Cardiology Flashcards
1
Q
how do you treat arterial thrombosis in coronary system- 3
A
aspirin and other antiplatelets
thrombolytic therapy- tissue plasminogen activator, streptokinase
reperfusion- catheter directed treatments and stents
2
Q
how do you treat arterial thrombosis in brain
A
aspirin and other anti-platlets
thrombolysis
3
Q
3 main antiplatelets
A
aspirin
clopidogrel
dipyridamole
4
Q
where would you find a venous thrombus
A
peripherally in leg and cerebral
5
Q
what is d dimer
A
a test to EXCLUDE dvt/ pe
6
Q
treatments for venous thrombosis- 3
A
DOAC (direct oral anticoagulation- tablet)
warfarin
heparin or low molecular weight heparin
7
Q
disadvantage of low molecular weight heparin
A
injectable only
8
Q
prevention for venous thrombosis
A
VTE prophylaxis- mechanical (like stockings) or chemical
early mobilization and good hydration
9
Q
difference between heparin and low molecular weight heparin
A
heparin- continuous IV infusion, requires monitoring with APTT , short half life
LMWH- subcutaneous injection in tummy, once a day , used for treatment and prophylaxis
10
Q
how does warfarin work
A
prevents synthesis of factor 2,7,9,10
antagonist of vitamin K
prolongs prothrombin time
11
Q
signs and symptoms of DVT
A
symptoms: leg pain, swelling
signs- tenderness, swelling, warmth, discoloration
12
Q
signs and symptoms of pulmonary embomism
A
signs- tachycardia, tachypnoea
symptoms- breathlessness, pleuritic chest pain
13
Q
what heart failure results from pulmonary embolism
A
right heart failure- cor pulmonale
14
Q
what conditions present with pleuritic chest pain and how to differentiate
A
pe, pneumothorax, pneumonia
cxr- pe= normal, pneumonia and pneumothorax is diagnostic
15
Q
what is in a athersoscleortic plaque structure
A
lipid
necrotic core
connective tissue
fibrous cap
16
Q
what are the major cell types in atherogenesis
A
endothelium
macrophages
smooth muscle cells
platelets
17
Q
risk factors for venous thromboembolism
A
VIRCHOWS TRIAD
- venous stasis (change in blood flow)- immobility- long haul flights, after surgery. you get aggregation of clotting factors
- Endothelial injury- smoking, trauma, surgery. damaged endothelim cant secrete anticoagulants
- Hypercoagubility- preggo, obesity, sepsis, contraceptives
18
Q
what does venous thromboemolim usually result in
A
PE
DVT
19
Q
presentation + scoring for dvt
A
sudden onset PLEURETIC CHEST PAIN
dyspnoea with evidence of dvt (swollen calf and immonilsation)
haemoptysis
tachycardic, hypotensive, ankle oedema
wells score for pe is >4= likely pe.
4 or less is unlikely
20
Q
investigations for PE
A
if pe is likely (wells score>4)- CTPA (CT pulmonary angiogram that looks for clots in the lungs)
1st line is D-dimer test (in blood)- if raised then PE is likely and should do a CTPA, if not raised then its not a PE- it excludes this but isnt diagnostic
x ray would look normal in a PE
21
Q
treatment for pe
A
if massive PE- thrombolytics
if not massive (more common)- give anticoagulants - DOAC- 1st line DOAC is apixaban/ rivaroxaban
if renal impairment- LMWH
22
Q
presentation of dvt + scoring
A
unilateral swollen calf with engorged leg veins- typically warm and oedematous
if complete occlusion- severe ischemic leg turns blue
on wells score, >1= likely DVT
23
Q
investigations for dvt (first line and gold standard
A
wells score less than 1- d dimer to exclude
if raised then do duplex ultrasound which is gold standard!
duplex ultrasound gives you an idea of blood flow and is always gold standard when investigating veins
24
Q
treatment for dvt
A
same as non-massive PE
- anticoagulant DOACs- apixaban and Rivaroxiban
- LMHW if renal impairment
25
differentials for dvt
cellulitis which presents with swollen inflamed calf-
but this will show leukocytosis which is indicative of infection on blood test while dvt doesnt. dvt also conformed with d-dimer and duplex ultrasound
26
definition of abdominal aortic aneurysm, where is it typically, what is false
weakening of arterial walls leading to dilation where diameter is >3cm
typically infrarenal (below renal arteries)
true aneurysm is where all 3 layers of vascular tunic are degraded (usually genetic)
27
risk factors for aaa
(basically risk factors for atherosclerosis)- smoking, obesity, hypertension, trauma, increasing age, family history
28
pathophysiology of aaa
smooth muscle, elastic and structural degradation in all 3 layers of the vascular tunic (intima, media, adventitia)
- if not all 3 layers then a pseudoaneurysm
dilation >3cn
above 5.5cm is a very high risk of rupture and a rurpture is a surgical emergency
29
presentation of aaa
asymptomatic until high rupture risk
pulsatile mass in abdomen
ruptured= sudden epigastric pain radiating to flank, hypotensive and tachycardic
30
diagnosis of aaa
1st line + diagnostic is abdominal ultrasound
also can do ct angiogram which is more detailed
31
treatment of aaa
non ruptured:
- manage rf- stop smoking, lower bmi, statins..
- if expanding 1cm+/year- surgery
- endovascular repair- stent though femoral artery
- open surgery- fewer complications but more invasive
ruptured:
- stabilise abcde, fluids
- AAA graft surgery- replace weakened walls with graft
32
diffential for aaa
differential is acute pancreatitis, but in that the mass is not pulsatile
33
definition of peripheral vascular disease
narrowing of the arteries supplying the peripheries (mostly calf- basically ihd of lower limb arteries)
34
risk factors for peripheral vascular disease
smoking, hypertension, ageing, obesity, CKD, T2DM
35
what are the stages of peripheral vascular disease
intermitted claudication
critical ischemia
acute- acute limb ischemia
36
pathophysiology and presentation of peripheral vascular disease- pathophysiology of each stage
caused by atherosclerotic plaque
intermittent claudication = least severe. astherosclortic partial lumen occlusion, crampy pain usually in calves after walking a certain distance. stops after few minutes of rest
critical limb ischemia= most severe. very big occlusion and blood supply is barely adequate to meet metabolic demand. pain at rest and risk of gangrene
- 6Ps!!!- present in critical limb ischemia but the more you have, the more life threatening, present in acute limb ischemia too
- pulselessness
- pallor
- pain- burning and worse at night
- perishingly cold
- parasthesia (pins and needles)
- paralysis
acute limb ischemia = complication where theres total occlusion of vessel due to embolic/ thrombolic formation at site of critical limb ischemia rapid onset of ischaemia in a limb
37
tests and indications of peripheral vascular disease
buerger test positive- elevate legs 45 degrees for one minute - pallor then reactive hyperemia when put down
skin changes on leg- cooler and ulcerations
ankle-brachial pressure index <0.9- lower perfusion to legs than arms and lack of lower leg pulse
38
treatment of peripheral vascular disease- different phases
drugs- atorvastatin, clopidogrel
intermittent claudication- RF management- smoking cessation, lower BMI, statins, aspirin/ clopidogrel
critical limb ischemia- revascularization surgery- endovascular by stent or surgical bypass
acute limb threatening ischemia- revascularization surgery within 4-6 hours
39
complication of peripheral vascular disease
amputations, permanent limb weakness, increased risk of cerebrovascular accidents
40
cardiomyopathy definition and categories
refers to diseases of the myocardium- heart muscular/ conduction defects
categorised into hypertrophic obstructive , restrictive, dilated
inherited cardiac condition
41
hypertrophic obstructive cardiomyopathy- cause
autosomal dominant genetic condition- defect in sarcomeres
42
hypertrophic obstructive cardiomyopathy- pathophysiology
left ventricle becomes hypertrophic, blocks blood flow out the left ventricle, decreased compliance and decreased CO
43
presentation of hypertrophic obstructive cardiomyopathy
often with sudden death, other is angina, exertional sob, syncope, palpitations
SAD
44
diagnosis of hypertrophic obstructive cardiomyopathy
ecg showing left ventricular hypertrophy, echo=definitive, genetic testing
45
treatment of hypertrophic obstructive cardiomyopathy
bb,ccb, amiodarone (anti-arrhythmic)
46
what cardiomyopathy is main cause of sudden death in young people
hypertrophic obstructive cardiomyopathy
47
dilated cardiomyopathy cause
autosomal dominant- often cytoskeleton gene mutation
48
what type of cardiomyopathy is most common
dilated cardiomyopathy
49
pathophysiology of dilated cardiomyopathy
dilated heart chambers- thin cardiac walls poorly contract- reduced CO
50
presentation of dilated cardiomyopathy
sob, heart failure, atrial fibrilation, thromboemboli
51
diagnosis for dilated cardiomyopathy
echo, ecg
52
treatment of dilated cardiomyopathy
treat underlying conditions and control symptoms
53
what is the rarest type of cardiomyopathy
restrictive cardiomyopathy
54
causes and pathophysiology of restrictive cardiomyopathy
causes- granulomatous disease- sarcoidosis, idiopathic
path- rigid fibrotic myocardium fills poorly and contracts poorly- reduced CO
55
presentation and diagnostic of restrive cardiomyopathy
px- dyspnoea, oedema, congestive hf
dx- ecg, echo, cardiac catherterisation is definitive
56
treatment of restrictive cardiomyopathy
tx- none- consider transplant
57
values for hypertension
clinical blood pressure >140/90
home/ ambulance > 135/85
58
causes of hypertension
most common= primary HTN= idiopathic
secondary HTN= bc of known secondary cause- ROPED- renal disease (ckd), obesity, pregnancy, endocrine (conns, cushings, phaeochromocytoma), drugs- (nsaids, steroids)
59
risk factors for hypertension
increased age
black ethnicity
overweight, lack of excersize, diavetes
stress
increased salt intake
family history
60
stages of hypertension
61
blood pressure targets
under 80- less than 140/90 or 135/85
over 80- less than 150/90 or 145/85
62
pathophysiology of hypertension
all mechanisms will increase raas and sns activity and tpt
blood pressure increases bc bp= co x tpr
63
presentation of hypertension
mostly asymptomtic
pulsatile headache, visual disturbances, seizures
consider secondary causes - phaeochromocytoma, cushings, conns
64
diagnosis of hypertension
bp reading in hospital 140/90 mmHg then ABMP for 24 hours to confirm (bp 135/85+ throughout the day)
asses end organ damage
- urinanalysis and egfr to check renal function
- echo/ecg to check LVH
65
treatment for hypertension
66
complications of hypertension
heart failure, severe increased risk of ihd, ckd, increased risk of cerebrovascular accident
67
what is the most common valvular disease
aortic stenosis
68
where do you hear the aortic valve
right of sternum, 2nd intercostal space
69
what is aortic stenosis
narrowing of aortic valve
70
causes of aortic stenosis
- idiopathic age-related calcification
- bicuspid aortic valve- congenital (its normally tricuspid)- need family screening after finding this
- rhematic heart disease
71
pathophysiology of aortic stenosis
- pressure gradianet develops between left ventricle and aorta- increased afterload
- left ventricle initially compensates by hypertrophying so it can eject more blood
- when the left ventricle compensatory mechanism of hypertropjy gets exhaused, the lv functon declines
72
presentation including heart sound for aortic stenosis
- triad: exertional synope, angina, exertional dyspnoea (SAD)
- slow rising carotid pulse and decreased pulse amplitude
- second heart sound (made by closing of aortic+ pulmonary valve) becomes soft or absent ( the aortic valve is not moving and therfore not closing)
- murmer- ejection systolic murmer- cresendo-decresendo character-radiates to carotid- louder and softer
73
gold standard investigation for aortic stenosis + what are you looking for
echocardiogram- look for left ventricular size and function, and aortic valve area (doppler derived). the aortic valve will barely open
74
treatment of aortic stenosis
- dental hygiene, consider infective endocarditis prophylaxis
- if symptomatic- surgery for aortic valve replacement TAVI- transcatheter aortic valve implant- stents the valve open
- in asymptomatic patients with severe as- consider intervention if adverse features on excersize testing
75
what is malignant hypertension
very high blood pressure causing immediate end organ damage- eg aki, acute stroke, acute coronary syndrome
76
in terms of dilation and hypertrophy, what do regurgitation and stenosis cause
regurgitation- proximal chamber dilation
stenosis- increases upstream pressure and causes proximal chamber dilation and hypertrophy
77
which valve disorders causes systolic murmers and which cause diastolic
systolic: asmr!- atrial stenosis, mitral regurgitation
diastolic: arms!- aortic regurgitation, mitral stenosis
78
how can you best hear murmers
rile!- right- inspiration
left- expiration
79
where do you hear mitral valve
left midclavicular line, 5th intercostal space
80
what is mitral regurgitation
backflow of blood from LV to LA during systole- volume overload
81
causes of mitral regurgitation
- MYXOMATIOUS MITRAL VALVE (mitral valve prolapse)- main cause
- IE
- rhematic heart disease
- dilated cardiomyopathy
82
pathophysiology of mitral regurgitation
volume overload- left atrial enlargement to compensate and lvh- get pulmonary hypertension- this causes exertional dyspnoea
progressive left ventricular volume overload leads to dilation and progressive heart failure
83
presentation + murmur type for MR
- ascultation: pansystolic blowing murmer at apex radiating to axilla- simmilarly in volume throughout systole
- murmer correlates to severity
- exertional dyspnoea - due to pulmonary hypertension from backlogged blood
- displaced apex beat because ventricle gets bigger
84
investigation for MR
gs= echocardiogram- la and lv size and function,
85
treatment for MR
- if severe/ symptoms at rest- - valve replace or repair,
- anticoag, bb, ccb if AF
86
what is aortic regurgitation
leakage of blood into lv during diastole due to ineffectve aoritc cusps
87
causes of AR
- biscuspid aortic valve- congenital (mc)
- rheumatic heart disease
- IE
88
presentation of AR
- wide pulse pressure- high systolic and low diastolic
- displaced apical pulse
- ascultation- early diastolic blowing murmur at left sternal border 2nd space and systiloc ejection murmur
- decrescendo
89
investigation for AR
gs= echo= evalulate aortic valve and root + dimension
90
treatment for AR
- consider ie prophylaxis
- serial echocardiograms to monitor progression
- medical management of any heart failure
- surgery if symptomatic with severe ar, and asymptomatic with lv systolic dysfunction
91
what is mitral stenosis
- rare
- obstruction of lv inflow that prevents proper filling during diastole
92
main cause of mitral stenosis
rhematic heart disease
93
patho of mitral stenosis
- rhd causes mitral inflammation, excacerbated over years with calcification. left atria dilates causing pulmonary hypertension- causing right heart failure symptoms
94
presentation of mitral stenosis
- malar cheek flush
- association with A.fib
- low pitched mid diastolic murmur- most prominent at apex- heard best when patients lying on elft
- intensity of murmer doesnt correlate with severity
95
investigation for mitral stenosis
echo- gs
96
treatment for mitral stenosis
- if present with a.fib- treat with anticoagulation
- asymptomatic- serial echocardiogram
- symptomatic- percutaneous mitral balloon valvotomy, mitral valve surgery or replacement
97
what do calcium channel blockers usually end in + give an example
-dipine
amlodipine
also verapamil
98
what do angiotensin 2 receptor blocker drugs end in
-artan
99
definition of aortic dissection
tear in intima of aorta, blood dissects into media. type of pseudoanyeurism, intramural
100
causes/ rf of aortic dissection
age, male, smoking, cholesterol, hypertension, sedentary lifestyle, CABG
101
main location of aortic dissection + types
right lateral area of arch- under the most stress. type a is ascending aorta before brachiocephalic. type b= descending aorta after left subclavian
102
pathophysiology of aortic dissection
blood dissects media, pools in the false lumen, can propagate forward or backward (anterograde or retrograde) causing low perfusion to end organs, organ failure and shock
103
presentation of aortic dissection
sudden onset ripping chest pain
(not mi- thats crushing and heavy)
back pain, abdomen pain
hypotension, hear an aortic regurg, syncope, low left arm peripheral pulse
104
investigation of aortic dissection
ct scan= gold standard
cxr shows widened mediastinum
toe = helpful
105
treatment of aortic dissection
surgical emergency
- type a= open surgery to remove section of aorta and replace with graft
- b- endovascular repair- catheter thry femoral and stent graft
medically- beta blocker- esmolol
if hypotensive- iv fluids, blood transfusion
106
complications of aortic dissection
mi, stroke, cardiac tamponade, death
107
what is cardiac tamponade
a medical or traumatic emergency that happens when enough fluid accumulates in the pericardial sac compressing the heart and leading to a decrease in cardiac output and shock
108
definition of peicarditis
typically acute inflammation of pericardium, with or without effusion
- effusion can be dry (fibrous) or wet (most common, exudative, hemorrhagic)
109
risk factors for pericarditis
male- age 20-50
viral infection
transmural mi
110
causes of pericarditis including main cause
idiopathic
main- VIRUS- coxsackie, ebv, cmv, herpes
bacteria- mycobacterium tuberculosis !
common- autoimmune- sle, sjrogens, RA
dresslers syndrome -post mi
111
pathophysiology of pericarditis
inflamed pericardial layers rub against eachother and cause further inflammation. inflammation causes narrowing of the pericardial space and if not treated it may remain dry or can lead to pericardial effusion
112
presentation of pericarditis overview
triad of signs: sharp chest pain, pericardial friction rub (to and fro sound when pt leans forward) and ecg changes
pain is worse lying down and worse with inspiration, better sitting forward
pain radiates to left shoulder and back (trapezius)
myalgia, tripod position to relieve pain,
signs of right sided heart failure (raised jvp and peripheral oedema)
113
in pericarditis- where is the pain and when is it better and worse
sharp chest pain that radiates to your left shoulder and back (traps)
its better in a tripod forward position and worse when lying down
114
what is the triad of signs for pericarditis
sharp chest pain
pericardial friction rub- leans forwards- a to and fro sound
ecg changes
115
investigations for pericarditis, which is diagnostic
ecg= diagnostic- widespread saddle shaped st elevation and pr depression
blood test shows raised wbc (infective), crp, esr (may show autoimmune)
cxr may show cardiomegalic heart
116
treatment for pericarditis
idiopathic + viral- NSAIDS eg aspirin + CHOLCHICINE (long term)
if bacterial consider abx
117
complications of pericarditis
pericardial effusion leading to CARDIAC TAMPONADE!, constrictive pericarditis
118
definition of atrial fibrilation- rhythm
electrical activity in the atria becomes disorganized, leading to random muscle twitching and an irregularly irregular pulse
119
causes of atrial fibrilation and what makes it worse
SMITH
-sepsis, mitral stenosis/regurgitation, IHD, thyrotoxocisis, hypertension
alcohol and caffeine make it worse
120
pathophysiology of A fib and why do you get complications
electric activity of heart is disorganized- san is overridden by random signals in atria- causes atria to twitch and contract at different times- causes irregularly irregular ventricular contraction
blood stagnates in atria forming a thrombus- may travel to brain causing ischaemic stroke (really high risk)
121
presentation of A fib
- palpitations
- irregularly irregular pulse
- thromboemoli (ischaemic stroke)
- chest pain, syncope, hypotension
122
diagnostic test of A fib and what you see
diagnostic= ecg.
- irregularly irregular pulse with narrow qrs <120ms
- no p waves and fibrillatory squigles
maybe echo later
123
treatment for a fib- both acute and chronic
acutely if unstable-/ syncope/ shock/ chest pain/ heart failure-synchronized cardioversion (shock)
stable/ long term- bb (heart rate and pulse), oral anticoag (stroke)
124
for a.fib- explain the scoring system to see if anticoag is needed
CHADS2-VASc-SCORE- stroke risk so anticoagulation needed
GREATER THAN 2= GIVE ORAL ANTICOAG (apixaban/ rivaroxaban)
congestive heart failure
hypertension
age > 76
DM
stroke
vascular disease
age 65-74
sex (female)
125
in a.fib, explain the score that asses risk of major bleeds in patients taking anticoagulation
- old age
- renal impairment
- bleeding previously
- iron- low hb
- taking antiplatelet
126
127
definition of atrial flutter
irregular organised atrial firing- 250-300bpm.
128
risk factors of atrial flutter
atrial fib. also similar aetiology to atrial fib
129
pathophysiology of atrial flutter
fast atrial ectopic firing (250-300bpm). causes atrial spasm but not as uncoordinated as A.Fib
130
presentation of atrial flutter
dyspnea, palpitations
131
diagnostic investigations of atrial flutter
ECG= diagnostic. saw tooth pattern on f wave. often with a 2:1 block (2 p waves for every QRS)
132
treatment, acute and stable of atrial flutter
acutely unstable- synchronized cardioversion
stable- beta blocker with oral anticoagulation
133
what do you call a large volume of fluid thats enough to impair ventricle filling
cardiac tamponade
134
what is pericardial effusion
accumulation of fluid in pericardial space accompanying pericarditis
135
causes/ rf of pericardial effusion
typically pericarditis
rf all pericarditis related- viral, autoimmune
136
presentation of pericardial effusions and its main complication
related to pericarditis
cardiac tamponade (effusion is large enough to raise intra-cranial pressure, squeezing the heart - reduced filling in diastole and decreased CO)-
- BECKS TRIAD (bless)- blood pressure lowered (hypotension), elevated JVP, soft/ muffled s1+s2 heart sounds
- pulsus paradoxicus- fall in systolic BC >10mmHg on inspiration- good indicator of tamponade
137
diagnostic investigation of pericardial effusion and other
effusion- echocardiogram= diagnostic- asses size fo effusion
cxr will show big globular heart
138
treatment of pericardial effusion and tamponade
effusion- treat underlying cause (usually nsaids and colchicine), drain effusion
cardiac tamponade- urgent paricardiocentesis
139
definition of heart block and bundle block and bundle branch block
when the av delays for too long
bundle block is when delay is in bundle of his (before split into r+l)- the r and l delay is bundle branch block
140
what is the av delay represented by on ecg and how long should this be
pr interval- 200ms/5 small boxes (120-200)
141
what is one small box on ecg equal to
0.04s
142
first degree heart block- what is it and treatment
the avn delay is just too long
prolonged pr interval (>200ms)
usually asymptomatic- so no treatment
143
what are the subcategories of type 2 heart block
mobitz 1/ wenckebach- progressive delay
mobitz 2- no progression, all or nothing
144
explain mobitz 1 in second degree heart block and treatment
MOBITZ 1/ wenckebach - delay gets progressively longer until you drop a beat
pr gets progressively longer until a beat is dropped and theres no qrs, and then normal pr returns
no tx unless theres symptoms eg syncope. tx= pacemaker
145
explain mobitz type 2 second degree heart block and treatment
MOBITZ 2- conduction through av node is all or nothing- atrial impulse goes through with no delay or it doesnt go through at all
pr interval is consistently prolonged (not progressively) and theres random dropped qrs , then the prolonged pr returns
treatment= pacemaker
146
what does a 3:1 heart block mean
p waves for every qrs is a 3:1 block
147
explain 3rd degree/ complete heart block and treatment
no impulses are conducted
ventricles recognixe they don’t get impulses so generate their own ventricular escape rhythm
the atria and ventricles now each have their own pacemaker and contract independantly of eachother- av dissasociation- reduced CO- syncope or sudden cardiac death
p and qrs waves appear at their own rates
NEEDS treatment- pacemaker.
148
cause of bundle branch block
usually caused by fibrosis- ischemia, heart attack , hypertension, CAD, cardiomyopathy
149
explain bundle branch block- how it works
conduction block on right bundle branch
sa node- atria contract- av node- bundle of his- at split it goes down left bundle first because right is blocked, so left ventricle contracts first, then to the right. (from left, spreads through purkinjie fibers to right)
150
on the leads what does bundle branch block look like
use chest leads- v1-v6
left- william - w in v1, m in v6
right- marrow- m in v1, w in v6
151
in structural heart defects, when is there cyanosis and when isnt there
blood shunts left to right- non cyanotic
right to left- cyanotic
152
what are the 4 features of tetralogy of fallot
- ventricular septal defect
- overriding aorta on top of the ventricular septal defect
- rv hypertrophy
- rv outflow obstruction
153
explain whats going on in tetralogy of fallot and what the baby looks like
- cyanotic, ventricular septal defect with rv outflow stenosis
- right vnetricule is higher pressure than the left, puncures hole in the ventricle, blue blood (deoxygenated) passes from RV to LV- patient is blue.
154
what position improves cyanosis in babies
knee to chest squat position
155
what would a chest x ray show in tetralogy of fallot and whats the treatment
boot shaped heart
full surgical repair within 2 years of life
156
explain coarctation of aorta- what is it whats happening
- aorta narrows at ductus arteriosus (pul artery to aorta)
- blood diverts through aortic arch branches- increased perfusion to upper body vs lower body
157
presentation, dx and tx of coarctation of aorta
- presentation- scapular bruits, upper body hypertension
- dx- cxr show dilated intercostal vessels, ct angiogram
- tx-surgical repair or stenting
158
what does ductus arteriosus do
connects pulmonary artery to aorta
159
what happens in a patent ductus arteriosus, presentation, dx and tx
fails to close after burth
- blood shunts from aorta to pulmonary trunk - risk of pulmonary overload + eisenmengers ( high pressure pul blood flow- damaage to pul vasculature- RV
- dyspnoea, failure to thrive- machine like murmur
- dx- echo
- tx- close it surgicially or percutaneously (medically first- ibuprofen, indomethacin)
160
what is an av septal defect , whats its presentation
hole down middle of heart
dyspnoea, exersize intolerant- eventually eisenmengers
161
what strucutal heart defect is downs syndrome most commonly associated with
atrioventricular septal defect
162
explain ventricular septal defect- whats happening, dx and tx
left to right- non cyanotic shunt. risk of eisenmangers + RVH
small vsd- asymptomatic
large vsd- excersize intolerance, failure to thrive,
dx- echo
tx- surgical closure or spontaneous
163
whats happening in an atrial septal defect, dx, tx
patient foramen ovale
shunt of blood left to right so non cyanotic
may overload right hand side circulation and cause rvh, worst case is eisenmengers
dx- echo
tx- spontaneous or surgical closure
164
define Infective endocarditis
infection of heart valve/ other endocardial strucutres in the heart
165
causes of carditis
- bacteria
- main cause= staph .aureus
- strep. viridans ( gram positive, a haemolytic, optochin resistant strep, associated with poor dental hygeine)
- s. boris- associated with colon cancer
- HACEK organisms- ***Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, and Kingella***
166
epidemiology of Infective endocarditis
elderly
young iv drug users
young with congenital heart disease
prostetic heart valves
167
what valve is affected in Infective endocarditis
ie typically affects MITRAL VALVE on left, but in IV drug users, affects more TRICUSPID
168
pathophysiology of Infective endocarditis
abnormal/ damaged endocardium have increased platelet , deposition- bacteria adheres to this and causes vegetations (mass of fibrin, platelets, bacteria and antibodies)
169
presentation of Infective endocarditis
FEVER+ NEW MURMUR!
fatigue, chest pain
janeway lesions- painless lesions in palms and soles due to microemboli
splinter haemorrhages in nail bed
osler nodes- painful, red lumps on tips of fingers and toes
roth spots- small ruptured capillaries in the eyewe- seen on funduscope
170
diagnosis of Infective endocarditis- gold standard, what a diagnosis is based on and blood test/ film results
GS= transoeseophageal echocardiography- can see vegetations on the valves through this
based on modified duke criteria- 1major+3minor or 5 minor
- major= persistently positive blood cultures (typical bacteria), echo toe shows vegitations
- minor- predisposing factors, fever, vascular phenomena, equivocal blood cultures
also have high esr, crp, neutrophillia
171
general treatment for Infective endocarditis
iv penicillin and gentamicin
172
treatment for Infective endocarditis if staph aureus is cause
vancomycin + rifampicin
173
treatment for Infective endocarditis if strep viridians is the cause
benzylpenicillin + gentamicin
174
complication of Infective endocarditis
heart failure + septic emobili + sepsis
175
what does one large square on the ecg mean
200ms
176
how to calculate heart rate on ecg
300/ no of big squares
eg- 2 big boxes (400ms)
300/2= 150 bpm
177
what does the st segment represent
isovulemic ventricular relaxation
178
what does the qrs complex show
ventricular depolarisation and atrial repolarisation
cant see atrial repolarisation bc its masked by ventricular depol
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how long is the p wave normally
<120ms wide
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how long is the pr interval and where is it
0.12-0.2 seconds (120-200ms) (3-5 small squares)
from start of p to q of qrs
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what does the t wave show
ventricular repolarisation
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what does a broad qrs show
ventricular conduction delay/ bundle branch block
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where is the qrs interval and what does it represent
start of qrs to end of t wave
ventricular depolarisation and repolarisation
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how do you know if something is a superventricular rhythms
qrs complex is narrow and tachycardia
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eg of supraventricular rhythms
atrial fib
atrial flutter
atrial tachycardia
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what do ventricular rhythms look like
broad qrs- just looks in general a broad rhythm
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what is cardiac failure
- state where the heart is unable to pump enough blood to satisfy the needs of metabolising tissues
- symptomatic condition- breathlessness, fluid retention and fatigue are associated with a cardiac abnormality that reduces cardiac output
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causes of cardiac failure
- IHD!!! main cause
- hypertension- (as arterial pressu reincreases it gets harder for lv to pump blood out- so lv hypertrophies needing more oxygen, extra muscles also squeeze coronary arteries so less blood to tissue)
- dilated cardiomyopathy
- restrictive cardiomyopathy
- valvular heart disease- mainly aortic stenosis
- pregnancy, hyperthryodiism, arrhythmias (anything increasing myocardial work)
- cor pulmonale
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rf for cardiac failure
- age (65+), smoking, obesity, previous MI, male
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systolic vs diastolic cardiac failure
- systolic
- decreased contractility of lv- causing decreased cardiac output- so DECREASED EJECTION FRACTION<40% and INCREASED EDV (bc more blood left over as less is pumped out, combined with diastolic filling)
- caused by ihd (low contractility as part of it was damaged), mi, hypertension, dilated cardiomyopathy (dilated and weakened)
diastolic:
- not enough blood is returning to heart
- normal ejection fraction and normal edv (as atria is capable of sqeezing more blood into ventricle)
- end diastolic pressure is HIGH as the venticle is not compliant
- causes: hypertension, cardiac tamponade, constrictive pericarditis
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high output vs low output cardiac failure
can also be low or high output- low output is decreased co and fails to increase with exertion- could be due to mitral regurgutation, pump failure, high output is like anaemia, pregnancy, hyperthyroidism
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patho of heart failure
- normally increased preload= increased afterload= increased CO (frank starling law)
- failing hearts= dysfunctional frank starling= reduced CO
- compensatory mechanism activates- RAAS & SNS (temporary increase bp with increase in aldosterone, adh, sns), causing vasoconstriction increasing afterload
- compensation soon fails- cardiac remodeling, the raas will exacerbate fluid remodeling and heart failure will affect both circuits - congestive heart failure
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cardinal signs of heart failure
SOBASFAT
sob
ankle swelling- fluid retention
fatigue
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left heart failure causes and presentation
heart failure with reduced ejection fraction. typically due to systolic (pumping) dysfunction
- IHD
- Hypertension
- Dilated cardiomyopathy (ventricle is dilated + weakened- restrictive is also a rarer cause)
- aortic stenosis
- presentation
symotoms:
- exertional dyspnoea
- paroxysmal nocturnal dyspnoea (sob attack at night)
- orthopnea (usually pt will lie on more pillows to help)
- fatigue
- weight loss
signs:
- cardiomegaly + displaced apex beat
- pulmonary oedema
- pleural effusion
- 3rd (and 4th) heart sounds
- crepitations in lung bases (crackles)
- tachycardia
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rifht heart failure causes and presentation
- left ventricular failure (increased pressure in pul artery makes it harder for right side to pump blood into it)
- hypertension
- pulmonanry stenosis
- cor pulmonale (lung disease)
- presentation
symptoms:
- sob
- peripheral oedema
- ascites
signs:
- raised JVP
- hepatomegaly
- pitting oedema
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classification of heart failure
NHYA- new york heart assocoiation- for hf severity
- class 1- asymptomatic- no limit on physical activity
- 2 and 3- mild hf - slight limit on moderate activity and symptomaticallt moderate/ marked limit on moderate and gentle activity
- class 4- symptomatically severe- symptoms even at rest!
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investigations 4 for heart failure
- bloods- brain natriuretic peptide (bnp)- released from stressed ventricles in response to increase mechanical stress
- CXR- (abcde)
- alveolar oedema (bat wings)
- kerley b lines
- cardiomegaly
- dilated upper lobe vessel of lung
- effusion (pleural)
- echo
- ecg- may show underlying cause
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what does a chest x ray show for heart failure
- alveolar oedema (bat wings)
- kerley b lines
- cardiomegaly
- dilated upper lobe vessel of lung
- effusion (pleural)
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treatment of heart failure
- lifestyle change- weight loss, excersize , stop smoking and drinking
- pharmacological: (ABAL) one after the other if it doesnt help
- Ace inhibitor (or arb)
- Beta blocker
- Aldosterone antagonist- spironolactone
- Loop diuretic- furosemide or thiazide
in severe- cardiac resynchronisation therapy, or heart transplant
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cause/ rf of stable angina
most common cause is ischaemic heart disease
age, smoking, family history (first relative and under 65ish), diabetes- hyperlipidemia, hypertension, obesity, stress, sedentery…
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exacerbating factor of stable angina
anemia, hypoexemia, hypertension, valvular heart disease
cold weather, emotional stress
big meals
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patho for stable angina
mismatch between hearts oxygen supply and demand- increase in demand and limited supply.
atherosclerosis:
- fatty streak appears in intimal wall- t cells and macrophages
- in intimediate lesiosn you get foam cells , t cells and vascular smooth muscle cells. platelet aggregates and adheres to site inside vessel lumen
- advanced lesion- foam cells, t cells, smooth muscle, fibroblasts, lipid decelop fibrous cap on top of lesion
symptoms will start when lumen is 70-80% occluded.
if plaque ruptures- progressive luminal damage
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presentation of stable angina
central crushing chest pain radiating to neck/jaw
brought on with exertion and worsens from time
relieved with 5 mins rest/ gtn spray
breathlessness
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1st line and gold standard investigations for stable angina
1st line is ecg- normal, wuth excersize shows ischaemia. may see st depression and t wave inversion
GS- CT angiography- shows stenosed athersoscleoric arteries- 70-80% occluded
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treatment for stable angina
- lifestyle modifying- low weight, stop smoking, healthy diet
- symptomatic- GTN spray
all pt should 1st line be on CCB- (AMLODIPINE) OR BETA BLOCKER
then ccb AND bb
then ccb and bb and another antianginal eg long acting nitrates
- contraindications of ccb= heart failure, bb is asthma
consider:- ace-i, aspirin, statin
if pharmacology is unceccessful- referal for revascularisation
- PCI- balloon stent coronary artery- less invasive but risk of restenosis
- CABG- bypass graft- more invasive but better prognosis
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what is prinzmetal angina- who do you see it in and what does it present with
prinzmetals angina due to coronary vasospasm- not due to cv vessel atherogenesis. seen in cocains users and ecg shows st elevation
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what is acs
umbrella term for unstable angina, NSTEMI, STEMI
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patho/ cause of acs
usually ischaemic heart disease (mc) -
usuallt result of thrombus from an atherosclerotic plaque blocking a coronary artery
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presentation of acute coronary syndrome
same as stable angina but resting pain with no relief- GTN doesnt help
severe palpitations and sense of impending doom
central, constricting chest pain
- levine sign is a sign of ischemic chest pain
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dx and ix for acs
ecg
biomarkers- troponin and creatine kinase
ct angiogram to show extent of occlusion
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long term treatment for acs
long term treatment: beta blocker, aspirin, (75mg life), atrovastatin, acei
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occlusion in unstable angina
partial occlusion of minor artery
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infarction in unstable angina
no- ischemia only
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ecg and troponin in unstable angina
- ecg normal (may be some st depression and t wave inversion)
- troponin lvls normal
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presentation of unstable angina
chest pain at rest
- chest pain with cresendo pattern
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treatment for unstable angina
MONAC
- morphine, o2 if sats are left than 94, nitrates (gtn) aspirin 300mg +clopidogrel (dual antiplatelet)
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occlusion and infarction of NSTEMI
occlusion- major partial/ total minor coronary artery
infarction- sub endothelium infarction- area far away from coronary artery
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diagnosis on? and other test/ investigation for nstemi
retrospective diagnosis based on troponin results (elevated)
ecg- st depression, t wave inversion, NO Q WAVES!
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treatment for nstemi
use GRACE score- if low risk coronary angiography later and if high risk then coronary angiography right there- consider pci
pci only- not thrombolytics
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occlusion and infarction of stemi
total of major coronary artery
transmural infarction through all layers
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diagnosis based on and other tests for stemi
diagnosis made on ECG at presentation
st elevation
pathological Q WAVES after some time
troponin elevated
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treatment for stemi
MONAC
PCI- stenting
if not- thrombolytics
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