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Year 1 > CV Physiology > Flashcards

CV Physiology Flashcards

1
Q

What is resting heart rate?

A

60-100bpm

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2
Q

What is bradycardia?

A

HR below 60 bpm

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3
Q

What is tachycardia?

A

HR above 100bpm

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4
Q

Autorhythmicity

A

excitation of heart originates from within itself (Sa node pacemaker cells)

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5
Q

Sinus rhythm

A

Heart driven by sinoatrial node pacemaker cells

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6
Q

Ionic mechanisms of SA node pacemaker potentials

A

To reach threshold - this is slow depolarization
- “funny” current Na+ influx
- superimposed on Closure of K+ channels, less K+ efflux
Rapid Depolarization
- Opening of transient Ca2+ channels, influx
- L-type Ca2+ channel opening, influx
Rapid Repolarization
- L-type channel closure
- K+ channel opens, K+ efflux

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7
Q

Route of excitation from SA node to ventricular cells?

A

Via AV node, bundle of His, R and L fibres and then purkinje fibres.
Cell to cell transmission via gap junctions throughout the heart!

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8
Q

Chronotropic?

A

Rate change

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9
Q

Inotropic?

A

Force contraction change

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10
Q

What is the role of AV node?

A

Point of contact between SA and ventricles, delayed conduction to allow atria to contract fully before ventricular systole

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11
Q

Ionic mechanisms of ventricular myocytes

A 
Rapid Depolarization
- Na+ influx through sodium channels
Peak/Plateau
-Na+ channels close (prevent influx) , K+ channels open (efflux) transiently
- L type Ca2+ channels open
Depolarization
- L type Ca2+ channels shut
- K+ channels reopen (efflux)
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12
Q

What is the significance of vagal activity of the heart?

A

Parasympathetic activity from vagus nerve exerts continuous influence on SA node.

  • Negative chronotropic effect, takes longer to reach ionic threshold
  • Slows the INTRINSIC heart rate from 100bpm to 70bpm
  • Increases AV nodal delay

Neurotransmitter is acetylcholine acting through M2 receptors. Atropine is LAMA used to compete with this in bradycardia.

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13
Q

What is the sympathetic supply of heart?

A

Sympathetic nerves supply SA, AV and myocardium. Inc. HR and shorten AV delay. Positive inotropic AND chronotropic effect.
Noradrenaline acts on B1 receptors!

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14
Q

P wave

A

atrial depolarization

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15
Q

QRS complex

A

Ventricular depolarization

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16
Q

T wave

A

Ventricular repolarization

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17
Q

PR interval

A

AV nodal delay

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18
Q

ST segment

A

ventricular systole

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19
Q

TP interval

A

ventricular diastole

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20
Q

Structure of cardiac muscle

A

Striated with filaments.
THIN filaments actin, THICk filaments myosin. Joined by cross bridge.
Filaments make up myofibril (units of muscle), myofibrils arranged into sarcomeres.

There are no neuromuscular junctions in these cells. Have GAP junctions to allow excitation to jump.
Ensures electrical excitation reaches all myocytes. ALL OR NONE.

Desmosomes anchor cells together.

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21
Q

How does cardiac muscle contract?

A

Sliding of filaments via cross bridge.
Extracellular Ca2+ released from sarcoplasmic reticulum due to depolarization frees cross bridge binding site by pulling away troponin units.
Cross bridge binding triggers power stroke that pulls filaments for contraction.

Diastole achieved when AP has passed and Ca2+ is resequestered by SR.

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22
Q

The importance of a long REFRACTORY PERIOD to the normal cardiac function?

A

Prevents generation of tetanic contractions of cardiac muscles.

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23
Q

Stroke Volume

A

the volume of blood ejected by each ventricle per heart beat

End Diastolic Volume (EDV) – End Systolic Volume (ESV)

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24
Q

End Diastolic volume

A

EDV is determined by venous return to the heart. It is the volume of blood at the end of diastole, this determines the length of the muscle fibres at diastole. Changes in EDV can therefore affect SV. They determine preload.

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25
Q

What is the Frank Starling law?

A

the more the ventricle is filled with blood during diastole (END DIASTOLIC VOLUME), the greater the volume of ejected blood will be during the resulting systolic contraction (STROKE VOLUME)

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26
Q

Significance of stretch in cardiac muscle?

A

Cardiac muscle stretches in response to increased return. I.e. increased return in R or L atria. This leads into increased Sv in aorta/pulmonary artery

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27
Q

What is afterload?

A

The resistance into which the heart is pumping. If this increases heart can’t eject full SV, so EDV increases. Continued leads to hypertrophy.

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28
Q

What is the effect of sympathetic simulation on ventricular contraction?

A

Increase peak ventricular pressure
rate of pressure change during systole increases - relaxes more during diastole and contracts harder during systole.
+ve ino and chrono effects
Less EDV needed for equal stroke volume - frank starling curve shift LEFT!!!

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29
Q

What is the effect of parasympathetic simulation on ventricular contraction?

A

Very little vagal innervation in ventricles.

Influence on rate but not contraction force

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30
Q

What is BP?

A

Pressure exerted outwardly (hydrostatic) on blood vessel walls during systole and diastole

31
Q

Calculate MABP?

A

(2xsystolic BP + diastolic bp)/3

TPR x CO / TPR x HR x SV

32
Q

Normal MABP

A

70-105

33
Q

Systolic BP normal

A

<140

34
Q

Diastolic BP normal

A

<90

35
Q

How to use sphygmonameter?

A

External pressure exceeds systolic pressure = silence there is no blood flow.
External pressure between systolic and diastolic - turbulent flow, audible.
Tighten cuff then release, hear first sound listen brachial artery = systolic BP estimate
Silence= diastolic BP estimate

36
Q

Why nothing heard through normal patent artery?

A

Laminar flow

37
Q

What are Krotokoff sounds?

A

Turbulent flow through cuff suggests pressure is between diastolic and systolic pressures. 1st sound is estimate systolic BP. 5th sound (silence) is estimate diastolic BP.

38
Q

Why does MABP have to be kept within a narrow range?

A
  • High enough to perfuse major organs brain heart kidneys

Low not cause damage vessels or place strain on heart

39
Q

What are the major resistance vessels?

A

Arterioles

40
Q

Baroreceptor role, function

A

Located aortic arch and carotids
Sensitive to stretch, firing increases in response to high BP, absence of high BP (postural hypotension) causes a decrease in baroreceptor afferent nerve firing. This leads to increase in CARDIAC sympathetic nerve firing.
Controlled by medulla
Affect heart and blood vessels
Moment to Moment impact, “normal” can be reset, negative feedback loop

41
Q

Characteristics specific to veins?

A

Capacitance vessels - contain most of blood volume during rest. , venous tissue must supply volume for heart to pump

42
Q

Resistance to blood flow is directly proportional to…

A

Positively : blood viscosity and length of blood vessel
Inversely: the radius of blood vessel to the power of 4!!
Therefore resistance is MAINLY controlled by vascular smooth muscle through changes in the radius of arterioles.

43
Q

Examples of extrinsic control of resistance to blood flow?

A

Baroreceptor reflex
Hormones (ADH, ANP, Aldosterone, Angiotensin II)
Sympathetic stimulation
Tonic discharge sympathetics

44
Q

Examples of chemical intrinsic control of resistance to blood flow?

A

Local metabolites ( Inc. extracellular K+ levels, CO2, H+, osmolarity/decrease PO2)
Vasodilation: Adenosine from ATP
Humoral factors - Vasodilatory inflammation (histamine, bradykinin, NO)
Vascontriction: Serotonin, Thromboxane A2, Leukotrienes, Endothelin

45
Q

Examples of physical intrinsic control of resistance to blood flow?

A

Intrinsic control can override extrinsic control. Has chemical and physical factors
Temperature
Stretch
Sheer Stress!

46
Q

Noradrenaline supplies what?

A

Vascular smooth muscle, supplied by sympathetic nerve fibres. It is a neurotransmitter that acts on alpha receptors!

47
Q

Adrenaline supplies what?

A

Adrenaline from adrenal medulla has organ specific effects.
acting on alpha receptors causes vasoconstriction
acting on beta2 receptors causes vasodilation
Helps with strategic redistribution such as during exercise.

48
Q

What is special about nitric oxide?

A

Continuously released by endothelium of arteries and arterioles.
Potent vasodilator with short life few secs
Maintenance of vascular health

49
Q

How does nitric oxide work?

A

Produced from amino acid L-arginine through enzymatic action of Nitric Oxide Synthase.
Shear stress or vasoactive chemical stimuli cause activation of NOS and NO.
NO diffuses through endothelium into adjacent smooth muscle cells. Activates cGMP and signals smooth muscle relaxation

50
Q

Why is endothelium important in vascular health?

A

Endothelial produced vasodilators are anti-thrombotic, anti-inflammatory and anti-oxidants, vasoconstrictors have opposite effect.
Factors are meant to help with maintenance of vascular health!

51
Q

What is the myogenic response to stretch?

A

MAP rise => automatically vasoconstrict to limit flow

MAP fall => automatically dilate to increase flow

52
Q

What is sheer stress and what are it’s short-term consequences?

A

Sheer stress is the force is applied to deform vessel walls, causes upstream blood vessels to dilate.

53
Q

What is shock? What are the consequences of shock?

A

Abnormality of CV system leading to inadequate tissue perfusion and oxygenation.
Anaerobic metabolism and accumulation of metabolic waste products, leads to cellular failure.

54
Q

What is hypovolaemic shock? What are the consequences of hypovolaemic shock?

A

Loss of blood volume, decreased venous return, decreased EDV, decreased SV, decreased CO and BP, inadequate perfusion.

55
Q

What is cardiogenic shock? What are the consequences of this type of shock?

A

Sustained hypotension due to decreased cardiac contractility. Decreased SV, decreased CO and BP, inadequate perfusion.
Results in a depression of the Frank Starling curve!

56
Q

What is obstructive shock? What are the consequences of this type of shock?

A

Increased intrathoracic pressure due to cardiac tamponade, pneumothorax, severe aortic stenosis, PE etc.
Decreased venous return, decreased EDV, decreased SV, decreased CO and BP, inadequate perfusion.

57
Q

What is neurogenic shock? What are the consequences of this type of shock?

A

Loss of sympathetic tone due to spinal cord injury usually.
Massive venous & arterial vasodilation, decreased venous return, decreased EDV, decreased SV, decreased CO and BP, inadequate perfusion.

58
Q

What is vasoactive shock? What are the consequences of this type of shock?

A

Vasoactive mediators due to sepsis or anaphylactic shock, release of vasoactive mediators
Increased permeability of capillaries and arterial vasodilation,decreased venous return, decreased EDV, decreased SV, decreased CO and BP, inadequate perfusion.

59
Q

Treatment of shock

A

ABCDE
High flow oxygen
Treat cause: Inotropes cardiac, immediate thoracocentesis pneumothorax/pericentesis tamponade. Vasopressors for septic shock adrenaline for anaphylactic shock.

60
Q

How long can compensatory mechanisms maintain BP?

A

Until >30% blood lost

61
Q

Compensatory mechanisms hypovolaemic shock?

A

Tachycardia via baroreceptor reflex
Sympathetic activity increase HR, contractility, attempt inc venous return inc venous vasoconstriction. Attempt inc. SV and EDV.
Fluid shift from interstitial fluid to plasma in attempt to increase blood volume and BP.
RAAS system activated VAT/PIS vasoconstriction, ADH, Thirst, inc. plasma vol and BP, retention of salt and water, decreased urine output

62
Q

What are the special adaptations of the coronary circulation?

A
  • High capillary density
  • High oxygen extraction (75% comp to body’s 25%), maximal can’t extract more if there’s problems
  • High flow, this can be increased if demand increases though
63
Q

Intrinsic mechanisms controlling coronary blood flow?

A
  • Low PO2 causes vasodilation
  • Adenosine (from ATP) potent vasodilator?
  • Metabolic hyperaemia increases flow (high metabolites K+, H+, PCO2)
64
Q

Extrinsinc mechanisms controlling coronary blood flow?

A

Overridden by metabolic hyperaemia
Sympathetic stimulation of ADRENALINE acts on Beta2 receptors causing VASODILATION! This is because sympathetics everywhere else promote inc. CO SV & HR.
They are also supplied by sympathetic vasoconstrictor nerves acting on ALPHA receptors.

65
Q

When does peak coronary flow occur?

A

During diastole, arteries not compressed

shortening diastole decreases coronary flow.

66
Q

What is the basic anatomy of cerebral circulation?

A 
Supplied by internal carotids and vertebral arteries. 
Basilar arteries (from vertebral) &amp; carotids anastamose to form Circle of Willis, major arteries arise from here.

Therefore cerebral perfusion should be maintained even if one carotid is obstructed.

Obstruction small branch = deprive blood area brain.

67
Q

What is the physiology of cerebral circulation?

A

Grey matter highly sensitive to hypoxia. Consciousness lost within seconds, irreversible cell damage within 3 mins.

BBB tight intercellular junctions, glucose crosses (brain needs it) but impermeable to hydrophilic substances such as ions etc

Skull tight box, increase in intracranial pressure can lead to failure autoregulation cerebral blood flow (injury or tumor)

68
Q

What are the intrinsic mechanisms of regulation of cerebral circulation?

A

Physical (1)
Autoregulation guards against changes in cerebral blood flow
MABP rise= automatic constriction MABP fall= automatic dilation
Maintained within range 60-160. If outwith autoregulation FAILS.

Chemical (2)
High PC02 causes vasodilation, low PC02 leads to fainting. Hyperventilation can lead to fainting because of this.
Metabolic hyperaemia - blood flow increases to active part of the brain.

69
Q

What is the significance of low blood pressures in the pulmonary circulation?

A

Low BP = absorptive forces exceed filtration forces to prevent pulmonary oedema.

70
Q

What is the effect of hypoxia on pulmonary circulation?

A

Vasoconstriction to help divert blood from poorly ventilated areas of lung.

71
Q

What is the effect of exercise on skeletal muscle?

A

Metabolic hyperaemia overcomes sympathetic vasoconstrictor activity

Adrenaline released during exercise acts on Beta 2 receptors causing vasodilation

Increases CO increases blood flow to tissues.

72
Q

Describe the effects of the skeletal muscle pump

A

Contraction of muscles aids venous return
One way venuous valves allow blood to move towards heart
Reduces chance of postural hypotension and fainting

73
Q

What is preload?

A

Measure of stretch of ventricular myocytes due to end diastolic volume

Year 1 (15 decks)

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