inversion in leads oriented towards LV eg I, AVL, V5, V6 when disease severe
333
valvular disease - aortic stenosis - diagnosis - echo
- LV size and function - LV hypertrophy, dilation, ejection fraction
- doppler derived gradient and valve area (AVA) - assessment pressure gradient across valve during systole
334
valvular disease - aortic stenosis - diagnosis - CXR
- LV hypertrophy
| - calcified aortic valve
335
valvular disease - aortic stenosis - treatment
- rigorous dental hygiene/care (increased IE risk in valvular heart disease) - consider IE prophylaxis in dental procedures
- mechanical problem so limited role for meds
- vasodilators CONTRAINDICATED (may trigger hypotension thus syncope)
- surgical aortic valve replacement
- transcutaneous aortic valve implementation (TAVI)
336
valvular heart disease - aortic stenosis - treatment - surgical aortic valve replacement indications
- ANY symptomatic patients w/ severe aortic stenosis (inc symptoms with exercise)
- any patient decreasing ejection fraction
- any patient undergoing CABG w/ moderate/ severe aortic stenosis
337
valvular heart disease - aortic stenosis - treatment - transcutaneous aortic valve implementation (TAVI)
- minimally invasive
- catheter up aorta inflate balloon across narrowed valve, crack calcification
- another catheter, leaves stent with a valve = new aortic valve
338
valvular heart disease - aortic regurgitation
-leakage blood into LV from aorta during diastole, due to ineffective coaptation (bringing together) of 3 aortic cusps
339
valvular heart disease - aortic regurgitation - epidemiology
```
-can associated with aortic stenosis
main causes:
-congenital bicuspid aortic valve (BAV) (chronic)
-rheumatic fever (chronic)
-infective endocarditis (acute)
```
340
valvular heart disease - aortic regurg - risk factors
- SLE (lupus)
- Marfan's, Ehlers-Danlos syndromes (connective tissue disorders)
- aortic dilatation
- infective endocarditis or aortic dissection
341
valvular heart disease - aortic regurg - pathophysiology
(reflux is during diastole)
- LV dilation and hypertrophy to maintain blood pumped into aorta / net CO
- progressive dilation = heart failure
- root aorta supplies coronary arteries via coronary sinus : coronary perfusion decreases
- LV hypertrophy = cardiac ischaemia
342
valvular heart disease - aortic regurg - clinical presentation
chronic regurg - patients remain asymptomatic many years
- exertional dysponea, palpitations, syncope
- angina
- wide pulse pressure
- apex beat displaced laterally
- hear sounds/murmurs
- collapsing water hammer pulse
- Quincke's sign, de Musset's sign, pistol shot femoral
343
valvular heart disease - aortic regurg - heart sounds
- diastolic blowing murmur at the left sternal boarder
| - systolic ejection murmur - due to increased flow across aortic valve
344
valvular heart disease - aortic regurg - Quincke's sign, de Musset's sign
Quincke's sign - capillary pulsation in the nailbeds
| de Musset's sign - head nodding with each heart beat
345
valvular heart disease - aortic regurg - differential diagnosis
- heart failure
- infective endocarditis
- mitral regurgitation
346
valvular heart disease - aortic regurg - echo
- evaluation of aortic valve and aortic route
- measurement LV dimensions and function
- cornerstone for decision making, follow up evaluation
347
valvular heart disease - aortic regurg - CXR
- enlarged cardiac silhouette and aortic route enlargement
| - LV enlargement
348
valvular heart disease - aortic regurg - ECG
- signs LV hypertrophy : 'volume overload'
- tall R waves, deeply inverted T waves in left sided chest leads
- deep S waves in right sided leads
349
valvular heart disease - aortic regurg - treatment
- IE prophylaxis (any valvular disease)
- symptomatic/ hypertensive: vasodilators eg ACEi eg Ramipril to improve SV, reduce regurg
- serial echos to monitor progression
- surgical valve replacement - if symptoms increasing eg enlarging heart on CXR, echo or ECG deterioration (T wave inversion lateral leads)
350
Infective endocarditis
- an infection of the endocardium or vascular endothelium of the heart
- known as subacute bacterial endocarditis
351
infective endocarditis - where does it occur?
- valves with conegn or acquired defects (usually left side of heart)
- right sided IE more common in IV drugusers
- normal valves with virulent organisms eg Streptococcus pneumoniae, Staphylococcus aureus
- prosthetic valves, pacemakers
352
infective endocarditis - epidemiology
- more common developing countries
- elderly / those with prosthetic valves
- young IV drug users
- young with congen heart disease
353
infective endocarditis - what caused by?
- Staphylococcus aureus most common (IVDU, diabetes, surgery)
- Pseudomonas aeruginosa
- Streptococcus viridans (dental problems) - GRAM POSITIVE, alpha haemolytic, optochin resistant (step mutans, strep sanguis, strep milleri, step oralis)
354
infective endocarditis - risk factors
- IV drug use
- poor dental hygiene
- skin and soft tissue infection
- dental treatment
- IV cannula
- cardiac surgery
- pacemaker
355
infective endocarditis - pathophysiology
consequences of
- presence of organisms in bloodstream
- abnormal cardiac endothelium (facilitates adherence and growth)
- bacteraemia (patient specific reasons)
- associated w/ diagnostic/therapeutic procedures
- infected vegetation (damaged endocardium promotes platelet, fibrin deposition, organisms adhere and grow)
356
infective endocarditis - pathophysiology - bacteraemia for patient specific reasons
- poor dental hygiene (bacteria tooth plaque - gum disease - bleeding, inflammation - brushing/ dental procedures bacteria enter bloodstream -> heart)
- IV drug use
- soft tissue infections
357
infective endocarditis - pathophysiology - associated with diagnostic / therapeutic procedures
- dental treatment
- intravascular cannulae
- cardiac surgery
- permanent pacemakers
358
infective endocarditis - pathophysiology - worsening heart failure
virulent organisms destroy valve they are on resulting in regurgitation, worsening heart failure
359
infective endocarditis - clinical presentation - HIGH CLINICAL SUSPICION
- new valve lesion/regurgitant murmur
- embolic events unknown origin
- sepsis unknown origin
- haematuria, glomerulonephritis, suspected renal infarction
- fever PLUS prosthetic material in heart, IE risk factor eg IVDU, newly developed ventricular arrhythmias/ conduction disturbances
360
infective endocarditis - clinical presentation - general
ANY pt w/ heart murmur, fever must exclude
- headache, confusion, malaise, fever, night sweats (unspecific - often misdiagnosed)
- finger clubbing
- Staph aureus -develop v quickly- high fever, feel ill rapidly- other virulent wont feel as ill
- embolisation of vegetations eg stroke, PE, bone infection, kidney dysfunction, MI
- arrhythmia, heart failure (valve dysfunction
361
infective endocarditis - clinical manifestations
- splinter haemorrhages (finger nail beds)
- embolic skin lesions (black skin spots)
- Osler nodes - tender nodules in digits
- Janeway lesions- finger haemorrhages, nodules
- Roth spots - retinal haemorrhages with white or clear centres seen on fundoscopy
- Petechiae- small red/ purple spots caused by bleeds in skin
362
infective endocarditis - diagnosis
- Duke's criteria
- Blood cultures
- Blood test
- Urinalysis - haematuria
- CXR (cardiomegaly)
- ECG (long PR interval at regular intervals)
- Echo (TTE vs TOE)
363
infective endocarditis - diagnosis - blood cultures and blood tests
- blood cultures: 3 sets from different sites over 24 hours, take BEFORE antibiotics started, identifies in 75% cases
- blood tests: CRP, ESR raised, normochromic and normocytic anaemia, neutrophilia
364
infective endocarditis - echo TTE vs TOE
- Transthoracic echo - safe, non invasive, no discomfort, often poor images (low sensitivity), identifies vegetations (2mm+) - neg TTE does not exclude possibility IE
- Transoesophageal echo - more sensitive, very uncomfy, useful visualising mitral lesions, possible aortic root abscesses - BETTER A DIAGNOSING
365
Infective endocarditis - treatment
- antibiotics (organism specific)
- treat complications (heart block, arrhythmias, embolism, abscess drainage)
- surgery
- prevention (eg good oral health, patient education symptoms may indicate IE)
366
infective endocarditis - treatment - antibiotics
4-6 weeks
- if NOT staphylococcus then Benzylpenicillin (IV penicillin) and Gentamycin
- If IS staph then Vancomycin and Rifampicin (if MRSA)
367
infective endocarditis - treatment - surgery
- removing valve, replacing with prosthetic one, operate if:
- if infection cannot be antibiotic cured
- to remove infected devices
- to remove large vegetations before they embolise
368
Hypertension (HTN)
- major cause premature vascular disease -> cerebrovascular events, IHD, peripheral vascular disease
- increases mortality
- commonest cause cardiac failure, major atherosclerosis, cerebral haemorrhage risk factor
369
Hypertension - epidemiology
- screening vital -often symptomless
- major risk factor CVD
- under diagnosed, under treated, poorly controlled in UK
- prevelant over 35s , more common men
- less than 140/90 = normotensive
370
Hypertension - stage 1 and stage 2
- Stage 1: more than/ equal to 140/90mmHg clinic BP. Daytime av ABPM/HBPM greater than equal to 135/85mmHg
- Stage 2: more than/equal to 160/100mmHg clinic BP. Daytime av ABPM/HBPM greater than/ equal to 150/95mmHg
371
Hypertension - severe hypertension
-clinic systolic BP greater than/ equal to 180mmHg and/or diastolic greater than/ equal to 110mmHg
(start immediate antihypertensive drugs)
372
Hypertension - essential/primary/idiopathic hypertension
- most cases are essential
- primary cause unknown - multifactoral: genetic susceptibility, excessive symp nervous system activity, abnormalities Na+/K+ membrane transport, high salt intake, abnormalities in RAAS
373
hypertension - secondary hypertension
- commonly caused renal disease/pregnancy
| - possibly endocrine causes, aorta coartication, drug therapy
374
secondary hypertension causes - renal disease
- can be both cause and result of HTN
- chronic kidney disease commonest cause secondary hypertension, diabetes is most common cause CKD
- acceleration atherosclerosis, endothelial cell dysfunction (vascular changes induced by hypertension) may cause or exacerbate renal disease
- chronic glomerulonephritis another potential cause (less common now)
375
secondary hypertension - endocrine causes (tumours are RARE)
- Cushing's syndrome -hypersecretion corticosteroids (enhcnace adrenalines=vasoconstriction)
- Conn's syndrome -adrenal tumor secretes aldosterone
- Pheochromocytoma - adrenal tumor secretes catecholamines (stimulate alpha and beta adrenergic receptors -vasoconstriction, increased cardiac contractility and HR)
376
secondary hypertension causes -coartication of the aorta
- systemic hypertension commonest features in cortication
- raised BP detected either arm, not legs
- femoral pulse delayed relative to radial
- undetected/untreated die cardiac failure, hypertensive cerebral haemorrhage, dissecting aneurysm
377
secondary hypertension causes - drug therapy
- corticosteroids eg Prednisolone
- cyclosporin
- erythropoietin
- some types oral contraceptive pill
- antidepressants, antismokings, antiADHDs
- alcohol, amphetamines, ecstacy, cocaine
378
Hypertension - risk factors
- ageing
- race (more common in black people)
- family history
- overweight and obese, little exercise
- smoking, too much salt in diet
- alcohol, diabetes, stress
379
hypertension - pathophysiology
- vascular changes - eg accelerates atherosclerosis
- heart - major risk factor IHD
- nervous system - intracerebral haemorrhages (death)
- kidneys
- malignant hypertension consequences
380
hypertension pathophysiology - vascular changes
- accelerates atherosclerosis
- thickening media (muscular arteries)
- smaller arteries, arterioles esp effected
- endothelial cell dysfunction associated w/ impaired NO mediated vasodilatation, enhanced secretion vasoconstrictors inc endothelins, prostaglandins
381
hypertension pathophysiology - kidneys
HTN can cause or be result of renal disease
| -kidney size often reduced, small vessels: intimal thickening medial hypertrophy, numbers sclerotic glomeruli increased
382
hypertension pathophysiology - what is malignant hypertension
- markedly raised diastolic blood pressure, usually over 120mmHg and progressive renal disease
- quite rare, can occur prev fit individuals, often black males 30s-40s
- prominent renal vascular changes, usually evidence acute haemorrhage, papilloedema (optic disc swelling: +intracran pressure)
383
hypertension pathophysiology - malignant hypertension consequences
- cardiac failure, LV hypertrophy + dilatation
- blurred vision (papilloedema, retinal haemorrhages)
- haematuria, renal failure (fibrinoid necrosis of glomeruli)
- severe headache, cerebral haemorrhages
384
Hypertension - clinical presentation
- usually ASYMPTOMATIC (except malignant hypertension)
| - found on screening
385
Hypertension - diagnosis
- end organ damage eg LV hypertrophy, retinopathy, proteinuria - indicates severity, duration HTN, associated poorer prognosis
- urinalysis
- blood tests
- fundoscopy/opthalmoscopy
- ECG, echocardiogram
- 24hr ambulatory BP monitoring
386
Hypertension - diagnostic tests - what are you looking for
Urinalysis: protein, albumin:creatinine ratio, haematuria
Blood tests: serum creatinine, eGFR, glucose (assess diabetes risk)
Fundoscopy: retinal haemorrhages, papilloedema
ECG, echo: LV hypertrophy
387
Hypertension - what is the treatment goal BP value?
140/90mmHg
388
Hypertension - treatment
- change diet (lots veg, fruits, low fat)
- regular physical exercise
- reduce alcohol and salt intake
- lose weight
- stop smoking
- drugs (using NICE 'ACD' pathway)
389
Hypertension - pharmacological treatment - NICE guidelines ACD pathway
- under 55: ACEi (ramipril, enalapril) or low cost ARB (candesartan, losartan) if cough
- over 55 or any age of black/afrocaribbean origin: calcium channel blocker (nifedipine, amlodipine)
- Step 2: calcium channel blocker AND ACEi/ARB
- Step 3: add thiazide like diuretic (bendroflumethiazide)
390
Hypertension treatment - beta blockers
eg bisoprolol, metoprolol
- consider in young people esp intolerant ACEi/ ARBs
- NOT first line treatment
- if higher dose not tolerated in some patients, consider BBs
391
Acute myocardial infarction - definition and 2 types
- necrosis cardiac tissue (myocyte death) due to prolonged myocardial ischaemia, due to COMPLETE occlusion of artery by thrombus
- STEMI vs NSTEMI/non Q infarction
392
acute myocardial infarction - STEMI
- COMPLETE occlusion MAJOR coronary artery prev affected by atherosclerosis
- full thickness damage heart muscle
- usually diagnosed ECG on presentation
- tall T waves, ST elevation subsequent pathological Q wave
- may present new LBBB on ECG
393
acute myocardial infarction - NSTEMI
- complete occlusion minor, or partial occlusion major coronary artery prev affected atherosclerosis
- partial thickness damage heart muscle
- RETEROSPECTIVE diagnosis after troponin results, sometimes other investigations
- ST depression, T wave inversion
394
acute MI - epidemiology
- STEMI most common medical emergency
- STEMI 5/1000 deaths per annum UK
- worse prognosis: elderly, those with LV heart failure
395
acute MI - risk factors
- age, being male
- history premature CHD
- premature menopause
- diabetes mellitus, smoking, hypertension
- hyperlipidaemia, obesity, sedentary lifestyle
- family history IHD, MI first degree relative below 55
396
acute MI - pathophysiology
- rupture/erosion vulnerable fibrous cap of coronary artery atheromatous plaque
- platelet aggregation, adhesion, local thrombus, vasoconstriction, distal thrombus embolisation - prolonged complete arterial occlusion - myocardial necrosis within 15-30mins in STEMI
397
acute MI - pathophysiology - specifically STEMI
- subendocardial myocardium initially affected, continued ischaemia, infarct zone extends through myocardium, producing transmural Q wave MI
- early reperfusion may salvage regions myocardium - reducing future mortality and morbidity
398
acute MI - clinical presentation
any severe chest pain more 20 mins - may be MI
- chest pain
- breathlessness
- fatigue
- distress and anxiety
- pale, clammy, marked sweating
- significant hypotension (low BP)
- bradycardia or tachycardia
399
acute MI - chest pain
- severe central ongoing, more 20mins
- pain radiate left arm, jaw, neck
- pain NOT respond sublingual GTN spray - opiate analgesia required
- substernal pressure, squeezing, aching, burning, sharp pain
- pain associated with nausea, vomiting, dyspnoea and/or palpitations
400
acute MI - differential diagnosis
- NSTEMI, unstable angina, stable angina
- pneumonia, pneumothorax, heart failure
- oesophageal spasm, GORD, acute gastritis
- pancreatitis, MSK chest pain, PE
- pericarditis, anxiety attack
401
acute MI - STEMI diagnosis
- diagnosed on presentation
- ST elevation, tall T waves
- LBBB
- T wave inversion and pathological Q waves follow
402
acute MI - NSTEMI diagnosis
- RETEROSPECTIVE diagnosis after troponin etc results
| - ST depression, T wave inversion
403
acute MI - diagnosis - ECG
- performed on admission to A+E
- continuous monitoring required - high likelihood significant cardiac arrhythmias
- ECG changes confined to leads that face infarction
404
acute MI - evolution STEMI on ECG
- after first few mins: T waves tall, pointed, upright, ST segment elevation
- after first few hours, T waves invert, R wave voltage decreases, Q waves develop
- after few days, ST segment normal
- after weeks or months, T wave may return upright , Q WAVE REMAINS
405
acute MI - diagnosis
Troponin I or T increased
Myoglobin increased
Transthoracic echo may help confirm MI - wall motion abnormalities detected early in STEMI
406
acute MI - treatment
- pre hospital (aspirin 300mg chewable, GTN sublingual, morphine)
- hospital (IV morphine, oxygen if sats below 95% or breathless, BB, P2Y12i - clopidogrel)
- coronary revascularisation (PCI, CABG)
- fibrinolysis (enhance breakdown occlusive thromboses acitvation plasminogen-plasmin)
407
acute MI - treatment - coronary revascularisation
- PCI - all patients with acute STEMI who can be transferred primary PCI centre within 120 mins first medical contact. If not, fibrinolysis, transfer PCI centre after infusion
- CABG
408
acute MI - risk factor modification
- stop smoking
- lose weight, exercise daily, healthy diet
- treat hypertension and diabetes
- low fat diet with statins
409
acute MI - secondary prevention (5)
- statins
- long term aspirin
- warfarin if large MI
- beta blockers
- ACE inhibitors
410
acute MI - 4 complications of myocardial infarction
-sudden death (within hours. ventricle fib)
-arrhythmias (few days. electrical instab,
pump failure, exces symp stimulation)
-persistent pain (12 hours - few days.
myocardial necrosis)
-heart failure (CO insufficient meet body metabolic demands. ventricular dysfunction after muscle necrosis also resulting in arrhythmias)
411
acute MI - 4 complications of myocardial infarction
- mitral incompetence(first few days-later. myocardial scarring preventing valve closure)
- pericarditis (transmural infarct=inflamm of pericardium, more common STEMI)
- cardiac rupture (early-result of shearing between mobile, immobile myocardium)
- ventricular aneurysm (stretching newly formed collagenous scar tissue)
412
acute MI - 8 complications of myocardial infarction
- sudden death
- pericarditis
- arrhythmias
- cardiac rupture
- ventricular aneurysm
- persistant pain
- heart failure
- mitral incompetence
413
Cardiac arrhythmias
```
'an abnormality of the cardiac rhythm'
can cause: sudden death
syncope
heart failure
chest pain
dizziness
palpitations
no symptoms
```
414
2 main types of cardiac arrhythmias
Bradycardia
| Tachycardia
415
Bradycardia
- heart rate slow - less than 60bpm (day) less than 50bpm(night)
- usually asymptomatic unless rate really slow
- normal in athletes: increased vagal tone thus parasymp activity
416
Tachycardia
fast HR - more than 100bpm
- more symptomatic when arrhythmia is fast and sustained
- supraventricular tachycardias arise from atria or AV junction
- ventricular tachycardias arise from ventricles
417
Sinus rhythm (normal) - the pathway
SAN - action potention - muscle cells of atria - depolarisation of AVN - slow - interventricular septum - bundle of His - R,L bundle branches - free walls both ventricles - Purkinje cells - ventricular myocardial cells
418
Sinus rhythm (normal)
- SAN @ junction beterrn superior VC and RA
- action potential travels through gap junctions to get to muscle cells
- AVN in lower interatrial septum
- slow spread action potential between AVN, ventricles allows for complete contraction atria before ventricles are excited
419
Sinus node function
- SAN=normal cardiac pacemaker
- depolarises spontaneously
- rate SAN discharge modulated by autonomic nervous system, normally parasymp predominates, slowing spontaneous discharge rate
- increased parasymp tone or decreased symp stimulation produces bradycardia (vice versa to produce tachy)
- women slightly faster sinus rhythm
420
How is normal sinus rhythm characterised on an ECG?
P waves that are upright in leads I and II but inverted in the cavity leads AVR and V1
(and each P wave followed by a QRS complex)
421
Sinus arrhythmia
- fluctuations autonomic tone result in changed sinus discharge rate
- during inspiration - parasympathetic tone falls, heart rate quickens
- during expiration - parasympathetic tone increases so heart rate fails
- this variation is normal esp children and young adults
422
Atrial fibrillation
-chaotic irregular atrial rhythm 300-600bpm, AV node respondes intermittently hence an irregular ventricular rate
423
atrial fibrillation - epidemiology
- most common sustained cardiac arrhythmia
- more males
- 5-15% patients over 75
- paroxysmal (self terminating) or persistant (continues without intervention)
424
atrial fibrillation - 5 clinical classifications
- Acute: onset within last 48 hours
- Paroxysmal: stops spontaneously within 7 days
- Recurrent: 2 or more episodes
- Persistent: continues for more than 7 days and not self terminating
- Permanent
425
atrial fibrillation - causes
- idiopathic (5-10%)
- Hypertension (most common developed world)
- Heart failure (most common heart failure)
- Coronary artery disease
- Valvular heart disease (esp mitral stenosis)
- Cardiac surgery (1/3rd patients)
- Cardiomyopathy (rare cause)
- Rheumatic heart disease
- Acute excess alcohol intoxication
- any condition results in raised atrial pressure, increased atrial mass, atrial fibrosis, inflamm, infiltration of atrium
426
atrial fib - risk factors
- older than 60
- diabetes
- hypertension
- coronary artery disease
- prior MI
- structural heart disease (valve problems/ congenital defects)
427
atrial fib - pathophysiology
- maintained by continuous rapid (300-600bpm) activation atria by multiple meandering re-entry wavelets
- often driven by rapidly depolarising automatic foci, located predom within pulmonary veins
- atria respond electrically at this rate but there is no coordinated mechanical action - only proportion impulses conducted to ventricles (no unified atrial contraction - atrial spasm)
428
atrial fib - pathophysiology - ventricular response
- depends on rate and regularity atrial activity, esp at entry to AV node and balance between sym and parasymp tone
- CO drops by 10-20% - ventricles not primed reliably by atria
429
atrial fib and thromboembolic events
- atria spasming = some parts not contracting - causes blood to pool in these parts, remain still - begins to clot = thrombus, easily embolism -> stroke
- ATRIAL FIB - GIVE BLOOD THINNER EG WARFARIN
430
atrial fib clinical presentation
- symptoms highly variable
- asymptomatic
- palpitations
- dyspnoea and/or chest pain (following onset atrial fib)
- fatigue
- apical pulse greater radial rate
- 1st heart sound variable intensity
431
atrial fib differential diagnosis
- atrial flutter
| - supraventricular tachyarrhythmias
432
Atrial fib diagnosis - ECG
ABSENT P WAVES
| IRREGULAR AND RAPID QRS COMPLEX
433
atrial fib acute management definition
when AF is due to acute precipitating event eg alcohol toxicity, chest infection, hyperthyroidism - provoking cause should be treated
434
atrial fib acute management
- cardioversion - conversion to sinus rhythm achieved electrically by DC shock eg defibrillator - give LMW-heparin eg Enoxaparin to minimise thromboembolism risk associated with cardioversion
- if fails - medically by IV infusion antiarrhythmic drug eg amiodarone
- Ventricular rate control - drugs that block AV node eg Ca channel blocker, BBs, digoxin, antiarrhythmic drug eg amiodarone
435
atrial fib - long term and stable patient management
- Rate control - AV node slowing agents plus oral anticoagulants - beta blocker - calcium channel blocker - last resort digoxin then amiodarone
- Rhythm control - advocated for younger, symptomatic, physically active patients - cardioversion to sinus rhythm, use BBs to surpress arrhythmia - can use pharma cardioversion eg Flecainide if no structural heart defect, Amiodarone if is - appropriate anticoagulation with cardioversion
436
CHA2DS2VASc score to calculate stroke risk thus need for anticoagulation
```
Congestive heart failure (1 point)
Hypertension (1 point)
Age greater/equal 75 (2 points)
Diabetes mellitus (1 point)
Stroke/TIA/thromboembolism (2 points)
Vascular disease (aorta, coronary, peripheral arteries) (1 point)
Age 65-74 (1 point)
Sex category female (1 point)
Score 1 - consider anticoag and or aspirin
Score 2 and above - requires oral anticoag
```
437
Heart block
- can occur any level in conducting system
- block in AV node or His bundle results in AV block
- block lower conducting system produces bundle branch block
438
heart block - AV block - 3 forms?
- first degree AV block
- second degree AV block
- third degree AV block
439
heart block - first degree AV block
- simple prolongation PR interval to greater than 0.22s
- every atrial depolarisation followed by conduction to ventricles but with delay
- causes: hypokalarmia, myocarditis, inferior MI, AV node blocking drugs eg BBs, Ca channel blockers, digoxin
- ASYMPTOMATIC - NO TREATMENT
440
heart block - second degree AV block
- some P waves conduct, others do not
- acute MI may produce it
- Morbitz I block vs Morbitz II block
441
heart block - second degree AV block - Morbitz I block
- Wenckebach block phenomenon
- progressive PR interval prolongation until beat is dropped and P wave fails to conduct (excitation completely fails to pass through bundle of his)
- PR interval before blocked P wave much longer
- causes: AVN blocking drugs BB, CCB, digoxin - inferior MI
- causes light headiness, dizziness, syncope
- does not require pacemaker unless poorly tolerated
442
heart block - second degree AV block - Morbitz II BLOCK
- PR interval constant, QRS interval dropped
- failure of conduction through His-Purkinje system
- causes: anterior MI, mitral valve surgery, SLE, lyme disease, rheumatic fever
- causes shortness of breath, postural hypertension, chest pain
- high risk developing sudden complete AV block, pacemaker should be inserted
443
heart block - third degree AV block - COMPLETE AV BLOCK
- all atrial activity fails to conduct to ventricles
- ventricle contractions sustained by spontaneous escape rhythm which originates below the block
- P waves completely independent of QRS complex
- causes: structural heart disease (transposition great vessels), IHD (acute MI), hypertension, endocarditis or lyme disease
444
heart block - third degree AV block - complete AV block - Narrow - complex escape rhythms
- QRS complex less than 0.12 seconds
- implies block originates in His bundle thus region block lies more proximally in AV node
- recent onset narrow complex AV block with transient causes may respond IV ATROPINE
- chronic narrow complex AV block requires permanent pacemaker if symptomatic
445
heart block - third degree AV block - complete AV block - broad - complex escape rhythm - B - below His
- QRS complex greater than 0.12 seconds
- implies block originates below bundle of his thus region of block lies more distally His-Purkinje system
- dizziness, blackouts
- permanent pacemaker required - treatment depends on aetiology - IV atropine
