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Cardiovascular Flashcards

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1
Q

Stenosis…

A

Leads to decreased blood flow, and establishes a collateral circulation

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2
Q

What does the lymphatic system transport?

A

Interstitial fluid
Bacteria
Cellular debris
Cells eg lymphocytes

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3
Q

Functions of the cardiovascular system (x 6)

A 
Distribute metabolic substrates to the tissues
Removal of waste
Movement of immune cells
Regulation of body water
Maintain internal temperature
Transport signalling molecules
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4
Q

What are the 3 types of pacemaker?

A

Main= sino-atrial node
Secondary- atrio-ventricular node
Back-up= myocytes

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5
Q

Electrical impulse

A
  1. AP initiated in SA node -> AV node
  2. Cells of AV slow the impulse
  3. -> ventricles via bundle of His
  4. AV bundle divides into L and R branches
  5. Spread to contractile cells of ventricle via Purkinje fibres
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6
Q

What is the function of gap junctions?

A

Allow spread of AP through myocardium

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7
Q

What is the refractory period?

A

Gap between heart beats to prevent tetanic contraction

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8
Q

Sinus arrythmia

A

Slowing of SA node on expiration, speeds up on inspiration

Helps preserve cardiac output

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9
Q

Complete heart block

A

Top and bottom of heart are not electrically connected => independent QRS

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10
Q

Ectopic beat

A

Extra heart beat => wider QRS

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11
Q

Atrial fibrilation

A

Strain on the top of heart => irregularly irregular beat

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12
Q

Ventricular fibrilation

A

Completely disorganised contraction => no QRS

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13
Q

Cardiac cycle

A
  1. Diastolic ventricular filling
  2. Isovolumic contraction
  3. Systolic ejection
  4. Isovolumic relaxation
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14
Q

Diastolic ventricular filling

A

Aortic valves open

Atria contract to fill

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15
Q

Isovolumic contraction

A

Aortic valves shut

Pressure but no flow

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16
Q

Systolic ejection

A

Valves open

Blood pushed out

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17
Q

Isovolumic relaxation

A

Early diastole

Valves shut

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18
Q

Cardiac power

A

= force x velocity

= pressure x flow rate

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19
Q

Stroke volume (SV)

A

= End diastolic volume (EDV) x end systolic volume (ESV)

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20
Q

Ejection fraction (LVEF)

A

= SV / EDV

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21
Q

Cardiac output (CO)

A

= heart rate x stroke volume

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22
Q

Blood pressure

A

Force exerted per unit blood

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23
Q

Variables for haemodynamics (x 7)

A 
Heart rate
Blood pressure
Volume
Flow
Blood velocity
Power
Vascular resistance
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24
Q

What does the endoderm induce in vasculogenesis?

A

Mesoderm (visceral/splanchnic) -> angioblasts -> endocardial tubes

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25
What do the endocardial tubes fuse laterally to form?
Primitive heart tube
26
What does the endocardium become?
Endothelial lining of the heart
27
What does the myocardium become?
The muscular wall of the heart
28
What does the epicardium become?
The outer surface of the heart and the coronary arteries
29
What is the function of cardiac jelly?
To separate the myocardium and endocardium
30
Which vessels are at the cranial end of the developing heart?
2 dorsal aortae -> 1 aorta
31
Which vessels are at the caudal end of the developing heart?
Sinus venosus (common cardinal, umbilical and vitelline veins)
32
Which 5 dilations does the heart tube grow into?
``` Ventricle Atrium Sinus venosus Truncus arteriosus Conus arteriosus ```
33
When does the heart tube fold into 4 chambers?
Day 23
34
Where does the bulbus cordis move?
Caudally, ventrally and to the R
35
Where does the primitive ventricle move?
To the L
36
Where does the primitive atrium move?
Cranially and dorsally
37
What forms the smooth walls of the ventricle?
Conus arteriosus
38
What forms the trabeculated part of the ventricle?
Primitive ventricle
39
How do the atria form?
LA wall outgrows into 1 pulmonary vein -> L and R -> bifurcate into 4
40
What happens to the left atrium at week 5?
Veins are intusscepted into the LA wall
41
When does septation occur?
Week 4
42
Interatrial septation
Septum primum divides atria and extends => foramen primum. | AV boundary lining -> dorsal/ventral cushions -> AV septum
43
At what week do the septum primum and AV septum fuse?
Week 6
44
By what week does the sinus venosus degenerate?
Week 5 - R horn -> smooth part of RA wall - L horn -> oblique vein of RA and coronary sinus
45
How does the foramen secundum form?
From the apoptosis of the septum primum
46
How does the septum secundum form?
From the dorsal wall of the atrium | - opening in it forms the foramen ovale
47
Interventriuclar septation
Muscular projection from the floor -> endocardial cushions. Leaves interventricular foramen- membranous part projects to close
48
Contruncal septation
Truncus arteriosus divided into 2 by conotruncal swellings -> fuse to form sprial septum (separates pulm. trunk and aorta)
49
In the foetus, how does blood pass from RA to LA?
Via the foramen ovale
50
Where does the poorly oxygenated blood in the RA pass through?
Ductus arteriosus
51
Ductus venosus ->
Ligamentum venosum
52
Foramen ovale ->
Fossa ovalis (greater pressue in LA on 1st breath)
53
Ductus arteriosus ->
Ligamentum arteriosum (increase in O2 sats, decrease in prostaglandins)
54
Dextrocardia
Abnormal cardiac looping or induced in gastrulation (wk 5). - associated with abnormal bv connection or septation
55
Patent ductus arteriosus
Allows blood to shunt aorta -> pulm artery => increase workload of heart => hypertension, ventricular hypertrophy and heart failure
56
Treatment of patent ductus arteriosus
Prostaglandins
57
Atrial septal defects
Failure of septa 1 and 2 to close at birth, due to probe patent foramen ovale
58
When is surgery required for atrial septal defects?
When pulmonary hypertension occurs
59
Ventricular septal defects
Allows L to R shunt of blood => RV hypertrophy and pulmonary hypertension
60
Which ventricular septal defect will resolve as the child grows?
Muscular
61
What are conotruncal defects due to?
Abnormal migration of neural crest cells
62
Persistent truncus arteriosus
Conotruncal septum is absent -> cannot fuse with IV septum | Blood mixes -> poor O2 delivery => cyanosis, breathlessness, lethargy and delayed growth
63
Transposition of the great vessels
Conotruncal septum is straight, so aorta from RV and pulm artery from LV Incompatible with life unless accompanying shunt
64
Tetralogy of Fallot
Unequal division of truncus arteriosus
65
What are the 4 features of tetralogy of Fallot?
Pulmonary stenosis VSD Overriding aorta RV hypertrophy
66
What is coarctation of the aorta?
Narrowing near the ductus arteriosus
67
Preductal coarctation
DA obliterates -> hypoperfusion of lower body | Prostaglandins needed to keep DA open
68
Postductal coarctation
Collateral circulation established
69
What enters cardiac muscle to initiate contraction?
Calcium
70
Cardiac functional reserve
The capacity to augment performance on demand eg exercise, illness and pregnancy
71
Cardiac reserve
Max cardiac output - cardiac output at rest
72
What is the effect of autonomic input on stroke volume?
Prolonged opening of Ca channels -> enhanced action of contraction coupling mechanisms
73
What do small changes in sarcomere length lead to?
Large variations in tension
74
What is the effect of stretching the LV?
Aids contraction -> increase in preload -> increased performance
75
How does muscle stretching lead to more contraction?
The myofibril is reduced -> filaments are closer together -> more myosin/actin interaction => more contraction
76
What causes a L shift on the Frank-Starling curve?
Exercise, adrenalin/noradrenaline pharma stimulation
77
What causes a R shift on the Frank-Starling curve?
Myocardial loss and pharma depression
78
When is preload best measured?
At end diastolic volume
79
How to NAd/Ad cause L shift?
Stimulate cAMP -> more calcium entry -> more cross linking
80
How does the body compensate for a failing ventricle?
The SNS overactivates, and RAAS systems kicks in to increase preload -> LV stretch
81
Mean systemic arterial pressure=
CO x total peripheral resistance
82
How is preload increased? (x 6)
``` Increased circulating vol Decreased venous compliance Increased atrial filling and contraction Decreased heart rate Increased ventricular compliance Increased aortic/pulmonary pressure ```
83
What is the Bowditch effect?
Increase in HR -> increased force of contraction
84
Systemic sympathetic actions
RAAS activation -> increased central venous P and total peripheral resistance Suprarenal stimulation -> catecholamines
85
What are the effects of angiotensin II?
Vasoconstriction | Salt and water retention
86
What are the effects of aldosterone?
Salt and water retention
87
What is the effect of vasopressin (ADH)?
Water retention
88
What are the parasympathetic actions on the heart?
Lower heart rate (chronotrophy) Decreased AV conduction (dromotrophy Decreased atrial contractility (inotrophy)
89
What are the sympathetic actions on the heart
Increased heart rate (chronotrophy) Increased AV conduction (dromotrophy) Increased atrial contractility (inotrophy) Increased myocardial relaxation (lusitrophy)
90
Receptors in the heart
B1/2- stimulate NAd release A2- inhibit NAd release B1- stimulates contraction
91
Receptors in blood vessels
B1/2 and A2- stimulate NAd release A1- stimulates contraction B1- stimulates relaxation
92
A1 adrenergic receptors
For hypertension- inhibit peripheral motor tone
93
Non-selective B2 antagonists
Hypertension and angina (lower heart rate and contractility)
94
Non-selective B1/A1 antagonists
Heart failure and severe hypertension
95
B1 selective antagonists
Hypertension and angina | eg. atenolol
96
Side effects of beta blockers
Bronchoconstriction, heart failure, bradycardia, hyperglycaemia, fatigue and cold extremities
97
Calcium channel blockers
Act on smooth and cardiac muscle to reduce vascular tone and contractility eg. amlodipine and veramapril
98
ACE inhibitors
Stop conversion of angiotension I -> II. For hypertension, LV hypertrophy and to prevent a secondary MI eg. ramipril, lisinopril
99
Angiotensin II receptor blockers
Prevent vasoconstriction, reduced ADH and aldosterone secretion. For hypertension, heart failure and nephropathy eg. valsartan, losartan
100
Nitrovasodilators
For angina, ACS, acute + severe hypertension and oedema | ed nitroprusside
101
Warfarin
Inhibits vit K epoxide reductase
102
Heparin
Unfractioned- targets thrombin and factor 10a
103
What are the 3 types of blood flow?
Laminar Turbulent Single-file
104
What is active hyperaemia?
An increase in local blood flow in response to an increase in local metabolic activity
105
Atherosclerosis
1) Endothelial injury 2) Lesion develops as a plaque in intima of artery wall- lipid core with fibrous cap 3) Cap calcifies 4) Collagen exposure stimulates thrombus formation

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