REVISION BDS > Cardiovascular system > Flashcards

Cardiovascular system Flashcards

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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
afterload
pressure that must be exceeded in order for the ejection to occur
26
regulation of stroke volume by
preload contractiltiy afterload
27
frank-stirling law =
greater preload, and therefore the volume, the greater the force of contraction (in a healthy heart)
28
cardiac control
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
29
blood vessels endothelial cells and their role
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
30
4 functions of endothelial cells in blood vessels
* 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
31
vascular smooth muscle in blood vessels
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
32
blood pressure =
systolic / diastolic e.g. 120/80mmHg
33
mean arterial pressure
MAP diastolic pressure + 1/3 pulse pressure MAP = average systemic BP
34
BP and MAP
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
35
Blood vessels macrostructure layers
tunica intima tunica media tunica externa
36
tunica intima
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
37
tunica media
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
38
tunica externa
contains a variety of nerves also vasa vasrum (vessels to vessels) this tissue anchors the vessel to surrounding tissues
39
blood vessel flow equation
Poiseuille Flow Rate = π (Pressure x Radius4 ) / 8 (Viscosity x Length of tube)
40
5 types of blood vessels
arteries arterioles capillaries venules veins
41
arteries
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
42
arterioles
regulate blood flow into the capillaries causes resistance between the vessel walls and the blood itself
43
capillaries
involved in the microcirculation where exchanges are carried out between blood and interstitium 1 cell thick + basement structure
44
venules
receieve blood from the capillaries and begin flow back toward the heart
45
veins
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
46
cardiovascular disease risk factors
irreversible * age * sex * family history reversible * smoking * obesity * diet * exercise * hypertension * hyperlipidaemia * diabetes * stress
47
CV disease risk modification by
information belief motivation behavioural change
48
primary prevention of CV disease
exercise diet stop smoking risk assessment (tx if high risk)
49
secondary prevention of CV disease
medical tx to reduce risk factors
50
antiplatelet drugs e.g.
-grel * aspirin * clopidogrel * dipyridamole
51
aspirin
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
clopidogrel
inhibit ADP induce platelet aggregation
53
dipyridamole
inhibits platelet phophdiesterase
54
oral anticoagulant e.g.
warfarin
55
warfarin
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
New Oral Anticoagulants e.g.
NOACs (-an) Rivaroxiban Apixaban Dabigatran
57
activated factor X inhibitors NOACs
rivaroxiban apixaban
58
direct thrombin inhibitors dTi NOACs
dabigatran
59
statins e.g.
simvastatin, atrovastatin, rosuvastatin (-in) inhibit cholesterol synthesis in liver interact with antifungals
60
beta-adrenergic blockers (beta blockers) e.g.
-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
diuretics e.g.
-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
nitrates
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
short acting nitrate e.g.
glycerly trinitrate spray (sublingual) emergency management of angina pectoris
64
long acting nitrate e.g.
isosorbide mononitrate - prevention of angina pectoris (transdermal and IV)
65
calcium channel blockers e.g.
nifedipine amolodipine verapamil N.B Gingival Hyperplasia (also seen with Cyclosporin and Phenytoin)
66
nifidipine and amlodipine Ca channel blockers
peripheral BVs relax and vasodilate
67
verapamil
Ca channel blocker cardiac muscle, slow conduction of pacing impulses
68
angiotensin converting enzymes (ACE) inhibitors
-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
angiotensin II blockers e.g.
-artan losartan inhibit same system but different mechanism as ACE inhibitors
70
2 types of acute coronary syndromes
BV narrowing BV occlusion
71
BV narrowing
poor O2 delivery, cramp in affected tissue/muscle
72
BV occlusion
No O2 delivery, severe pain, loss of tissue function
73
Dx of acute coronary syndromes
history ECG findings STEMI (ST elevation MI or NSTEMI) biomarkers - troponin
74
CVS major issues 7
artherosclerosis atheroma thrombosis embolism aneurysm ischaemia infarction
75
artherosclerosis
fatty streak -\> fibrolipid plaque -\> complicated plaque precursor to more serious CV disease
76
atheroma
fat in tunic intimi synonymous with artherosclerosis
77
thrombosis
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
embolism
mass of material floating free in vascular system able to lodge into a vessel to block its lumen often thrombotic or atheromatous debris
79
aneurysm
permanent vasodilation causing a bulge in the vessel wall ballooning
80
ischaemia
inappropriate reduction of blood supply to organ or tissue
81
infarction
death of tissue due to ischamia
82
Angina pectoris
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
angina pectoris tx
**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
peripheral vascular disease
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
ischeamia -\> infarction
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
5 types of MI
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
spontaneous MI
primary coronary event plaque fissure/rupture
88
MI secondary to ischaemia due to
imbalance in supply and demand
89
2 tx modes for MI
aspirin thrombolysis
90
MI on ECG
ST elevation (can vary in position) Q waves - indicate previous MI
91
hypertension is
raised BP systolic - \> 140mmHg diastolic - \> 90mmHg taken as 3 separate measurements whilst sitting
92
risk factors for hypertension
Usual risk factors but also drugs (NSAIDs, Corticosteroids, Oral Contraceptives, Sympathomimetics for symp nerve system stim.) Stress, family history, pregnancy, alcohol
93
aetiology of hypertension
None usually Rarely : Renal Artery Stenosis, Endocrine Tumours- Phaeochromocytoma (Adrenaline) Conn’s Syndrome (Aldosterone) Cushing’s syndrome (Cortisol)
94
investigations for hypertension
urinalysis serum biochemistry (electrolytes, urea and creatinine) serum lipids ECG occasionally renal ultrasound, renal angiography, hormone estimations
95
tx hypertension
* single daily drug dose (compliance) * thiazide diuretic (gout) * beta blocker (COPD and asthma) * calicum channel antagonist * ACE inhibitor (PVD)
96
heart failure
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
3 types of heart failure
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
aetiology of valve disease
congenital abnormlaity myocardial infarction - papillary muscle rupture rheumatic fever - immunological reaction to streptococci dilation of the aoritc root - syphillis and aneurysm formation
99
2 e.g. valve diseases
valve stenosis bicuspid aortic valve
100
valve stenosis
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
bicuspid aortic valve
normally tricuspid can lead to aortic or valve stenosis dilation of the ascending aorta valve infection
102
2 types of valve replacments
porcine - well acccepted by body, but shorter lifespan mechanical - longer lasting but need lifelong antibiotic prophylaxis
103
5 congental heart defects
tetralogy of fallot ventricular septal defect artrial septal defect co-artication of the aorta patent ductus arteriosus
104
tetralogy of fallot
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
ventricular septal defect
cause a mixing of oxygented and deoxygenated blood
106
artrial septal defect
can cause pulmonary hypertension
107
co-artication of aorta
narrowing in aorta in the region of the ligamentum arteriosus
108
patent ductis arteriosus
failure of the natal ductus arteriosus to close after birth causes blackflow of blood towards the lungs = shortness of breath, inc pulmonary pressure
109
noraml sinus rhytm
110
ventricular fibrilation
111
atrial fibrilation
112
ventricular tachycardia
113
SDCEP guidance on anticoagulant/antiplatelet guidelines vit k agonists
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
SDCEP guidance on anticoagulant/antiplatelet guidelines injectable anticoagulant (parins)
e.g. Heparin, Dalteparin, Enoxaparin, Tinzaparin consult with GMP or specialist for more info applies for multiple drug combos with antiplatelets/anticoagulants
115
SDCEP guidance on anticoagulant/antiplatelet guidelines NOACs
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
SDCEP guidance on anticoagulant/antiplatelet guidelines antiplatelets
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
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