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Kine 3012 - Physiology II > Lab 3 Questions - EKG > Flashcards

Lab 3 Questions - EKG Flashcards

1
Q

Why is the myocardium able to contract?

A

Due to the cells being electrically conductive which allows them to squeeze

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2
Q

How does the myocardium get stimulated if it is electrically conductive?

A

Self-stimulation in the absence of neural input; A.K.A. Automaticity

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3
Q

What cells in the right atrium regulate the electrical cycle of the myocardium?

A

SA node and AV node (made of specialized cells)

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4
Q

Explain the transmission of a signal from the SA node

A
  1. SA node initiates electrical signal spreading across right and left atria (causes contraction of atria)
  2. Signal sent to AV node (base of atria) where conduction velocity is slowed (makes sure entirety of atria is contracted)
  3. Signal then rapidly transmitted over to Bundle of His
  4. Splits and forms Left and Right Bundle branches
  5. Impulse conducted to apex of ventricles where network of thin, branching Purkinje Fibres transmit the electrical signal to ventricular muscle to contract both ventricles
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5
Q

Isoelectric activity means?

A

When the voltage is 0
* PR, ST and TP segmen are periods of isoelectric activity

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6
Q

Explain each segment & complex on an EKG. Note issues that can occur along the EKG

A
  1. Mass depolarization of atrial muscle fibres creates P-wave (precedes atrial contraction)
  2. PR Interval - Interval between P wave and initiation of QRS complex (too long = AV node block); Time required for depolarization of atria and AV node
  3. PR segment - Zero voltage; delay in conduction of electrical signal through AV node (allows atria to contract and ventricles to fully fill)
  4. QRS complex - Rapid depolarization of ventricular muscle fibres; Too long = Bundle branch conduction or Ventricular hypertrophy
  5. ST segment - 0 Voltage; Rapid ejection of blood from ventricles (A.K.A. Ventricular Systole); Too long = myocardial ischemia
  6. T wave - Electrical changes associated with ventricular repolarization (Repolarization time > Depolarization time)
  7. TP segment - Zero voltage; Ventricles early diastole ==> Filling with blood
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7
Q

Purpose of ECG signal

A

Tells you info about the heart rate, rhythm, presence or absence of cardiac hypertrophy, ischemia, infarction

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8
Q

What are some heart issues you could recognize on an ECG?

A
  • Bradycardia (slow HR)
  • Tachycardia (Fast HR)
  • Premature ventricular contractions (extrasystoles)
  • Atrial Flutter
  • 1st, 2nd, 3rd degree heart blocks
  • Atrial & Ventricular fibrilation
  • Myocardial ischemia & myocardial infarction
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9
Q

What are the mechanical events of the cardiac cycle?

A

Cardiac muscle contraction, Opening/Closing of heart valves, blood flow

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10
Q

Mechanical events in the heart cause low and high frequency vibrations, what is contributing to low and what is contributing to high?

A

Low: Muscle contraction
High: Valve action + Blood Flow

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11
Q

What is the Lub and Dub associated with on the EKG?

A

Lub is the closing of the AV valves (Ventricular systole)
Dub is coinciding with closing of aortic and pulmonary semilunar valves at ventricular diastole

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12
Q

Phonocardiography is?

A

Technique of recording and displaying heart sounds

Note: Both electrical and mechanical events of the cardiac cycle occur on the EKG but electrical events happen before mechanical

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13
Q

What happens to blood flow for someone who is lying in supine position

A
  • Blood returning back to heart does not have to fight against gravity
  • Venous return ↑ ==> SV ↑
  • Arterial BP will increase causing baro-receptors to fire and ↓ sympathetic outflow and ↑PNS outflow to heart
  • Peripheral vasodilation is stimulated so that BP goes ↓

Purpose: Homeostatic Mechanism to maintain MAP

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14
Q

What happens to blood flow for someone who is standing up?

A
  • Blood pools in extremeties
  • ↓Venous Return and ↓SV
  • ↓Arterial BP causes less baroreceptor activity and ↑SNS to Heart and Vasculature
  • ↑HR and Contractility which stimulates peripheral vasoconstriction and BP↑

Purpose: Homeostatic mechanism to maintain MAP

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15
Q

What is the purpose of the Valsava manuever?

A

Test for autonomic nervous system dysfunction

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16
Q

What is the Valsalva maneuver intertwined with?

A

Baroreceptor reflex and heart rate

Note: You must forcibly exhale while keeping your glottis closed (pretend like you’re constipated)

17
Q

How does the Valsalva maneuver work?

A
  1. ↑ Intrathoracic Pressure
  2. ↓Venous return (↓CO and ↓SV)
  3. Decreases cause HR to ↓ as well
  4. Baroreceptors fire less frequently and activate the SNS outflow while ↓ PNS outflow
18
Q

What is the end result of the Valsalva maneuver?

A

↑HR + ↑Contractility + ↑Peripheral vasoconstriction = ↑BP

19
Q

What happens when the Valsalva maneuver is released?

A

Intrathoracic Pressure ↓ ==> Venous return restored ==> Reverses effects of baroreceptor ==> BP increases ==> SNS ↓ while PNS ↑ ==> HR and Contractility ↓ and vasoconstriction is inhibited ==> ↓BP

20
Q

As we know, Action Potentials spontaneously initiated by SA node cells spread through myocardium to give heartbeat. How can we modify the frequency of action potentials?

A
  • Neurotransmitters secreted by PNS and SNS of the ANS
  • Hormones, Ions, Drugs
21
Q

If the frequency of depolarization ↓ what does this mean? What about when the opposite occurs

A
  • When AP’s ↓, reduction in HR
  • AP’s ↑ ==> Increase in HR
22
Q

What is the cardiac action potential characterized by?

A

A long refractory period where you cannot initiate another action potential for a short period of time; followed by relative refractory period which the heart only acts on given a very strong stimulus

23
Q

Pithed animal?

A

Brain & Spinal Cord destroyed; Heart beats for several hours

24
Q

What does a force transducer do to a frog heart connected to it?

A

When the heart contracts, the force transducer causes a deflection of the force’s transducer level in which the mechanical signal is converted to an electrical signal

25
Q

What happens to Heart Rate when you add Pilocarpine?

A

It mimics the effects of PNS and reduces frequency of depolarization of SA nodal cells

NOTE: NO EFFECT ON FORCE OF MYOCARDIAL INFARCTION

Binds to muscarinic cholinergic receptors

26
Q

What does Atropine do to the Heart?

A

Parasympathetic antagonist; blocks Ach receptor which will ↑HR

Similar to Pilocarpine, PNS has no effect on contractility so force is not affected

27
Q

How does epinephrine affect HR?

A
  • Increases contractility by binding to Beta-receptors
  • Binding initiates events leading to opening of L-type calcium channels which increase Ca2+ in cardiac muscle and that brings in more Ca2+ from SR (sarcoplasmic reticulum)
  • ↑HR + ↑Contractility
28
Q

F-type Na+ Channels and T-type Ca2+ channels in the SA nodal cells can be increased by what hormone?

A

Epinephrine; ↑the pacemaker cells to threshold sooner; thus APs generated more frequently

29
Q

How does Digitalis work?

A
  • Disrupts the effects of the Na+/K+ ATPase pump causing Na+ to not move against concentration gradient (inside to out)
  • Na+/Ca2+ exchanger protein will cause Na+ to move back into the cell because it follows [Na+] gradient & [Ca2+] moves out of cytosol
  • However there is little movement of Na+ outside the cell so most of it is already in the cell so not much will move into the cell
  • If less Na+ is moving in then less Ca2+ is moving out which means cytosolic Ca2+ remains elevated

↑Cytosolic Ca2+ = ↑Contractility and ↓HR

30
Q

What does Calcium do to the heart?

A
  • Disrupts conduction of electrical impulses within heart and have drastic consequences on cardiac function - hypercalcemia
  • Decreases HR
  • Severe cases - Asystole
31
Q

What does Potassium do to the Heart?

A
  • ↓Contractility + ↓HR
  • Resting membrane potential of cardiomyocytes depends on K+ efflux
  • High levels of K+ retained in cell and RMP becomes -70
  • Elevated levels of K+ eventually cause inactivation of Na+ channels which makes cell in hyperpolarized state
  • Ventricular fibrillation develops leading to ↓ forced production
32
Q

Clinical significance of digitalis

A

Frequently used to treat congestive heart F, Atrial flutter, A-Fib
1. ↑ force contraction
2. ↓Cardiac rate (inhibiting SA node and stimulating vagus nerve)
3. ↓Rate of conduction of Bundle of His, ↑P-R Interval

33
Q

Clinical significance of Atropine?

A

Blocks effects of PNS; used in dilating eyes, soldiers also carry atropine injectors to treat nerve gas poisoning

34
Q

Clinical significance of Pilocarpine

A
  • Eye drops for managing glaucoma (excess fluid flushed away)
  • Sjogren’s syndrome: disease attacking lacrimal and salivary glands
  • PNS stimulating secretions and pilocarpine helps with that
  • Induce sweating in patients to check for cystic fib.
35
Q

Two main factors involved in regulating blood flow?

A
  1. Pressure
  2. Resistance

Q = ΔP/R

Q is indicative of cardiac output/blood flow

36
Q

Formula for Total Peripheral Resistance

A

R = L x n / r^4

L = length of tube
n = viscosity
r is radius

37
Q

Relationship amongst the TPR formula?

A
  • Length and viscosity are directly proportional to resistance
  • Radius is inversely proportional to resistance
38
Q

Diseases/conditions affecting blood viscosity

A

Blood doping & Polycythemia
* ↑ viscosity => ↓Blood flow

39
Q

Diseases/conditions affecting blood vessel radius?

A

Atherosclerosis & Pulmonary Embolism
* ↓radius => ↓Blood Flow

Kine 3012 - Physiology II (30 decks)

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