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CP+R > CV System > Flashcards

CV System Flashcards

1
Q

Function if cv system

A 
Gaseous exchange 
Nutrition and waste transport 
Hormones 
Immune system function 
Temperature regulation
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2
Q

Artery supping brain

A

Carotid artery

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3
Q

Artery supplying arms

A

Subclavian artery

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4
Q

Artery supplying stomach and intestines

A

Mesenteric artery

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5
Q

Artery supplying liver

A

Renal artery

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6
Q

Artery supplying lower limbs

A

Iliac artery

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7
Q

Layers of the heart

A 
Endocardium 
Myocardium 
 - 75% of heart muscle mass 
 - electrical signals pass through 
Epicardium 
Pericardium
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8
Q

Stages of the cardiac cycle

A 
Artrial contraction 
Isovolumetric contraction
Ventricular ejection 
Isovolumetric relaxation 
Artrial filling 
Ventricular filling
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9
Q

Describe the SA node

A

Located in RA
Pacemaker
Naturally beats at 100 bmp
Altered by sympathetic and parasympathetic

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10
Q

Why does the AV node delay the impulse slightly

A

Allows time for atria to fully contract and blood to enter the ventricles

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11
Q

Stages of an ecg and what they show

A

P wave - atrial depolarisation
QRS complex - ventricular depolarisation
T wave - ventricular repolarsation

PR interval - time between atrial and ventricular depolarisation

ST segment - ventricular repolarisation

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12
Q

Describe cardiac cells

A

Involuntary
Striated
Branched

Intercalated discs
Gap junctions
Desmosomes
Increased mitochondria

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13
Q

3 layers of blood vessels

A

Tunica externa - fibrous outer layer
Tunica media - muscular layer
Tunica intima - inner layer, secretes key nutrients and signals

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14
Q

Name the left Coronary arteries and where the supply

A

Left coronary artery - LA and LV
Left anterior descending - LV, septum and bundle of his
Circumflex - posterior or heart

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15
Q

Name the right coronary arteries

A

Right coronary artery - RA, RV and LV
Posterior descending
Right marginal artery

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16
Q

Stages of atherosclerosis

A

Damaged endothelium
LDL penetrates into the intima and attracts monocytes
Monocytes attach your LDL to form foam cells and clusters to make fatty plaques
When the foam cells die they release lipid signalling, smooth muscles cells migrate to intima
Cells divide and form protein and collagen matrixes enlarging plaque size
Plaque is prone to rapture and thrombus formation

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17
Q

What is angina

A

Pain experienced when O2 demand exceeds O2 supply

Ischemia causing pain

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18
Q

Signs and symptoms of angina

A

Tightness, burning or dull pain in chest pain or heavy feeling in left arm
Pain or discomfort radiating to jaw
Breathlessness on exertion

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19
Q

Role of valves

A

Prevent backflow

Open and close with pressure changes

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20
Q

Name the 4 main heart valves and their location

A

Mitral - LA->LV

Aortic valve -LV -> aorta

Tricuspid - RA -> RV

Pulmonary - RV-> pulmonary artery

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21
Q

Arrhythmia

What?

A

Not a sinus rhythm

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22
Q

Causes of arrhythmia

A 
Heart attack 
Mi 
Heart failure 
Valve disease 
Cardiomyopathy
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23
Q

Describe atrial fibrillation

A

Most common
Rapid/irregular impulses in atria
Caused by numerous abnormal foci

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24
Q

Symptoms of atrial fibrillation

A

Palpitations
Irregular pulse
HTN at high HR

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25
Q

AF care pathway

A 
Diagnose - ecg, 24h ecg, loop recorder 
Prevent stroke - anti coagulation drugs 
Rate control - slow HR and protect LV 
Rhythm control - anti-arrhythmias 
Interventions - cardioversion, catheter ablation
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26
Q

Describe atrial flutter

A

Electrical impulse from SA node form an irregular current
Impulse circulates very fast
Ventricles can’t beat that fast
Often progresses to AF

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27
Q

Bradycardia

A

HR <60bpm

Causes

  • normal/fitness
  • SA node issue
  • heart block

Only a concerned when combined with dizziness

28
Q

Describe Ventricular tachycardia

A

Rapid hr in ventricles
Can’t fill and contract efficiently
May be brief and harmless
Long lasting cab become life threatening

29
Q

Describe Ventricular fibrillation

A

Radio chaotic electrical impulse causes ventricles to quiver ineffectively

May occur after a Mi
Can escalate to cardiac arrest and be fatal

30
Q

Ectopic beat

A

Early or extra heart beat originating somewhere other than the SA node

Common and usually harmless
Can develop into life threatening arrhythmia

31
Q

Method to diagnose arrhythmias

A

Alivecore

Loop recorders

Ecg

32
Q

Arrhythmia interventions

A

Cardioversion

  • shock heart back into normal rhythm
  • treats symptoms not cause

Cardio ablation

  • uses guide catheter
  • stimulate heart to have an arrhythmia to see where it originates
  • burn it freeze cels causing it
33
Q

Describe pacemakers

A

Artificially replace the hearts intrinsic pacing

Can be single, dual or biventricular

34
Q

Describe what the 4 numbers on a pacemaker stand for

A

I - which chamber being paced - A,V or D
II - sensing for hearts intrinsic signals - if it sensed a natural signal, it will not stimulate - 0 A, V or D
III - the response to II - inhibited, triggered or Dual
IV - rate responsiveness, special sensor detects movement and helps HR adjust to meet demand

35
Q

What do ICDs do

A

Send inplules to regulate abnormal and dangerous rhythms

36
Q

what is stenosis

A

when a valve doesnt open properly

reduces blood flow

37
Q

what is a regergitant valve

A

a valve that doesnt close properly

blood back flows

38
Q

effect of atrial stenosis

A

increased LV workload

LV hypertrophy - not functional, reduced LV size

39
Q

effect of atrial regergitation

A

increased LV workload, LV dilation

40
Q

what is mitral stenosis and effect

A

fulid on the lungs

41
Q

what is the effect of mitral regergiataion

A

LA dilation

LV failure

42
Q

causes of a murmur

A

Rheunmatic fever - not common in UK
calcifiation - atherscolersis, progressive
bicuspid - 2 leaflets rather than three

43
Q

symptoms of a heart murmur

A

dysponea
syncope
angina
fatigue

44
Q

diagnosis of a murmur

A

echocardiogram

45
Q

medications

A

Reduce HTN

anti coagulatants

46
Q

interventions of a heart murmuer

A

valve replacement

TAVI

47
Q

pros and cons of a mechanical valve

A

last indefinetly

require anti coagulant medication
open heart surgery

48
Q

what is hypertrophic cardiomyopathy

A

LV becomes thickened and stiff reducing ability to contract and relax
weaker contractions

49
Q

what is dialted cardiomyopthay

A

LV becomes weak and enlarged which reduces it abilty to pump

50
Q

what is arrhythmogenic cardiomyopthy

A

fat and scar tissue infiltrates heart muscle effecting electrical pathways

51
Q

causes of cardiomyopthay

A

genetic
lifestyle
pregency/virus

52
Q

symptoms of cardiomyopathy

A 
teird
dizzy 
SOB 
chest pain 
swelling in stomach and ankles
53
Q

how is left ventricle dysfunction measured

A

using ejection fraction

50-70% is normal

54
Q

what is heart failuer

A

inability of heart to meet oxygen demands of the tisues

55
Q

classes of heart failure

A

I - no symptoms
II - mild symptons, occasional swelling, activites somehwat limited
III - noticable limitaions, comforatble only at rest
IV- unable to do any form of PA, symptoms at rest

56
Q

Symptoms of heart failure

A

fatigue
SOB
Chest pain
swelling in stomach and ankles

57
Q

diagnosis of heart failure

A

ECHO - ultrasound of the heart, non invasive, structure and function of heart, allows you to take measurements

Cardiac MRI - non invasive, high res image

58
Q

causes of myocaridal infarction

A

reputed plaque and thrombus formation which occludes the lumen
irreversible death of cardiac tissue

59
Q

presentation of an MI

A

similar to angina

  • intense pain/pressure in the chest
  • radiation to throat and arm
  • indigestion
  • nausea/vomiting
  • weakness
  • breathlessness
  • fear of impending doom
60
Q

what is a STEMI

A

st elevated MI

ST elevation on ecg
raised troponin

= full thickness heart damage

61
Q

whats is a NSTEMI

A

no st elevation
raised troponin

= partial thickness damage to heart muscle

62
Q

mycocardial perfusin test

A

thallium injected into veins
ischemic or necrotic cells will not take up thallium
shows site and size of ischemia
can be done at rest or exercise

63
Q

angiography

A

radioplaque dye injected via cathetre into coronary arteres
visible of xray, CT and MRI
local anaesthetic
Measures
- site, number and severity of stenosis
- helps determine best cause of treatment

64
Q

CT Coronary angiogram

A

much less invasive
xray blood flow through heart
dye injected into vein in arm

65
Q

CT fractional flow reserve

A

new technique
computer based non-invasive CTCA
coronary mapped out
evaluates the haemodynamic relveance of stenosis
- measures flow rate before and after stenosis size change and treatments

CP+R (5 decks)

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