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Cardiopulmonary > Factors affecting cardiac performance and S&S of CVD > Flashcards

Factors affecting cardiac performance and S&S of CVD Flashcards

1
Q

What is pericardium

A

 Forms a fibrous covering around the heart holding it in a fixed position in thorax
 A tri-layer sac consisting of a tough, outer fibrous layer and a thin, inner serous layer
 Inner serous layer consists of a visceral layer and parietal layer
 Visceral layer (also known as epicardium) covers entire heart and great vessels

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2
Q

What does pericardium do

A

Provides physical protection and barrier to infection

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3
Q

What is myocardium

A

 Muscular portion of heart, forms the wall of atria and ventricles
 Dense structures, intercalated discs (unique to cardiac muscle), separate the cardia muscle fibres from neighbouring cardiac muscle cells

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4
Q

What is endocardium

A
  • Thin, three-layered membrane that lines the heart

- Innermost layer consists of smooth endothelial cells supported by a thin layer of connective laye

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5
Q

What blood flows in right side of heart

A
  • Receives deoxygenated blood from body

- pumps deoxygenated blood to lungs

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6
Q

What blood flows in left side of heart

A
  • receives oxygenated blood from lungs

- pumps oxygenated blood to body

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7
Q

what is systemic circulation

A

carries oxygenated blood away from heart to body tissues, and oxygen-depleted blood back to heart

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8
Q

what is pulmonary circulation

A

carries oxygen-depleted blood away from heart to lungs, and oxygenated blood back to heart

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9
Q

What is diastole

A

ventricles relax for filling

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10
Q

What is systole

A

ventricles contract to rapidly eject blood from ventricle

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11
Q

What is HR

A

no of times heart beats per min

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12
Q

what is Sv

A

volume of blood pumped from ventricles in 1 heart beat

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13
Q

what is CO

A

total volume of blood pumped by heart.min

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14
Q

what is ejection fraction

A

% of EDV (end-diastolic volume) pumped in one heart beat

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15
Q

Explain normal electrophysiology of heart

A

 SA node generates impulse atrial contraction begins
 Impulse displayed at atrioventricular node (AV node)
 Impulse passes to heart apex and ventricular excitation begins
 Ventricular excitation complete

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16
Q

What are functions of CV system

A

 Transport transporting oxygen, nutrients, meds, waste products for elimination
 Control system:distribution of Hormones
 Temperature regulation important to deliver heat to surface

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17
Q

What are the determinants of CO

A
  • HR
  • Preload
  • Contractility
  • Afterload
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18
Q

What are normal CO values at rest

A

5L/min

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19
Q

What are normal CO values with strenouse activity

A

15L/min

-in atheletes= 35L/min

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20
Q

What is the CO with severe heart failure

A

less than 4L/min

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21
Q

what is normal SV

A

60-130mL

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22
Q

what is the effect of PNS and SNS on HR

A

PNS–>decreases HR

SNS–.> increases HR

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23
Q

What are effects of increased HR on EDV and preload

A

end-diastolic volume falls and preload decreases

24
Q

what is the effect of chronotropes on HR

A

+ve chronotropes= increased HR

-ve chronotropes= decreased HR

25
Q

What is tachycardia

A

HR that exceeds the normal resting HR, hence a resting HR of >100 beats/min

26
Q

What is bradycardia

A

slower than normal HR, hence usually between 60-100 beats/min

27
Q

What is BP

A

pressure exerted by blood on arterial walls

28
Q

whats is BP regulated by

A
  • Arterial pressure
  • Effect of Cardiac Output (Q)
  • Effects of Total Peripheral Resistance (TPR)
  • Effect of hormones
29
Q

what is systolic and diastolic BP

A
  • Systolic BP: pressure during ventricular contraction (systole)
  • Diastolic BP: pressure during ventricular filling (diastole)
30
Q

what are the effects of CO on BP

A
  • If CO increases, arterial blood volume increases and therefore arterial pressure
  • If CO decreases, arterial blood pressure will decrease
31
Q

What is TPR

A
  • total peripheral resistance

- Determined by changes in diameter of the arterioles

32
Q

what are the effects of TPR on BP

A
  • Vasoconstriction: increases arterial pressure (AP)

- Vasodilation: decreases AP

33
Q

Effects of hormones on BP

A
  • ADH–> antidiuretic hormone

- causes reabsorption of water in kidneys= decreased blood volume

34
Q

What is Frank-Starling law

A
  • Within physiological limits, the force of contraction (of the heart) is directly proportional to the initial length of the muscle fibres
  • The ability of the heart to change its force of contraction and therefore stroke volume in response to changes in venous return
35
Q

define preload

A
  • Tension or stretch of myocardial fibres before contraction begins
  • Workload imposed upon the ventricle prior to contraction
  • Represents the amount of blood the heart must pump each beat
  • Largely determined by venous return to heart and accompanying stretch of the cardia muscle fibres
36
Q

Define afterload

A
  • The force required to eject blood from the heart–> force against which heart must pump
  • It is the work presented to the heart after contraction–>i.e. the ‘left over’ blood
  • The systemic arterial blood pressure is the main source of afterload work on the left heart and pulmonary arterial pressure is the main source of afterload work on the right heart
37
Q

Factors affecting preload

A
  • changes in circulating blood volume
  • changes in distribution of blood volume
  • atrial contraction
  • intrapericardial pressure,
  • pumping action of skeletal muscle
38
Q

How does circulating blood volume affect preload

A
  • decreased total blood volume= decrease preload

- increased total blood volume= increase preload

39
Q

How does distribution of blood volume affect preload

A
  • gravity causes blood to pool in LL, hence not much in thorax
  • if head-down tilt= increase in blood volume in thorax= increase preload
40
Q

How does atrial contraction affect preload

A

increased atrial contraction= increased preload

41
Q

READ NOTES

A

ON PRELOAD

42
Q

What factors affect afterload

A
  • Peripheral resistance

- Tension in ventricular wall

43
Q

How does peripheral resistance affect afterload

A
  • Compliance and radius of BV’s
  • Blood viscosity–>start to produce more haemoglobin to pick up oxygen= increases blood viscosity, making blood thicker= more work for heart

-Changes in pressure within vessels–>biggest determinant of right ventricular afterload will be constriction

44
Q

what is inotropic state of myocardia contractility

A

-Change in force and speed of shortening of heart muscles that in independent of changes in preload/afterload

45
Q

What are positive and negative inotropes

A
  • Positive inotropes–> digitalis, calcium, adrenaline/noradrenaline, caffeine
  • Negative inotropes–>beta blockers
46
Q

What are some factors related to contractility

A
  • SNS stimulation (fight and flight)
  • inotropes
  • phhysiological depresents
  • damage to myocardium, valves, conducting system
47
Q

What are the variables used to assess contractility

A
  • SV–> good indicator of ventricular performance; directly related to myocardial fibre shortening
  • Ejection Factor (EF)
  • Rate-pressure product (RPP)
48
Q

READ NOTES

A

ON RESPONSE TO INCREASED PRE/AFTERLOAD

49
Q

Define orthostatic intolerance

A
  • The inability of the cardiopulmonary system to maintain BP and adequate cerebral perfusion pressure against gravity
  • Development of S&S during upright standing that are relieved by recumbency
50
Q

how does bed rest for 24hrs or longer effect orthostatic intolerance

A
  • negative fluid balance occurs
  • Peripheral vasodilation occurs and cardiac filling pressure are reduced
  • decrease in SV below the excepted normal for individual in supine
  • Blood becomes more viscous–> increased risk of venous stasis, thromboembolism and DVT
  • diuresis (urine output)–> loss of blood volume
51
Q

effect of lying-standing on Blood distribution

A
  • 700ml blood loss from thorax
  • Decreased SV and CO
  • Compensatory increase in HR and peripheral vasoconstriction to increase peripheral vasoconstriction
52
Q

effect of standing-lying on Blood distribution

A
  • Acute increase in thoracic blood volume which results in an increased preload (venous return)
  • Hence increase in SV and CO
  • In order to maintain constant BP, compensatory decrease in HR, peripheral vascular resistance and diastolic BP occurs
53
Q

effect of standing inactively for 20mins on Blood distribution

A
  • increased hydrostatic pressure in feet
  • Leads to transudation of fluid from vasculature into interstitial tissues
  • Results in increase in plasma volume interstitial tissues
  • Net effect within body is a reduced absolute blood volume
  • Called Relative Hypovolaemia–>systemic BP is reduced as a result
54
Q

Orthostatic intolerance S&S

A
  • Decreased BP
  • Increased HR–>in an attempt to compensate the low stroke volume
  • Weak pulse–>it is a result of the reduction in SV and BP (this reflects the low pulse volume)
  • SNS–> dizziness, fainting (syncope), pallor, sweating, tremor, nausea
55
Q

Orthostatic intolerance management

A
  • Acute–>activate muscle pump, elevate legs
  • Prevention
  • Avoid/correct hypovolaemia–> decreased volume of circulating blood in body
  • Gravitational stimulus
  • Early mobilisation–> dangling, sit out of bed

Cardiopulmonary (4 decks)

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