Functional Anatomy and Innervation of the Heart

●​ Four Chambers: Remember the two atria (right and left) receiving blood and the two
ventricles (right and left) pumping blood out.
●​ Valves: Pay close attention to the atrioventricular valves (tricuspid on the right,
mitral/bicuspid on the left) and the semilunar valves (pulmonary and aortic). Understand
their function in ensuring unidirectional blood flow.
●​ Layers of the Heart: Epicardium, myocardium (the muscular layer – crucial for
contraction), and endocardium (lining the chambers).
●​ Pericardium: The sac surrounding the heart. Know its layers (fibrous and serous) and the
pericardial fluid.
●​ Blood Supply to the Heart: Coronary arteries (left and right) are vital. Understand their
origin from the aorta and their major branches. Be aware of potential blocks leading to
myocardial infarction. Coronary veins drain deoxygenated blood.
●​ Innervation:
○​ Autonomic Nervous System: The heart is innervated by both sympathetic and
parasympathetic fibers.
■​ Sympathetic: Originates from thoracic spinal cord, increases heart rate and
force of contraction (fight or flight). Neurotransmitter: Norepinephrine.
■​ Parasympathetic: Originates from the vagus nerve (cranial nerve X),
decreases heart rate (rest and digest). Neurotransmitter: Acetylcholine.
○​ Intrinsic Conduction System: The heart has its own ability to generate electrical
impulses. Key components:
■​ Sinoatrial (SA) Node: The "pacemaker" located in the right atrium. Initiates
the heartbeat.
■​ Atrioventricular (AV) Node: Located in the interatrial septum. Delays the
impulse allowing atrial contraction before ventricular contraction.
■​ Bundle of His: Extends from the AV node into the interventricular septum.
■​ Right and Left Bundle Branches: Travel down the septum towards the apex
of the heart.
■​ Purkinje Fibers: Spread throughout the ventricular myocardium, ensuring
rapid and coordinated ventricular contraction.

Specialised Conduction Pathway

●​ This essentially reiterates the intrinsic conduction system mentioned above (SA node
\rightarrow AV node \rightarrow Bundle of His \rightarrow Bundle Branches \rightarrow
Purkinje Fibers).
●​ Understand the inherent firing rates of each component. The SA node has the highest
rate and thus dictates the heart rate under normal conditions.
●​ Clinical relevance: Arrhythmias (abnormal heart rhythms) often arise from issues within
this conduction pathway.

Properties of Cardiac Muscle

 ●​ Automaticity (Autorhythmicity): The ability of cardiac muscle cells (specifically in the
SA and AV nodes) to spontaneously depolarize and generate action potentials.
●​ Excitability: The ability to respond to an electrical stimulus.
●​ Conductivity: The ability to transmit the electrical impulse to adjacent cells.
●​ Contractility: The ability to shorten and generate force in response to an action potential.
●​ Long Refractory Period: Unlike skeletal muscle, cardiac muscle has a prolonged
refractory period. This is crucial to prevent tetanus and allow the ventricles to fill properly
before the next contraction.

Cardiac Action Potential

●​ Understand the different phases of the cardiac action potential in ventricular muscle cells:
○​ Phase 0 (Rapid Depolarization): Influx of \text{Na}^+ ions.
○​ Phase 1 (Early Repolarization): Inactivation of \text{Na}^+ channels and transient
outward current of \text{K}^+ ions.
○​ Phase 2 (Plateau Phase): Balance between \text{Ca}^{2+} influx and \text{K}^+
efflux. This prolonged depolarization is unique to cardiac muscle and contributes to
the long refractory period.
○​ Phase 3 (Rapid Repolarization): Inactivation of \text{Ca}^{2+} channels and
increased outward current of \text{K}^+ ions.
○​ Phase 4 (Resting Membrane Potential): Maintained by \text{Na}^+/\text{K}^+
pump and \text{K}^+ leak channels.
●​ Compare and contrast the action potential of pacemaker cells (SA and AV nodes) which
have a slower, gradual depolarization (pacemaker potential or funny current) due to
\text{Na}^+ influx and decreased \text{K}^+ efflux.

Cardiac Cycle
●​ The sequence of events that occur during one heartbeat. It includes systole (contraction)
and diastole (relaxation) of both the atria and ventricles.
●​ Atrial Systole: Atria contract, pushing the remaining blood into the ventricles.
●​ Ventricular Systole:
○​ Isovolumetric Contraction: Ventricles begin to contract, but all valves are closed,
so there is no change in volume, but pressure increases rapidly.
○​ Ejection Phase: Ventricular pressure exceeds aortic and pulmonary artery
pressure, forcing the semilunar valves open and blood is ejected.
●​ Ventricular Diastole:
○​ Isovolumetric Relaxation: Ventricles relax, and all valves are closed, so there is
no change in volume, but pressure decreases rapidly.
○​ Ventricular Filling: AV valves open when ventricular pressure drops below atrial
pressure, and blood flows passively from the atria into the ventricles.
●​ Understand the pressure changes in the atria, ventricles, and major arteries during each
phase.
●​ Relate the cardiac cycle to the ECG waveforms (P wave, QRS complex, T wave).

JVP Pulse (Jugular Venous Pulse)

 ●​ The waveform of the blood pressure in the internal jugular vein, which reflects pressure
changes in the right atrium.
●​ Understand the different waves and descents:
○​ 'a' wave: Atrial contraction.
○​ 'c' wave: Ventricular contraction causing bulging of the tricuspid valve into the right
atrium.
○​ 'x' descent: Atrial relaxation and downward movement of the tricuspid valve during
ventricular systole.
○​ 'v' wave: Passive filling of the right atrium during ventricular systole.
○​ 'y' descent: Opening of the tricuspid valve and rapid filling of the right ventricle.
●​ Clinical significance: Abnormalities in the JVP waveform can indicate various cardiac
conditions (e.g., tricuspid regurgitation, atrial fibrillation, cardiac tamponade).

Heart Sounds
●​ Normal heart sounds (S1 and S2):
○​ S1 ("lub"): Closure of the AV valves (mitral and tricuspid) at the beginning of
ventricular systole.
○​ S2 ("dub"): Closure of the semilunar valves (aortic and pulmonary) at the
beginning of ventricular diastole.
●​ Abnormal heart sounds (murmurs, clicks, rubs): Understand their timing in the cardiac
cycle (systolic or diastolic) and what they might indicate (e.g., valve stenosis or
regurgitation).

Heart Rate
●​ The number of heartbeats per minute. Normal resting heart rate is typically between
60-100 bpm.
●​ Factors affecting heart rate:
○​ Autonomic Nervous System: Sympathetic stimulation increases heart rate,
parasympathetic stimulation decreases it.
○​ Hormones: Epinephrine, thyroid hormones increase heart rate.
○​ Age: Generally higher in infants and decreases with age.
○​ Fitness Level: Lower resting heart rate in well-trained individuals.
○​ Body Temperature: Increased temperature increases heart rate.
○​ Emotions: Stress, anxiety can increase heart rate.

Cardiac Output (CO)

●​ The volume of blood pumped by each ventricle per minute.
●​ Formula: \text{CO} = \text{Heart Rate (HR)} \times \text{Stroke Volume (SV)}
●​ Normal resting cardiac output is around 5 liters/minute.

Factors Affecting Cardiac Output

●​ Heart Rate (HR): As discussed above.
 ●​ Stroke Volume (SV): The volume of blood ejected by each ventricle per beat. Influenced
by:
○​ Preload: The degree of stretch on the ventricular muscle fibers at the end of
diastole (end-diastolic volume). Increased preload generally leads to increased
stroke volume (Frank-Starling mechanism).
○​ Contractility: The force of contraction of the ventricular muscle fibers at a given
preload. Influenced by sympathetic stimulation, hormones (e.g., epinephrine), and
certain drugs. Increased contractility leads to increased stroke volume.
○​ Afterload: The resistance the ventricles must overcome to eject blood (e.g., aortic
pressure, pulmonary artery pressure). Increased afterload decreases stroke
volume.

Measurement of Cardiac Output

●​ Direct Methods (invasive): Fick principle, indicator dilution method.
●​ Indirect Methods (non-invasive): Echocardiography, Doppler ultrasound.
●​ For BDS, a basic understanding of the concept and the factors influencing CO is more
important than the detailed methodology of measurement.

Regulation of Cardiac Output

●​ Intrinsic Regulation (Frank-Starling Mechanism): The heart's ability to adjust its stroke
volume based on venous return. Increased venous return leads to increased preload and
thus increased stroke volume.
●​ Extrinsic Regulation:
○​ Autonomic Nervous System: Sympathetic stimulation increases both heart rate
and contractility, leading to increased CO. Parasympathetic stimulation primarily
decreases heart rate, leading to decreased CO.
○​ Hormonal Control: Epinephrine and norepinephrine (from the adrenal medulla)
increase heart rate and contractility.

Blood Pressure (Types)

●​ Arterial Blood Pressure: The pressure exerted by blood on the walls of arteries. Usually
measured in the brachial artery.
●​ Systolic Blood Pressure: The peak pressure during ventricular contraction (systole).
●​ Diastolic Blood Pressure: The lowest pressure during ventricular relaxation (diastole).
●​ Pulse Pressure: The difference between systolic and diastolic pressure (Systolic -
Diastolic).
●​ Mean Arterial Pressure (MAP): The average arterial pressure during one cardiac cycle.
Estimated as: \text{MAP} \approx \text{Diastolic Pressure} + \frac{1}{3} \text{Pulse
Pressure}. MAP is a better indicator of tissue perfusion than systolic pressure alone.
●​ Hypertension: High blood pressure. Classified into primary (essential) and secondary
hypertension.
○​ Primary Hypertension: Elevated blood pressure with no identifiable underlying
cause (idiopathic). Multifactorial involving genetics, lifestyle factors (diet, obesity,
stress, smoking).
 ○​ Secondary Hypertension: Elevated blood pressure due to an underlying medical
condition (e.g., kidney disease, endocrine disorders, cardiovascular disorders).

Factors Affecting Blood Pressure

●​ Cardiac Output (CO): Increased CO tends to increase blood pressure.
●​ Total Peripheral Resistance (TPR): The resistance to blood flow in the systemic
circulation. Increased TPR tends to increase blood pressure. Influenced by:
○​ Vessel Diameter (Vasoconstriction increases TPR, Vasodilation decreases
TPR).
○​ Blood Viscosity.
○​ Blood Vessel Length.
●​ Blood Volume: Increased blood volume tends to increase blood pressure.
●​ Elasticity of Arterial Walls: Reduced elasticity (arteriosclerosis) increases systolic blood
pressure.

Regulation of Blood Pressure

●​ Short-Term Regulation (Neural Reflex Mechanisms): Primarily involves the autonomic
nervous system and baroreceptor reflexes.
○​ Baroreceptors: Pressure-sensitive receptors located in the carotid sinuses and
aortic arch. They detect changes in blood pressure and send signals to the
brainstem (cardiovascular center).
○​ Cardiovascular Center (in the Medulla Oblongata): Integrates information from
baroreceptors and other receptors and adjusts sympathetic and parasympathetic
output to the heart and blood vessels to regulate blood pressure.
■​ Increased Blood Pressure: Baroreceptors fire more frequently, leading to
increased parasympathetic stimulation (decreased HR) and decreased
sympathetic stimulation (vasodilation, decreased HR and contractility),
resulting in a decrease in blood pressure.
■​ Decreased Blood Pressure: Baroreceptors fire less frequently, leading to
decreased parasympathetic stimulation and increased sympathetic
stimulation (vasoconstriction, increased HR and contractility), resulting in an
increase in blood pressure.
○​ Chemoreceptors: Sensitive to changes in blood oxygen, carbon dioxide, and pH.
Play a role in blood pressure regulation during hypoxia, hypercapnia, or acidosis.
●​ Intermediate-Term Regulation (Hormonal):
○​ Renin-Angiotensin-Aldosterone System (RAAS): Decreased blood pressure
leads to renin release from the kidneys, eventually causing vasoconstriction and
increased sodium and water retention, increasing blood pressure and volume.
○​ Antidiuretic Hormone (ADH) or Vasopressin: Released by the posterior pituitary
in response to low blood volume or high blood osmolarity. Causes vasoconstriction
and increased water reabsorption in the kidneys, increasing blood pressure and
volume.
○​ Atrial Natriuretic Peptide (ANP): Released by the atria in response to high blood
volume or pressure. Promotes vasodilation and increased sodium and water
excretion, decreasing blood pressure and volume.
 ●​ Long-Term Regulation (Renal Mechanisms): The kidneys play a crucial role in
long-term blood pressure regulation by controlling blood volume through adjusting fluid
intake and output.

Short-Term Regulation of Blood (Neural Reflex

Mechanisms)
●​ This reiterates the baroreceptor and chemoreceptor reflexes discussed above. Make sure
you understand the sensory receptors, the integrating center (cardiovascular center in the
medulla), and the effector mechanisms (heart and blood vessels) involved in these rapid
adjustments of blood pressure.
Remember to connect these concepts to their clinical relevance, especially in the context of oral
and dental procedures. For example, understanding blood pressure is crucial when managing
patients with hypertension or during surgical procedures where bleeding is a concern.
Knowledge of cardiac function is important when dealing with patients with underlying heart
conditions.