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Module 3: Cardiovascular Sciences > Cardiovascular Physiology > Flashcards

Cardiovascular Physiology Flashcards

1
Q

Calculating Flow - Equation

A

Flow = Pressure (PA-PV) / Resistance

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2
Q

Usual range for MAP

A

70 -110 mmHg

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3
Q

TPR = ?

A

TPR = MAP x CO

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4
Q

Factors which affect flow within vessels

A
  • Vessel diameter - Vessel length - Fluid viscosity
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5
Q

Effects of changes in vessel radius (numerical)

A

19 % increase in vessel diameter doubles flow (vasodilation) 16 % decrease in vessel diameter halves flow (vasoconstriction)

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6
Q

Regulation of blood flow: Active Hyperaemia

A

Increased blood flow to local tissues in response to exercise/increase metabolic demand

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7
Q

Regulation of blood flow: Autoregulation

A

Regulation of local blood flow over a range of perfusion pressures. Independent of neuronal and endocrinal influence. Occurs in tissues such as the brain, heart and kidney.

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8
Q

Regulation of blood flow: Reactive hyperaemia

A

An increase in local blood flow that occurs following an occlusion in blood supply to the tissue. The occlusion leads to a build-up of respiratory by-products and vasodilatory chemicals. Hyperaemic response occurs when blood supply is restored.

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9
Q

Factors affecting arteriolar radius

A
  • Local metabolic controls. Vasodilators: Increased CO2, potassium, adenosine. Decreased O2 and pH Autoregulation - Hormonal controls Constrictors: Epinephrine, angiotensin II, vasopressin Dilators: Epinephrine, Atrial Naturetic Peptide (ANP) - Neural controls: SNS
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10
Q

G-proteins for alpha (1 and 2) and beta receptors

A

Alpha 1: Gq Alpha 2: Gi Beta: Gs

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11
Q

Autoregulatory mediators of blood flow

A
  • Sphincters - Metabolic status: K, H, lactic acid - Endothelial derived substances: Endothelin-1 (constrictor), prostacyclin (dilator) - Increased shearing forces: Increased strain on endothelial cells due to increased perfusion pressure leads to synthesis of NO by eNOS (NO synthase)
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12
Q

NO production

A

Local mediators prompt NO production. Calcium is released from the endoplasmic reticulum. eNOS is activated and produces NO. No diffuses into smooth muscle cells, a decrease in calcium influx is seen. Muscle contraction is inhibited.

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13
Q

ECG - Basis

A
  • A graph: Voltage vs time - Measures the electrical activity created by action potentials - Lead II is the rhythm strip as it holds the closest value to the mean electrical activity of the heart
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14
Q

Milieu Interior

A

Homeostasis. Maintaining activity within physiological limits.

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15
Q

Components controlling the cardiovascular (CV) system

A
  • Baroreceptors: Carotid sinus and aortic arch - Stretch receptors: In the atrium - Hormonal control
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16
Q

Hormonal control of the cardiovascular system

A

ANP (Atrial Natriuretic peptide): Is released in response to increased atrial stretch. Causes vasodilation, increased sodium and water release and decreases ADH release. Decreases MAP

Aldosterone: Increases sodium and water retention. Increases MAP.

Erythropoietin: Increases the viscosity of the blood, increases MAP -

Anti-diuretic peptide: Increases sodium and water retention. Increases MAP

Cortisol: Increases sympathetic activity, increases MAP (as HR is increased)

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17
Q

Name the location and outline the function of Baroreceptors

A

CAROTID SINUS AND ARCH OF THE AORTA

  • When increased stretch is experienced they signal via IX to the medulla oblongata.
  • Subsequently, autonomic activity is adjusted accordingly.
    • Sympathetic innervation affects SAN, AVN and ventricles
    • Parasympathetic innervation only affects the SAN and AVN
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18
Q

Factors affecting BP

A
  • Heart rate (CO) - Stroke volume (CO) - Viscosity - Radius of vessels (vaso- dilation/constriction) - Length of vessels (pregnancy and obesity) - Fluid retention by the kidneys
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19
Q

Describe the histological structure of blood vessels

A

Tunica Intimia: Squamous epithelial cells joined by gap junctions Internal elastic lamina Tunica media: High smooth muscle content. More elastin seen in aorta, elastic arteries rather than muscular. External elastic lamina. Tunica adventitia: External connective tissue. For larger vessels a blood supply may be seen.

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20
Q

Define hypertension

A

Blood pressure greater than 140/90 Where treatment does more good than harm

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21
Q

Outline the type of hypertension

A
  • Primary (idiopathic cause) - Secondary (aetiology known) > Both may be benign (stable over many years) or malignant (dramatic rise over a short period of time) Causes of secondary hypertension: Renal disease, endocrine disorders (hyperthyroidism), tumours, cardiovascular disorder (coarctation), medication (contraceptive), iatrogenic
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22
Q

Venous return

A

Valves: Compartmentalise the blood flow Muscle pump: Movement of muscles stimulates opening and closing of valves as they are compressed by contraction.

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23
Q

Pathology of arterioles

A

Hypertension causes constant smooth muscle activation within the arteries. This leads to hypertrophy of the vessels. Collagen is layed down to provide support. This leads to a loss in flexibility. The wall thickens and hardens (arteriosclerosis). Damage is seen within end organs as blood supply can no longer be controlled.

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24
Q

Phaeochromocytoma

A

Rare pathological cause of secondary hypertension. A tumour of the neuroectodermal cells (hormone responsive).

25
Q

Flow

A

Flow = Pressure / Resistance

26
Q

Inherent Heart Rate

A

The inherent rhythm of the heart is 105 bpm. Parasympathetic input constrains the heart at 70 bpm

27
Q

Stroke volume

A

SV = EDV-ESV

28
Q

Pulse Pressure

A

PP = SBP - DBP

29
Q

Net Filtration Pressure (NFP)

A

NFP = Filtration Forces - Absorption Forces - Can do Arterial NFP - Venous NFP

30
Q

Local vasodilators

A

NO (nitric oxide) – produced by vascular endothelial cells eg. In response to high perfusion pressure ACh – binds to muscarinic GPCRs inducing NO formation by NO synthase. Bradykinin – also binds to GPCRs to cause NO formation by NO synthase. Endothelin-1 – produced by vascular endothelial cells

31
Q

Control of blood flow: Hormonal Vasoconstrictors

A

Epinephrine

Angiotensin II

Vasopressin

32
Q

Control of blood flow: Hormonal Vasodilators

A

Epinephrine

Atrial Natriuretic Peptide

33
Q

Control of blood flow: Increase Resistance

A

Antidiuretic Peptide Cortisol Erythropoietin: Increases RBCs, increases viscosity

34
Q

Response of the heart to exercise

A
  • HR increases - SV increases and then plateaus. It is limited by Frank-Starling Mechanism (Due to Pre-load and stretch (Length-tension relationship)) - Combined increases in HR and SV lead to an increased CO
35
Q

Heart Block: First Degree

A

Delays between P and the QRS

36
Q

Heart Block: Second Degree - Mobitz Type I

A

Signals are delayed until the heart skips a beat, P is not followed by QRS, and then regular rhythm returns. Patients often feel dizzy.

37
Q

Heart Block: Second Degree - Mobitz Type II

A

Electrical impulses do not pass to the ventricles. The rate is more irregular than type I.

38
Q

Heart Block: Third Degree

A

P wave isn’t always followed by QRS. None of the electrical signals reach the ventricles.

39
Q

Heart Block rhyme

A

Longer, longer, longer - drop, then you have a Wenkeback, If some Ps don’t get through then you have a Mobitz II

40
Q

Describe vessel characteristics and functions

A

Arterioles have lots of smooth muscle to allow control of the flow of blood. Arteries are wide bore, thick elastic vessels. Venous vessels have wide and thin walls, as the pressure is lower

41
Q

Describe the pressure differences across the cardiovascular system

A

Greatest pressure in the aorta, decreases throughout with the lowest seen in the vena cava (remember intermediate vessels, arteries, veins etc.)

42
Q

Describe circumstances of altered metabolic demand which may require changes to blood flow

A

Periods of exercise, post-prandial periods

43
Q

Describe the relationship between blood flow, arterio-venous pressure and resistance to flow

A

Flow = (Pa - Pv) / resistance

44
Q

Describe the terminologies active hyperaemia, auto regulation and inactive hyperaemia

A

Active hyperaemia: Increased blood flow in response to increased physical activity. Under neural, endocrine and metabolic control Auto regulation: Normal level of blood flow to tissues, independent of neural and endocrine input. IMPORTANT IN THE HEART, BRAIN AND KIDNEYS Inactive hyperaemia: An increase in blood flow to tissues following occlusion of a vessel to the tissue. Occlusion leads to the build up of products from cellular respiration and vasodilator molecules. Hyperaemic response occurs when blood flow is restored

45
Q

Describe autonomic, endocrine and metabolic substances which mediate control of tissue perfusion

A

Autonomic: Sympathetic nervous system (!parasympathetic generally has no effect!) Endocrine vasodilator: Atrial naturetic peptide (ANP), epinephrine Endocrine vasoconstrictor: Aldosterone, cortisol, angiotensin II, epinephrine, vasopressin (ADP) Metabolic vasodilator: decreased oxygen or pH. Increased CO2, potassium and adenosine

46
Q

How does NO induce vasodilation

A

Diffusion of NO into smooth muscle causes an overall reduction in calcium influx, inhibiting muscle contraction

47
Q

Physiology underpinning CV response to increased metabolic demand in muscles

A

Heart needs constant ATP supply, cannot build up a deficit. Uses a variety of energy sources. Heart must increase heart rate and stoke volume in order to generate the increased cardiac output required for increased metabolic demand of skeletal muscles

48
Q

Describe the regulation of HR (central and peripheral)

A

HR: increased by sympathetic nerves, NA and A. SV: increased by sympathetic nerves Peripheral input: baroreceptors (carotid sinus and aortic arch), mechanoreceptors (muscle spindle and Golgi tendon organ), peripheral and central chemoreceptors

49
Q

Describe the regulation of SV

A

Determined by 4 factors: pre-load, stiffness, inotropy and after-load **Frank-Starling Law

50
Q

Describe how the heart responds to changes in metabolic demand

A

Increased rapidly until a plateau is met.

HR: Increases due to increased sympathetic input and decreased parasympathetic input. Heart rate continues to rise as temperature increases, feedback from proprioceptors and accumulation of metabolites.

51
Q

Describe how changes in coronary blood flow are elicited

A

Coronary vasodilation occurs in response to metabolites released from cardiac myocytes: adenosine, vasodilatory prostaglandins, CO2, decreased O2, NO Smaller arterioles also have beta-adrenoreceptors that mediate vasodilation in response to sympathetic activation

52
Q

What factors allow for increased cardiac output during exercise

A

Increased heart rate and stroke volume. Both increase proportionately but stroke volume reaches its maximum at around 40-60% VO2max

53
Q

Describe the changes in blood distribution seen during exercise

A

The amount of blood directed to muscles increases during exercise

54
Q

Describe the cardiac changes seen during dynamic exercise

A

CO increased, TPR decreased **TPR is decreased due to increased vasodilation. This decreases resistance and therefore decreases TPR

55
Q

Describe the cardiac changes seen during resistance exercise

A

CO increased, TPR increased ** TPR increases due to only a few muscle groups being active and therefore less vasodilation occurs, causing increased resistance and therefore increased TPR. Also, the contracting muscles undergo vasoconstriction due to force of contraction

56
Q

Outline the 7 stages of the cardiac cycle

A

Atrial diastole, isometric contraction, rapid ejection, reduced ejection, isovolumetric relaxation, rapid filling, diastasis

57
Q

Describe the components which control the cardiovascular system

A

Autonomic nervous system - sympathetic (NA/A) and parasympathetic (ACh) (no real effect on MAP though)

Baroreceptors (carotid sinus and aortic arch)

Chemoreceptors

Endocrine influences such as cortisol, aldosterone, ADP, ANP, ADH

58
Q

Outline the relative distribution of water in the body

A
59
Q

Describe the action potentials of contractile and autorhythmic cardiac cells

A

Module 3: Cardiovascular Sciences (10 decks)

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