Applied Anatomy of Heart Flashcards
Cardiac plexus location
Anterior to bifurcation of trachea
Posterior to aortic arch
Parasympathetic innervation pathway
Cardioinhibitory centre in medulla
Vagus Nerve
To SA + AV nodes
Sympathetic innervation pathway
Cardioacceleratory centre in medulla
Preganglionic sympathetic neurones in thoracic spinal cord
Postganglionic sympathetic neurones to SA + SV node and to coronary vascular smooth muscle
Cardiac Pain
Caused by ischaemia
General visceral afferent nerve fibres ascend to CNS through cardiac branches of sympathetic trunk
Pain referred
Referred Cardiac Pain
T1-4
Medial arm + neck/jaw
To epigastrium T5-9
Because heart + skin share same pathway
Anterior surface of heart
Right ventricle
Base of heart
Left atrium
Coronary Artery Dominance
70% right dominant
Defined by where posterior interventricular artery comes from- if from RCA, right dominant, if from Circumflex, left dominant
LCA blood supply
Anterior 2/3rd heart
RCA blood supply
Posterior 1/3rd heart
SA node supply
60% RCA
AV node supply
80% RCA
Inferior part of heart ECG leads
II, III, aVF
Septal part of heart ECG leads
V1, V2
Anterior part of heart ECG leads
V3, V4
Lateral part of heart ECG leads
I, aVL, V5, V6
Mitral Valve Stenosis
Atrial Enlargement
Increased atrial pressure- pulmonary congestion (oedema)
Reduced ventricular filling- reduced CO
Can lead to atrial fibrillation due to atrial enlargement
Mainly rheumatic in origin- rare diastolic murmur
Aortic Regurgitation
Backflow into LV during diastole Chronic Vol Overload--> stretching + elongation myocardial fibres LV dilatation Congestive HF Decreased CO output Pre-load elevation DIASTOLIC MURMUR
Valvular Disease
Inflammation of valve Fibrosis Calcification Stenosis (narrowing) Regurgitation Cusps fibrose + cordae tendinae soften
Mitral regurgitation
Most common form valvular disease
Mitral valve doesn’t close properly- regurgitation of blood back into LA
SYSTOLIC MURMUR
Heard @ apex
Left atrial enlargement + LV eccentric hypertrophy
Pulmonary oedema + reduced CO
Aortic Stenosis
LV generates increased pressure to overcome stenotic aortic valve blockage
LV hypertrophy- increased muscle mass to help
Hypertrophied myocardium has reduced compliance + decreased coronary blood flow reserve
Heard @ Right 2nd intercostal space
Concentric Hypertrophy
PRESSURE OVERLOAD
Wall thickness increase
Compliance reduced (stiffy boi)–> vol. overload
Vent. filling compromised
Eccentric Hypertrophy
VOLUME OVERLOAD Chamber dilation - aortic + mitral regurgitation, systolic dysfunction, vol overload Elevates O2 demand Lowers mechanical efficacy
S1
Lub
Mitral + tricuspid closing
S2
Dub
Aortic + pulmonary closing
Concentric Hypertrophy causes
Physiological- strength training
Pathological- hypertension, aortic constriction
Eccentric Hypertrophy causes
Physiological- Endurance training e.g. swimming
Pathological- Valve disease
Concentric Hypertrophy Remodelling
Sarcomeres added in parallel
Increase myocyte cell width
Eccentric Hypertrophy Remodelling
Sarcomeres added in series
Increase myocyte cell length
Remodelling issues
Myocyte ratio will outweigh capillary ratio
Insufficient angiogenesis- decreased blood supply
Increased fibrous tissue
Increase in resistance
Bundle Branch Block
Impulses not conducted right
Different pathways used for depolarisation
Impulse travels through myocytes- QRS complex prolonged
Loss of Vent. synchrony
e.g. if RHS block, need to go first via LHS then RHS
Pathological cardiac hypertrophy
Non reversible
Physiological cardiac hypertrophy
Reversible
