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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
Flow
Flow = Pressure / Resistance
26
Inherent Heart Rate
The inherent rhythm of the heart is 105 bpm. Parasympathetic input constrains the heart at 70 bpm
27
Stroke volume
SV = EDV-ESV
28
Pulse Pressure
PP = SBP - DBP
29
Net Filtration Pressure (NFP)
NFP = Filtration Forces - Absorption Forces - Can do Arterial NFP - Venous NFP
30
Local vasodilators
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
Control of blood flow: Hormonal Vasoconstrictors
Epinephrine Angiotensin II Vasopressin
32
Control of blood flow: Hormonal Vasodilators
Epinephrine Atrial Natriuretic Peptide
33
Control of blood flow: Increase Resistance
Antidiuretic Peptide Cortisol Erythropoietin: Increases RBCs, increases viscosity
34
Response of the heart to exercise
- 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
Heart Block: First Degree
Delays between P and the QRS
36
Heart Block: Second Degree - Mobitz Type I
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
Heart Block: Second Degree - Mobitz Type II
Electrical impulses do not pass to the ventricles. The rate is more irregular than type I.
38
Heart Block: Third Degree
P wave isn't always followed by QRS. None of the electrical signals reach the ventricles.
39
Heart Block rhyme
Longer, longer, longer - drop, then you have a Wenkeback, If some Ps don't get through then you have a Mobitz II
40
Describe vessel characteristics and functions
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
Describe the pressure differences across the cardiovascular system
Greatest pressure in the aorta, decreases throughout with the lowest seen in the vena cava (remember intermediate vessels, arteries, veins etc.)
42
Describe circumstances of altered metabolic demand which may require changes to blood flow
Periods of exercise, post-prandial periods
43
Describe the relationship between blood flow, arterio-venous pressure and resistance to flow
Flow = (Pa - Pv) / resistance
44
Describe the terminologies active hyperaemia, auto regulation and inactive hyperaemia
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
Describe autonomic, endocrine and metabolic substances which mediate control of tissue perfusion
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
How does NO induce vasodilation
Diffusion of NO into smooth muscle causes an overall reduction in calcium influx, inhibiting muscle contraction
47
Physiology underpinning CV response to increased metabolic demand in muscles
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
Describe the regulation of HR (central and peripheral)
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
Describe the regulation of SV
Determined by 4 factors: pre-load, stiffness, inotropy and after-load \*\*Frank-Starling Law
50
Describe how the heart responds to changes in metabolic demand
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
Describe how changes in coronary blood flow are elicited
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
What factors allow for increased cardiac output during exercise
Increased heart rate and stroke volume. Both increase proportionately but stroke volume reaches its maximum at around 40-60% VO2max
53
Describe the changes in blood distribution seen during exercise
The amount of blood directed to muscles increases during exercise
54
Describe the cardiac changes seen during dynamic exercise
CO increased, TPR decreased \*\*TPR is decreased due to increased vasodilation. This decreases resistance and therefore decreases TPR
55
Describe the cardiac changes seen during resistance exercise
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
Outline the 7 stages of the cardiac cycle
Atrial diastole, isometric contraction, rapid ejection, reduced ejection, isovolumetric relaxation, rapid filling, diastasis
57
Describe the components which control the cardiovascular system
**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
Outline the relative distribution of water in the body
59
Describe the action potentials of contractile and autorhythmic cardiac cells

Module 3: Cardiovascular Sciences (10 decks)

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