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REVISION BDS > Cardiovascular system > Flashcards

Cardiovascular system Flashcards

1
Q

layers of heart

A

pericardium

epicardium

myocardium

endocardium

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2
Q

pericardium

A

made of fibrous and serous pericardium (which in turn has a visceral (inner) and parietal (outer) component)

at inferior edge of pericardium is teh pericardial space which is filled with fluid to allow movement between pericardium and epicardium

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3
Q

epicardium

A

with coronary blood vessels

slippery tissue which has the vessels that supply the heart contained within

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4
Q

myocardium

A

with trabeculae carnae

cardiac muscle responsible for hearts pumping action

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5
Q

endocardium

A

endothelial lining of the chambers of the heart which is continuous with the vessels supplying the heart

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6
Q

right artrium

A

receives deoxygenated blood from SVC and IVC

blood then passes though tricuspid valve

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7
Q

right ventricle

A

series of ridges known as trabeculae carnae made of myocardium projections

some of these trabeculae from papillary mauscles which connect to the tricuspid valve via chordae tendineae

deoxygenated blood then passes from RV to the L and R Pulmonary arteries through the pulmonary valve to the lungs

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8
Q

left atrium

A

receives oxygenated blood from the 4 pulmonary veins

blood passes through the LA to the LV via the bicuspid (mitral valve)

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9
Q

left ventricle

A

blood passess from LA to LV and is then ejected via the aortic (semilunar) valve

the blood passes into the ascending aorta and out to the body

some blood also goes to the coronary vessels

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10
Q

conduction of heart carried out by

A

Autorhythmic fibres

these fibres set the rhythm of the heart but also the path in which the rhythm is conducted

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11
Q

sequence of heart conduction

A
  1. Starts at Sino Atrial Node in the RA with spontaneous depolarisation
  2. Reaches the Atrioventricular Node which is the junction between RA and RV
  3. The conduction then reaches the Bundle of His which is the only site where Atrio-Ventricular conduction can occur as the fibrous skeleton of the heart usually separates A from V
  4. The fibres then branch left and right into the bundle branches through the interventricular septum
  5. Finally large diameter purkinje fibres conduct the action potentials into the trabeculae carnae of the myocardium to aid with ventricular contraction
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12
Q

cardiac action potention

A

contractile working fibres after SA node

depolariation

plateau

repolarisation

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13
Q

depolarisation stage in cardiac action potential

A

stage 0

rapid depolarisation by Na+ ions efflux

channels close soon after

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14
Q

plateau stage in cardiac action potentials

A

stages 1 and 2

Ca2+ ions maintain the depolaristion level by equalising the K+ outflow

increased calcium ion concentration ultimately triggers heart muscle contraction

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15
Q

repolarisation stage in caridac action potential

A

stage 3

Ca2+ begin to close

K+ channels begin to open

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16
Q

production of ATP in the heart

A

mostly comes from oxidation of glucose and fatty acids

  • smaller contributions from Lactic Acid, amino acids and ketone bodies
  • some also produced by creatinine phosphate

dying/injured cells release creatinine into the blood - diagnostic sign

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17
Q

electrocardiogram ECG

A
  1. Raising part of P-Wave = Depolarisation of Atrial contractile fibres
  2. Descending part of P- Wave = Atrial Systole
  3. QRS complex = Depolarisation of Ventricular contractile fibres
  4. Flat portion following QRS = Ventricular Systole
  5. Repolarisation of Ventricular contracile fibres = T-wave
  6. Ventricular diastole (relaxation) = flat end point/beginning next cycle
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18
Q

caridac output

A

volume of blood ejected from either

  • LV -> Aorta
  • RV -> Pulmonary trunk

per min

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19
Q

stroke volume =

A

volume of blood ejected in a contraction

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20
Q

heart rate =

A

bpm

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21
Q

CO=

(cardiac output)

A

SV (ml/beat) x HR (bpm)

stroke volume x heart rate

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22
Q

typical adult male CO =

A

SV x HR

70 x 75

= 5250ml/min

5.25L/min

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23
Q

preload

A

degree of stretch of the heart before it contracts

(how much space can it make)

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24
Q

contractility

A

force of contraction

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25
Q

afterload

A

pressure that must be exceeded in order for the ejection to occur

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26
Q

regulation of stroke volume by

A

preload

contractiltiy

afterload

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27
Q

frank-stirling law =

A

greater preload, and therefore the volume, the greater the force of contraction (in a healthy heart)

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28
Q

cardiac control

A

Both branches of the autonomic nervous system can affect cardiac output by altering HR or SV (symp only)

  • The sympathetic nervous system also affects blood vessels so effects on blood pressure can be complex

Changes in cardiac output will be detected by baroreceptors and information on blood pressure fed back to the CVS control centre in the brain

CNS control allows BP to be modulated during sleep and by emotions such as rage etc

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29
Q

blood vessels

endothelial cells and their role

A

Line ALL vessels and the inside of the heart chambers

  • Important for local blood pressure control
  • Prevent platelet aggregation and blood clot formation
  • Angiogenesis + vessel remodelling
  • Permeability barrier for nutrients/fluid between plasma and interstitial fluid
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30
Q

4 functions of endothelial cells in blood vessels

A
  • Release constrictors- endothelin, thromboxane + dilators- nitric oxide, prostacyclin
  • Can influence proliferative state of smooth muscle cells- hypertension
  • Can release free radicals which can oxidise LDL
  • Can express molecules which tether inflammatory cells
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31
Q

vascular smooth muscle in blood vessels

A

In all vessels apart from smallest capillaries

determiens vessel diameter

can expand and contract

secret ECM - provides elasticity

can proliferate in hypertension = inc vascular resistance

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32
Q

blood pressure =

A

systolic / diastolic

e.g. 120/80mmHg

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33
Q

mean arterial pressure

A

MAP

diastolic pressure + 1/3 pulse pressure

MAP = average systemic BP

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34
Q

BP and MAP

A

BP = MAP = CO x TPR

TPR and therefore MAP can be modified by α-Adrenoceptor Antagonists

α1 selectives e.g Prazosin, Doxazosin = Decrease Vasoconstrictor tone, with no direct change in HR/CO = dec. BP

non-selectives e.g Phentolamine = Blocks α1 receptors on vessel and α2 receptors at synaptic bulb that releases NA neurotransmitter to activate α1 so both pathways essentially

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35
Q

Blood vessels macrostructure

layers

A

tunica intima

tunica media

tunica externa

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36
Q

tunica intima

A

innermost layer is endothelium

basement membrane deep to the endothelium with collagen fibres = confers tensile strength

internal elastic lamina - looks like swiss cheese and allows nutrients to diffuse from tunica media to the intima and vice versa

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37
Q

tunica media

A

mainly smooth muscle and elastic fibres

varies in size and structure for different vessels

external elastic lamina on the outside same function as the IEL

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38
Q

tunica externa

A

contains a variety of nerves

also vasa vasrum (vessels to vessels)

this tissue anchors the vessel to surrounding tissues

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39
Q

blood vessel flow

equation

A

Poiseuille

Flow Rate = π (Pressure x Radius4 ) / 8 (Viscosity x Length of tube)

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40
Q

5 types of blood vessels

A

arteries

arterioles

capillaries

venules

veins

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41
Q

arteries

A

muscular so have por recoil so can’t really propel blood along but rather just maintain pressure

ability to recoil and remain partially contracted is know as vascular tone

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42
Q

arterioles

A

regulate blood flow into the capillaries

causes resistance between the vessel walls and the blood itself

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43
Q

capillaries

A

involved in the microcirculation where exchanges are carried out between blood and interstitium

1 cell thick + basement structure

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44
Q

venules

A

receieve blood from the capillaries and begin flow back toward the heart

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45
Q

veins

A

lack teh IEL and EEL and their tunics area musch thinner than arteries

also contain infolds of the tunica intima that form valves to stop backflow of blood because its at low pressure

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46
Q

cardiovascular disease risk factors

A

irreversible

  • age
  • sex
  • family history

reversible

  • smoking
  • obesity
  • diet
  • exercise
  • hypertension
  • hyperlipidaemia
  • diabetes
  • stress
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47
Q

CV disease risk modification by

A

information

belief

motivation

behavioural change

48
Q

primary prevention of CV disease

A

exercise

diet

stop smoking

risk assessment (tx if high risk)

49
Q

secondary prevention of CV disease

A

medical tx to reduce risk factors

50
Q

antiplatelet drugs e.g.

A

-grel

  • aspirin
  • clopidogrel
  • dipyridamole
51
Q

aspirin

A

inhibits platelet aggregation, thromboxane a2 and prostacyclin

works for the life of the platelet

new APDs like Prasugrel and Ticagrelor being used with this

52
Q

clopidogrel

A

inhibit ADP induce platelet aggregation

53
Q

dipyridamole

A

inhibits platelet phophdiesterase

54
Q

oral anticoagulant e.g.

A

warfarin

55
Q

warfarin

A

inhibits vit K dependent clotting factors (II, VII, IX, X) - slow

inhibits protien C+S - Fast, often used concurrently with Heparin

interacts with amoxicillin, metronidazole, erythromycin and NSAIDS

56
Q

New Oral Anticoagulants e.g.

A

NOACs (-an)

Rivaroxiban

Apixaban

Dabigatran

57
Q

activated factor X inhibitors

NOACs

A

rivaroxiban

apixaban

58
Q

direct thrombin inhibitors dTi

NOACs

A

dabigatran

59
Q

statins e.g.

A

simvastatin, atrovastatin, rosuvastatin (-in)

inhibit cholesterol synthesis in liver

interact with antifungals

60
Q

beta-adrenergic blockers (beta blockers) e.g.

A

-olol

atenolol and propanolol

Stop arrhythmias leading to VF, and reduce heart muscle excitation, cause postural hypotension

Reduce heart efficiency and beta receptors in lungs make asthma more difficult to treat

61
Q

diuretics e.g.

A

-ide

thiazide diuretics (bendroflumethiazide)

loop diuretics (frusemide)

inc salt and water loss

therefore reduce cardiac workload and plasma volume

Xerostomia in the elderly and Na+/K+ imbalance if not monitored

62
Q

nitrates

A

Dilate veins (red. Preload)

Dilate resistance arteries (red.Afterload (cardiac workload)) and cardiac O2 consumption

Dilate Colateral Coronary artery supply (reduce Anginal pain)

  • Sublingual spray- short acting
  • Transdermal and IV- long acting

Inactivated by 1st pass metabolism

63
Q

short acting nitrate e.g.

A

glycerly trinitrate spray (sublingual)

emergency management of angina pectoris

64
Q

long acting nitrate e.g.

A

isosorbide mononitrate - prevention of angina pectoris

(transdermal and IV)

65
Q

calcium channel blockers e.g.

A

nifedipine

amolodipine

verapamil

N.B Gingival Hyperplasia (also seen with Cyclosporin and Phenytoin)

66
Q

nifidipine and amlodipine

Ca channel blockers

A

peripheral BVs

relax and vasodilate

67
Q

verapamil

A

Ca channel blocker

cardiac muscle, slow conduction of pacing impulses

68
Q

angiotensin converting enzymes (ACE) inhibitors

A

-pril

enlapril, ramapril, lisinopril

inhibit conversion of angiotensin I to II

prevents aldosterone dependent reabsorption of salt and water

reduce BP

N.B cough, hypotension, angio-oedema and lichenoid reaction

69
Q

angiotensin II blockers e.g.

A

-artan

losartan

inhibit same system but different mechanism as ACE inhibitors

70
Q

2 types of acute coronary syndromes

A

BV narrowing

BV occlusion

71
Q

BV narrowing

A

poor O2 delivery, cramp in affected tissue/muscle

72
Q

BV occlusion

A

No O2 delivery, severe pain, loss of tissue function

73
Q

Dx of acute coronary syndromes

A

history

ECG findings

STEMI (ST elevation MI or NSTEMI)

biomarkers - troponin

74
Q

CVS major issues

7

A

artherosclerosis

atheroma

thrombosis

embolism

aneurysm

ischaemia

infarction

75
Q

artherosclerosis

A

fatty streak -> fibrolipid plaque -> complicated plaque

precursor to more serious CV disease

76
Q

atheroma

A

fat in tunic intimi

synonymous with artherosclerosis

77
Q

thrombosis

A

solid mass of blood constituents formed within vascular system during life

Virchow’s triad

  1. surface of BV
  2. pattern of blood flow
  3. blood constituents
78
Q

embolism

A

mass of material floating free in vascular system able to lodge into a vessel to block its lumen

often thrombotic or atheromatous debris

79
Q

aneurysm

A

permanent vasodilation causing a bulge in the vessel wall ballooning

80
Q

ischaemia

A

inappropriate reduction of blood supply to organ or tissue

81
Q

infarction

A

death of tissue due to ischamia

82
Q

Angina pectoris

A

Reversible ischaemia of heart muscle

Classic- worse with exercise

Unstable- pain at rest with no biomarkers

Central crushing chest pain (arm, back and jaw)

Symptoms include

  • Anaemia,
  • Hyperthyroidism
  • Hypovolaemia (dec. blood vol. systemically)
83
Q

angina pectoris tx

A

Reduce O2 demand of heart, Increase O2 Delivery to tissues

Non Drug therapy

  • Live within limits,
  • modify risk factors (smoking, diet, exercise, cholesterol)

Drug Therapy

  • Reduce risk of MI- aspirin
  • HBP- diuretics, ace inhibitors, beta blockers
  • Reduce preload/dilate coronary vessels- Nitrates
  • Emergency treatment- GTN spray
  • Surgical- Coronary Artery Bypass Graft (CABG), Angioplasty + Stenting w/ dual antiplatelet therapy to prevent thrombosis
84
Q

peripheral vascular disease

A

Angina of tissues, Atheroma of femoral/popliteal vessels causes infarction, claudication pain on exercise

Poor wound healing, limitation of function

Tissue necrosis and gangrene (feet esp.)

85
Q

ischeamia -> infarction

A
  1. Atheroma in vessels
  2. ulcerated plaques with platelet aggregates
  3. thrombosis on the surface
  4. Thrombosis can enlarge rapidly to block vessel
  5. Plaque surface/ platelets detach travel downstream and BLOCK vessels
  6. no blood flow to that area - infarction

Infarction tends to occur in

➡Heart- Coronary Artery Atheroma

➡Limb- Femoral and Popliteal arteries

➡Brain- Carotid Arteries

86
Q

5 types of MI

A

spontaneous

MI secondary to ischaemia

sudden death with symptoms of ischaemia and evidence of ST elevation or thrombus

MI from PCI

MI from CABG

87
Q

spontaneous MI

A

primary coronary event

plaque fissure/rupture

88
Q

MI secondary to ischaemia due to

A

imbalance in supply and demand

89
Q

2 tx modes for MI

A

aspirin

thrombolysis

90
Q

MI on ECG

A

ST elevation (can vary in position)

Q waves - indicate previous MI

91
Q

hypertension is

A

raised BP

systolic - > 140mmHg

diastolic - > 90mmHg

taken as 3 separate measurements whilst sitting

92
Q

risk factors for hypertension

A

Usual risk factors but also drugs (NSAIDs, Corticosteroids, Oral Contraceptives, Sympathomimetics for symp nerve system stim.)

Stress, family history, pregnancy, alcohol

93
Q

aetiology of hypertension

A

None usually

Rarely : Renal Artery Stenosis, Endocrine Tumours- Phaeochromocytoma (Adrenaline) Conn’s Syndrome (Aldosterone) Cushing’s syndrome (Cortisol)

94
Q

investigations for hypertension

A

urinalysis

serum biochemistry (electrolytes, urea and creatinine)

serum lipids

ECG

occasionally renal ultrasound, renal angiography, hormone estimations

95
Q

tx hypertension

A
  • single daily drug dose (compliance)
  • thiazide diuretic (gout)
  • beta blocker (COPD and asthma)
  • calicum channel antagonist
  • ACE inhibitor (PVD)
96
Q

heart failure

A

output of the heart is incapable of meeting the demands of the tissues

high output - anaemia, thrytoxicosis

low output failure - cardiac defect e,g, MI, valve disease

97
Q

3 types of heart failure

A

right sided - backs up in the area that collects ‘used’ blood

left sided - failure to properly pump blood to the body

congestive heart failure - fluid backs up to the lungs and tissues

98
Q

aetiology of valve disease

A

congenital abnormlaity

myocardial infarction - papillary muscle rupture

rheumatic fever - immunological reaction to streptococci

dilation of the aoritc root - syphillis and aneurysm formation

99
Q

2 e.g. valve diseases

A

valve stenosis

bicuspid aortic valve

100
Q

valve stenosis

A

can affect mainly aortic and mitral valevs - can form thrombi or block blood flow to the rest of the body

common in the elderly and Down’d pts

101
Q

bicuspid aortic valve

A

normally tricuspid

can lead to aortic or valve stenosis

dilation of the ascending aorta

valve infection

102
Q

2 types of valve replacments

A

porcine - well acccepted by body, but shorter lifespan

mechanical - longer lasting but need lifelong antibiotic prophylaxis

103
Q

5 congental heart defects

A

tetralogy of fallot

ventricular septal defect

artrial septal defect

co-artication of the aorta

patent ductus arteriosus

104
Q

tetralogy of fallot

A

P ulmonary stenoiss

R ight ventricular hypertrophy

O veriding aorta

V entricular septal defect

central cyanosis due to >5g/dl of deoxygenated Hb in blood

finger clubbing

105
Q

ventricular septal defect

A

cause a mixing of oxygented and deoxygenated blood

106
Q

artrial septal defect

A

can cause pulmonary hypertension

107
Q

co-artication of aorta

A

narrowing in aorta in the region of the ligamentum arteriosus

108
Q

patent ductis arteriosus

A

failure of the natal ductus arteriosus to close after birth

causes blackflow of blood towards the lungs = shortness of breath, inc pulmonary pressure

109
Q

noraml sinus rhytm

A
110
Q

ventricular fibrilation

A
111
Q

atrial fibrilation

A
112
Q

ventricular tachycardia

A
113
Q

SDCEP guidance on anticoagulant/antiplatelet guidelines

vit k agonists

A

e.g. warfarin, acenocoumarol or phenindone

check INR

  • no more than 24hrs before procedure
  • up to 72hrs if stably anticoagulated
  • if tx without interruption
    • limit the initial tx area
    • activaly consider suture and packing

if INR is >4, delay tx or refer if urgent

114
Q

SDCEP guidance on anticoagulant/antiplatelet guidelines

injectable anticoagulant (parins)

A

e.g. Heparin, Dalteparin, Enoxaparin, Tinzaparin

consult with GMP or specialist for more info

applies for multiple drug combos with antiplatelets/anticoagulants

115
Q

SDCEP guidance on anticoagulant/antiplatelet guidelines

NOACs

A

e.g Apixiban, Rivaroxiban (activated Factor X inhibitors) and Dabigatran (Direct Thrombin inhibitor)

Low Bleeding risk e.g Simple extractions, I+D of abcesses, 6pt chart, RSI, Restorations w/ subgingival margins

  • Treat w/o interruption
  • Conditional recommendation - low evidence for this!

High Bleeding risk e.g Complex extractions, >3 extractions at once, flap raising procedures

If treating w/o interruption

➡ Limit the initial treatment area

➡ Actively consider suture + packing

➡ advise on dose schedules

Apixiban/Dabigatran - 2x p/d usually - for treatment miss morning dose and take evening tablet as norm

Rivaroxiban - 1x p/d either in morning or evening

➡ Morning - Delay morning dose and take 4hrs after haemostasis in the evening

➡ Evening - treat in morning and take tablet at usual time in evening

116
Q

SDCEP guidance on anticoagulant/antiplatelet guidelines

antiplatelets

A

Traditional Antiplatelets - e.g Aspirin

  • treat without interruption, use local haemostatic measures

Alternative Antiplatelets - e.g Clopidogrel, Dipyridamole, Prasugel, Ticagrelor

  • Treat w/o interruption
  • except if history of prolonged bleeding
  • consider staging procedures at different times

REVISION BDS (43 decks)

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