Cardiac Diseases Flashcards
3 main causes of HF?
IHD (70%)
Non-ischaemic dilated cardiomyopathy (25%)
HTN (5%)
causes of L heart failure?
IHD
Non-ischaemic dilated cardiomyopathy
HTN
Mitral or Aortic valve disease
Physical signs of L heart failure?
Displaced apex beat-dilated LV/cardiomegaly
Mitral regurge- pansystolic murmur radiating to axilla
Gallop rhythm, S3
Lung base crepitations
Dependent pitting oedema- RAAS activation
causes of R heart failure?
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
Physical signs of R heart failure?
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
when are nitrates administered in HF patients and why?
08:00 and 14:00 BD, as with chronic use, tolerance develops.
Non pharmacological HF management?
Revascularisation
Biventricular pacemaker or implantable cardioverter defibrillator (ICD)
cardiac transplant
left ventricular assist device (LVAD) and artificial heart
Drug management in HF LT?
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.
Considerations in ACEI therapy for HF?
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.
troponins specific for the myocardium?
TnI and TnT
define pulmonary HTN?
mean pulmonary arterial pressure (mPAP) of more than 25mmHg at rest, as measured on R heart catheterisation.
how can emphysema cause pulmonary HTN, and subsequently lead to RHF?
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.
symptoms and signs of pulmonary HTN?
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.
vaccination in HF and pulmonary HTN pts?**
influenza
pneumococcal pneumonia
when might Ca2+ blockers be useful in pulmonary HTN pts?
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.
how does sildenafil work in the tment of pulmonary HTN (also used in erectile dysfunction)?
phosphodiesterase type 5 inhibitor producing vasodilation in pulmonary vasculature, provides symptomatic relief and increases exercise capacity.
chest pain in pericarditis relieved by doing what?*
sitting forward
what feature on pt examination may suggest that aortic stenosis is severe?
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*
why might a heart failure pt have a soft S1?
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.
what feature may be present other than RF delay in a pt with coarctation of the aorta?
upper limb HTN
management of acute HF?
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.
general management in HF?
vaccinations- influenza and pneumococcal diet-low salt smoking cessation low level exercise education daily weighing at home- can titrate own diuretic therapy
NYHA classification of HF?
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
complications of MI?
cardiogenic shock arrhythmia HF severe MR VSD myocarditis ruptured ventricle ruptured papillary muscle
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.
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.
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.
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.
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
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.
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
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)
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.
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
factors that increase likelihood of arrhythmia development in pt with hypertrophic cardiomyopathy?**
myocardial scar tissue seen on MRI
severe degree of obstruction (HOCM)
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.
CA occlusion required for symptoms to be produced?
more than 50% occlusion in exercise, and more than 70% at rest
what is myocardial oxygen demand determined by?
HR
contractility
wall tension
why might a pt with CAD be asymptomatic?
occlusion less than 50%
*
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
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.
3 defining characteristics of unstable angina?
at rest and last for more than 20mins
severe, frank pain
new onset or crescendo pattern
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.
most common symptoms of HCM?
dyspnoea
exertional angina
causes of a raised Troponin?
MI tachyarrhythmias aortic stenosis- outflow reduction causes ischaemia myocarditis heart failure PE sepsis renal failure-usually assoc. HTN anaemia
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.
main drug for thrombolysis in STEMI in district general hospitals?
reteplase*
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.
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
how does pericardial fluid drain into the R pleural space?
via the thoracic duct and R lymphatic duct
characterising features of acute pericarditis?
chest pain
pericardial friction rub
serial ECG changes
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
*pathophysiology of acute pericarditis?
infiltration of neutrophils and pericardial vascularisation
*bread and butter appearance
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
5 features of pericardial pain?
like pleurisy: sharp, worse on inspiration
like angina: central chest pain, radiating to L shoulder
specific: eased sitting forward
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
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*
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
define prinzmetal’s angina
cyclical angina at rest due to coronary artery spasm
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.
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.
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
commonest cause of aortic regurge?
rheumatic fever
ECG evidence of aortic regurge?
LV hypertrophy- tall R waves in V5, V6*
