Pathology Revision

Cardiovascular Pathology
Pacemaker Tissue
Unstable membrane potential, slow
depolarization (prepotential), prior to
threshold triggers action potential. Slow
decline in K+ efflux.
Abnormal pacemaker:
ectopic focus discharges faster than SA Node
focus may be atria or ventricles and may be
multiple foci. Excitation, sympathetic tone and
drugs may influence ectopic activity.
Ectopics
Atrial Ectopics
Morphology of P-waves abnormal; premature
and longer PR interval; QRS complex normal;
multiple supra-ventricular ectopics may cause
atrial flutter/fibrillation

Ventricular Ectopics:
Broad, erratic morphology of QRS complex;
isolated or multiple; multiple VEs cause VT or VF.

LV dysfunction (HF) & LVH predispose to ectopics

Long QT Syndromes
delayed repolarisation of heart following
heartbeat

Acquired ischaemia, drugs

Congenital Romano-ward syndrome

Torsades-de-pointes (twisting of the points)

Sudden death (unexpected) in young adults.

Valvular Disease
Valve Stenosis: Narrow or obstructed valve

Valve Regurgitation (or incompetence): leaky valve

Valve diseases will usually worsen with time and
cause progressive cardiac damage unless they are
correctly managed

Cardiac Murmurs
Abnormal blood flow
causing turbulence which
generates vibrations of
audible frequency.
Valve stenosis causes
increased flow and velocity
across narrowing.
Regurgitation when there is
high velocity flow from
higher to lower pressure due
to imperfect valve closure
Abnormal passage from high
to low pressure e.g.
Ventricular-septal defect
Mitral Stenosis
99% Rheumatic fever; congenital very rare. Inflammation
leads to cusp thickening adhesion and commissure fusion.
Thickening, shortening and fusing of chordae tendinae.
Causes raised LA pressure -> leads to dilatation and AF, stiff
oedematous lung, raised pulmonary artery pressure and RHF
Symptoms dyspnoea, exertional dyspnoea, orthopnoea,
paroxysmal nocturnal dyspnoea (PND), cough and
haemoptysis, fatigue, palpitations (AF)
Signs AF, tapping apex beat (palpable first heart sound),
pulmonary hypertension
Investigations ECG (AF); CXR (LAH, enlarged Pulmonary
veins); Echo (mitral valve thickening)
Management - diuretics, digoxin and warfarin, valvoplasty,
valve replacement
Mitral Regurgitation
Rheumatic, infective endocarditis, mitral valve prolapse (floppy
valve) is usually myxomatous degeneration, papillary muscle
stretch/rupture (IHD), congenital (ASD)
Systolic regurgitation of blood from LV to LA; increase LA pressure -
> pulmonary oedema, dyspnoea, pulmonary hypertension.
Reduced CO (fatigue), LV strain dilatation and failure, Pulmonary
HT causes RV failure, dilatation.
Symptoms exertional dyspnoea, PND, orthopnoea; fatigue,
cough, fluid retention (ankle oedema)
Signs AF, normal pulse wave but red. Volume, displace apex beat,
apical pan-systolic murmur, RHF (heightened JVP, hepatomegaly,
oedema)
Investigations ECG (AF, LVH); CXR (LVH); Echo (mitral valve
prolapse)
Management diuretics, (loop + spironolactone) ACE Is, B-blocker
(if LV dysfunction), digoxin+warfarin for AF, mitral valve
repair/replacement

Aortic Stenosis
Congenital (bi-cusp aortic valve); rheumatic;
degenerative (calcification)
Obstructed flow from LV to aorta, reduced CO, left
ventricular strain (LVH, LVF)
Symptoms exertional dyspnoea, fatigue, angina,
syncope, sudden death
Signs small volume, slow rising pulse, ejection systolic
murmur, later signs of Cardiac failure
Investigations ECG (LVH); CXR (normal/calcification);
Echo (cusp thickening and impaired opening)
Management diuretics (if pulmonary congestion)
statin (if hyperlipidaemia); valve replacement,
palliative care if unfit for surgery
Aortic Regurgitation
Rheumatic, infective endocarditis, degenerative (lipids), aortic
dissection, syphilis, Marfans, inflammation (A. Spondylitis, JRA)
Diastolic regurgitation of blood from aorta to LV, progressive LV
dilatation with LVH and LVF eventual. Leading to pulmonary
oedema, PHT, RHF.
Symptoms dyspnoea, fatigue, cough, fluid retention oedema
and ascites
Signs Large volume quick rising collapsing pulse, increase pulse
pressure (dec. diastolic BP), displace apex beat and LV heave, early
diastolic murmur at LSE 2ICS, crepitations and fluid retention (late)
Investigations ECG (LVH), CXR (dilated ascending aorta), Echo
(regurgitant aortic valve)
Management diuretics, ACE Is, B-blockers, aortic valve
replacement

Heart Failure
Cardiac Output is insufficient to deliver adequate
oxygen to meet bodys demands. It is a clinical
syndrome that represents the final pathway for a wide
variety of diseases that affect the heart.
Aetiology: CAD, Hypertension, Valvular Heart Disease,
Cardiomyopathy, Pericardial diseases
Ejection Fraction :
EF = EDV-ESV/EDVx100% - most techniques give normal
as >50%
However not much use diagnostically as normal or
reduced LVEF present in wide range of conditions
predisposing to HF. Knowing LVEF allows categorising of
patient into two broad categories HF-NormalEF and
HF-ReducedEF (HF-NEF and HF-NEF respectively)

Adaptive Mechanisms
Frank-Starling mechanism of beat by beat adaptation. Extra
cardiac muscle stretch from increased venous return
(preload) -> increase inotropy

Ventricular Remodelling structural change in ventricle in
response to change in loading condition. Hypertrophy and
dilation, due to increased afterload, preload and myocardial
injury

Sympathetic NS left ventricle damage -> adrenergic support
to enable chronotropic and inotropic stimulation and RAAS


Adaptive Mechanisms 2
Peripheral Vascular Disease
Atherosclerosis of lower limb vessels
Age adjusted prevalence (~12%, ABPI<0.9)
Identical risk factors to CHD
40% experience symptoms
Intermittent Claudication (IC)
1% progress to critical ischaemia

Classification :
Stage I Asymptomatic;
Stage II Intermittent Claudication
Stage III ischaemic rest pain
Stage IV ulceration/gangrene
Sites of Intermittent Claudication
Based on site of obstruction


Aorta/iliac buttock, hip, thigh
Femoral and branches thigh, calf
Popliteal calf, ankle, foot
ABPI
IC is measured by ABPI (ankle brachial
pressure index measure of ratio of ankle and
brachial blood pressures.
Should be 1. <0.9 is worry, IC shows changes
dependent on occlusion (as claudication is
intermittent!).
Lower ABPI = poorer prognosis.
Selecting Patients for Surgical
Revascularisation
For severe symptoms, job affected, no
response to exercise program, stenosis or
short occlusion, proximal, unilateral disease

Against short history, continued smoking,
angina or COPD, long occlusion, distal, multi-
vessel disease.

Priorities for Prevention
People with established atherosclerotic CV
disease

Asymptomatic but CVD risk >20% over 10yrs

People with diabetes

elevated single risk factors (BP >160/100; TC :
HDL > 6.0; familial dyslipidaemia)
Interventions and Treatments
Interventions (delay progression)
Smoking cessation, blood pressure reduction, LDL
reduction, anti-platelet therapy, diabetes control,
atrial fibrillation control.

Treatments
Tight BP control <145/80; RAAS blockade (ACE,
ARB); Statin therapy; anti-platelet therapy
(aspirin +/- clopidogrel); anticoagulation
(INR>2.5) for AF;