Block 2 (+ repeat muscle, belong to block 2)

The normal heart rate for adults is between 60 - 100 bpm.

Maximal heart rate is calculated using the formula: 220 - age.

The normal blood pressure for adults is 120/80 mmHg.

Pulse pressure is the difference between systolic and diastolic pressure, normally around 40 mmHg.

MAP can be calculated using the formulas:

1. MAP = Systolic pressure + 2 x Diastolic pressure / 3
2. MAP = Diastolic pressure + 1/3 Pulse Pressure

The normal value of MAP in the periphery is 93 mmHg.

Stroke volume (SV) is calculated as: SV = End Diastolic Volume (EDV) - End Systolic Volume (ESV).

Normal values are approximately:

• EDV: 140-150 mL
• ESV: 60-70 mL

The normal stroke volume is 70-80 mL per heartbeat.

Cardiac output is the volume of blood pumped from the ventricle in one minute, with a normal value of 5-6 L/min.

CO = HR × SV or CO = MAP/TPR

Ejection fraction is the percentage of the ventricular volume that is ejected, representing the percentage of blood ejected from the ventricles. The normal value is 50-70%.

Ejection fraction = (SV/EDV) × 100%

They are equal.

MAP = (systolic pressure + 2 × diastolic pressure) / 3

MAP = 90 mmHg

CO = 60 × 100 = 6000 mL = 6L

TPR = MAP/CO

TPR = 15

Ejection fraction = (100/150) × 100% = 66.6%

Pulse pressure = systolic pressure - diastolic pressure = 110 - 80 = 30 mmHg.

Cardiac cycle = 60/HR

0.8 seconds

270 ms

530 ms

The MAP should increase.

Cardiac output increases.

The Goltz reflex is triggered by increased abdominal pressure, such as from hitting the cardia or abdominal wall. This reflex activates the vagus nerve, leading to a decrease in heart rate (HR↓).

The Occulo-cardiac reflex occurs when there is increased pressure against the eyeballs, similar to the Cushing reflex. This pressure raises intracranial pressure, signaling through the ophthalmic nerve to the heart, which results in a decrease in heart rate (HR↓) due to vagus nerve activation.

In the cerebellar spinal fluid, the concentrations of potassium and glucose are lower than those in plasma, indicating a difference in composition that may have physiological implications.

The heart rate increases due to the Loven reflex.

1 mm in the ECG paper is approximately 40 ms.

A normal ECG is composed of a P wave, a QRS complex, and a T wave.

The P wave is caused by electrical potentials generated when the atria depolarize before they contract.

The QRS complex represents the electrical potentials generated when the ventricles depolarize before they contract, with atrial repolarization hidden in this complex.

The T wave represents ventricular repolarization and has a duration of less than 200 ms.

The P-R interval duration is 120-200 ms.

The U wave indicates the repolarization of the papillary muscle.

The QRS complex duration is 40-100 ms.

Heart rate is calculated using the formula:

Heart Rate (bpm) = 60 / R-R interval (in seconds). For an R-R interval of 1 second, the heart rate is 60 bpm.

The QT interval duration is 0.37-0.42 seconds (or 370-420 ms).

False. The correct duration is 0.08 s.

True. It is hidden in the QRS complex.

1st degree AV-block, as the PR interval is too long (should be between 120-200 ms).

75 bpm, calculated as ( \frac{60}{0.8} ).

False. We place 10 electrodes on the patient to measure 12 leads.

False. We have 3 bipolar leads and 9 unipolar leads.

In leads V1, V2, and aVR.

By observing an abnormal QRS followed by a compensational pause.

Einthoven's triangle is used to determine the electrical axis of the heart by measuring the electrical potential differences between the limbs.

Einthoven's Law states that the sum of the potentials recorded in leads I and III will equal the potential in lead II, expressed as II = I + III.

In Goldberger's augmented leads, two limbs are connected to the negative terminal of the electrocardiograph, while the third limb is connected to the positive terminal, resulting in leads aVR, aVL, and aVF.

The ejection fraction decreases because the stroke volume decreases.

14 mmHg

15 mmHg

70-80 mL

50-70%

93 mmHg

• Ventricular pressure increases
• Ventricular volume remains unchanged
• Semilunar valves and AV-valves are closed

The closure of the AV-valves is the main component of the first heart sound. Both AV-valves close simultaneously, resulting in no split between them.

• Ventricular pressure increases
• Ventricular volume decreases
• Semilunar valves are open
• AV-valves are closed

• Ventricular pressure stops increasing
• Ventricular volume continues to decrease
• Semilunar valves are open
• AV-valves are closed

Both the semilunar valves and AV-valves are closed during isovolumetric contraction.

The protodiastole phase is a short period of 40 ms where nothing significant happens in the heart.

During isovolumetric relaxation, ventricular pressure decreases, ventricular volume remains unchanged, and both AV and semilunar valves are closed. The closure of the semilunar valves marks the second heart sound.

In the fast filling phase, blood moves from the atriums to the ventricles, accounting for 70-80% of cardiac filling. Ventricular pressure slightly decreases then increases, ventricular volume increases, semilunar valves are closed, and AV-valves are open. The third heart sound may be heard due to vibrations of the ventricular wall.

The slow filling phase is similar to the fast filling phase, where the ventricles continue to fill with blood, but at a slower rate. Ventricular pressure slightly increases, ventricular volume increases, semilunar valves are closed, and AV-valves are open.

During atrial systole, the ventricles continue to fill with blood (20% of total filling). Ventricular pressure slightly increases, ventricular volume increases, semilunar valves are closed, and AV-valves are open. The ventricular volume does not change significantly during this phase.

Isovolumetric relaxation.

The first heart sound.

Fast filling phase.

Isovolumetric contraction.

All diastolic phases (Protodiastole, Isovolumetric relaxation, fast filling phase, slow filling phase, atrial systole) and isovolumetric contraction.

Rapid/fast ejection phase and slow ejection phase.

Fast filling phase, slow filling phase, and atrial systole.

With a stethoscope or PCG (Phonocardiography).

Closure of AV valves.

Closure of semilunar valves.

Rapid filling phase, vibration of the ventricular wall.

Pathological (atrial systole).

The three major types of cardiac muscle are atrial muscle, ventricular muscle, and specialized excitatory and conductive muscle.

Cardiac muscle fibers communicate through gap junctions, which allow the action potential to spread to adjacent cells, enabling the atria and ventricles to function as two functional syncytia despite being electrically isolated.

The structural and functional unit of cardiac muscle is the sarcomere, which contains Z-lines, thin filaments (actin, tropomyosin, troponin), and thick filaments (myosin).

During contraction, the I-band and H-band decrease in size, while the M-lines and Z-lines get closer together.

In isometric (isovolumetric) contraction, the strain (pressure) increases without a change in length, while in isotonic contraction, the muscle shortens and work can be measured, such as when the ventricles contract and the semilunar valves open.

Ectopic impulse generation occurs when the electrical impulse develops outside the SA node, which is the normal pacemaker of the heart. This can happen when the SA node ceases to generate impulses, leading to pacemaker activity from another site, such as the AV node.

An extrasystole is a premature cardiac contraction that occurs independently of the normal rhythm of the heart. It can be characterized by a coupling time and may include a complete or incomplete compensatory pause.

The main components of the heart's conduction system are the SA node, AV node, bundle of His, bundle branches (Tawara bundles), and Purkinje fibres.

The SA node is the main generator of the heart, activating the atrial muscles and generating 60-100 action potentials per minute, which corresponds to the heart rate.

If the SA node fails, the AV node can take over with a heart rate of 40-60 bpm. If the AV node also fails, the His-bundle can take over with a rate of 12-25 bpm, which is insufficient for human life.

The conduction velocity through the AV node is between 0.02-0.05 m/s.

1. SA node generates impulse; atrial excitation begins.

2. Impulse is delayed at the AV node.

3. Impulse passes to the heart apex; ventricular excitation begins.

4. Ventricular excitation is complete.

The conduction velocity of the Purkinje fibres is 4 m/s.

SA-node -> atrium -> AV-node -> His bundle -> Tawara bundles/right and left bundle branches -> Purkinje fibres -> Ventricular muscle.

1. Purkinje fibres
2. Bundle of His and Tawara bundles
3. Atrial muscle
4. Ventricular muscle
5. AV node
6. SA node

1. SA node
2. AV node
3. Ventricular muscle
4. Atrial muscle
5. Bundle of His and Tawara bundles
6. Purkinje fibres

Purkinje fibres.

Gives time for ventricular filling.

1st Stannius ligature is placed between the sinus venosus and the atrium, causing the atria and ventricles to stop contracting temporarily, then contract at a lower rate due to atrial pacemaker activity. The 2nd Stannius ligature is placed between the atrium and ventricle, stopping the ventricles while the atria continue contracting, leading to a lower frequency of ventricular contractions than atrial contractions.

The order is: 1. Sinus venosus (fastest) 2. Atria 3. Ventricles

The apical piece does not contract on its own due to lack of impulse generation capability, but it contracts when mechanically stimulated with a pinprick.

They remain unaffected after placing the Stannius ligatures.

By stimulating the ventricle after the first Stannius ligature with electrical impulses, it was shown that the heart responds to every suprathreshold stimulus with the same maximal contraction, regardless of stimulus intensity.

No, there are no pacemaker cells in the apex of the ventricles.

False, according to the Bowditch 'all or nothing' law, once the threshold is reached, the contraction force remains the same regardless of stimulus intensity.

Heart muscle cannot be tetanized because the duration of an action potential is almost equal to the duration of the mechanical response (contraction).

Ventricular diastole.

Coupling time is the interval from R-wave of last sinus beat to R-wave of an extrasystole.

Compensatory pause is an impulse generation after an extrasystole.

Nonselective cation channels, also known as the funny current, primarily allow Na+ inflow which contributes to the slow diastolic depolarization in nodal tissue action potentials.

T-type calcium channels facilitate Ca2+ inflow, which is crucial for both the slow diastolic depolarization and the early phase of the action potential in nodal tissue.

L-type calcium channels allow Ca2+ inflow, which further increases the membrane potential during the action potential, contributing to its peak phase.

Voltage-gated potassium channels are responsible for K+ outflow, which leads to repolarization of the membrane potential after the action potential peaks.

The action potential starts from a resting membrane potential of around -65 mV, rises slowly due to T-type Ca2+ channels, peaks with L-type Ca2+ channels, and then repolarizes due to K+ channels opening.

The action potential in cardiac muscle is longer and includes a plateau phase due to the involvement of L-type slow calcium channels in addition to fast sodium channels. In contrast, the action potential in skeletal muscle is primarily caused by fast sodium channels that open briefly, resulting in a shorter action potential.

1. Depolarization: Fast voltage gated sodium (Na+) channels open, causing sodium inflow and evoking the action potential.

2. Early Repolarization: Early voltage gated potassium (K+) channels open, potassium outflows, and fast sodium channels close.

3. Chloride Inflow: Voltage gated chloride (Cl-) channels open, allowing chloride inflow, contributing to repolarization.

4. Plateau Phase: L-type calcium (Ca2+) channels open, leading to calcium inflow.

5. Late Repolarization: Late voltage gated potassium (K+) channels open, potassium outflows, completing the repolarization process.

The plateau occurs because there is a simultaneous potassium outflow that balances the membrane potential.

L-type Ca2+ channels and voltage-gated potassium (K+) channels are found in both.

Fast voltage-gated sodium channels are found only in the atrial and ventricular muscle.

Non-selective cation channels and T-type Ca2+ channels are found only in the nodal tissue.

The maximal diastolic membrane potential is most negative in the ventricular muscle.

• Nodal tissue: 200 ms
• Ventricular muscle: 300 ms

ECG stands for electrocardiogram and provides information about the heart's electrical activity, rate, and rhythm.

In a standard clinical ECG, 12 leads are recorded using 10 electrodes placed on the patient.

The standard speed of the ECG paper is 25 mm/s.

The aVR lead is significant because it records the electrical activity of the heart from the right arm and is inverted compared to standard limb leads, providing a different perspective on the heart's electrical activity.

aVR

Negative QRS complex.

The normal electrical axis of the heart is -30 to 100 degrees.

Normal electrical axis.

Right deviation.

Left deviation.

Extreme right deviation.

False, it's too high. 10mV = 100mm.

aVR

aVR

aVR, V1 and V2.

The right hand.

Vector I will be negative.

Normal electrical axis.

Ventricular extrasystole is characterized by an abnormal QRS complex that is too wide, with no P wave preceding it. It is followed by a compensational pause due to the absolute refractory period, which prevents the next heartbeat from occurring immediately. This condition can be caused by low levels of magnesium.

Supraventricular extrasystole originates from the atrium, resulting in a normal QRS complex. Unlike ventricular extrasystole, there may not be a compensational pause following the extrasystole.

A 1st degree AV-block is defined by a P-R interval that is longer than 200 ms.

In a 2nd degree AV-block, some action potentials are stopped by the AV node, while in a 3rd degree AV-block, all action potentials are stopped by the AV node, leading to a complete dissociation between atrial and ventricular activity.

Phonocardiography (PCG) is a technique that graphically represents and visualizes heart sounds using a special microphone placed over the heart. It is significant for the detection and monitoring of valve diseases and is used in conjunction with ECG.

The auscultation points for heart sounds are as follows:

The first heart sound ('lub') is due to the closure of the atrioventricular valves, while the second heart sound ('dub') is due to the closure of the semilunar valves.

The third heart sound is caused by extremely fast ventricular filling, leading to a vibration in the ventricular wall. It is best heard over the cardiac apex and can be prominent in young people who exercise regularly.

The three basic percussion sounds are:

1. Resonant - heard over normal lung tissue.
2. Tympanic - heard over most portions of the normal abdominal cavity.
3. Dull - heard over solid organs (e.g., liver) and muscles.

Percussion can provide an estimate of a patient's heart size by assessing the magnitude of cardiac dullness, which can be increased in cases of cardiomegaly or the accumulation of pericardial fluid.

The normal borders of the lungs are:

• Parasternal anterior: 5th intercostal space
• Medio clavicular line: 6th intercostal space
• Anterior axillary line: 7th rib
• Middle axillary line: 8th intercostal space
• Scapular line: 10th intercostal space
• Paravertebral line: 11th intercostal space

The vagus nerve (X) provides parasympathetic innervation to the heart, with the right vagus innervating the SA node and atrial muscle, and the left vagus innervating the AV node and atrial muscle.

The neurotransmitter associated with the vagus nerve in the heart is acetylcholine.

Inhibitors of acetylcholine esterase, such as eserine, physostigmine, and neostigmine, decrease the heart rate.

A very low dose of epinephrine decreases blood pressure by binding to β-2 receptors, causing vasodilation and a decrease in total peripheral resistance (TPR).

An alpha-receptor blocker does not change the heart rate.

Choline acetyl transferase catalyzes the synthesis of acetylcholine in the heart muscle.

Acetylcholine esterase catalyzes the degradation of acetylcholine in the heart.

The parasympathetic innervation has a negative chronotropic effect, leading to a decrease in heart rate (HR).

The heart rate will decrease when the vagus nerve is stimulated electrically.

Atropine increases the heart rate by inhibiting muscarinic acetylcholine receptors, blocking the parasympathetic effect on the heart.

Cutting the vagus nerve (vagotomy) will increase the heart rate.

Eserine decreases the heart rate by inhibiting the degradation of acetylcholine (ACh).

Stimulation of the right vagus nerve decreases the heart rate, resulting in a longer R-R interval on the ECG.

Stimulation of the left vagus nerve slows down the AV node, increasing the atrioventricular conduction time and resulting in a longer P-R interval, with a decrease in heart rate.

Warming up the SA node increases the heart rate by generating more action potentials.

Intravenous acetylcholine will decrease the heart rate due to its parasympathetic effects.

The sympathetic innervation causes an increase in heart rate due to the release of norepinephrine, which acts on β-1 receptors in the heart.

When sympathetic fibers are stimulated, the heart rate increases.

Cutting sympathetic fibers results in a decrease in heart rate.

β-blockers cause a decrease in heart rate by blocking the action of norepinephrine on β-1 receptors.

Administering a β-blocker antagonist results in an increase in heart rate.

The heart rate will increase because the effect of the parasympathetic nervous system, which decreases heart rate by 30-40 bpm, is stronger than that of the sympathetic nervous system, which increases heart rate by 10 bpm.

It increases contraction force and heart rate, but the heart stops in systole.

It decreases contraction force and heart rate, and the heart stops in diastole.

Mild hyperkalaemia can cause ventricular fibrillation, while more severe hyperkalaemia can lead to cardiac arrest in diastole.

Epinephrine increases both contraction force and heart rate.

Propranolol prevents the effects of epinephrine, reducing contraction force and heart rate.

Acetylcholine increases contraction force and heart rate.

Atropine prevents the effects of acetylcholine, leading to an increase in contraction force.

Baroreceptors detect changes in blood pressure through transmural pressure in the arteries, particularly in the carotid sinus and aortic arch. They send signals to the brain via the glossopharyngeal nerve (from the carotid sinus) and the vagus nerve (from the aortic arch) to regulate blood pressure through sympathetic or parasympathetic responses.

When a ligature is placed on the common carotid artery, the pressure in the carotid sinus decreases. This lower transmural pressure is detected by baroreceptors, which signal the brain to activate the sympathetic nervous system, resulting in increased blood pressure, heart rate, cardiac output, stroke volume, and total peripheral resistance (TPR). This response is known as the pressor reflex.

Ligation of the external carotid artery increases the transmural pressure in the carotid sinus, which is detected by baroreceptors. This leads to the activation of the vagus nerve, resulting in decreased blood pressure, heart rate, and cardiac output. This response is referred to as the depressor reflex.

Baroreceptor activity is directly proportional to blood pressure. Therefore, when blood pressure is low, the activity of these receptors is also low.

Peripheral chemoreceptors are located in the aortic body and carotid body.

Yes, chemoreceptors can be activated in cases of very severe hypercapnia, although their primary stimulus is hypoxia.

The neurotransmitters of the peripheral chemoreceptors are dopamine and ATP.

If the common carotid artery is constricted, blood pressure will increase due to low pressure in the carotid body, which activates the sympathetic nervous system.

In cases of baroreceptor hypersensitivity, the heart rate decreases.

Atropine causes an increase in heart rate (HR ↑) and can lead to a decrease in blood pressure (BP ↓).

A β-receptor agonist causes an increase in heart rate (HR ↑).

A β-receptor antagonist causes a decrease in heart rate (HR ↓).

Acetylcholine causes a decrease in heart rate (HR ↓) and can lead to a decrease in blood pressure (BP ↓).

The stimulus of the pressor reflex is low blood pressure. The response includes increased blood pressure, heart rate, and respiration rate.

The depressor reflex is triggered by increased blood pressure. Its physiological response includes decreased blood pressure, heart rate, and breathing rate.

Peripheral chemoreceptors located in the carotid body and aortic body sense low oxygen levels, activating the sympathetic nervous system, which leads to increased heart rate and blood pressure.

The Bainbridge reflex occurs when there is an increase in venous return. It is detected by low pressure baroreceptors in the atrium, leading to an increase in heart rate and blood pressure as the brain activates sympathetic fibers.

The heart rate increases when you lay down because the venous return increases. Blood from the lower extremities does not have to flow against gravity, as they are at the same level as the heart, prompting an increase in heart rate.

The heart rate decreases when standing up quickly after laying down.

The Bezold Yarish reflex involves coronary dilation during diastole to compensate for the increased heart rate during exercise. This reflex allows more blood to flow to the heart muscle, counteracting the reduced blood flow due to shortened diastole, primarily through the activation of B-2 adrenergic receptors by epinephrine and norepinephrine.

During ischemia, receptors on the wall of the left ventricle detect overload and activate the afferent vagus nerve, which informs the brain. This leads to activation of the efferent vagus nerve, resulting in a decrease in heart rate and an increase in diastole duration, improving coronary circulation and reducing heart workload.

The Loven reflex is evoked by pain, activating the sympathetic nervous system, which results in an increase in heart rate, cardiac output, total peripheral resistance (TPR), and blood pressure.

The Cushing reflex occurs when intracranial pressure is high, activating the autonomic nervous system. It results in a decrease in heart rate (HR↓) due to vagus nerve activation, while the sympathetic system constricts vessels, leading to an increase in blood pressure (BP↑). This reflex is significant in cases of brain tumors, hemorrhage, or swelling, as it can compress the medulla oblongata, which is critical for respiratory and cardiovascular function.

No, the brain is not involved in the pressor reflex.

No, the brain is not involved in the depressor reflex.

The heart rate decreases in the case of the Bezold Yarish reflex.

The heart rate decreases in the case of the Cushing reflex.

The heart rate increases in the case of the brain bridge reflex.

The heart rate increases in the case of the pressor reflex.

The heart rate increases in the case of the Loven reflex.

High intracranial pressure can occur due to a brain tumour, brain haemorrhage, or swelling.

The Goltz reflex is caused by a hit in the abdominal wall, leading to a decrease in heart rate.

The heart rate decreases in the Occulo-cardiac reflex.

The mechanism of autoregulation is the Bayliss effect. When blood pressure is high, transmural pressure increases, opening mechanosensitive Ca2+ channels, leading to Ca2+ inflow and smooth muscle contraction (vasoconstriction). Conversely, when blood pressure is low, there is no Ca2+ inflow, resulting in vasodilation.

Autoregulation is effective when the mean arterial pressure (MAP) is between 60 and 160 mmHg.

The brain receives the same amount of blood during sleep, training, or praying. However, certain parts of the brain may be used more during these activities, leading to increased blood flow to those specific areas.

At rest, the blood flow rates are as follows:

Hypercapnia acts as a vasodilator in the brain, while hypocapnia acts as a vasoconstrictor.

Fainting during hyperventilation is caused by a decrease in the partial pressure of CO2, leading to hypocapnia, which results in vasoconstriction in large parts of the brain.

Hypoxia acts as a vasodilator in the periphery and a vasoconstrictor in the pulmonary circulation.

Heterometric regulation refers to the heart's ability to increase its force of contraction and stroke volume in response to an increase in venous return and hence preload.

Homeometric regulation is the heart's ability to increase contractility and restore stroke volume when the afterload increases, occurring independently of cardiomyocyte fibre length, via the Bowditch effect.

Increasing venous return leads to an increase in EDV, SV, CO, and BP. The heart rate remains unchanged because there is no Bainbridge reflex in this preparation, and the heart lacks sympathetic and parasympathetic innervation when removed from the chest.

The pressure in the aorta will increase. This is because peripheral resistance is proportional to afterload.

The ESV will increase when afterload is increased. This occurs because the aortic valve opens later, resulting in more blood remaining in the ventricle at the beginning of the ejection phase.

• Arterial blood pressure
• Central venous pressure
• Volume of the ventricles (EDV, ESV)
• Blood temperature

• Venous return
• Peripheral resistance
• Temperature of the blood

Increasing blood temperature causes the heart rate to increase due to the warming of the SA node, which generates more action potentials.

If venous return increases, the heart rate increases.

The resistance vessels are the arterioles, which can easily increase and decrease their diameter, thereby affecting resistance.

The capacitance vessels are the veins, which are responsible for storing blood.

The sympathetic nervous system innervates all blood vessels except for the capillaries, which do not have parasympathetic innervation.

Local vasodilators include:

• NO (endothelin derived/releasing)
• Histamine
• Bradykinin
• Prostacyclin (Pgl₂)
• Adenosine
• Hypocapnia
• Lactate
• Local acidosis
• Hyperkalaemia

In the lungs, hypoxia causes vasoconstriction to prevent blood flow to poorly ventilated alveoli, ensuring blood is directed to well-ventilated areas for effective gas exchange.

CO2 diffusion is much better through the lipid bilayer compared to O2.

The order of blood flow velocity is:

1. Arteries (fastest)
2. Veins
3. Arterioles
4. Venules
5. Capillaries (slowest)

Blood flows from areas of higher pressure to areas of lower pressure in the circulatory system.

The blood pressure hierarchy at rest is:

1. Left ventricle (lowest)
2. Arteries
3. Arterioles

Hypoxia acts as a vasodilator in the periphery and a vasoconstrictor in the pulmonary circulation.

Hypercapnia is a vasodilator in the brain.

Hypocapnia is a vasoconstrictor in the brain.

High blood temperature results in low blood viscosity.

Hematocrit does not affect the viscosity of blood plasma, as plasma contains no cells.

When the velocity of blood flow is high, the viscosity of the blood is low.

No, plasma viscosity is the same in both big arteries and arterioles because plasma is a Newtonian fluid.

Blood viscosity is higher in big arteries and lower in arterioles.

There is no fluid in the alveoli to allow for gas exchange to occur.

The hydrostatic pressure in the pulmonary circulation is significantly lower, with blood pressure in the pulmonary artery at 24/9 mmHg compared to 120/80 mmHg in the periphery, making it insufficient to induce filtration under normal conditions.

Edema occurs in the periphery in the case of right ventricular failure.

Pulse is the elastic dilation and retraction of the arteries according to the cardiac rhythm, resulting in a palpable, periodic pulsation due to the elasticity of vessel walls, allowing continuous blood flow in veins.

Pulse can be examined by palpation with fingers or with devices, both non-invasive and invasive.

The palpation points include:

1. Carotid artery
2. Superficial temporal artery
3. Maxillary artery
4. Subclavian artery
5. Radial artery
6. Ulnar artery
7. Cubital artery
8. Dorsalis pedis artery
9. Posterior tibial artery
10. Popliteal artery
11. Femoral artery

The Physical Fitness Index (PFI) is measured using the Harvard step test, which involves:

1. Patients step up and down on a 50 cm high step at a rate of 30 steps per minute for 5 minutes.
2. Pulse is recorded 3 times for 30 seconds at 1, 2, and 3 minutes after exercise.
3. The 3 pulse values are summed to calculate PFI using the formula: PFI = (duration of exercise (sec) x 100) / (2 x sum of pulse rates during recovery).

Capillary permeability can be increased by several molecules that contract the endothelial cells of the capillary wall, enlarging the pores. These molecules include:

• Histamine
• Serotonin
• Bradykinin and other kinins
• Leukotrienes

Curare inhibits the nicotinic acetylcholine (Ach) receptors on the muscle.

When the maximal threshold is reached, the maximal recruitment of muscle fibers is also reached, and the amplitude of the contraction cannot increase further.

The equipment used includes:

1. Stimulator (placed over the nerve)
2. Ground electrode
3. Electrode pair (2x)
4. EMG electrode
5. AD-setup

The grip force decreases due to muscle fatigue.

Factors that can influence muscle fatigue include:

• Nutrition
• Drug
• Sleep
• Physical state
• Mentality

During exercise, the systolic pressure primarily increases as more blood needs to be pumped out of the heart.

All living cells have membrane potential. Only excitable cells like skeletal, neural, and cardiac cells can generate action potential.

2-2.2 um

The titin is as long as the sarcomere, while the nebulin is as long as the actin.

Both thick and thin filaments.

Thin filaments.

Thick filaments.

Curare is a non-depolarising muscle relaxer that does not change the membrane potential; it inhibits the nicotinic Ach receptors.

Reversible

Direct stimulation involves stimulating the muscle directly, while indirect stimulation involves stimulating the nerve that stimulates the muscle.

There will be a contraction only when stimulated directly, as curare inhibits the receptors on the muscle membrane, preventing contraction during indirect stimulation.

1. Resting phase: Myosin heads are not bound to actin (bound to ATP).
2. Depolarization: Action potential causes Ca2+ inflow, leading to depolarization.
3. Activation: Ca2+ binds to calmodulin, activating myosin light chain kinase, which phosphorylates myosin head.
4. Contraction: Phosphorylated myosin binds to actin, forming cross bridges, leading to sliding filament mechanism.
5. Maintaining phase: Unique to smooth muscle, uses a few ATP molecules.
6. Repolarization: ADP dissociates, Ca2+ levels normalize via Ca2+ pump and Na+/Ca2+ exchange.
7. Relaxation: Ca2+ decreases, myosin head detaches from actin, returns to 90°, binds new ATP.

• Tonic contraction: Long action potential with plateau phase, resulting in long-lasting contraction.
• Phasic contraction: Short-lasting and rhythmic contraction.

Ca2+ is sourced both intracellularly and extracellularly.

Smooth muscles are innervated by the autonomic nervous system, making them involuntary.

The resting membrane potential of smooth muscle ranges from -40 mV to -70 mV, which is unstable.

The duration of action potential in smooth muscle is longer compared to that in skeletal muscle, lasting approximately 25 times longer.

• Ligand gated Ca2+ channels
• K+ channels
• Voltage gated Ca2+ channels

Dens plaque.

ATP.

Activate MCL (myosin light chain) kinase.

Yes, both muscles are working simultaneously.

• Increased oxygen uptake capacity
• Increased glucose uptake capacity
• Increased number and function of mitochondria
• Increased aerobic capacity
• Increased anaerobic glycolysis
• Increased lactate tolerance

• Troponin I inhibits the binding of actin and myosin.
• Troponin C binds to calcium.

Intracellular.

Yes.

Smooth muscle contraction is initiated by calmodulin, which binds calcium ions and activates myosin light chain kinase (MLCK).

Calcium ions increase in the cytosolic fluid due to influx from extracellular fluid and release from the sarcoplasmic reticulum, leading to the activation of calmodulin and subsequent phosphorylation of myosin light chains.

Most calcium ions needed for smooth muscle contraction come from the extracellular space during action potentials or other stimuli, unlike skeletal muscle which primarily relies on the sarcoplasmic reticulum.

The two types of action potentials in smooth muscle are: 1. With plateau phase (e.g., arteries) 2. Without plateau phase (e.g., antrum pyloricum).

The actin to myosin ratio in smooth muscle is 15/1, while in skeletal muscle it is 2/1.

In a neurogenic lesion at rest, there is fibrillation and fasciculation, indicating spontaneous activity. The waveform shows increased motor potential with larger amplitude and duration over time due to regeneration.

In normal conditions, the motor unit potential is 0.5-1.0 mv with a duration of 5-10 msec. In myogenic lesions, the motor unit potential is characterized by small units with early recruitment, indicating a reduced size and function of motor units.

In neurogenic lesions, the interference pattern shows a reduced fast firing rate and a reduced slow firing rate, leading to a decreased count of motor units. In contrast, normal conditions exhibit a full interference pattern.

The increase in motor unit size in neurogenic lesions over time indicates regeneration and results in a huge motor potential with increased amplitude and duration, reflecting the body's attempt to compensate for lost motor units.

Smooth muscle cells are 1-5 um in diameter and 20-500 um in length. They are composed of myocytes, which are thin elongated cells with a single nucleus, containing organelles like mitochondria and filaments (actin and myosin). The arrangement of actin and myosin filaments differs from that in skeletal muscle, with actin filaments attached to dense bodies, which serve a similar role to Z-disks in skeletal muscle.

The two types of smooth muscle are:

1. Multi-unit smooth muscle:

   • Cells function separately.
   • Contraction is initiated by a transmitter, not by action potentials.
   • Examples: uterus, respiratory muscles (bronchi, bronchioles).

2. Single-unit smooth muscle:

   • Cells form a functional unit with stimuli spreading through gap junctions.
   • Contractions are usually caused by action potentials (phasic contractions).
   • Examples: pupillary muscle (pupillary sphincter and dilator muscle), arrector pili.

Smooth muscle can contract as much as 80 percent of its length, while skeletal muscle can only contract about 30 percent of its length. This is due to the unique arrangement of actin and myosin filaments in smooth muscle, allowing for more extensive contraction.

Myasthenia gravis is a chronic autoimmune neuromuscular disease that causes weakness in the skeletal muscles due to the production of antibodies against the nicotinic acetylcholine receptors (N-Ach-R) at the neuromuscular junction.

Malignant hyperthermia is caused by a mutation of the ryanodine receptors, leading to a severe reaction to certain anesthetic drugs. Activation of these receptors results in muscle activation and increased body temperature (hyperthermia).

The main treatment for malignant hyperthermia is the administration of dantrolene. Anaesthesiologists give this drug immediately if malignant hyperthermia is suspected, stop the anesthetic, and the surgeon ends the surgery as soon as possible.

In neurogenic lesions, there is spontaneous activation of the muscle even when the patient is asked to relax, resulting in EMG signals. The motor unit potential is typically larger than 1 mV, and there is no complete interference.

In myogenic lesions, the amplitude of the motor unit potential and maximal contraction is smaller than normal, with no resting/spontaneous activity (isoelectric line during relaxation). Complete interference is present but with small amplitude, unlike neurogenic lesions which show larger potentials and spontaneous activity.

The transducer converts the mechanical signal into an electrical signal.

The amplifier increases the amplitude of the electrical signal.

The filter removes parts of the noise; for example, to examine signals between 0.5Hz and 50Hz, a 0.5Hz high pass filter and a 50Hz low pass filter are used.

The minimum stimulus threshold is the single pulse with the lowest intensity that can induce a single twitch.

The amplitude of the contraction force stops increasing above a certain stimulus intensity called the maximal recruitments threshold.

If a second action potential arrives before the muscle is fully relaxed, the force of the next contraction will be greater, a phenomenon known as summation or superposition.

If the stimulus frequency is increased and the muscle does not relax completely, the individual twitches will fuse into a single sustained contraction. If the individual twitches are still recognizable, it is called incomplete tetanus; if they fuse completely, it is called complete tetanus.

Type I-A muscle fibers are red fibers caused by myoglobin, are slow-twitch, utilize aerobic glycolysis, show muscle fatigue later, are antigravitational muscles, and have lots of mitochondria. They are typically associated with activities like marathon running.

Type II-A muscle fibers are fast-twitch, have a moderate amount of mitochondria, and utilize both aerobic and anaerobic glycolysis. Type II-B muscle fibers are white fibers caused by glycogen, are fast-twitch, utilize anaerobic glycolysis, show muscle fatigue early, produce more lactate, and are associated with activities like 100m sprints and weightlifting.

Regular workouts do not increase the number of muscle fibers; instead, they lead to an increase in size known as hypertrophy.

The effects of training on muscle include:

1. Hypertrophy (bigger, stronger muscles)
2. Increased O2 uptake
3. Increased function and number of mitochondria
4. Increased aerobic enzyme capacity with low intensity long training
5. Increased anaerobic enzyme with high intensity interval training
6. Increased lactate tolerance

Muscle strain is caused by microtrauma, which leads to sterile inflammation in the muscle.

EMG stands for electrical myography and it records the electrical activity of skeletal muscle.

Surface electrodes have a low risk of infection and are less precise, while deep electrodes have a high risk of infection, are painful, but provide more precise measurements.

Both ATP and calcium are required for muscle activation during contraction.

When troponin C binds to calcium, it changes conformation, which also alters the conformation of the troponin-tropomyosin complex.

During muscle contraction, the angle between the myosin head and neck is 45°, while during relaxation it is 90°.

The myosin head binds to the actin site and tilts from 90° to 45°, allowing it to slide towards the Z-line and bind to the next actin, facilitating contraction.

The action potential reaches the axon terminal, opening voltage-gated calcium channels, leading to calcium inflow which is crucial for neurotransmitter release.

Acetylcholine is released into the neuromuscular junction and binds to nicotinic acetylcholine receptors, causing sodium outflow and depolarization of the muscle cell membrane.

The sliding filament mechanism involves the change in angle of the myosin head from 90° to 45°, allowing myosin to bind to actin and cause muscle contraction.

Yes, DHP receptors are present in the heart.

Yes, ryanodine receptors are present in the heart.

Nebulin is as long as the actin filament and functions to support it.

The H-band and I-band get shorter during contraction.

During relaxation, there are no calcium signals, and ATP is needed to relax the muscle. Calcium is moved back to the sarcoplasmic reticulum by the calcium-ATPase transporter.

The troponin-tropomyosin complex occupies the myosin binding site on the actin filament, preventing interaction between actin and myosin during relaxation.

The troponin-tropomyosin complex consists of Tropomyosin, Troponin I (inhibits), Troponin C (binds to calcium), and Troponin T.

The optimal length of a sarcomere to exert maximal contraction force is between 2-2.2 micrometers (um).

The sarcomere consists of:

• Thin filaments: Actin, Dystrophin, Nebulin, Tropomyosin, Troponin I, Troponin C, Troponin T
• Thick filaments: Myosin
• Structural proteins: M-protein (M-line), Titin, Z-lines

Titin connects the Z-line to the myosin and back, anchoring the myosin to the Z-line and is as long as the sarcomere itself.

The A-band is as long as the myosin itself and contains both thick and thin filaments.

The H-band is the length between the two actin molecules and contains only thick filaments.

The I-band is from the end of one myosin to the next and contains only thin filaments.

Muscle fatigue is a reversible decrease in the ability of skeletal muscle to exert force in response to physical activity. Its significance is to protect the body from complete depletion.

The types of muscle fatigue are:

1. Peripheral: Involves motoneurons and/or muscle fibers.
2. Central: Involves the CNS, primarily caused by hypoglycemia.
3. Mental (psychic): Involves factors like motivation, tolerance, attention, and focus.

The causes of peripheral fatigue include:

• Lactic acid formation leading to decreased pH
• Hypoxia
• Hypoglycemia
• Hyperthermia
• Dehydration

The order in which muscle uses energy sources is:

1. ATP
2. Phosphocreatine
3. Muscle glycogen
4. Liver glycogen

When there is no ATP, the muscle cannot contract or relax, leading to a condition known as 'Rigor Mortis', where the muscle becomes stiff.

The functional unit of skeletal muscle is the muscle fibre, which varies in length depending on the specific muscle.

A-alpha motoneurons have the following characteristics:

• Conduction velocity: 70-120 m/s
• Diameter: 15 μm
• Myelinated axons
• Associated glia cells: Schwann cells

A motor unit consists of the motoneuron and all the muscle fibres it innervates. Each muscle fibre is innervated by only one motoneuron, while one motoneuron can innervate numerous muscle fibres (10-1000).

The motor unit potential is the sum of action potentials from one motor unit.

No, one muscle fibre is only innervated by one motoneuron.

The innervation ratio varies depending on the type of muscle:

• Smaller muscles with finer movements have a lower innervation ratio (e.g., extraocular muscles: 3-10 muscle fibres per motoneuron).
• Larger muscles like the quadriceps have a higher innervation ratio, with one motoneuron innervating around 1000 muscle fibres.

Voltage-gated calcium channels open when the action potential reaches the axon terminal, allowing calcium ions to flow into the terminal due to the electrochemical gradient. This calcium inflow is crucial for the release of neurotransmitters from vesicles into the neuromuscular junction.

The action potential travels in a saltatory manner from one node of Ranvier to the next, which increases the conduction velocity of the action potential.

The release of neurotransmitters is triggered by the inflow of calcium ions into the axon terminal, which occurs when voltage-gated calcium channels open in response to an action potential.

The electrochemical gradient causes calcium ions to flow into the axon terminal when voltage-gated calcium channels open, as the intracellular concentration of calcium is lower than that in the extracellular space, facilitating neurotransmitter release.

Acetylcholine is the neurotransmitter that binds to muscle type nicotinic acetylcholine receptors, which are ligand-gated ion channels. This binding opens sodium channels, allowing sodium to flow into the muscle cell, leading to a change in membrane potential.

The resting membrane potential of skeletal muscle is normally -90 mV, maintained by the sodium-potassium-ATPase pump, which pumps out 3 Na+ ions and brings in 2 K+ ions.

During depolarization, the membrane potential becomes less negative, reaching a threshold that opens voltage-gated sodium channels, resulting in an influx of sodium and the generation of an action potential.

During repolarization, the membrane potential returns to a more negative value after depolarization. Hyperpolarization occurs when the membrane potential becomes more negative than the resting membrane potential, going below -90 mV.

The end plate potential is the depolarization that occurs when acetylcholine binds to receptors, and if it reaches the threshold, it triggers the opening of voltage-gated sodium channels, leading to the generation of an action potential that spreads throughout the muscle fiber.

The triad consists of 1 T-tubule (transverse tubule) and 2 Terminal cisternae (connected to longitudinal tubules).

The action potential penetrates through the muscle fiber via transmission along the T-tubules, which are internal extensions of the cell membrane.

DHP receptors sense the voltage change when the action potential reaches the T-tubule, triggering the ryanodine receptors to release calcium.

Calcium binds to troponin-C inside the cell, which is crucial for muscle contraction.

The main function of the sarcoplasmic reticulum is to store and release calcium ions, which are essential for muscle contraction and relaxation.

DHP receptors are situated in the wall of the T-tubule and their function is to activate ryanodine receptors.

Ryanodine receptors are located in the wall of the terminal cisternae and their function is to release calcium.

The space inside the T-tubule is extracellular.

The calcium source for muscle contraction in skeletal muscle is intracellular, coming from the sarcoplasmic reticulum, which is inside the cell.

One molecule of troponin C can bind to 4 calcium ions.