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HSC1007 > Cardiovascular System > Flashcards

Cardiovascular System Flashcards

(40 cards)

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1
Q

Function of the Heart

A

Meet metabolic needs of the body and is achieved by ensuring adequate exchange of fluids dependent on vessel integrity and sufficient pressure and output

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2
Q

Impulse conduction of the heart

A
  1. SA node activity and atrial contraction begins
  2. Stimulus spreads across atrial surface and reaches AV node
  3. 100msec delay at AV node. Atrial contraction begins
  4. Impulse travels along interventricular septum within AV bundle and bundles of branches to Purkinje fibers and by moderator band, to papillary muscles of right ventricle
  5. Impulse distributed by Purkinje fibers and relayed throughout ventricular myocardium. Atrial contraction completed and ventricular contraction begins
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3
Q

Pacemaker cells

A

Sinoatrial node, Atrioventricular Node, bundle of his, Purkinje fibers

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4
Q

Pacemaker ability

A

Action potential in heart =/= Action potential in NS
Rate of AP generation
- SA node: 70 - 80 AP/min
- AV node: 40 - 60 AP/min
- Bundle of His and Purkinje: 20 - 40 AP/min

SA node is the fastest and sets the pace

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5
Q

Electrical activity of the heart

A

Done by specialized myocardial fibers; not motor neurons
- Contractile cells: 99% of cells do pumping
- Autorhythmic cells: Initiate and conduct AP generation for contraction of working cells

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6
Q

How is heart rate controlled

A

Controlled by autonomous nervous system
- increased sympathetic stimulus = increased HR
- increased parasympathetic stimulus = decreased HR
- both are active but one will dominate based on certain condition

Cardiovascular Control Centre
- affected by pain, chemoreceptor, baroreceptor, respiratory center

Control SA node
- affected by epinephrine and temperature
- acts only on SA node; not ANS

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7
Q

Interpret ECG

A

P wave: atrial depolarization (SA node fires)
PR segment: AV node delay
QRS complex: Ventricular depolarization and atrial repolarizing simultaneously
ST segment: Ventricules contracting and emptying
T wave: Ventricular repolarization
TP segment: ventricules relaxing and refiling

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8
Q

When is there no electrical activity recorded?

A

AV node delay (PR segment)
Ventricules completely depolarized and cardiac cells undergo plateau phase (ST segment)
Heart muscles relaxed and ventricules filling (TP segment)

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9
Q

What makes SA node weird in ECG

A

SA node firing is not detected as it does not create sufficient electrical activity to reach body surface and not recorded
Impulse spreading through atria is recorded

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10
Q

Define cardiac ouput

A

Volume of blood pumped out by each ventricle per min

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11
Q

Factors of cardiac ouput

A

Heart rate: beats per min
Stroke volume: volume of blood pumped per beat
CO = HR x SV

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12
Q

Ejection fraction

A

Fraction of blood ejected from ventricle per heartbeat
Measured by echocardiography
Measure of cardiac contractility and definite measurement by cardiac catherisation
EF = SV/EDV x 100% (Normal range = 55 - 75%)

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13
Q

Parasympathetic effects on Heart rate

A

Decrease contractility and weaken contraction of atrial muscles
Decrease excitability and increase AV node delay
Decrease rate of depolarization to threshold of SA node

No effect
- ventricular conduction pathway
- ventricular muscles
- adrenal medulla (endocrine gland)
- veins

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14
Q

Sympathetic effects on heart rate

A

Increased rate of depolarization to threshold of SA node

Increased excitability and decrease in AV node delay

Increased contractility of atrial and ventricular muscles

Increased conduction through bundle of His and Purkinje fibers of ventricular conduction pathway

Increased venous return and increased cardiac contraction via intrinsic control of veins

Increased epinephrine secretion

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15
Q

What is EDV

A

End diastolic volume

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16
Q

Frank Starling Law of the heart

A

Intrinsic relationship between EDV and SV
- ↑ diastolic filling = ↑ EDV = ↑ stretching of heart = ↑ length of cardiac muscle fibers = ↑ cardiac contraction = ↑ stroke volume
- basically ↑ EDV = ↑ SV
- sympathetic stimulus = ↑ heart contraction

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17
Q

What are the factors of Stroke volume

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A

Determined by extent of venous return and by sympathetic activity

SV = EDV - ESV

Intrinsic control = extent of venous return

Extrinsic control = sympathetic stimulus of heart

18
Q

Stroke volume and cardiac output factors

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A

Strength of cardiac muscle contraction
- Extrinsic control - varies extent of sympathetic stimulus
- Intrinsic control - varies initial length of muscle fibers dependent on ventricular filling

↑ Sympathetic stimulus = ↑ cardiac output by ↑ SV and HR

19
Q

Define Cardiac output

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A

Volume of blood pumped out by each ventricle per min

20
Q

Factors of cardiac output

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A

Preload (volume of filling)
Heart (contractility and heartrate)
Afterload (peripheral resistance)

21
Q

Define cardiac failure

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A

Occurs when cardiac output is insufficient to meet metabolic requirements of tissues

22
Q

Causes of cardiac failure

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A

Congestion in pulmonary and or systemic circulations

23
Q

Compensatory measure for heart failure

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A

Sympathetic stimulation and retention of salt and water by kidneys to ↑ blood volume

24
Q

What supplies blood to heart

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A

Coronary circulation during diastole flows to heart and adjusts to changing requirements such as ↑ O2 demands

25
Explain process of more O2 rich blood entering heart
1. ↑ metabolic demand of cardiac muscle cells 2. ↑ adenosine 3. vasodilation of coronary vessels 4. ↑ blood flow to cardiac muscle cells 5. ↑ O2 available
26
Types of coronary heart disease
Angina Pectoris - Myocardial ischemia causes chest pain (usually epigastric region such as neck and shoulder) - Common symptom Acute myocardial Infarction - Heart disease - Irreversible death (necrosis) of part of heart muscle secondary to ischemia
27
Causes of Coronary Heart Disease
Thrombus - abnormal clot in vessel wall Embolus - abnormal particle floating in blood vessel Thromboembolism - obstruction of blood vessel by blood clot dislodged from another site Atherosclerosis - progressive degenerative arterial disease which causes occlusion of affected blood vessels and low blood flow
28
Treatment methods of Coronary Heart Disease
Coronary Artery Bypass Grafting (CABP) Percutaneous Transluminal Coronary Angioplasty (PTCA)
29
Why is AV node delay called as such
PR interval is 0.12 - 0.20s (Average 0.16s) Time for signal to travel from SA to AV node, AV node delay, out to bundle of His. Bulk of time is AV node delay hence the name
30
Difference between AP in Autorhythmic cells and AP in Cardiac contractile cells
Purpose - Autorhythmic cells responsible for autogeneration of AP (impulses) whereas cardiac contractile cells is responsible for contracting upon receiving the impulses Related to - autorhythmic cells related to rate and rhythm of heartbeat whereas cardiac contractile cells are related to contraction Ca2+ - autorhythmic cells necessary for self-induction of AP compared to Nervous system - cytosolic Ca2+ directly involved for contraction Plateau phase - autorhythmic cells do not have this; only cardiac contractile cells have
31
Similarity between AP in autorhythmic cells and cardiac contractile cells
All ions (Na+, K+, Ca2+) are important to occur
32
Process of Autorhythmic cells to cardiac contractile cells
Autogeneration of impulses in autorhythmic cells > impulse spreads > AP in cardiac contractile cells > ↑ cytosolic Ca2+ in cardiac contractile cells > contraction
33
When does atrial systole and atrial diastole start and end
Atrial systole - 0msec to 100msec Atrial diastole - 100msec to 800msec Ventricular systole - 100msec to 370msec Ventricular diastole - 370msec to 100msec
34
Process of atrial and ventricular systole and diastole
1. Atrial contraction - forces small amount of additional blood into relaxed ventricles (atrial systole) 2. Atrial systole ends, atrial diastole starts - atria relaxes after contraction 3. Ventricular systole - ventricular contraction pushes AV valves closed but not create enough pressure to open semilunar valves. As ventricular pressure ↑ and > pressures in arteries, semilunar valves open and blood is ejected 4. Ventricular diastole - As ventricles relax, pressure in ventricles decreases, blood flows against cusps of semilunar valves and forces them closed. Blood flows into relaxed atria and
35
4 phases of heart blood flow
1. Passive filling and atrial contraction 2. Ventricular contraction 3. Ventricular depolarization and diastole 4. Ventricular refilling
36
Explain passive filling and atrial contraction
- Atrial P >Ventricular P - Blood flows into ventricles - Ventricular volume ↑ - SA node fires and impulse spreads through atria - Ventricular volume ↑ = Ventricular pressure ↑ - Atrial contraction ends - End diastolic volume = 135 mL
37
Explain ventricular contraction
- impulse spreads through AV node - occurs at QRS complex of ECG - Ventricular P increases sharply - AV valve closes (1st Heart sound) - Isovolumetric ventricular contraction - Ventricular P > Aortic P; Aortic valves open and blood is ejected - aortic pressure ↑ as blood is pumped into aorta faster than blood can drain off - ventricular P decreases
38
Explain ventricular depolarization and diastole
- End systolic volume = blood not pumped out - ventricular repolarization (T wave) - Ventricular P < Aortic P so aortic valve closes and created notch on aortic pressure curve called "dicrotic notch" - all valves closed, no changes to chamber volume
39
Explain ventricular refilling
- ventricular P < atrial P (AV valves open) - atrial P ↑ due to constant blood flow from veins - Pool of blood in atria rush into ventricles when AV valves open - Filling of blood slows down - SA node fires and cardiac cycle repeats
40
What does extracellular fluid consist of
Interstital fluid + plasma

HSC1007 (18 decks)

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