PHYSIOLOGY LAB FINAL!
Breathe with constricted airways, and determine what changes happen to the TV, IRV, ERV and VC.
All decrease
Explain how action potentials travel between nodal cell and cardiac myocytes.
- The impulses start from the pacemaker cells (small group of myocytes). SA node: primary pacemaker of the heart. ON POWER POINT
Identify the typical deflections of an ECG tracing for Lead II
- to + means upward (positive deflection) + to - means downward (negative deflection)
· Discuss the differences between 1st, 2nd, and 3rd generation beta blockers.
1: non-selective antagonist (blocking both B1 and B2 receptors) 2: semi-selective antagonist (more cardio selective, more selective for B1-receptors) 3: highly selective antagonist for B-1 receptors)
Explain vectors. What does a vector represent?
A vector describes the movement of charge (spread of electrical activity).
Describe the action potential in a cardiomyocyte and the refractory period in a cardiomyocyte.
Action potential: slide 4 with ions??????????? ON POWER POINT For the cardiac myocytes because of the plateau phase, the time is extended. The mechanical event is initiated before the muscle is completely relaxed. Refractory period: Period of time after the muscle initiates an AP to where it cannot initiate another AP. Skeletal muscle: refractory period, very brief! We can see summation and tetany for this. For cardiac myocytes: the muscle has contracted and almost fully relaxed before another stimulus. We do not see summation or tetany in cardiac myocytes which is a good thing! Must almost fully contract and relax before another stimulation can occur. Refractory period: the time following an action potential during which a new action potential cannot be initiated
· Explain a beta blocker's mechanism of action and its physiological effects on the heart.
Antagonists of β-adrenergic receptors, known as β-blockers, have been used effectively for over four decades and have beneficial effects in the treatment of cardiovascular diseases A beta blocker's mechanism of action is to reduce sympathetic nervous system activity through the blockade of Beta-adrenergic receptor subtypes. Basically blocking the adrenergic receptor so that NE can't bind!
Explain how changes in location of blood pressure measurement relative to the heart impact measured blood pressure.
Arm = lower pressure above heart Arm = normal pressure at heart Leg = high pressure, gravity pulls blood down and there is less blood flow to the heart. Laying down: Effect of gravity is evenly distributed Standing up: Greater pressure at the bottom of column. As you stand, blood pools in the legs (bc veins are compliant). Less blood returns the heart = decreased venous return decreased SV decreased b/p. BUT baroreceptor reflex saves you... usually.
Explain the length-tension relationship in the heart (Starling's law).
As cardiac muscle is stretched, it's ability to generate tension increases.
Describe how stimulus intensity is related to magnitude of individual muscle twitch and how this phenomenon relates to motor unit recruitment and control of contractile force.
At low stimulus strengths, no motor nerves are depolarized and no muscle contraction is seen. As stimulus strength is increased, some motor neurons are brought above their threshold potential and an action potential is fired. This results in contraction of all muscle fibers in that motor unit, which causes a twitch (one complete cycle of contraction and relaxation) in the muscle. Twitch force increases progressively as more motor nerve fibers are excited. A twitch involves one complete cycle of contraction and relaxation. The greater the stimulus strength means greater the number of activated motor units and thus greater the muscle tension. This phenomenon is known as twitch or motor unit recruitment.
· Discuss which beta-adrenergic receptor subtypes are expressed by the heart and in what ratio.
B1 and B2 Ratio:4:1
· Explain the signal transduction cascade for beta-1 adrenergic receptors, including how this pathway increases contractility in cardiac myocytes.
Beta receptors, in general, are activated by noradrenaline and adrenaline. Beta 1 receptors are coupled to a G protein. So, when a B1 receptor is activated, there is a change in conformation of cardiomyocytes which leads to the activation of the G proteins, which will cause GTP -> GDP. As this happens, this allows for activation of a G alpha and G-beta gamma complex to be activated, which leads to, in short, a pathway that results depolarization down the L channel and calcium release into the sarcoplasmic reticulum. This will allow for phosphorylation of myofilaments, which allows for increased sensitivity of troponin, allowing for a contraction to occur.
o How are changes in blood gas levels monitored by the body?
Chemoreceptors - Central: In ventral surface of medulla - Peripheral: carotid sinus and aortic body
What two variables contribute to a vector?
Direction and magnitude
Explain the baroreceptor reflex from initiation to the heart and vascular responses.
Draw out chart
Compare the terms electrical axis and cardiac axis.
Electrical axis: - Overall vector of electrical activity at a given moment during the cardiac cycle. - As the cardiac cell depolarizes, it creates its own small vector - All the small vectors are added together, giving the overall vector (electrical axis) - Changes over time Cardiac axis: - The mean electrical axis (QRS vector) during ventricular depolarization - Tells us the orientation of heart within chest cavity - Always the same
Explain the relationship between electrical and mechanical activity in the heart.
Electrical event ALWAYS proceeds to mechanical event Electrical event triggers the mechanical event (contraction) in myocytes. Mechanical: You have action potential which enters from adjacent cells. Then voltage-gated Ca2+ channels open. Ca2+ enters the cell. Ca2+ induces Ca2+ release through the RyR channels. This is called calcium induced calcium release.
Describe and explain the effects of various neurotransmitters on the performance of the heart.
Epinephrine: Increases HR - Isoproterenol increases HR AND force of contraction (SNS) - Atropine increases HR (PNS) Acetylcholine: Decreases HR. - Propranolol decreases HR and force of contraction. - Pilocarpine decreases HR.
· Explain how spike rates (discharge rates) in ballistic muscle contractions change following training.
Following training, spike rates (discharge rates) in ballistic (muscle contractions that exhibit maximum velocities and accelerations over a very short period of time) muscle contractions are adaptable. If you train the spike rate is going to increase. It will respond to lack of training by decreasing.
Define hydrostatic pressure and explain how this contributes to changes in location of blood pressure measurements relative to the heart.
Hydrostatic pressure: force exerted by a fluid on an object due to gravity. LEGS: High hydrostatic pressure because gravity is pulled down and all blood pools in the legs.
Explain what upward and downward deflections represent on an ECG tracing.
If we have an upward deflection, it is depolarization from the electrical impulse moving towards the electrode. If the depolarizing current is moving away from the electrode, we have a downward deflection. It is the same concept, but the opposite for the repolarization. If the electrical impulse is moving away from the electrode, it is an upward deflection, and if the electrical impulse is moving towards the electrode, it is a downward deflection.
Explain how variables that contribute to mean arterial blood pressure change during exercise in in a healthy individual and a patient with chronic hypertension. Particularly, note differences in how diastolic blood pressure changes and explain why these changes in diastolic blood pressure are usually observed.
In a healthy individual, systolic b/p is supposed to increase and diastolic b/p is supposed to decrease during exercise. However, in a patient with chronic hypertension, there is an increase in systolic b/p and an increase in diastolic b/p. WHY? Because there is a increase in TPR, due to the resistance arteries tightening, and basically becoming more resistant. This causes the diastolic b/p to elevate.
Describe how the magnitude of the isometric tension developed by a muscle depends on the muscle length at which the tension is measured.
Isometric: constant length. Think of pulling the muscle (lengthening it) When you pull you are increasing elasticity (passive forces) and it will produce a lot of force when It contracts. The muscle is able to generate higher levels of tension. Think of a rubber band! As you lengthen you increase passive
Calculate mean arterial blood pressure.
MABP = DBP + [PP/3] OR MABP = CO X TPR PP = SBP - DBP
Discuss variables that contribute to mean arterial blood pressure There are two equations...
MAP = CO X TPR OR MAP = SBP - [PP/3] PP = SBP - DBP
Calculate cardiac axis of a heart using the hexaxial system, given an ECG sample ECG rhythm strip.
Make sure I can calculate the numbers like on the chart, then put them onto the circle thing.
Evaluate normal versus deviated cardiac axes.
Memorize circle! Normal: I +, II +, avF + Left axis deviation: I +, II -, avF, - Right axis deviation: I -, avF + Indeterminate: I -, avF -
Describe and explain the effects of muscle stretch, summation, and tetanus.
Muscle stretch: Summation: If a second stimulus arrives before the muscle has relaxed, a second twitch occurs on top of the first and a greater peak tension is developed. The steady rise in calcium translates into summation of twitches. Therefore, twitch force can also be increased by increasing the frequency of action potentials in motor units. Tetanus: As the frequency of stimulation increases, the time for the muscle fiber to relax between stimuli decreases. Eventually, the contractions fuse and a smooth powerful contraction is seen (straight line on graph)! It is the state of sustained maximal muscle contraction.
Compare the influence of the sympathetic and parasympathetic nervous systems on heart rate, including: Effects of NE and Ach Effects of sympathetic agonists and antagonists Effects of parasympathetic agonists and antagonists
NE: Increases Heart Rate Ach: Decreases Heart Rate Increase HR AND force of contraction. - Agonist: Isoproterenol (↑ HR) - Antagonist: Propranolol ( Decrease HR - Agonist: Pilocarpine (↓ HR) - Antagonist: Atropine
· Discuss key anatomical abnormalities in a patient with COPD.
Narrowed airways and floppy lungs. Risk of death due to hypoxia. Right-sided heart problems, a complication of her COPD. FEV1/FVC ratio decreased Shortness of breath, struggles to carry out simple tasks without getting out of breath.
Discuss how tension generated by a muscle varies following nerve stimulation versus muscle stimulation.
Nerve stimulation: Inject current into sciatic nerve to stimulate action potential Muscle stimulation: Inject current into gastrocnemius muscle itself. BUT... This is not directly exciting the muscle tissue. It still works through the NMJ and release of Ach b/c that is the path of least resistance. Requires a higher threshold stimulus because the current must travel through lots of CT layers to get to NMJ so you need more!!!
Compare nodal cells and cardiac myocytes.
Nodal cells: non-contractile cells. Their job is to generate electricity... by themselves...at a regular interval... and then moving that electricity through the heart in a specific way (will come back to that). Spontaneous depolarization generates Aps. Significant features at rest: Electrical charge difference across plasma membrane (cytsol is negative relative to IF) = RMP! (~ -60mV) Contain specific v-gated channels, including v-gated cation channels and v-gated Ca2+ channels and v-gated K+ channels Autorhythmicity: capable of depolarizing and initiating an AP spontaneously, without external stimulation - Possible because these cells don't have a stable RMP Nodal cells are located in discrete regions in the heart - associated with the conduction system Myocytes: Contractile cells. 99% of cardiac cells = form the myocardium - Their Job: contract! Which is what pumps blood through the chambers
When is optimal tension generated? Why?
Optimal tension is generated in a resting-length muscle (or when the sarcomeres are at their resting length). Because of the optimal alignment of actin and myosin!
Discuss how different components of the ECG waveforms correspond to events of the heart's electrical activity.
P wave: - to + : upward deflection Q wave: + to - : downward deflection R wave: - to + : upward deflection S wave: + to - : downward deflection T wave: - to + : upward deflection
Illustrate how a parent vector can be resolved from two daughter vectors.
Parallelogram rule or tip to tail method. One arrow on the hexaxial (lead I) and then another arrow on hexaxial avF, maybe a stronger magnitude, meaning further arrow. The middle of the two will be a little more to the larger/longer arrow side.
Determine pulmonary ventilation and FEV1/FVC ratio.
Pulmonary ventilation is the expired minute volume. FEV1 (how much air a person can forcibly expire in 1 second)/FVC (the max amt of air a person can forcibly expire after maximal inspiration) ratio: allows us to know the fraction of FVC that was able to be expired in one second .The lower the ratio, the more likely It is that the airways are obstructed. A healthy person will have a ratio of 0.8 or 80% or more.
· Discuss whether rate coding plays a more prominent role in fast or slow contractions and explain why.
Rate coding plays a more prominent role during the muscle force during fast contractions. The capacity of motor neurons to discharge action potential at rates on the plateau of the force frequency relation during the rapid contractions suggests that rate coding is limited during slow change in force during isometric contractions.
Discuss the significance of the heart's refractory period, as it relates the cardiac myocyte action potential.
Refractory period is the time during which the muscle cell cannot be stimulated again----it has not yet repolarized so it cannot depolarize again The plateau phase delays repolarization. This is important so we can ensure that the heart chamber completely fills with blood before the next contraction.
o What is the response to changing blood gas levels?
Regulate breathing to maintain homeostatic levels of pO2 and pCO2. increasing breathing rate and depth.
· Discuss the central regulation of breathing under normal conditions and in the context of the "paper-bag breathing" experiment. o How does respiratory rate change?
Respiratory rate changed because it increases.
· Label and identify static and dynamic lung parameters on a spirometer recording.
STATIC: TV, IRV, ERV, RV, TLC, FRC,
Explain the length-tension relationship.
Sarcomere too short: myosin and actin get in the way of each other Ideal sarcomere length = lots of force Sarcomere too long: no overlap between myosin and action = no force generation The length-tension relationship is how much tension a muscle generates is related to the degree of overlap between thick and thin filaments.
· Discuss whether spike rates (discharge rates) are higher for shortening or lengthening of a muscle and explain why.
Spike rates (discharge rates) are higher for shortening of the muscle (contraction) because more motor units are recruited (higher metabolic demand). For lengthening of the muscle, the discharge rate is lower because fewer motor units are recruited (less metabolic demand).
Apply the Frank-Starling law of the heart to explain the relationship between stretch of cardiac muscle and the force of the subsequent contraction.
Starling's law of the heart explains how when cardiac muscles are at rest, that is not at optimal length or tension (whereas for skeletal muscle it is). As we stretch the heart more and more, more tension is produced, and that is the optimal length. Why? Because the heart is stretching as blood is entering. The filling during the relaxation part is what stretches the heart. We want it at an optimal alignment. All in all, the greater the stretch, the greater the force of contraction!
Explain the terms subthreshold, threshold, submaximal, maximal, and supramaximal - as they are related to stimulation of a muscle in order to generate tension.
Subthreshold: Stimuli below the threshold. They do not initiate a mechanical response. Threshold: Point where the intensity (voltage) of the stimulus brings a response. Submaximal: Maximal: Marks the point where all the fibers in the muscle are stimulated and responding all-or-none Supramaximal: Stimuli above the maximal stimulus.
Explain the physiological cause of summation and tetany.
Summation: If a second stimulus arrives before the muscle has relaxed, a second twitch occurs on top of the first and a greater peak tension is developed. Tetany: As the frequency of stimulation increases, time for the muscle fiber to relax between stimuli decreases. Eventually, the contractions fuse and a smooth powerful contraction is seen.
Explain the regulation of blood pressure during exercise.
Systolic pressure is supposed to rise, whereas diastolic pressure is supposed to decrease. Exercising requires more blood flow than resting, so the TPR must go wayyyyyy down! Don't want resistance! CO goes wayyyyy up! Want more blood pumped out of the heart!
Explain systolic blood pressure and diastolic blood pressure.
Systolic: turbulent? Artery is maximally stretched during ventricular systole Diastolic: artery recoils no further during ventricular diastole (relaxation)
· Discuss how lung volumes change in a patient with obstructive lung disease.
TV, IRV, ERV decrease, RV increases
identify static and dynamic lung parameters and capacities. Pulmonary function parameters such as, TV, IRV, ERV, VC.
TV: Tidal Volume: The volume we inspire and expire during restful breathing. IRV: Inspiratory reserve volume: The maximum volume above tidal volume that we can inspire into our lungs. ERV: Expiratory tidal volume: The maximum below the tidal volume htat we can expire from our lungs. VC: Vital capacity: All the air that can be expired from a maximal inspiration
Discuss how tension in a whole skeletal muscle is regulated, as it relates to motor unit recruitment.
Tension is controlled at the level of motor units. To increase tension, we recruit more motor units. A motor unit is a motor neuron and all the muscle fibers it innervates. The smallest motor units are recruited first. Then increasingly larger ones. Tension generated with each contraction increases until the point of maximum contraction = when all motor units have been recruited.
o How are blood gas levels altered in this experiment?
The CO2 in the blood increased, which triggers the sympathetic nervous system - the chemoreceptors to detect this change and increase the breathing rate.
What are the differences between active and passive forces? How do they contribute to tension that can be generated by a muscle?
The active force is generated by the contraction when the fibers are stimulated. The passive forces reflect the contributions of elastic elements in the muscle, both extracellularly and within the fibers themselves. Passive curve: tension that is measured at various muscle lengths BEFORE muscle contraction. - Generated by elastic elements of a muscle; CT elements and intrinsic elasticity Active curve: Tension that is measured at various muscle lengths DURING muscle contraction - Generated by myofilament crossbridge cycling.
· Define rate coding
The force exerted by a muscle during a voluntary contraction depends on the number of motor units recruited for the action and the rates at which they discharge action potentials.
Discuss the relationship between the ECG and the finger pulse.
The relationship between the ECG and the pulse wave shows that there is a delay in the pulse wave. The timing of the QRS complex in the ECG and the beginning of the pulse do not coincide because the electrical activity in the heart is a mechanical contraction/event (one after another). This is initiated by the electrical depolarization, so if SA node depolarizes, it precedes atrial contraction.