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Cardiovascular > basics of physiology > Flashcards

basics of physiology Flashcards

1
Q

What part of the CVS is in series?

A

Pump to the lungs and pump to the tissues

Gut to the liver

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2
Q

What part of the CVS is in parallel?

A

Most body tissues

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3
Q

Which organs take the largest amount of blood?

A

Abdominal organs, Kidneys and skeletal muscle

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4
Q

Which organs take the smallest amount of blood?

A

Heart, skin

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5
Q

Which organs take the largest amount of oxygen?

A

skeletal muscle, abdominal organs

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6
Q

Which organs take the smallest amount of oxygen?

A

skin, kidney

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7
Q

Equation: Flow in a tube =

A

Change in pressure / Resistance
The pressure difference is the mean atrial pressure – the central venous pressure. The resistance is controlled by the radius.

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8
Q

What is regional distribution of blood controlled by?

A

Arterioles

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9
Q

What is fractional distribution of blood controlled by?

A

venules

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10
Q

What is the excitation - contraction coupling in the heart called?

A

Functional syncytium

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11
Q

What does a functional syncytium involve?

A
  • Gap junctions = Electronic connection

- Desmosomes = Physical connection (intercalated discs)

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12
Q

Where does Ca 2+ come from in the cardiac muscle

A 
Sarcoplasmic reticulum (Doesn't saturate)
Outside cells (Regulation of cardiac contraction)
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13
Q

key features of a cardiac muscle contraction

A
  • Long AP
  • Long refractory period
  • No tetanus
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14
Q

What are pacemaker cells ?

A

Unstable resting membrane potential and will spontaneously depolarise.
AP occurs because of a Ca2+ increase.
Found in SA node

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15
Q

Only non-conducting part of the heart

A

Annulus fibrosis

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16
Q

What is the delay box of the heart?

A

AV node

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17
Q

Path of electrical signal through the heart

A 
SA node
Atrial contraction 
VA node 
Bundle of his 
Purkinje system 
ventral contraction
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18
Q

What are the key elements of a ECG

A

P wave corresponds to atrial depolarisation
QRS complex corresponds to ventricular depolarisation
T wave corresponds to ventricular repolarisation

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19
Q

What is 1st degree block

A

Increase between p and QRS complex

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20
Q

What is 2nd degree block

A

Increasing delay between P and QRS

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21
Q

What is 3rd degree block

A

No p waves

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22
Q

What is atrial flutter

A

Rapid depolarisation. Saw tooth pattern.

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23
Q

What is atrial fibrillation

A

Less crazy looking than atrial flutter

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24
Q

What is ventricular fibrillation

A

Totally uncoordinated

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25
Q

What is standard limb lead I

A

L arm to R arm

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26
Q

What is standard limb lead II

A

L leg to R arm

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27
Q

What is standard limb lead III

A

L leg to L arm

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28
Q

On SLL II what does a depolarisation moving toward the L leg look like ?

A

Upward spike

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29
Q

On SLL II what does a repolarisation moving toward the L leg look like ?

A

Downward spike

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30
Q

On SLL II what does a depolarisation moving away the L leg look like ?

A

Downward spike

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31
Q

On SLL II what does a repolarisation moving away the L leg look like ?

A

Upward spike

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32
Q

What is the PR interval?

A

normally 0.12 s Time from P to start of QRS

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33
Q

What is the QT interval?

A

normally 0.42 s Time from start of QRS to end of T

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34
Q

Why is R bigger than P and T ?

A

SLL II lead in same direction that the bulk of the ventral depolarisation is in

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35
Q

How many ALLs are there

A

3

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36
Q

How many SLLs are there

A

3

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37
Q

How many PCLs are there

A

6

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38
Q

What plane the PCLs look at

A

Transverse

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39
Q

Will V1 be -ve or +ve

A

negative

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40
Q

Rhythm strip settings

A

25mm/sec

Calibrating pulse should be 0.2s so that it lies over 1 box

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41
Q

Difference between STEMI and NSTEMI ?

A

ST elevation in STEMI

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42
Q

What is the normal range for the QRS complex?

A

2-4 little boxes

43
Q

What heart rate is considered bradycardia and what is considered tachycardia?

A

Over 100 or under 60

44
Q

Stages of cardiac cycle

A 
Late diastole 
Atrial systole 
Isovolumetric ventricular contraction 
ventricular ejection 
isovolumic ventricular relaxation
45
Q

What is the ejection fraction?

A

SV/EDV

46
Q

What is a phonocardiogram ?

A

Heart sounds as a result of turbulence

47
Q

When are heart sounds heard?

A

Closure of mitral and tricuspid valves
Closure of aortic and pulmonary valves
(Rapid passive filling and active filling phases)

48
Q

What causes systolic murmour

A

Aortic/pulmonary stenosis

mitral/tricuspid regurgitation

49
Q

What causes a diastolic murmur?

A

Aortic / pulmonary regurgitation

mitral / tricuspid stenosis

50
Q

What causes a continuous murmur?

A

Septal defect

51
Q

Regulation of the heart

A
  • Pacemakers
  • Sympathetic NS noradrenaline B1 in SA depolarise
  • Adrenal medulla Adrenaline B1 in SA
  • Parasympathetic (vagus) AcH muscarinic SA hyperpolarise
52
Q

energy of contraction proportional too

A

initial length of muscle fibres

53
Q

The greater the volume of blood in the heart …

A

The longer the muscle fibres and stronger the contraction to a certain length of muscle fibres.

54
Q

What is the afterload?

A

The load against which the muscles tried to contract i.e. the resistance in the rest of the system

55
Q

what is stroke volume ?

A

The volume of blood that is pushed out of the heart in each contraction

56
Q

What is preload?

A

How full the ventricles are before starting contracting

57
Q

Cardiac output =

A

heart rate x stoke volume

58
Q

What is the systemic filing pressure?

A

pressure difference which move blood back to the heart

59
Q

Where is blood flow the greatest ?

A

Largest vessels because they have a smaller total lumen size

60
Q

Things which influence flow in the veins

A
  • Gravity
  • Skeletal muscle pump
  • Respiratory pump
  • Vasomotor tone
  • Systemic filling pressure
61
Q

What is the skeletal muscle pump?

A

Contraction of the leg muscles pushes blood back

62
Q

What is the respiratory pump ?

A

Increased rate and depth of breathing lowers the pressure in the heart pulling blood in.

63
Q

What is the vinometer tone?

A

Smooth muscle contraction of vessels moves blood

64
Q

Endothelium mechanisms which prevent clot forming in the wrong place

A

Prevents blood contracting collagen
Prostacyclin’s and nitric oxide stops platelets binding to each other
Tissue factors inhibit thrombin production
Thrombomodulin and heparin inactivated thrombin
Tissue plasminogen converts plasmin and digests clots

65
Q

Which direction does hydrostatic pressure push blood?

A

out of capillaries

66
Q

How much blood goes out of the capllarie?

A

20l

67
Q

How much blood goes into the capillaries ?

A

17 l

68
Q

How is peripheral circulation regulated?

A
  • Control arteriolar radius
69
Q

Levels of control of smooth muscle

A

Local (flow to meet the needs of individual tissues)

Central (total peripheral resistance)

70
Q

types of local control

A

Active hyperaemia - Ions causes endothelium to produce signalling molecules which increased flow
Autoregulation - Decrease in perfusion causes decrease in flow
Reactive hyperaemia - occlusion causes increased blood flow
Injury response - Increased blood flow

71
Q

types of central control

A 
Sympathetic nerves decrease flow 
coronary circulation 
cerebral circulation 
pulmonary circulation 
renal circulation
72
Q

How is MAP regulated

A

Baroreceptors in the aortic (Vagus) arch and carotid sinus (Glossopharyngeal)
Chemoreceptors

73
Q

What is the Valsalva manoeuvre

A

forced expiration when not allowing air out

74
Q

Stages of the Valsalva manoeuvre

A
  • Increase in BP
  • Reduced filling pressure
  • Reduced venous return
  • reduced end diastolic volume
  • reduced stoke volume
  • Reduced cardiac output
  • Reduced mean atrial pressure
  • Baroreceptors kick in
  • Manover ends and decreased thoracic pressure passes through the heart causing a further drop in BP
  • return to normal
75
Q

Long term mediation of BP

A

Kidneys

76
Q

Kidney process used to regulate BP

A

Renin-angiotensin-aldosterone system. Reacts to a drop in BP by increasing BP.
Antidiuretic factor. reacts to a drop in BP by increasing BP.
ANO and BNP react to an increase in BP and lower BP

77
Q

What is an acute coronary syndrome?

A

New onset collection of symptoms relating to a problem in the coronary artery.

78
Q

What evidence do you need in order to diagnose myocardial infarction?

A

Evidence of cardiac cell death (Detected on a blood test) i.e. Troponin
+ symptoms or ECG changes or etc

79
Q

What is dual antiplatelet therapy?

A

300mg of Aspirin given immediately and then 75-100mg each day thereafter. + the P2Y12 inhibitors

80
Q

Treatment for STEMI

A
  • Thrombolysis
  • Dual antiplatelet therapy
  • Get in Cath lab ASAP for reperfusion therapy
81
Q

How do most thrombolytic agents work?

A

They are serine proteases converting plasminogen to plasmin. Plasmin then breaks down clots.

82
Q

Treatment for NSTEMI and other ACSs

A
  • Aspirin (Dual platelet)
  • Ticagrelor
  • Platelet aggregation i.e. P2Y12 inhibitors
  • Beta blockers
  • GTN
83
Q

What is the ending of CCBs

A

-pine

84
Q

What is the ending of ACEis?

A

-pril

85
Q

What is type I MI ?

A

Spontaneous MI due to a primary coronary event

86
Q

What is type II MI ?

A

Due to imbalance of supply and demand of oxygen

87
Q

On an ECG what is used to determine if a patient has a STEMI or NSTEMI ?

A

ST elevation normally or ST depression

88
Q

Surgical intervention for ACSs

A 
Reperfusion therapy (In a cath lab with a balloon and stents)
Also called a PCI or angiogram. There are some risks of bleeding.
89
Q

What is a stoke?

A

Neurological deflect which has sudden onset and lasts more than 24 hours and has vascular origin int he brain.

90
Q

Two types of stoke

A

Haemorrhages (Rupture in the vessel wall) high death rate

Ischemic (blockage)

91
Q

Three types of ischemic stoke

A

Large artery disease i.e. carotid stenosis where there is thrombus formed at the bifurcations, emboli then occurs.
Cardioembolic stoke. I.e. atrial fibrillation causes a clot to from in the LA
Small vessel stoke where little vessels in the brain get occluded. Lots of damage because nerves are so close together.

92
Q

Treatment for stoke

A
  • Get patient into a stoke unit
  • Give them aspirin
  • Alteplase (A type of thrombolysis)
  • Clot retrieval
93
Q

Name of Classification system used for stoke

A

Vaughan-William classification system

94
Q

What are class 1A Antiarrhythmics

A

Moderate sodium channel blockers i.e. Quinidine

95
Q

What are class 1B Antiarrhythmics

A

Weak sodium channel blockers i.e. Lidocaine

96
Q

What are class 1C Antiarrhythmics

A

Strong sodium channel blockers i.e. Flecainide

97
Q

What are class 2 Antiarrhythmics

A

B- adrenergic receptor antagonist’s i.e. Atenolol, and Bisoprolol

98
Q

What are class 3 Antiarrhythmics

A

Prolong refractory i.e. Aminodarone

99
Q

What are class 4 Antiarrhythmics

A

Calcium channel blockers i.e. Diltiazem and verapamil

100
Q

other important antiahhyrmias

A

Digoxin - Inhibits sodium potassium pump

101
Q

Important anticoagulation drugs

A
  • Warfarin
  • Dabigatran
  • Rivaroxaban (All end in Ban)
102
Q

What system is used to determine if a patient is at risk of stoke?

A

CHADSVASC

103
Q

What scoring system is used to determine the risk of giving warfarin ?

A

HADBLED

Cardiovascular (2 decks)

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