Cardiac Diseases Flashcards
1
Q
3 main causes of HF?
A
IHD (70%)
Non-ischaemic dilated cardiomyopathy (25%)
HTN (5%)
2
Q
causes of L heart failure?
A
IHD
Non-ischaemic dilated cardiomyopathy
HTN
Mitral or Aortic valve disease
3
Q
Physical signs of L heart failure?
A
Displaced apex beat-dilated LV/cardiomegaly
Mitral regurge- pansystolic murmur radiating to axilla
Gallop rhythm, S3
Lung base crepitations
Dependent pitting oedema- RAAS activation
4
Q
causes of R heart failure?
A
Pulmonary parenchymal diseases: COPD ILD e.g. sarcoidosis adult resp distress syndrome chronic lung infection or bronchiectasis Pulmonary vascular diseases: PE or pulmonary HTN Cardiac causes: Tricuspid or Pulmonary valve disease L to R shunts e.g. ASD/VSD Isolated RV Cardiomyopathy RV infarction L sided HF
5
Q
Physical signs of R heart failure?
A
rasied JVP, with or without V waves of tricuspid regurge
Cardiomegaly, and may give rise to functional tricuspid regurge- systolic murmur*
hepatic enlargement-tender and smooth
ascites
dependent pitting oedema
6
Q
when are nitrates administered in HF patients and why?
A
08:00 and 14:00 BD, as with chronic use, tolerance develops.
7
Q
Non pharmacological HF management?
A
Revascularisation
Biventricular pacemaker or implantable cardioverter defibrillator (ICD)
cardiac transplant
left ventricular assist device (LVAD) and artificial heart
8
Q
Drug management in HF LT?
A
diuretics: step 1=furosemide 40mg, and titrate up if needed, 2= change to bumetanide if not working, 3=add thiazide for complete diuresis- must monitor Us and Es.
ACEI- improve signs and symptoms of all HF grades, improve ET, increase survival and slow disease progression. Should be maintained on highest dose they can tolerate. Monitor renal function carefully after starting and after each dose titration.
ARBs- good evidence for cadesartan and valsartan
beta blocker- in chronic stable HF, e.g. carvedilol or bisoprolol. NOT if shock or heart block. start low and go slow. Safe to start if systolic BP more than 100, and HR more than 60, with no HB and no significant postural drop.
ivabradine (reduces HR by specific inhibition of If funny Na+ current in pacemaker cells) useful if can’t tolerate beta blocker, or resting HR more than 75bpm despite beta blocker. also doesn’t lower BP.
spironolactone
IV inotropes e.g. dobutamine and dopamine if acute LV failure with hypotension. If hospitilised or present with severe HF in spite of vasodilator, beta-blocker and diuretic therapy, and in those with rapid AF, consider digoxin- weak inotrope and arterial vasodilator.
nitrates- isosorbide mononitrate and vasodilator hydrazaline (NOTE can cause lupus) can be useful in combination to reduce mortality if pt cannot tolerate ACEI or ARB, or in those with resistant CCF.
amlodipine to treat co-morbid HTN and/or angina.
anticoagulation- if in sinus rhythm, consider if previous VTE, LV aneurysm or intracardiac thrombus. May use warfarin or NOACs. Use if AF, and consider if suspicion of pulmonary thromboembolic disease. Consider if severe CCF and ventricular aneurysm.
9
Q
Considerations in ACEI therapy for HF?
A
do not initiate in pt clinically suspected of haemodynamically unstable valvular disease, until valve disease been assessed by a specialist. not usually recommended if aortic stenosis and heart failure as ACEI unlikely to reduce afterload on heart, and may cause dangerous hypotension.
risk of hyperkalaemia if used alongside spironolactone.
10
Q
troponins specific for the myocardium?
A
TnI and TnT
11
Q
define pulmonary HTN?
A
mean pulmonary arterial pressure (mPAP) of more than 25mmHg at rest, as measured on R heart catheterisation.
12
Q
how can emphysema cause pulmonary HTN, and subsequently lead to RHF?
A
emphysema= destruction of air spaces distal to terminal bronchioles. This causes loss of pulmonary capillaries, destroying the vascular bed.
*COPD-hypoxic pulmonary vasoconstriction- pulmonary HTN.
13
Q
symptoms and signs of pulmonary HTN?
A
dyspnoea fatigue weakness angina syncope abdominal distension
o/e: L parasternal heave, loud S2, soft pan systolic murmur with tricuspid regurge (assoc. with RV hypertrophy and RH failure?) or early diastolic murmur with pulmonary regurge.
JVP distension, ascites, hepatomegaly, peripheral oedema.
may be signs of assoc. disease e.g. systemic sclerosis e.g. telangiectasia, raynauds, oesophageal dysmotility and chronic liver disease e.g. jaundice, dupuytren’s, spider naevi, ascites.
14
Q
vaccination in HF and pulmonary HTN pts?**
A
influenza
pneumococcal pneumonia
15
Q
when might Ca2+ blockers be useful in pulmonary HTN pts?
A
those with IPAH who respond to a vasodilator challenge- reduction in mean PAP of 10mmHg or more, to reach an absolute mean of 40mmHg or less with increased or unchanged CO.
16
Q
how does sildenafil work in the tment of pulmonary HTN (also used in erectile dysfunction)?
A
phosphodiesterase type 5 inhibitor producing vasodilation in pulmonary vasculature, provides symptomatic relief and increases exercise capacity.
17
Q
chest pain in pericarditis relieved by doing what?*
A
sitting forward
18
Q
what feature on pt examination may suggest that aortic stenosis is severe?
A
absence of S2 when listening over the aortic area- this may occur as aortic valve is so stiff that the valve leaflets are unable to become fully apposed again once open*
19
Q
why might a heart failure pt have a soft S1?
A
during diastole, the AV valves are unable to open fully as have to push against blood already in the ventricles due to poor ventricular ejection during systole, so they are almost closed when systole starts.
20
Q
what feature may be present other than RF delay in a pt with coarctation of the aorta?
A
upper limb HTN
21
Q
management of acute HF?
A
IV bolus or infusion of diuretic- furosemide 40mg-500mg daily, if 50mg ampoules for IV then give multiples of this. Must monitor Us and Es, fluid input and output, and daily weighing. Give higher dose than what pt already taking at home if already on diuretic!
consider inotropes e.g. dobutamine, dopamine, only if potentially reversible cardiogenic shock-must be given in CCU or HDU.
consider IV nitrates if underlying ischaemia, HTN or reurgitant aortic or mitral vave disease. Caution if aortic or mitral valve stenosis, HOCM or pericardial constriction.
after stabilisation, continue beta blocker if already taking, not if HR less than 50bpm, 2nd or 3rd degree AVN block, or shock!
start or restart beta blocker if acute HF due to LVSD once condition stabilised- e.g. no longer need IV diuretics. ensure stable on this for at least 48hrs before discharge.
offer ACEI and aldosterone antagonist durng hosp admission if acute HF and reduced LVEF.
22
Q
general management in HF?
A
vaccinations- influenza and pneumococcal diet-low salt smoking cessation low level exercise education daily weighing at home- can titrate own diuretic therapy
23
Q
NYHA classification of HF?
A
class 1= no limitation of physical activity 2= slight limitation of physical activity, symptomatically mild HF 3= marked limitation of physical activity, symptomatically moderate HF 4= symptoms at rest, symptomatically severe HF
24
Q
complications of MI?
A
cardiogenic shock arrhythmia HF severe MR VSD myocarditis ruptured ventricle ruptured papillary muscle
25
considerations other than pharmacological management when discharging pt following ACS?
CVD risk management- smoking cessation, diet modification, low salt diet, exercise, lose weight, good diabetes control
F/U in 6 wks?*
no work for 1 month
no driving for 1 month if car driver, but don't need to inform the DVLA themselves, if bus, coach, or lorry HGV driver, then need to inform the DVLA and can't drive for at least 6 weeks.
26
aims of cardiac resynchronisation therapy (CRT)?
improve efficacy of cardiac contraction by pacing both the left and right ventricles
improves symptoms, reduces mortality and HF hospitilisations.
27
CRT indications in pts with class IV HF (symptomatically severe HF-symptoms at rest)?
if QRS duration less than 120ms, then no therapy should be conisdrered.
if 120ms or more, consider CRT-P. Defibrillator not indicated.
28
CRT indications in pts with class I-III HF? (where LVEF 35% or less.)
if QRS less than 120ms, consider ICD only if high risk of sudden cardiac death.
if QRS 120-149ms, and no LBBB, consider ICD.
if QRS 120-149ms and LBBB, consider ICD if class I, CRT-D of class II, and CRT-D or -P if class III.
if QRS 150ms or more, with or without LBBB, consider CRT-D in class I-III, or CRT-P in class III.
29
causes of HF related to impaired ventricular contractility or increased afterload (systolic HF)?
IHD- previous MI, transient myocardial ischaemia
chronic volume overload- mitral regurge, aortic regurge
dilated cardiomyopathies
aortic stenosis
severe HTN
30
when does pulmonary oedema develop in the presence of normal plasma oncotic pressure?
when pulmonary capillary wedge pressure, which reflects LV diastolic pressure, exceeds 25mmHg.
31
how can morphine be used in the tment of a pt with acute pulmonary oedema?
can be given IV to reduce anxiety and as a venous dilator to permit pooling of blood periperally
32
define heart failure
cardiac output fails to meet metabolic demands of body, or meets those demands only if the cardiac filling pressures are abnormally high.
Chronic= HF with reduced EF (LVSD), and HF with preserved EF (diastolic dysfunction)
33
body's compensatory mechanisms initially in HF?
preload augmentation with increased SV via Starling mechanism: increased EDV due to reduced ventricular emptying increases stretch on mycoardial fibres, and subsequent force of contraction, hence increases SV during next ventricular systole to increase CO.
neurohormonal systems activation e.g. RAAS- AngII cuases peripheral arterial vasoconstriction to increase TPR and maintain systemic BP hence tissue perfusion e.g. to the kidneys- require 25% of our CO, and also acts to increase IV volume through aldosterone release and ADH- produced by hypothalamus- OVLT and STN, and released from post pituitary, aldosterone acting on DCT to increase Na+ reabsorption so LV preload raised to increase myocardial stretch, contraction force and SV. Also SNS, ADH and natriuretic peptides.
ventricular hypertrophy- help maintain contractile force, but hypertrphied wall is stiffer, and there are higher than normal end diastolic ventricular pressures.
34
factors that may precipitate symptoms in pts with chronic compensated HF?
increase met demands: infection, fever, anemia,hyperthyroid, tachycardia, preg
impaired contractility: myocardial ischaemia or infarct, excess alcohol, -ve inotropic meds e.g. bisoprolol
increased CV and hence preload: excess dietary sodium , renal failure, excess fluid admin
increased AL: uncontrolled HTN, PE
not taking prescribed meds
excessively slow HR
35
factors that increase likelihood of arrhythmia development in pt with hypertrophic cardiomyopathy?**
myocardial scar tissue seen on MRI
| severe degree of obstruction (HOCM)
36
how can upright tilt testing be used if suspected vasovagal/neurocardiogenic syncope?
pt secured to table tilted +60 degrees to the vertical for 45 mins or more
ECG and BP monitored throughout
+ve test for vasovagal if hypotension occurs, sometimes bradycardia and presyncope/syncope, and supports diagnosis.
37
CA occlusion required for symptoms to be produced?
more than 50% occlusion in exercise, and more than 70% at rest
38
what is myocardial oxygen demand determined by?
HR
contractility
wall tension
39
why might a pt with CAD be asymptomatic?
occlusion less than 50%
| *
40
3 defining characteristics of stable angina?
poorly localised pain
brought on by exercise/emotion, doesn't occur on its own at rest
relieved by GTN/rest
41
what is silent ischaemia? what are the RFs and how can it be investigated?
presence of objective finding suggestive of myocardial ischaemia that is not associated with angina or anginal equivalent symptoms.
Objective evidence found with exercise testing or ambulatory monitoring showing ECG changes, or nuclear imaging studies showing myocardial perfusion defects, or regional wall abnormalities shown on ECHO.
at risk: diabetics, HTN, previous MI, surgical revascularisation, advanced aged.
42
3 defining characteristics of unstable angina?
at rest and last for more than 20mins
severe, frank pain
new onset or crescendo pattern
43
ECG criteria for a STEMI?
ST elevation in 2 consecutive leads (i.e. for the same territory) or new onset LBBB- which in this case can't really comment on the ST.
44
most common symptoms of HCM?
dyspnoea
| exertional angina
45
causes of a raised Troponin?
```
MI
tachyarrhythmias
aortic stenosis- outflow reduction causes ischaemia
myocarditis
heart failure
PE
sepsis
renal failure-usually assoc. HTN
anaemia
```
46
why caution with nitrate use in aortic stenosis?
shouldn't give as reduction in cardiac output with aortic stenosis plus nitrate induced reduction in preload and lowering of TPR with arteriolar vasodilation may massively reduce BP compromising vital organ perfusion.
47
main drug for thrombolysis in STEMI in district general hospitals?
reteplase*
48
timing to allow PCI to take place?
door to needle time of less than 90mins- from pt first having chest pain to PCI must be less than 90mins.
49
thrombolysis indications?
less than 12 hrs from onset of pain and any 1 of:
ST elevation more than 1mm in 2 or more consecutive limb leads
ST elevation more than 2mm in 2 or more consecutive chest leads
posterior infarct
new onset LBBB
50
how does pericardial fluid drain into the R pleural space?
via the thoracic duct and R lymphatic duct
51
characterising features of acute pericarditis?
chest pain
pericardial friction rub
serial ECG changes
52
clinical features of acute pericarditis?
central chest pain, worse on inspiration or lying flat, may be relieved by sitting forward
pericardial friction rub
may be evidence of pericardial effusion-dyspnoea, raised JVP, bronchial breathing at L base- Ewart's sign- left lower lobe compressed by large effusion or cardiac tamponade- tachycardia, hypotension, raised JVP, pulsus paradoxus, kussmaul's sign, muffled heart sounds.
fever may occur
53
*pathophysiology of acute pericarditis?
infiltration of neutrophils and pericardial vascularisation
| *bread and butter appearance
54
causes of acute pericarditis?
viral (most common)- coxsackie B, give symptomatic tment and observe for development of pericardial tamponade
idiopathic
TB-a cause of constrictive pericarditis, along with bacterial infection and rheumatic heart disease-can cause diastolic HF but differentiate from constrictive cardiomyopathy as constrictive pericarditis can usually be fully treated with pericardium resection.
bacterial- causes purulent pericarditis, need Abx for at least 4 wks and drainage of pericardial fluid, devlops from direct pulm extension, haematog spread, myocardial abscess, endocarditis, penetrating injury to chest wall, subdiaphragmatic suppurative lesion
CVD- MI, dresslers syndrome*
neoplasm- lung Ca, metastatic disease
renal failure- need intensive dialysis
inflammatory- RA, sarcoidosis, SLE
55
5 features of pericardial pain?
like pleurisy: sharp, worse on inspiration
like angina: central chest pain, radiating to L shoulder
specific: eased sitting forward
56
pericarditis tment?
treat the cause if found!
bed rest and oral NSAIDs- high dose aspirin, indometacin or ibuprofen, but NOT post MI as NSAID assoc. with myocardial rupture*
corticosteroids have been used if disease does not subside rapidly
colchicine?- consider before steroids or immunosupressants if relapse or continuing symptoms occur.
further tment: pericardial window
pericardiectomy
57
symptoms and signs of acute myocarditis?
```
fatigue
dyspnoea
chest pain
fever
palpitations
tachycardia
soft S1
S4 gallop
```
+ve TnI or T confirms diagnosis in proper clinical setting and absence of MI- e.g. a confirmed with non-occluded CAs in angiogram*
58
causes of MI secondary to ischaemia due to increased O2 demand or decreased supply?
```
coronary spasm e.g. assoc. with illicit drug use e.g. cocaine-causes massive vasoconstriction
coronary embolism
anaemia
arrhythmias
hypertension
hypotension
```
59
define prinzmetal's angina
cyclical angina at rest due to coronary artery spasm
60
prasugrel to treat STEMI is restricted to which pts in UHL?
those under the age of 75 who weigh more than 60kg and have had no previous TIA or stroke.
61
TnI should be measured when in presentation of ACS, and how often?
should be measured on admission, and rpted 3 hrs later if admission trop was less than 6 hrs from onset of chest pain
rpt troponin with rise more than 30ng/ml is significant
if 1st trop done 6hrs or more from chest pain onset don't need to rpt.
62
causes of aortic regurgitation?
- rheumatic fever (commonest cause)-group A beta haemolytic strep
- bicuspid valve
- marfans syndrome
- ehler-danlos syndrome
- infective endocarditis
- ankylosing spondylitis
- RA
- SLE
- tertiary syphilis
63
commonest cause of aortic regurge?
rheumatic fever
64
ECG evidence of aortic regurge?
LV hypertrophy- tall R waves in V5, V6*
65
*explain the process of atherosclerosis?*
initiated by arterial wall damage e.g. high circulating LDLss, HTN, cigarette smoking or area of shear stress e.g.bifurcation.
Collagen deposition to form fibrous plaque.
Free O2 radicals produced and macrophages form foam cells.
Formation of a plaque, which can rupture to produce a thrombus which if occludes a CA can lead to myocardial ischaemia and subsequent cell necrosis hence MI.
66
F/U required for myocarditis pts?
must r/v LV function
67
effect of adenosine of AF and atrial flutter?
can slow them down, but will not terminate them as re-entry independent of the AVN.
68
why are beta blockers of particular use in LT treatment of VT in pts unsuitable for revascularisation and/or ICD therapy?
reduce ischaemia which is often the underlying cause of VT
69
signs of aortic regurgitation?
collapsing pulse (wide pulse pressure)
other signs: Quincke's sign- capillary pulsation in nail beds, De Musset's sign- head nodding with each heartbeat, Pistol shot femorals- a sharp bang heard on auscultation over femoral arteries in time with each heartbeat.
displaced apex beat
high-pitched early diastolic murmur heard best over L sternal edge 5th IC space with pt leaning forward and breath held in expiration. "lub taaarr".
70
define infective endocarditis
```
a microbial infection of:
normal heart valves
prosthetic heart valves
endothelial surface of heart
congenital defect- VSD, PDA or valve defect
```
71
organisms implicated in infective endocarditis?
most common= streptococcus viridans
also URT commensals
S.aureus- skin infections, abscesses, central lines, IV drug abusers
72
infective endocarditis incidence?
6 per 100,000 annually in UK
73
consequences of infective endocarditis?
heart murmurs from defected heart valves- aortic and mitral regurge, due to valve cusp disruption
embolised vegetations
immune complex deposition- splinter haemorrhages, Osler's nodes, Janeway lesions, microscopic haematuria- glomerulonephritis and ARF may occur, roth spots- boat shaped retinal haemorrhage with pale centre- retinal infarct.
74
pathophysiology of infective endocarditis?
endothelial damage or damaged valve- from high pressure jets of blood
platelet and fibrin deposition- sterile fibrin-platelet vegetation
bacteraemia- bacteria brought to valve surface
adherence and colonisation of bacteria
fibrin aggregates protect bacteria vegetation from host defence mechanisms
75
why are bacteria colonising valve in infective endocarditis protected from host immune system?
due to fibrin aggregates which were deposited in response to valve damage e.g. from high pressure jets of blood.
76
clinical presentation of infective endocarditis?
HEART MURMUR and FEVER
clinical picture reflects systemic infection, valvular/cardiac damage, embolisation and immune vasculitis.
systemic infection: pyrexia, myalgia, weight loss, fatigue, malaise, subacute or chronic disease presentation can present quite non-specifically-symptoms above plus loss of appetite, abdo symptoms, pleuritic pain, back pain-immune complex deposition in disc spaces
valve/cardiac damage: changing murmur- aortic and mitral regurge- early diastolic murmur and pansystolic murmur, aortic regurge most common, heart failure and conduction abnormalities.
embolisation: cerebral, pulmonary, coronary, renal. ?IE in pts with fever who present with stroke or TIA.
immune vasculitis: roth's spots, oslers nodes-painful red to purple lesions on fingers, janeway lesions, splinter haemorrhages, glomerulonephritis- microscopic haematuria, clubbing.
petechiae e.g. dorsum of hands and feet, chest and abdo wall
77
name given to criteria used to diagnose infective endocarditis?
Duke's criteria
78
how many criteria required for infective endocarditis diagnosis?
2 major OR
1 major, 3 minor OR
5 minor
79
Duke's criteria for infective endocarditis diagnosis?
major criteria: +ve blood culture for IE: typical organism in 2 separate cultures OR persistently +ve cultures- 3 sets at different times from different places at peak temp.
evidence of endocardial involvement: +ve ECHO- vegetation, abscess, prosthetic valve damage-valve dehiscience, OR new valvular regurgitation.
minor criteria: predisposition
fever more than 38 degrees C
vascular/immunological signs
+ve blood culture that doesn't meet major criteria e.g. atypical organism
+ve ECHO but doesn't meet major criteria.
need 2 major, 1 major and 3 minor, or 5 minor.
80
IE investigations?
blds: FBC- ?anaemia, raised WCC
raised CRP/ESR
Us and Es
LFTs
3 blood cultures- with 6 hrs in between each, unless severe sepsis/septic shock at presentation- 2 blood cultures within 1 hr separate from 1 another before commencing empirical Abx therapy.
CXR- part of inital assessment, ?chest infection as differential- fever, fatigue, or Ca- weight loss, malaise.
ECG- look for conduction defects that may develop with cardiac damage
ECHO- perform within 24hrs- TTE, follow with rpt TTE/TOE 7-10 days later if 1st negative but clinical suspicion remains high. TTE also on completion of Abx therapy to evaluate cardiac and valve morphology and function, may do F/U ECHO if cardiac complications or suboptimal response to tment.
Urinalysis- ?microscopic haematuria due to glomerulonephritis from immune vasculitis.
may serologically test for coxiella and bartonella ir -ve blood cultures, and consider brucellosis if risk of exposure.
81
IE treatment?
A to E, stabilise pt
involve microbiologist and cardiologist
depends on organism, but empirical tment= BENZYLPENICILLIN and GENTAMICIN, tment often at least 4 wks of IV Abx
82
at risk pts for IE?
```
IV drug user
prosthetic heart valve
previous endocarditis
acquired valve disease
structural congenital heart disease
```
83
what must be explained to pts at high risk of developing IE?
benefits and risks of antibiotic prophylaxis and why no longer routinely recommended for interventional procedures e.g. tooth extraction, as little evidence for benefit, and risks of adverse effects for pts and antibiotic resistance.
must maintain good oral health
symptoms of IE and when to seek help
risks of undergoing invasive procedures e.g. body piercing or tattooing.
84
IE prognosis?
staph- 30% mortality
strep- 10% mortality
mortality approaches 100% without tment.
85
use of oxygen therapy in ACS?
use if pt SOB or presence of heart failure
in unstable angina or NSTEMI, use if SpO2 less than 90%
in STEMI, use if SpO2 less than 95%
86
what is dressler's syndrome?
occurs between 2 and 10 weeks following MI.
A secondary pericarditis thought to be due to Abs being produced against the heart.
It is clinically indistinguishable from postcardiotomy syndrome.
The pain is associated with a pericardial rub, transient pleural effusions, pyrexia, anaemia, and elevated ESR. NSAIDs are helpful, but occasionally steroids or colchicine may be required.
87
features of grade 1 hypertensive retinopathy?
increased tortuosity of retinal vessels and increased reflectiveness (silver wiring)
88
features of grade 4 hypertensive retinopathy?
papilloedema (optic disc swelling), retinal oedema and hard exudates around the fovea, producing a 'macular star'.
89
features of grade 2 hypertensive retinopathy?
'nipping' of the venules at arteriovenous crossings.
90
features of grade 3 hypertensive retinopathy?
flame-shaped retinal haemorrhages and soft 'cotton-wool' exudates.
91
what features of the history may suggest HTN is secondary (non-essential)?
young pt
severe HTN
unresponsive to medications
sudden onset
92
how does HTN cause arterial damage?
elevated pressure causes smooth muscle cell hypertrophy, endothelial cell dysfunction and fatigue of elastic fibres.
chronic hypertensive trauma to the endothelium promotes atherosclerosis, possibly by disrupting the normal protective mechanisms such as NO secretion.
93
goals in the management of HTN?
treat the high BP
reduce overall CVS risk
minimise end organ damage
94
1st line HTN tment for 35yr old pt of afro-caribbean origin?
Ca2+ channel blocker e.g. amlodipine- a dihydropyridine- acts on peripheral smooth muscle cell receptors-Gq
if not tolerated e.g. due to ADR of oedema, consider a thiazide-like diuretic e.g. indapamide.
95
if a beta blocker is used 1st line in HTN tment e.g. in a younger pt intolerant of ACEI/AngII blocker, what 2nd drug should be avoided?
diuretics so as to reduce risk of DM developing.
96
classic triad of symptoms in phaeochromocytoma?
episodic headache
sweating
palpitations
97
initial therapy in STEMI?
- morphine 2.5-5mg until symptomatic relief, plus anti-emetic with 1st dose e.g. metoclopramide 10-20mg IV or cyclizine 50mg IV to reduce N and V.
- controlled O2 if SOB or HF, or SpO2 less than 95%, use 35% mask or nasal cannula, and monitor with pulse oximetry.
- aspirin 300mg chewable tablet.
- GTN 2 puffs SL
98
STEMI tment following initial therapy?
prasugrel- platelet ADP receptor antagonist, 60mg, only if pt under age of 75 yrs, weighs more than 60kg and no prev history of TIA or stroke. Then 10mg daily for up to 1 year. Used in pres. of STEMI requiring PCCI. If can't be used, use clopidogrel instead LD of 600mg, consider 150mg for a wk before 75mg OD. Also use if treat with thrombolysis. Also consider ticagrelor if can't use prasugrel.
PPCI if presenting within 12hrs of symptom onset. Ideally door to needle time of 90mins. Ideally PPCI within 2 hrs of 1st met contact, if not give a thromolytic drug. In PPCI, give UFH 70-100 IU/kg. Also give abciximab if clear evidence of thrombus.
aspirin and enoxaparin if reperfusion not appropriate.
should remain in hosp for 3 days.
aspirin 75mg for life
beta blocker e.g. bisoprolol for at least 1 yr.
ACEI e.g. ramipril 2.5-5mg
atorvastatin 80mg
99
ADR of ticagrelor to be aware of which can occur at rest?
dyspnoea
100
NSTEMI and unstable angina tment following initial therapy?
ticagrelor 180mg, then 90mg BD for 1 year.
101
absolute contraindications to thrombolysis in setting of acute STEMI?
Recent stroke (2 months)
Recent head trauma (4 weeks)
Recent surgery - including dental extraction (2 weeks) Lumbar puncture (within 4 weeks)
Pregnancy or less than 18 weeks postnatal
Active peptic ulceration or other GI blood loss Concurrent anticoagulation (unless INR less than 2·0)
Severe liver disease or clotting disorder
Acute pancreatitis
Aortic dissection
Active pulmonary disease with cavitation
Oesophageal varices
Cerebral neoplasm
Uncontrolled hypertension (BP more than 180/110 mmHg)*
102
define stage 1 HTN?
clinic systolic BP 140-159mmHg/diastolic BP 90-99mmHg, and subsequent ABPM daytime average or HBMP average 135/85mmHg or higher.
103
define stage 2 HTN?
clinic systolic BP 160-179mmHg/diastolic BP 100-109mmHg and subsequent ABPM daytime average or HBPM average 150/95 or higher.
104
define severe HTN?
clinic systolic BP 180 or more mmHg OR diastolic BP 110mmHg or more.
105
investigations in STEMI presentation?
```
FBC
Us and Es
LFTs
glucose
lipid profile
HbA1c in known or suspected diabetic pts
CK
TnI
12 lead ECG
portable CXR
```
106
considerations in setting of STEMI with 'triple anticoag'?
pt already taking warfarin for AF or VTE and then being commenced on dual anti-platelet therapy for STEMI will be at HIGH risk of BLEEDING.
clopidogrel less likely with aspirin and warfarin to cause bleeding than with prasugrel or ticagrelor.
if in setting of warfarin tment with AF, may just give dual anti-platelet therapy for a few mnths then restart warfarin later.
107
give 8 complications following MI, in the order that they would occur.
```
sudden cardiac death e.g. VF, and arrhthymias
cardiogenic shock and acute HF
pericarditis
VS rupture or papillary muscle rupture-severe MR
cardiac tamponade
PE-few days later
stroke and mesenteric thrombosis
Dressler's syndrome-2-10 wks after
```
108
what is pulsus paradoxus and pulsus alternans?
pulsus paradoxus- decrease in BP with inspiration e.g. in cardiac tamponade.
pulsus alternans- pulse alternates between strong and weak beats e.g. in LV systolic impairment, acute HF.
109
describe the use of risk stratification in ACS*
GRACE risk score- global registry of acute coronary events, predicts mortality in hospital to 6mnths. Helps to determine need for aggressive management and setting goals with the patient and their families base on their prognosis. Can avoid inappropriate interventions and long hosp stays as can be discharged early if deemed low risk.
Based on age, HR, systolic BP, creatinine, cardiac arrest on adm, ST deviation on ECG, raised cardiac enzymes and evidence of HF/CG shock.
for unstable angina/NSTEMI, risk score more than 3-med risk or more than 6-high risk for 6mnth mortality should be considered for inpt angio.
TIMI score: best known chest pain risk score tool. Estimates mortality for those with unstable angina or NSTEMI. Based on age 65 or over, known CAD-stenosis of 50% or more, 3 or more CAD risk factors, aspirin use in past 7 days, severe angina, ECG ST changes and +ve cardiac marker.
110
Score used to assess need for anticoag tment in AF?
```
CHADSVASC score:
CHF
HTN
age 75 or over- 2 points, 65-74-1 point
DM
prev TIA, stroke or TE-2
known vasc disease
female
```
111
symptoms of acute LV failure?
acute SOB
cough and pink frothy sputum
orthopnoea and PND
collpase, arrest, cardiogenic shock
112
signs of acute LV failure?
distressed, pale and sweaty- SNS activation with CO reduction
tachycardic
fine crepitations bilaterally
gallop rhythm: 3rd heart sound
113
commonest causes of acute LV failure?
myocardial ischameia
HTN
aortic stenosis or incompetence
mitral incompetence
114
acute LV failure management?
```
A to E
sit upright
100% O2 via non-rebreather mask
IV access and monitor ECG
morphine 2.5-5mg IV (with antiemetic)
if SBP more than 100mmHg, give nitrate IV infusion
furosemide 40-80mg IV
CPAP
```
investigations: ECG- arrhythmia, AF, sinus tachy, MI, LVH-tall R waves V5 and V6
blds-FBC-?anaemia, raised WCC-infection as trigger, Us and Es, CK, Tn I
CXR
ABG
ECHO-regional wall motion abnormalities, quantify LVEF and assess valvular function.
115
define cardiac tamponade
pericardial effusion causing haemodynamically significant cardiac compression- pericardial pressure increases reducing venous return to the heart, causing CO reduction, hypotension and SHOCK (mechanical).
116
acute causes of cardiac tamponade?
```
trauma
iatrogenic- cardiac surgery, cathet, anticoag
aortic dissection
spontan bleed-uraemia, thrombocytopenia
cardiac rupture post-MI
```
117
subacute causes of cardiac tamponade?
```
malignancy
idiopathic pericarditis
uraemia
infection includ. TB
radiation
```
118
presentation of cardiac tamponade?**
```
cardiac arrest
hypotension
confusion
shock
if slowly developing: SOB
cough, hiccups, dysphagia
```
119
signs of cardiac tamponade?
Beck's triad: raised JVP, decrease BP and muffled heart sounds
tachycardia
Kussmaul's sign- JVP increased with inspiration
pulsus paradoxus- decrease in palp pulse and systolic BP on inspiration.
120
name given to triad of signs in cardiac tamponade?
Beck's triad
121
cardiac tamponade management?
EMERGENCY:
ABC, IV access and fluids, ECG and blds
get senior help
pericardiocentesis- needle inserted at level of xiphisternum, aim for tip of left scapula, aspirating continuously. blind-compl risk of 5-50%, only if emergency, USS guided-relat safe.
send pericardial fluid for microbiology and cytology.
drain may be left in temp. to allow sufficient release of fluid.
122
management of NSTEMI/unstable angina?
initially: aspirin 300mg and LMWH-med and high risk pts for 1st 48hrs. Rpt ECG at frequnet intervals but if no changes and no raised TnI consider early discharge. Consider pre-discharge treadmill testing or functional testing if high index of suspicion.
if NSTEMI, ticagrelor LD 180mg, then 90mg BD for 1 yr. if very high risk, may not start as can the procedd to revasc sooner. should stop at least 5 days before CABG.
123
What are the dangers of using oxygen therapy in ACS patients?
If COPD, may retain co2 causing co2 narcosis and loss of rep drive to breathe.
Cause production of free oxygen radicals which can directly lead to myocyte death, and can trigger arrhythmias e.g. VT. also vascular effects of oxygen so if high this raises angI causing vasoconstriction and so prolonging ischaemia and increasing risk of HF.
124
what is meant by coronary artery dominance?
this refers to the CA which supplies the posterior descending artery
a R dominant system means the RCA supplies the posterior descending artery
a L dominant system means the L circumflex supplies the PDA
125
causes of long lasting chest pain e.g. around 1 week?*
MSK most likely
| ?GI
126
define restrictive cardiomyopathy
myocardial disease that impairs ventricular filling, with normal or near-normal systolic heart function and wall thickness that is usually secondary to increased stiffness.
127
causes of restrictive cardiomyopathy?
usually no underlying cause found-idiopathic
infiltrative myocardial disease
endomyocardial fibrosis assoc. with Loffler's syndrome
amyloidosis-most common cause in western world, but poor prognosis with poor tolerance of CVS med. and poor results from transplantation
sarcoidosis
haemochromatosis-raised LFTS, serum Fe, ferritin and decrease TIBC, transferrin sat more than 80%, blood glucose may be raised due to DM from pancreas infiltration
fabry's disease-infiltrated by glycolipids
128
cause of a fixed raised JVP?
SVC obstruction
129
what does a raises TnI level tell us?
it tells us the risk of this event happening again
| it is NOT a marker of severity
130
amiodarone ADRs?
```
grey skin colouring
danger with long sun exposure
hyper/hypo thyroid
liver toxicity
pulmonary fibrosis
```
131
how can a cardiac wheeze due to L sided HF be distinguished from a respiratory wheeze?
response to tment- cardiac wheeze responds to furosemide
132
why can left sided HF cause MR?
dilation of the LV and the mitral valve annulus
133
why might a pt with isolated LV dysfunction develop ankle oedema in the absence of R heart failure?
as reduced CO triggers RAAS system activation as reduced renal perfusion and SNS stimulation, so AngII and aldosterone mediate increased water retention and peripheral oedema.
134
causes of heart failure?
IHD (90%)
HTN
arrhythmias e.g. AF
inherited cardiomyopathies- dilated, hypertrophic and arrhythmogenic RV cardiomyopathy
non-ischameic dilated cardiomyopathy can be due to infective causes, alcohol, drugs, pregnancy and idiopathic
valvular disease- AS, MS
thyrotoxicosis
viral myocarditis- coxsackie B, EBV and CMV-immunocompromised host
alcohol
restrictive-amyloidosis, sarcoidosis, Fabry disease, haemochromatosis, idiopathic
anaemia- high output heart failure-both systolic and diastolic function of the heart is normal with a normal ejection fraction but heart unable to provide a sufficient cardiac output to meet the demands of the body due to a higher than normal demand
deficiencies-vit B12, folate, thiamine-wet beri-beri, niacin-pellagra disease
radiotherapy, herceptin
lyme disease
cor pulmonale
135
why do we classify experience of symptoms in heart failure using the NYHA?
mechanism for communicating the health of a patinet
| is the basis for trial data
136
what are BNP measurements useful for in the context of HF?
can be used to measure response to tment
| BNP more than 35pg/ml
137
what might an ECG show that is helpful in diagnosing heart failure?
signs of a cause: IHD- pathological Q waves following previous MI, LVH- tall R waves V5 and V6 due to HTN or AS or HOCM, axis deviation due to hypertrophy, arrhythmias e.g. AF
138
mechanism of action of isosorbide mononitrate and hydralazine in HF?
venodilation to reduce heart preload
| acute HF- IV nitrate infusion can reduce pulmonary oedema**
139
reasons as to why we would like to request an ECHO in suspected HF?
quantify LVEF
assess severity of valvular dysfinction- mitral and tricuspid valve regurgitation
look for regional wall motion abnormalities from previous MI
140
what CT disease can hydralazine be implicated in the development of?
SLE
141
importance of ACEI and beta blocker therapy post MI?
aid myocardial remodelling
142
indications for surgery in infective endocarditis?
valve abscess
heart failure
ascending/descending infection
143
when should PCI be considered in NSTEMI/unstable angina?
raised TnI
recurrent angina/ischaemic ECG changes despite optimal medical therapy
features of HF
poor LV function
haemodynamic instability
PCI less than 6mnths ago or previous CABG
144
key investigations in HTN?
blds-plasma glucose, Us and Es- e.g. low potassium and high sodium in conn's syndrome, creatinine, eGFR- may be low with CKD, serum total cholesterol and HDL cholesterol-assess for other CVD risk factors, HbA1c.
urine- protein, send sample for ACR and test for haematuria-query renal parenchymal disease, dip-glomerulonephritis?
fundoscopy for signs of hypertensive retinopathy
12 lead ECG
ECHO-if suggestion of LVH, valvular disease or LVSD or diastolic dysfunction.
24hr urine catecholamines-assess for phaeochromocytoma, but must image afterwards as often incidental findings.
145
complications of severe aortic stenosis?
L sided HF and congestive HF
sudden death
infective endocarditis
systemic emboli
146
why do we use ECHO in the setting of all ACS cases?
look for regional wall motion abnormalities-may result from ischaemic damage.
assess valvular dysfunction
147
name given to the narrow complex irregular tachycardia of AF?
AF with fast ventricular response
148
mainstays of AF treatment on hospital presentation?
rate control-beta blocker
rhythm control-IV fleicanide- not if IHD or structural heart disease
cardioversion-DCCV if haemodynamically unstable
anticoag-?CHADSVASC score and HASBLED score
149
features o/e of pt with AF which may help confirm the diagnosis?
irregularly irregular pulse
features of mitral stenosis- rumbling mid-diastolic murmur hear over the mitral area and accentuated by asking pt to lean over onto their L side
features of hyperthyroidsism/hypo? e.g. hair loss, dry skin*
features of acute HF e.g. S3 gallop, raised JVP, bilateral pitting ankle oedema, bibasal medium inspiratory crackles, displaced apex beat
features of HTN? or hypotension and cardiogenic shock-cold and clammy extremities*
150
what may be used to stimulate the SAN in pt experiencing asystoles and awaiting a pacemaker?
isoprenaline- Na+ channel agonist*
151
when might digoxin be the preferential tment in a pt with AF?
if pt also as HF
152
what investigations might we want to perform in a pt presenting to ED in AF as identified on ECG?
TFTs-identify a cause?
other blds-TnI-have they had a silent MI?
ECHO-identify a cause?-structural heart disease, previous MI-regional wall motion abnormalities, valvular disease-mitral stenosis?
CXR-is there a penumonia that has caused the AF?
153
in what acute situations might intra-aortic balloon pumping be used for circulatory support?
acute heart failure- improve CO if transient or reversible depression of LV function
unstable angina-improves coronary flow and decreases afterload
unsuitable if severe aortic regurge, dissection and severe PVD
can cause aortic dissecction, emboli and leg ischaemia, but embolic complications reduced by anticoag with heparin.
154
characteristics of dilated cardiomyopathy?
dilatation of ventricular chambers and systolic dysfunction with preserved wall thickness.
155
NICE guidelines on statin tment for primary prevention of CVD?
offer statin tment if lifestyle modification ineffective or inappropriate, after risk assessment
offer atorvastatin 20mg to those with a 10% or greater 10-year risk of developing CVD for primary CVD prevention, using QRISK2 for risk determination.
consider atorvastatin 20mg for those aged 85 or older to reduce risk of non fatal MI
156
components to assessment required before starting statin treatment?
smoking status
alcohol consumption
BP
BMI or other measure of obesity
total cholesterol, non HDL cholesterol, HDL cholesterol and triglycerides
HbA1c-DM may be cause of dyslipidaemia
renal function and eGFR
transaminase level-liver disease may be cause of dyslipidaemia, and statins can raise transaminase levels
TSH-?looking for hypothyroidism as cause of dyslipidaemia
157
role of statins in ACS?
do not delay starting statin tment
known benefit on mortality
measure lipid profile at baseline and after 3 mnths
atorvastatin 80mg
158
definition of severe aortic stenosis from ECHO?
pressure gradient more than 50mmHg across the valve
OR
valve area less than 1cm^2
159
drugs for the secondary prevention of CVD in patients with stable angina?
consider aspirin 75mg
consider ACEIs if angina and DM
offer statin tment in line with NICE guidelines-atorvastatin 80mg
offer tment for HTN
160
an anterior STEMI occurs with occlusion of which coronary artery?
LAD: left anterior descending/anterior interventricular artery
161
why is AF common in patients with idiopathic restrictive cardiomyopathy?
incompliant ventricle due to increased myocardial stiffness raises L atrial pressure and causes atrial dilatation which increases the potential for reentry loop development
162
how can restrictive cardiomyopathy be distinguished from constrictive pericarditis?
MRI-3D visualisation of heart and relationship to thoracic structures, can quantify cardiac volumes and function, and provides info regarding tissue characterisation to detect focal scar and fatty infiltration.
may have to do cardiac biospy- in restrictive cardiomyopathy, RV biopsy positive for congo red staining
