The Cardio-Vascular System - Part 2 (week 8) Flashcards

1
Q

state 2 facts about cardiac muscle

A
  1. have 1-2 nuclei centrally located
  2. sliding filament mechanism
  3. branching cells with gap junctions crucial to being stimulated
  4. have large mitochondria
  5. autorhythmicity/automaticity - node cells have the ability to generate their own AP’s
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2
Q

what percentage of cardiac muscle cells are replaced yearly

A

the heart has a limited ability to replace its muscle cells. only about 1% of heart muscle cells are replaced yearly

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3
Q

what percentage of muscle cells do not function in contraction (2 things)

A
  1. about 1% of muscle cells do not function in contraction

2. these cells form the conduction system and are in electrical contact with the cardiac muscle via gap junctions

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4
Q

state the effect of the sympathetic nervous system on the heart

A

the sympathetic nervous system innervates the entire heart muscle and node cells by the release of norepinephrine

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5
Q

state the effect of the parasympathetic nervous system on the heart

A

the parasympathetic nervous system innervates the node cells and releases primarily acetyl choline

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6
Q
  1. what type of receptors are on cardiac muscle for norepinephrine
  2. state another hormone which exerts the same effects
A
  1. beta-adrenergic receptors
  2. the hormone epinephrine (from the adrenal medulla) binds to the same receptors as norepinephrine and exerts the same actions on the heart
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7
Q

what type of receptors are on the cardiac muscle for acetyl choline

A

muscarinic receptors

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8
Q

state the 4 steps of the conduction pathway

A
  1. signal starts at the SA node (approx. 75 signals/min)
  2. wave of depolarisation travels through inter-nodal pathway via gap junctions to the AV node
  3. signal has a 0.1s delay to allow atria to contract and totally fill the ventricles before they contract
  4. the purkinje fibres also supply the papillary muscles and tell them to contract before the rest of the atria to help prevent back flow through the valves
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9
Q

state what it is meant by the key term - electrocardiogram (ECG)

A

an ECG shows a graphic record of the heart’s electrical activity. the reading is a composite of the electrical activity, not a single action potential

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10
Q

state what it is meant by the key term - P wave

A

the result of the depolarisation wave from the SA node to the AV node. atria contract 0.1s after P wave

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11
Q

state what it is meant by the key term - QRS complex

A

the result of ventricular depolarisation and precedes ventricular contraction. the atria repolarisation is also observed by the QRS complex

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12
Q

state what it is meant by the key term - T wave

A

caused by ventricular repolarisation

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13
Q

state what it is meant by the key term - cardiac output (Q)

A

the volume of blood ejected from the left ventricle per minute (Q = HR x SV)

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14
Q

state what it is meant by the key term - stroke volume (SV)

A

the difference between end diastole volume (EDV) and end systolic volume (ESV) - (SV = EDV - ESV)

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15
Q

state what it is meant by the key term - positive chronotropic factors

A

positive chronotropic factors are factors which cause the HR to increase

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16
Q

state what it is meant by the key term - negative chronotropic factors

A

negative chronotropic factors are factors which cause the HR to decrease

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17
Q

state what it is meant by the key term - Frank Starling mechanism

A

concept: the ventricles contract more forcefully when it has been filled to a greater degree during diastole (this is due to the length-tension relationship)

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18
Q

state 2 facts about the Frank Starling mechanism

A
  1. EDV is determined by how stretched the ventricular sarcomeres are before contraction
  2. the greater the EDV, the more the muscles are stretched, and thus the greater the contraction
19
Q

state what it is meant by the key term - contractility (in relation to VR)

A

concept: norepinephrine acts on beta-adrenergic receptors to increase ventricular contractility (the strength of contraction at any given EDV)

20
Q

state 2 facts about contractility

A
  1. plasma epinephrine also increases contractility

2. increased contractility results in increased SV due to a more complete ejection of the EDV

21
Q

state the calculation to work out - mean arterial pressure

A

diastolic pressure + 1/3(systolic pressure - diastolic pressure)

22
Q

mean arterial pressure is dependent upon what

A

cardiac output (Q) x total peripheral resistance (TPR)

23
Q

state 3 facts about arterial baroreceptors

A
  1. respond to changes in arterial pressure as nerve endings are highly sensitive to stretch/distortion
  2. degree of stretching is directly proportional to BP
  3. at normal mean arterial pressure (MAP) there is already a steady rate of neuronal discharge
24
Q

talk about arteriole baroreceptors ST and LT adaptation

A

ST - respond to changes in BP

LT - adapt to BP and only way to adjust BP is by changing blood volume

25
Q

state what it is meant by the key term - medullary cardio-vascular centre

A

located in the medulla oblongata and is the primary integrating centre for the baroreceptor reflex in a network of connected neurones

26
Q

state 3 facts about the medullary cardio-vascular centre

A
  1. the neurones receive input from the various baroreceptors
  2. input determines AP frequency from the CV centre
  3. not just neural, but also alters angiotensin 2 generation and vasopressin secretion
27
Q

state the physiological responses to hypertension (high BP) - 9 steps

A
  1. increased atrial pressure
  2. kidneys increase urinary loss of Na+ and H2O
  3. decreased plasma volume
  4. decreased blood volume
  5. decreased venous pressure
  6. decreased venous return
  7. decreased EDV
  8. cardiac muscle decreases SV
  9. decreased Q
28
Q

state 4 methods of treating hypertension

A
  1. diuretics
  2. beta-adrenergic receptor blockers
  3. calcium channel blockers
  4. angiotensin-converting enzyme (ACE) inhibitors
29
Q

explain how diuretics can be used to treat hypertension

A

increase the excretion of sodium and water, decreasing Q with no peripheral resistance

30
Q

explain how beta-adrenergic receptor blockers can be used to treat hypertension

A

reduce Q

31
Q

explain how calcium channel blockers can be used to treat hypertension

A

reduce the entry of calcium in vascular smooth muscle cells = weaker contractions = lower peripheral resistance

32
Q

explain how angiotensin-converting enzyme (ACE) inhibitors can be used to treat hypertension

A

final step in the formation of angiotensin 2 (a vasoconstrictor) is mediated by an ACE. blocking this enzyme causes vasodilation lowering peripheral resistance

33
Q

state the action of aldosterone in the renin-angiotensin system

A

slow acting steroid hormone that stimulates sodium re-absorption by kidney tubercles

34
Q

state the action of vasopressin (anti-diuretic hormone) in the renin-angiotensin system

A

rapid acting peptide produced by the pituitary gland which stimulates water re-absorption

35
Q

explain how the kidneys regulate blood pressure

A

intra-renal baroreceptors detect changes in stretching due to lower blood volumes which stimulates an increase in the production of Renin

36
Q

cardiac cells produce what to help with the renin-angiotensin system

A

atrial natriuretic peptide (ANP)

37
Q

atrial natriuretic peptide (ANP) has what 3 effects

A
  1. inhibits Na+ reabsorption by kidney tubercle cells
  2. acts on renal blood vessels to increase filtration rate causing sodium excretion
  3. inhibits aldosterone action
38
Q

what 4 things happen within hours of blood loss ?

A
  1. compensatory movement of interstitial fluid into capillaries to increase plasma volume
  2. redistribution not replacement
  3. slower effects: increase in thirst, decrease in Na+ and H2O secretion
  4. mediated by hormone and kidney function (renin, angiotensin, and aldosterone)
39
Q

what happens within days of blood loss

A
  1. erythropoiesis

2. haematopoiesis

40
Q

state the 4 steps (in order) of the cardiac cycle

A
  1. isovolumetric ventricular contraction
  2. ventricular ejection
  3. isovolumetric ventricular relaxation
  4. ventricular filling
41
Q

state 3 characteristic about the stage of the cardiac cycle - isovolumetric ventricular contraction (step 1)

A
  1. during 1st part of systole, ventricles are contracting, but all valves are closed so no blood is ejected
  2. ventricle walls develop tension + squeeze blood they enclose raising BP
  3. as blood is incompressible, ventricle fibres can’t shorten so is termed isometric
42
Q

state 2 characteristic about the stage of the cardiac cycle - ventricular ejection (step 2)

A
  1. once pressure in ventricles exceeds that in aorta and pulmonary trunk, SL valves open
  2. blood is forced out aorta + pulmonary trunk as the contracting ventricle muscles shorten
43
Q

state 2 characteristic about the stage of the cardiac cycle - isovolumetric ventricular relaxation (step 3)

A
  1. during 1st part of diastole, ventricles begin to relax and the SL valves close
  2. at the same time, AV valves are closed so no blood is entering or leaving the ventricles
44
Q

state 3 characteristic about the stage of the cardiac cycle - ventricular filling (step 4)

A
  1. AV valves open and ventricular filling occurs as blood flows in from atria
  2. atria contraction occurs at end of diastole, after most ventricular filling has occurred
  3. ventricles receive approx 80% throughout diastole before the atria contract