Endocarditis
A patient who is an IVDU develops Infective Endocarditis. What valve is most likely to be affected and why?
Tricuspid regurg/stenosis
IVDU enters the systemic circulation --> return to the R side of the heart (encountering tricuspid valve first)
Define congestive cardiac failure?
Failure of both sides of the heart
Features of fluid overload
Further classified into systolic dysfunction (HFrEF) and diastolic dysfunction (HFpEF)
What are the shockable and non-shockable rhythms?
Shockable = ventricular fibrillation, pusleless ventricular tachycardia
Non-shockable = pulseless electrical activity, asystole
Differentiate type 1 vs type 2 myocardial infarction?
Type 1 - troponin elevation AND ischaemic symptoms, ECG changes, wall motion abnormalities or thrombus
Type 2 - troponin elevation AND supply/demand mismatch
Infective Endocarditis
List some organisms you'd expect to find in a patient with a prosthetic heart valve vs normal valveProsthetic valves - coagulase negative Staphylococci (e.g. S. epidermidis)
Low virulent Streptococcus viridans, Enterococcus, HACEK in abnormal valves
Vs highly virulent S. aureus in normal valves
Which drugs are used in heart failure not because they reduce mortality but because they help with symptoms?
Thiazide diuretics
Loop diuretics
Improve symptoms (pulmonary and systemic congestion)
What is the QRS polarity in leads I, II, III in a right axis deviation?
Negative lead I
Positive in leads II and III
What is 'restrictive cardiomyopathy'? Compare it to dilated cardiomyopathy? Describe the changes on echo?
Restrictive = diastolic dysfunction
Proliferation of connective tissue = reduced elasticity of cardiac tissue
Reduced diastolic filling but normal ejection fraction (EF = SV/EDV x 100), impaired contractility and SV but also impaired EDV
Dilated = systolic dysfunction
Eccentric hypertrophy with dilated ventricles= reduced contractility
= systolic dysfunction (reduced EF)
You are taking a history from a patient with ?Infective Endocarditis. What risk factors should you enquire about?
Prosthetic valves
Valvular disease - aortic stenosis, mitral stenosis, congenital valvular conditions etc.
Hx of rheumatic heart disease
Previous IE
IVDU, any IV devices
Recent dental procedures
What are the possible causes for L-sided heart failure?
Secondary to increased preload on the LV - aortic or mitral regurgitation
What is Paroxysmal Nocturnal Dyspnoea? What does it suggest?
Sudden SOB, coughing at night
Suggests LHF
What are the possible causes for R-sided heart failure?
L-sided heart failure with backpressure onto R heart
Tricuspid regurgitation increasing preload on the R heart
Pulmonary hypertension increasing afterload on the R heart
List the extracardiac manifestation of Infective Endocarditis.
Splinter haemorrhages
Janeway lesions
Osler's nodes
Roth spots
What is HFrEF? Describe the causes and the resulting consequences of HFrEF?
Heart failure with reduced ejection fraction <50% (i.e. systolic dysfunction)
Damaged or loss of contractile myocytes (in MI, ischaemic)
Infiltration - amyloid, haemochromatosis, sarcoidosis
> decreased contractility and CO = reduced perfusion
What are the clinical features of someone who is 'fluid overloaded'?
Peripheral oedema +/- sacral oedema
Elevated JVP
Bibasal crackles
3rd heart sound
Dyspnoeic
Draw a table to compare Rheumatic Fever and Infective Endocarditis in terms of the pathophysiology/aetiology and clinical features.
RF - Strep pyogenes infection (GAS), molecular mimicry between streptococcal M protein and cardiac myosin = type 2 HSR (antibody-mediated) = tissue damage to valves
IE - bacteraemia, damaged valves, colonisation of valves, destruction of valve
JONES PEACE in RF
FROM JANE in IE
Modified Duke Criteria - 2 major, 1 major + 3 minor, 1 major + 5 minor
MAJOR - positive BC or TOE findings of IE
MINOR - clinical signs (Janeway lesions etc.), predisposing factors (IVDU, prosthetic valves)
Outline the RAAS system.
Discuss why RAAS blockers are useful in heart failure.
Bonus: what is neprilysin?
Renin from kidney converts angiotensinogen from liver into angiotensin I. ACE from lungs convert ang I to ang II which binds to ang II receptor type 1 = vasoconstriction, aldosterone, ADH, thirst...
ACEi - perindopril, inhibit ACE from converting angiotensin I into angiotensin II. No angiotensin II = no aldosterone, vasoconstriction or ADH. Reduced afterload (vasconstriction) and preload (aldosterone).
ARB - blocks angiotensin II from binding to receptor.
ARNI - ARB and neprilysin inhibitor (blocks neprilysin from degrading natriuretic peptides which promote natriuresis and diuresis to reduce preload as well as inhibit RAAS).
What investigations would you order for ?heart failure and why?
ECG - underlying arrhythmia or ischemia as a cause
U&E (renal impairment from reduced CO), LFT (congestion in RHF)
BNP - ventricular stretching
CXR - cardiomegaly, pulmonary oedema
Echo (TTE) - gold standard, evaluate EF, ventricle size and thickness, aetiology (valves)
What are the 4 main drugs used in heart failure? How do they work?
B blocker
ARNI/ACEi
Spironolactone
SGLT2i