Basic Anatomy & Physiology: Cardiovascular Heart Anatomy
Basic Anatomy & Physiology: Cardiovascular Heart Anatomy
Basic Anatomy & Physiology: Cardiovascular Heart Anatomy
Cardiovascular
Heart Anatomy:
Location:
o Snugly enclosed within the middle mediastinum (medial cavity of thorax). Contains:
Heart
Pericardium
Great Vessels
Trachea
Esophagus.
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Fibrous Skeleton of the Heart:
o Functions:
Reinforces Myocardium
Anchors muscle fibres + valves + great vessels
Electrically isolates
o 2 Parts:
Septums:
Flat sheets separating atriums, ventricles & left and right sides of the heart.
Electrically isolates the L&R sides of the heart
Rings:
Rings around great vessels & valves stop stretching under pressure
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Landmarks of the Heart:
Coronary Sulcus (Atrioventricular Groove):
o Encircles the junction between the Atria & Ventricles like a ‘Crown’ (Corona).
o Cradles the Coronary Arteries (R&L), Coronary Sinus, & Great Cardiac Vein
Anterior Interventricular Sulcus:
o Cradles the Anterior Interventricular Artery (Left Anterior Descending)
Posterior Interventricular Sulcus:
o Continuation of the Anterior Interventricular Sulcus
o Cradles the Posterior Descending Artery
Coronary Circulation:
The myocardium’s own blood supply
Arteries lie in epicardium – prevents the contractions inhibiting bloodflow
Arterial Supply:
o Aorta Left & Right coronary arteries
Left Coronary Artery
1. Left Anterior Descending Apex, Anterior LV, Anterior 2/3 of IV-Septum.
2. Circumflex Artery L atrium + Lateral LV
Right Coronary Artery Marginal & Post-Interventricular Artery
R-Atrium
Entire R-Ventricle
Posterior 1/3 of IV-Septum
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Heart Valves:
Ensure unidirectional flow of blood through the heart.
2x AtrioVentricular (AV) (Cuspid) Valves:
o Prevent backflow into the Atria during Contraction of Ventricles
Papillary muscles contract before the ventricle to take up the slack in the chordae tendinae
Prevents ballooning of valves under ventricular contraction.
o Tricuspid Valve (Right ):
3 flexible ‘cusps’ (flaps of endocardium + Conn. Tissue)
o Mitral Valve (Left):
2 Leaflets - resembles the 2-sided bishop’s miter [hat]
Valve Sounds:
S1 ( Lubb ):
o AV Valve Closure
o (M1 = Mitral Component)
o (T1 = Tricuspid Component)
S2 ( Dupp ):
o Semilunar Valve Closure
o (A2 = Aortic Component)
o (P2 = Pulmonary Component)
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Electrophysiology & ECGs
2 Types of Cardiac Muscle Cells:
- Conductile/Nodal: (Intrinsic)
o Have Spontaneous Electrical Activity Cannot Maintain a Resting Membrane Potential
Spontaneously Depolarises to Threshold (Due to Leaky Na+ Membrane Ion Channels)
NB: Na+ brings to threshold, but Ca+ is responsible for Depolarisation.
Slow ‘Pacemaker’ Action Potentials
o Heirarchy of control depending on Intrinsic Rate.
(SA is fastest :. takes control)
o Conduction Path:
SA node
AV node (delays signal – ensures coordinated contraction)
Bundle of His (further delay 0.04secs)
R and L bundle branches
Purkinji fibres
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- Contractile:
o Fast Non-Pacemaker Action Potentials
o Have stable membrane potentials.
Depolarisation:
Conductile AP Opens Fast Na+ Channels Massive Na+ influx Depolarisation
Plateau:
Fast Na+ channels close; Voltage-Gated Ca+ channels to open
o Ca Influx + Ca release from Sarcoplasmic Reticulum
[Ca+] causes muscular contraction.
o (Plateau is balanced by Ca+ influx & K+ efflux)
Repolarisation:
Influxing Ca+ channels close; but the effluxing K+ channels remain open;
Excess Ions?:
Excess Na+ & K+ deficit is dealt with by the Na/K-ATPase.
Excess Ca+ from the Plateau Phase is eliminated by a Na/Ca Exchanger.
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ElectroCardioGrams (ECG):
- Recording of all Action Potentials by Nodal & Contractile Cells in the heart at a given time.
o NB: It IS NOT a single action potential.
o NB: A “Lead refers to a combination of electrodes that form an imaginary line in the body, along
which the electrical signals are measured.
Ie. A 12 ‘lead’ ECG usually only uses 10 electrodes.
- Graphic Output:
o X-axis = Time
o Y-axis = Amplitude (voltage) – Proportional to number & size of cells.
- Understanding Waveforms:
- ECG Waves:
o P Wave:
Depolarisation of the Atria
Presence of this waves indicates the SA Node is working
o PR-Segment:
Reflects the delay between SA Node & AV Node.
Atrial Contraction is occurring at this time.
o Q Wave:
Interventricular Septum Depolarisation
Wave direction (see blue arrow) is perpendicular to the Main Electrical Axis results in a
‘Biphasic’ trace.
Only the –ve deflection is seen due to signal cancellation by Atrial Repolarisation.
Sometimes this wave isn’t seen at all
o R Wave:
Ventricular Depolarisation
Wave Direction (blue arrow) is the same as the Main Electrical Axis Positive Deflection.
R-Wave Amplitude is large due to sheer numbers of depolarizing myocytes.
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o S Wave:
Depolarisation of the Myocytes at the last of the Purkinje Fibres.
Wave Direction (black arrow) opposes the Main Electrical Axis Negative Deflection
This wave is not always seen.
o ST Segment:
Ventricular Contraction is occurring at this time.
Due to the lag between excitation & contraction.
o T Wave:
Ventricular Repolarisation
Positive deflection despite being a Repolarisation wave – because Repol. Waves travel in
the opposite direction to Depol Waves.
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Effects of the Autonomic Nervous System:
- Parasympathetic NS:
o Innervates SA & AV Nodes
Heart Rate
- Sympathetic NS:
o Innervates the SA & AV Nodes & Ventricular Muscle (& also via Noradrenaline).
Heart Rate
Contractility
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Mechanical Events of The Cardiac Cycle
Terms:
- Systole = Myocardial Contraction
- Diastole = Myocardial Relaxation
- Stroke Volume = Output of Blood from the Heart Per Contraction (≈80mL of blood)
- Heart Rate = #Heart Beats/Minute
- Cardiac Output:
o Volume of Blood Ejected from the Heart Per Minute (Typically ≈5L/min)
o Cardiac Output = Heart Rate x Stroke Volume
o Chronotropic Influences:
Affect Heart Rate
o Inotropic Influences:
Affect Contractility (& :. stroke volume)
o Dromotropic Influences:
Affect AV-Node Delay.
- End Diastolic Volume = Ventricular Volume @ end of Diastole (When Ventricle is Fullest)
- End Systolic Volume = Ventricular Volume After Contraction (Normal ≈ 60-65%)
- Preload = The degree of Stretching of the Heart Muscle during Ventricular Diastole.
o ( Preload = cross linking of myofibrils = Contraction (“Frank Starling Mechanism”)
- Afterload = The Ventricular Pressure required to Eject blood into Aorta/Pulm.Art.
o ( Afterload = SV due to ejection time)
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CardioDynamics:
- Cardiac Output:
o Determined by 2 Things:
1. Stroke Volume....&
2. Heart Rate
o A erage CO L min (ie. The entire blood supply circulates once per minute)
- Heart Rate:
o Depends on Tissue-Satisfaction with Nutrients & O2.
o Terms:
BradyCardia: HR Slower than normal. (too fast stroke volume & CO suffers)
TachyCardia: HR Faster than normal.
o Regulation of HR:
Autonomic Nervous System:
Parasympathetic: (Vagus Nerve)
o Decrease Heart Rate (-ve Chronotropic Effect)
o Increase AV-Node Delay (-ve Dromotropic Effect)
o NB: ONLY A TINY EFFECT ON CONTRACTILITY
Sympathetic: (Sympathetic Chains)
o Increase Heart Rate (+ve Chronotropic Effect)
o Increase Force of Contraction (+ve Inotropic Effect).
Reflex Control:
Bainbridge Reflex (Atrial Walls):
o Venous Return Heart Rate
o Responsible for 40-60% of HR increases.
BaroReceptor Reflex (Aortic & Carotids):
o BP HR & Contractility (+ Vasodilation)
ChemoReceptor Reflex:
o Low O2 or CO2 in Peripheral-Tissue HR & Resp. Rate
- Stroke Volume:
o Blood output per heart-beat.
o Stroke Volume = End Diastolic Volume End Systolic Volume
o :. SV is by:
Ventricular Filling Time (Duration of Ventricular Diastole)
Venous Return
Arterial BP (Higher harder to eject blood ESV Increases)
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Control of Circulation (Haemodynamics & BP Regulation)
Resistance:
- 3 Factors Influencing Resistance:
o 1. Blood Viscosity (Fairly Constant)
o 2. Total Vessel Length (Fairly Constant)
o 3. Vessel Diameter (Highly Variable)
Control of MAP:
- 3 Main Regulators:
o 1. Autoregulation (@ the Tissue Level):
‘Automatic Vasodilation/constriction @ the tissue relative to metabolic requirements.’
o 2. Neural Mechanisms:
Vasomotor Centres (Medulla):
Baroreceptors & Chemoreceptors
Autonomic Nervous System:
Sympathetic HR & Contractility MAP
Parasympathetic Heart Rate MAP
o 3. Endocrine Mechanisms (Kidney Level):
**Antidiuretic Hormone (ADH) AKA. Vasopressin:
ADH Water Retention Released MAP
Angiotensin II:
AT-II VasoConstriction MAP
Erythropoietin:
EPO Haematopoiesis Blood Volume MAP
Natriuetic Peptides (Released by the heart):
Stretch on Heart NP Release Diuresis Reduces BP & Volume.
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Blood Vessels
Introduction to Blood Vessels:
- 3 Classes:
o Arteries Carry blood away from the heart
Elastic Arteries Eg. Aorta & Major Branches (Conducting Vessels)
Muscular Arteries Eg. Coeliac Trunk & Renal Arts. (Distributing Vessels)
Arterioles Eg. Intra-Organ Arteries (Resistance Vessels)
Terminal Arteriole Eg. Afferent Arteriole in kidney
o Capillaries Intimate contact with tissue facilitate cell nutrient/waste transfer
Vascular Shunt
True Capillaries
o Veins Carry blood back to the heart
Post-Capillary Venule (Union of capillaries)
Small Veins (Capacitance Vessels – 65% of body’s blood is venous)
Large Veins (Capacitance Vessels – 65% of body’s blood is venous)
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Foetal Circulation:
B passes Shunts of foetal circulatory system:
o Ductus Venosus
Directs the oxygenated blood from the placental vein into inferior vena cava heart
Partially bypasses the liver sinusoids
o Foramen Ovale
An opening in the interatrial septum loosely closed by a flap of tissue.
Directs some of blood entering the right atrium into the left atrium Aorta.
Partially bypasses the lungs.
o Ductus Arteriosus
Directs most blood from right atrium of the heart directly into aorta
Partially bypasses the lungs
o **All of these “shunts” are occluded at birth due to pressure changes.
NB: The Foramen Ovale can take up to 6 months to close.
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