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VAP II > Cardio > Flashcards

Cardio Flashcards

1
Q

Primary Cardiovascular Disturbances

A

Congenital = Valve defects, wall of heart defects, major blood vessel defects, clotting disorders Acquired = Haemorrhage, clotting, primary cardiac disease, parasitic infection

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2
Q

Secondary Cardiovascular Disturbances

A

Vomiting, diarrhoea = cause heart arrhythmias, heart failure
Septic shock = blood poisoning
Anaesthetic overdose = depress central nervous system and heart function

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3
Q

Describe the components of the cardiovascular system & their primary functions

A

Heart, Blood Vessels, Blood= pumps and supplies blood to body, supplies oxygen, nutrients, removes waste
Blood functions-
Transport of gases, nutrients, waste
Regulation of temperature and pH (homeostasis)
Protection – clotting and immune functions

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4
Q

Describe in detail the basic composition of blood

A

Plasma = matrix
Erythrocytes - RBC
leukocytes - WBC
thrombocytes - platelets

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5
Q

Erythrocytes properties

A

Properties – Biconcave, flexible, live for 2-6 months, lack nuclei and organelles ** reptiles contain nuclei

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6
Q

Plasma function

A

Plasma = contains proteins and electrolytes
Proteins – globulin (immune function), albumin (fluid balance of blood), fibrinogen (clotting, inflammation)
Electrolytes – Na+, Cl-

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7
Q

Name the erythrocyte in cattle and why it is different to other mammals

A

Anisocytosis (variation in RBC size) - cattle

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8
Q

Name the type of RBC that varies in shape, and in what animal

A

Poikilocytosis (variation in RBC shape) – goats, cattle

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9
Q

Describe Erythropoiesis

A

production of erythrocytes (no nucleus thus cannot undergo mitosis) Performed by stem cells
Rate is determined by erythropoietin in the kidneys = under endocrine control

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10
Q

Explain blood component formation

A

haematopoiesis is where Erythrocytes and leucocytes develop by mitosis and differentiation from stem cells within the bone marrow

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11
Q

Describe clinical haematological tests

A

Collect sample – use anticoagulant (EDTA) to stop clotting
Haematocrit (Hct) – Packed cell volume (PCV), erythrocyte composition
% affects viscosity and fluidity of blood

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12
Q

What is the type of haemoglobin measurement

A 
Mean Corpuscular (cell) Haemoglobin (MCH) =
Mean Corpuscular (cell) Haemoglobin Concentration (MCHC) = [Hb]/Hct
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13
Q

What does high protein in blood indicate

A
  • Haemoconcentration eg. dehydration

– Increased globulin production eg. inflammation or infection

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14
Q

What can low protein in blood indicate

A

– Loss of protein via the kidneys (protein losing nephropathy)
– Loss of protein via the gastrointestinal system (protein losing enteropathy) – Loss of lymph
– Chronic or severe blood loss
– Lack of plasma protein production by liver

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15
Q

How is bloody typed

A

Blood cross match testing - detect presence of haemagglutinating & haemolysing antibodies in serum of donor & recipient animals

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16
Q

What is major and minor cross matching

A

Major cross-match = donor RBCs + recipient plasma

Minor cross-match = donor plasma + recipient RBCs

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17
Q

What role do white blood cells (leucocytes) play

A

Leukocytes are larger than red blood cells, have an immune function and contain a nucleus, organelles and cytoplasmic vesicles

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18
Q

Name the two types of WBC

A

arangulocytes

granulocytes

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19
Q

name and describe two types of aragulocytes

A

LYMPHOCYTE – Large, spherical, slightly indented nucleus– dark purple stain
- Specific immune response function (B and T lymphocytes)
MONOCYTE – Variable shape, blue/grey staining
- Phagocytic function, contain lysosomes

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20
Q

name and describe the three types of granulocytes

A

EOSINOPHIL – large, uniform, bilobed nucleus, red/orange staining
- Kills parasitic worms, modulate inflammation, allergic reactions
BASOPHIL – U/S shaped nucleus, blue/purple staining (rare in cats, dogs, horses, ruminants) - Immediate hypersensitivity reactions (contain histamine and heparin)
NEUTROPHIL – predominant granulocyte, irregular, knobbly nucleus, lilac staining
- Initiate immune system, 1st line of defence against bacteria and some fungi

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21
Q

Explain the role of platelets in primary haemostasis.

A

PLATELETS- also called thrombocytes, non-nucleated
ROLE – homeostasis and clotting
ACHIEVE HOMEOSTASIS BY – minimise or prevent blood loss
1) contraction of injured blood vessel
2) Formation of platelet plug
3) Coagulation of blood

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22
Q

Describe the mechanisms involved in primary haemostasis

A

PRIMARY –
VASCULAR PHASE- Reflex vasoconstriction temporarily restricts blood flow
Direct mechanical input on smooth muscle of vessel wall, release of vasoactive substances
30 min
PLATELET PHASE – damage to endothelium stimulates platelet adhesion and plug formation

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23
Q

Describe the mechanisms involved in secondary haemostasis.

A

SECONDARY – COAGULATION
Occurs at the same time as primary haemostasis
Causes consolidation of temporary platelet plug – blood clot formation
‘Coagulation cascade’ of enzymatic processes – intrinsic, extrinsic, common pathways Coagulation – conversion of soluble plasma protein fibrinogen into insoluble threads of fibrin, this traps RBCs and form gelatinous clot

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24
Q

describe the contents of the mediastinum

A

MEDIASTINUM – space in the medial thorax region, extending from thoracis inlet to the diaphragm

consists of

  • cranial vana cava
  • lymph nodes
  • thymus (immune system)
  • phrenic nerve (controls diaphragm)
  • vagus nerve (internal organ functions)
  • oseophagus
  • aorta
  • heart
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25
Q

describe the three layers of the pericardium

A

OUTER-FIBROUS LAYER- Fibrous pericardium INNER SEROUS MEMBRANES –
Parietal Pericardium: Attached to fibrous layers
Visceral Pericardium: Attached to heart (epicardium)
PARICARDIAL CAVITY – space between two serous layers

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26
Q

Describe the function of the four heart chambers

A

ATRIUM- Left and right, bounded by auricle
Collect blood, deliver to ventricle through valves
VENTRICLE – left and right
Pump blood to lungs by the right ventricle and to the body tissues by the left ventricle
PULMONARY TRUNK – right ventricle sends deoxygenate blood through the trunk
AORTA – left ventricle sends oxygenated blood through the aorta

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27
Q

How does blood flow through the mammalian heart

A

RECEIVING CHAMBERS – Right atrium (deoxygenated), Left atrium (oxygenated)
DISTRIBUTING CHAMBERS – Right ventricle (pumps deoxygenated blood to the lungs), Left ventricle (pumps oxygenated blood to the body)
VEIN – blood returning to the heart (not always deoxygenated, vein returning from the lungs to the left atrium through pulmonary veins is oxygenated)
ARTERY – blood leaving the heart (not always oxygenated, artery leaving right ventricle to the lungs is deoxygenated)
** RIGHT IS ALWAYS DEOXYGENATED, LEFT IS OXYGENATED**

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28
Q

To describe the structure of atrioventricular and semilunar valves and their fibrous skeleton

A

ATRIOVENTRICULAR VALVES
CUSP – flaps of membranous material, attach to fibrous ring of heart
CHORDAE TENDINAE – fibrous strands that join the cusps
PAPILLARY MUSCLES – muscular projections, each muscle connected to 2 cusps
SEMILUNAR VALVES – aortic and pulmonary
3 flaps – open when ventricular pressure increases, closes when pressure decreases

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29
Q

Explain how impulse generation occurs within the heart

A
  • Autorhythmic cells spontaneously depolarise, forming Action Potential. The initiate heartbeat and determine pace of heart
  • Pacemaker (autorhythmic) cells located in Sinoatrial Node (located in Right Atrium wall)
  • Pacemakers in SAN undergo slow depolarisation (leaky sodium channels) until membrane potential reaches threshold value
  • Cardiac action potential differs from neural action potential like in skeletal muscle
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30
Q

how does the cardiac conduction contract the ratio and ventricles

A
  • Cardiac muscle cells form syncytium (functional network) where cells contract in synchrony and relax together
  • Myocardium of atria are separated from ventricles by annulus fibrous, no electrical connections (gap junctions) can cross this layer
  • Conducting system acts as electrical window through fibrous layer Conducting system is formed from autorhythmic cells
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31
Q

what is the role of the Atrioventricular node

A

Collection of modified cells, located at bottom of septum, separate the 2 atria
Cells in AV node conduct action potentials more slowly than normal muscle cells
Delay in impulse transmission between atria and ventricles allows ventricles to be filled fully before contraction

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32
Q

What is the role of the Bundle of Hiss

A

Bundle of hiss
Penetrates annulus fibrosis, divides left and right bundle branches, they divide into:
Purkinje fibres-
Extensive network of fibres, branch into ventricular myocardium and allow rapid transmission of action potential to both ventricles

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33
Q

Explain contraction of the heart

A

Depolarisation begins in SA node, rapidly spreads through atrial muscle,
Delayed into AV node to allow ventricular filling
Atria contract but depolarisation does not pass annulus fibrosis
Depolarisation crosses AV node into ventricles along conducting system (bundle branches and purkinje fibres)
= Contraction!!

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34
Q

what is an electrocardiogram?

A
  • Graph made by voltmeter, plotting voltage over time, measuring electrical activity of the heart
  • Detects and amplifies electrical charges on the skin caused by cardiac muscle depolarisation during a heartbeat
  • Difference in electrical potential occurs during depolarisation of certain parts of the muscle Voltage difference causes ionic currents in tissues and body fluid surrounding the heart – induce voltage changes that can be measures
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35
Q

How are electrocardiograms recorded?

A

Electrodes applied to skin either side of the heart
Voltage recorded between a pair of electrodes (positive and negative)
Lead system: different leads examine heart from different angles, can show problems in certain areas of the heart

  • Einthoven’s triangle: heart located in centre of the lead triangle
    Lead I: left arm to right arm (1 L – Lead 1) Lead II: right arm to left leg (2Ls – Lead 2) Lead III: left arm to left leg (3Ls – Lead 3)
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36
Q

explains the responses of the ECG

A

PR INTERVAL
- time between the start of trial depolarisation and start of ventricular depolarisation

QRS DURATION
- time required for ventricular depolarisation

QT INTERVAL
- start of ventricular depolarisation to end of ventricular repolarisation

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37
Q

name and describe clinical applications of the ECG

A

Respiratory sinus arrhythmia – naturally occurs during variation in HR, occurs during breathing cycle – decreased parasympathetic activation in inspiration and increased during expiration (can see ECG go up and down) –
Arrhythmias – deviations from normal regular rhythm, Bradycardia (slow), Tachycardia (fast) Abnormal impulse generation- sinus tachycardia and bradycardia

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38
Q

What is a premature beat and ectopic beat

A

PRE MATURE - occasional extra atrial or ventricular beats (common). May arise from SA node, AV node, Atrial or Ventricular myocardium

ECTOPIC - rhythm created by extra beat or beat skipped caused by premature beat

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39
Q

What can disturb ECG impulses

A

Atrioventricular block
Atrial fibrillation - irregular beat
Ventricular fibrillation – random contraction and relaxing of myocardium, ventricles fail to pump – reversal by defibrillation.

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40
Q

Describe a single circuit pump in cyclostomes (jawless fish) with single chambered heart

A

Single circuit = blood only goes through the heart once in the cycle

  • gas exchange body capillaries
  • deoxygenated blood to
    - sinus venousus
    - atrium
    - ventricle push out to
    - bulbus aterious
  • gas exchange at the gill capillaries
  • cycle back through
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41
Q

Describe a single circuit pump in cartilaginous fish (sharks and rays)

A
  • 2 chambers
  • deoxygenated blood to sinus venousus
  • blood is then collected in the atrium
  • atrium to ventricle
  • ventricle to conus ateriosus
  • blood to body by ventral aorta
  • deoxygenated blood to the gills
42
Q

Describe a single circuit pump in teleost (bony fish)

A

similar to cyclostomes and cartilaginous except Bulbus arteriosus instead of conus arteriosus
Bounded by bulbar valve

43
Q

what is a double circuit pump (heart)

A

Air breathing vertebrates. Two circuits (systemic and pulmonary), heart to lungs to heart to tissue

44
Q

Describe how blood flows through the heart in a single circuit pump species

A

blood returns to the heart via liver and body tissues into the sinus venous which fills passively

sino- atrial valve opens due to increase in pressure in the sinus venous - blood flows into atrium

atrium contracts, sino atrial valve closes and atrioventricular valve opens

ventricle contracts forcing blood through conus arterioles towards the gills, thus causes the atrioventcular valve to close, the sinuses venous fills, sino atrial valve opens and begins to fill the atrium again

45
Q

What are the four modifications of the heart

A
  1. Separation of oxygenated and deoxygenated blood
  2. Partial separation of ventricle into two chambers
  3. Development of spiral valve
  4. Modifications to ventral aorta
46
Q

Describe how the heart of reptiles accommodates diving

A

Compartmentalisation via interatrial and interventricular septa - atria completely divided, ventricle incompletely divided in lizards, snakes, turtles, ventricle completely divided in crocodiles
Sinus Venosus retained
Conus arteriosus becomes three vessels = Truncus arteriosus,
Pulmonary trunk; right and left aorta

47
Q

Describe the differences in the crocodilian heart compared with the turtle heart.

A

Incomplete septum in turtle heart

48
Q

Describe major differences in the avian heart compared with the mammalian heart.

A

Single aorta bends to the right whereas mammals it bends to the left
Fully compartmentalised heart
Atrioventricular Valves - 1-2 cusp, right side muscular
Semilunar Valves - openings in aortic and pulmonary trunks
Atria and Ventricles completely separated - interatrial and interventricular septum Sinus Venosus - Vestigial
Single aorta which bends to the right
Two Brachiocephalic Arteries

49
Q

describe the development cardiogenic plate from embryonic mesoderm

A

Condensation of cells within the splanchnopleuric mesoderm
Cranial to caudal neural plate
Ventral to coelomic cavity

50
Q

describe the formation of the primary heart tube

A

Formed by lateral folding -brings tubes together, coalescing around tubes forms primitive myocardium
Thin walled squamous epithelium creates future inner lining (endocardium), chambers of the heart

51
Q

describe how the primary heart tube expands and loops to form chambers

A

Constrictions (or Sulci) partition the heart Sinus venosus – part of atrial wall (SAN)
Common Cardinal Veins Vitelline Veins
– By describing the formation of the primary heart tube.
Formed by lateral folding -brings tubes together, coalescing around tubes forms primitive myocardium
Thin walled squamous epithelium creates future inner lining (endocardium), chambers of the heart
- - - - -
- -
Umbilical Veins
Single Atrium
Single Ventricle
Bulbus Cordis – right ventricle Truncus Arteriosus
Looping of Heart
Heart increases in size faster than pericardial cavity U-shaped bend
Bulboventricular loop
Draws atrium into cavity
As embryo grows - Atrium occupies position dorsal to ventricle No separation of pulmonary or systemic

52
Q

Explain how the heart functions as a pump

A

Heart contains 2 pumps (ventricles)
Systole – contraction of ventricles
Diastole – relaxation and refilling of ventricles

53
Q

How is stroke volume regulated

A
  1. Ventricular contractility
  2. End diastolic volume
  3. Afterload
54
Q

What is a Regurgitant murmur

A

occur when valve meant to be fully closed

55
Q

What is a Stenotic murmur

A

occur when valve meant to be fully open

56
Q

What is a Systolic murmurs

A

during ventricular systole: Valve incompentance (failure to close completely), Stenosis (valve fails to open fully), Ventricular septal defect (hole in heart)

57
Q

What is a Diastolic murmurs

A

during ventricular diastole: Stenosis (valve cannot open properly), valve incompetence

58
Q

What is a Machinery murmurs

A

throughout systole and diastole, due to patent ductus arteriosus (opening between aorta and pulmonary artery fail to close after birth)

59
Q

what are the Consequences of cardia defects

A

Abnormally high or low blood flow or blood pressure

Increase workload – cardiac hypertrophy: adaptation to exercise or in response to abnormal pressures

60
Q

Name the three types of atrial arteries

A
  1. Elastic Arteries – aorta, brachiocephalic trunk, common carotid, subclavian, pulmonary
  2. Muscular Arteries –thickest tunica media, less elastin, radial, femoral, coronary
  3. Arterioles – terminal branches, supple capillary beds
61
Q

What is the role of venous

A

blood from capillary beds returns to heart through veins
Increase in diameter as blood flow returns to heart
thinner walls in comparison to arteries,
work under a much lower pressure,
skeletal muscle assists in venous return to heart
1. Venules – postcapillary, collecting, muscular
2. Veins – small, medium, large

62
Q

Factors affecting blood flow:

A
  1. Greater pressure difference = increased flow rate
  2. Higher viscosity (resistance) = decreased flow rate
  3. Flow rate is extraordinary sensitive to luminal radius
63
Q

Relationship between pressure, flow and resistance

A 
Cardiac Output (CO) = Aortic pressure / Total peripheral resistance (TPR)
High oxygen demand, high blood flow, high resistance, large amounts of pressure requires to overcome resistance
64
Q

Describe how blood pressure can be measured

A

Indirect: Non-invasive. Cuff wrapped around extremity, oscillometer used to determine flow Direct: Requires catherization of artery
pulse pressure
hypertension
hypotension

65
Q

Factors that determine blood pressure

A

fluid column effects (pressure increases due to deep arteries)
systolic blood pressure
diastolic blood pressure

66
Q

To describe the fate of the aortic arches

A

Embryos have six arches but the first two disappear very early in development
- Arch III contributes to the carotid arteries. In the embryo this arch communicates with arch IV (via
ductus caroticus) to form the common carotid arteries. This connection is lost in adult.
- Aorta(e) arise from the Arch IV and form the systemic arteries.
- Pulmonary arteries arise from the Arch VI to vascularise the lung bud. In the embryo this arch
communicates with Arch IV via the ductus arteriosus. This connection is lost in the adult.
- Arch V is lost except in terrestrial urodeles, some limbless lizards and snakes

67
Q

describe the features of the capillaries

A

Smallest blood vessels, consist of a single layer of endothelial cells
Small radius enables capillaries to withstand substantial pressures as their wall tension is small
LaPlace’s Law: T = Δ Pxr
S=T/t, Wall stress (S), Wall tension (T), thickness of wall (t)
Wall stress determines whether a. vessel can resist internal pressure, if stress exceeds a critical limit, tearing of the vessel will occur.

68
Q

Role of capillaries

A

site for exhcange of water and solutes between blood stream and interstitial fluid

69
Q

Diffusion is influenced by

A

features of capillary wall and substance being exchanged

70
Q

what are Continuous capillaries

A

Continuous capillaries – most tissues – uninterrupted endothelial

71
Q

what is Fenestrated

A

– larger openings, enable larger molecules to move through (selective filter), appears in intestines, endocrine glands, pancreas, kidney

72
Q

what is Discontinuous - fenestrated

A

Discontinuous - fenestrated capillaries with incomplete or absent basement membrane. Form irregularly shaped vessels (sinusoids) in tissues where it is important to have free exchange of substances such as liver, spleen, bone marrowcapillaries with incomplete or absent basement membrane. Form irregularly shaped vessels (sinusoids) in tissues where it is important to have free exchange of substances such as liver, spleen, bone marrow

73
Q

describe Brain capillaries

A

very small pores, allow only water and very small molecules past. Protect brain neurons from toxic substances. Facilitated diffusion of glucose through specialised carrier molecules in cell membrane of endothelial cells

74
Q

describe blue low in relation of the capillaries

A

Bulk flow: mass movement of water and dissolved substances by pressure differences across capillary wall. Determine by hydrostatic and colloid osmotic forces
Filtration – fluid flow out of capillary
Absorption – fluid flow into capillary

75
Q

What are the driving forces for fluid exchange in the capillaries Starling Forces:

A

Capillary pressure (Pc)
Intersitial fluid pressure (Pif)
Plasma colloid osmotic pressure (Pp)
Interstital fluid osmotic pressure ( Pif)

76
Q

role of the lymphatic system

A

removes fluid excess (lymph) by transporting it to large veins of systemic circulation

Extensive branched network of lymph capillaries (larger than blood capillaries)
Capillaries converge to form larger lymph vessels (contain valves, smooth muscle)
Lymph eventual returns via thoracic duct

77
Q

What is the role of the lymphatic system in the lung

A

reduced hydrostatic pressure in lungs helps reduce filtration

78
Q

what is Oedema and what causes it

A

accumulation of excessive interstitial fluid

Causes: imbalances of Starling forces, alteration in capillary permeability, impairment of lymphatic drainage

79
Q

how does hydrostatic pressure effect oedema

A

Increased hydrostatic pressure – constriction of veins impedes venous return, increase in venous pressure. Blood backs up in veins and capillaries, Pc increases leading to excessive filtration

80
Q

how does increased venous pressure effect oedema

A

occurs in heart failure from pulmonary oedema, pleural effusion, ascites and peripheral oedema

81
Q

what effects pulmonary oedema

A

due to increased hydrostatic pressure, increased capillary permeability (histamine release)

82
Q

what is Lymphoedema

A

Lymphoedema – lymphatic obstruction

83
Q

what is intrinsic blood flow

A

Arterioles affected by both mechanisms, but local mechanisms predominate in critical tissues Intrinsic (autoregulation) – exerted by local mechanisms within the tissues

84
Q

what is extrinsic control of blood flow

A

Arterioles affected by both mechanisms, but local mechanisms predominate in critical tissues

Extrinsic (neurohormonal regulation) – mechanisms from outside the tissue (nerves or hormones)

85
Q

how can arteriolar diameter and resistance be effected

A

Vasodilation- increases vessel diameter, increases blood flow
Vasoconstriction- decreases vessel diameter, decreases blood flow
Explain in detail the intrinsic (local) control of blood flow
Acute: rapid changes in local vaso- dilation or constriction of arterioles, metarterioles and precapillary sphincters

86
Q

describe the vasodilator theory that effects arteriolar diameter

A

increased metabolic rate results in increased formation of vasodilator substances (eg. Adenosine, adenosine phosphate compounds, CO2, histamine, K+, H+ ) which are released into the intercellular fluid and cause intense vasodilation.

87
Q

describe the O2 nutrient lack theory that effects arteriolar diameter

A

Smooth muscle of precapillary sphincters requires O2 to remain contracted. When O2 is high sphincters close, when O2 is low sphincters open. Deficiency of other nutrients may also result in vasodilation.

88
Q

what things can effect arteriolar diameter

A

Pressure - critical organs possess additional mechanisms- ensure constant perfusion despite altering arterial pressures
Metabolic – predominates (as above)
Myogenic – high pressure results in sudden stretch of vessels causing vasoconstriction, low pressure causes dilation
Long term: slow, controlled changes in flow over time. Due to increase or decrease in size, numbers of blood vessels supplying the tissues

89
Q

What are the consequences of prolonged vascular compression

A

O2 (nutrient) lack theory: Smooth muscle of precapillary sphincters requires O2 to remain contracted. When O2 is high sphincters close, when O2 is low sphincters open. Deficiency of other nutrients may also result in vasodilation.
Pressure - critical organs possess additional mechanisms- ensure constant perfusion despite altering arterial pressures
Metabolic – predominates (as above)
Myogenic – high pressure results in sudden stretch of vessels causing vasoconstriction, low pressure causes dilation
Long term: slow, controlled changes in flow over time. Due to increase or decrease in size, numbers of blood vessels supplying the tissues
Know the consequences of prolonged vascular compression.
Mechanical compression can reduce blood flow to tissues
If period of ischemia is prolonged – irreversible cell death can occur (infarction)
High alveolar pressure can compress pulmonary blood vessels

90
Q

Explain the role of the endothelial cell in autoregulation of blood flow.

A

Endothelial cells can produce substances that mediate relaxation or constriction of vascular smooth muscle

Activated by local: pO2, stretch, endothelial damage
Release: Nitric oxide and prostacyclin for dilation and endothelin 1 and thromboxane A2 for constriction

91
Q

Explain how neurohormonal (extrinsic) mechanisms regulate blood flow to non-critical organs.

A

Predominant in control of blood flow to non-critical organs (kidneys, splanchnic organs, resting skeletal muscle
If cardiac output is sufficient to maintain normal arterial pressure, blood flow to organs is determined by intrinsic mechanisms to match blood flow to metabolic needs
If CO cannot be increased to prevent decreased blood pressure, vasoconstriction of non-critical organs occurs

92
Q

what does neurohormonal control effect

A

primary function of neurohormonal regulation of arteriolar diameter = to adjust peripheral resistance (remember MAP = Q X TPR)

93
Q

what can influence neurohormonal control

A

adrenaline Sympathetic activity causes arteriolar constriction –
Direct effect- stimulate sympathetic nerves, release noradrenaline within individual = contraction of veins and arterioles
Indirect effect- sympathetic nerves to adrenal medulla cause secretion of noradrenalin and adrenaline into blood

94
Q

how is blood pressure controlled in the short term?

A 
effect of autonomic nervous system on TPR and cardiac pumping ability
- arterial baroreceptor reflex 
- chemoreceptor 
- muscle and joint receptor 
atrial volume receptor
95
Q

how does arterial baroreceptor reflex control blood pressure

A

pressure-sensitive nerve ending, monitor blood pressure, located in walls of carotid arteries and aortic arch. Detect stretching of walls, send afferent impulse to CNS – reflex alteration of cardiac output and vascular resistance to maintain BP Action potentials generated in baroreceptor afferent neurons

  • effected by posture as it changes the function
96
Q

how does arterial Chemoreceptors control blood pressure

A

sensitive to decreased oxygen and increased carbon dioxide. Located in aortic and carotid bodies

97
Q

how does Muscle and joint receptors control blood pressure

A

vasoconstriction or vasodilation of the arteries to send blood where its needed the most

98
Q

how does Atrial volume receptors control blood pressure

A

Sensory receptors in the large thoracic

veins and atria detect small changes in blood volume.

stretch receptors here will be affected.

Activation of atrial volume receptors has same effect as activation of baroreceptors.
Also act to alter blood volume by changes in water, salt (Na+) levels.

99
Q

Long term regulation of arterial blood pressure

A

primarily based on regulation of blood volume, mediated by kidneys and urinary output

100
Q

cardiovascular responses during exercise

A

local mechanisms increase blood flow to muscles, neural control via ANS cause increase in Q and vasoconstriction in non-critical organs, muscle and respiratory pump aid venous return

101
Q

cardiovascular response during decreased cardiac output eg haemorrhage

A

decreased preload, pressure and cardiac output. TPR increased due to vasoconstriction in the kidneys and splanchnic circulation, allows blood to critical organs. Immediate affects minimised by compensatory mechanisms initiated by baroreceptors and volume receptor reflexes
Long term affects cause lowering of capillary hydrostatic pressure, increasing fluid reabsorption, stimulation of thirst and restore plasma proteins and RBCs (takes longer)

102
Q

cardiovascular response during decreased cardiac output eg heart failure

A

reduced contractility limits cardiac output
Can lead to decompensation = exercise intolerance, oedema, uraemia and renal failure, septic shock
Left sided heart failure – pulmonary oedema
Right sided heart failure – systemic tissue oedema

VAP II (3 decks)

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