Cardiovascular system Flashcards
layers of heart
pericardium
epicardium
myocardium
endocardium
pericardium
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
epicardium
with coronary blood vessels
slippery tissue which has the vessels that supply the heart contained within
myocardium
with trabeculae carnae
cardiac muscle responsible for hearts pumping action
endocardium
endothelial lining of the chambers of the heart which is continuous with the vessels supplying the heart
right artrium
receives deoxygenated blood from SVC and IVC
blood then passes though tricuspid valve
right ventricle
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
left atrium
receives oxygenated blood from the 4 pulmonary veins
blood passes through the LA to the LV via the bicuspid (mitral valve)
left ventricle
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
conduction of heart carried out by
Autorhythmic fibres
these fibres set the rhythm of the heart but also the path in which the rhythm is conducted
sequence of heart conduction
- Starts at Sino Atrial Node in the RA with spontaneous depolarisation
- Reaches the Atrioventricular Node which is the junction between RA and RV
- 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
- The fibres then branch left and right into the bundle branches through the interventricular septum
- Finally large diameter purkinje fibres conduct the action potentials into the trabeculae carnae of the myocardium to aid with ventricular contraction
cardiac action potention
contractile working fibres after SA node
depolariation
plateau
repolarisation
depolarisation stage in cardiac action potential
stage 0
rapid depolarisation by Na+ ions efflux
channels close soon after
plateau stage in cardiac action potentials
stages 1 and 2
Ca2+ ions maintain the depolaristion level by equalising the K+ outflow
increased calcium ion concentration ultimately triggers heart muscle contraction
repolarisation stage in caridac action potential
stage 3
Ca2+ begin to close
K+ channels begin to open
production of ATP in the heart
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
electrocardiogram ECG
- Raising part of P-Wave = Depolarisation of Atrial contractile fibres
- Descending part of P- Wave = Atrial Systole
- QRS complex = Depolarisation of Ventricular contractile fibres
- Flat portion following QRS = Ventricular Systole
- Repolarisation of Ventricular contracile fibres = T-wave
- Ventricular diastole (relaxation) = flat end point/beginning next cycle
caridac output
volume of blood ejected from either
- LV -> Aorta
- RV -> Pulmonary trunk
per min
stroke volume =
volume of blood ejected in a contraction
heart rate =
bpm
CO=
(cardiac output)
SV (ml/beat) x HR (bpm)
stroke volume x heart rate
typical adult male CO =
SV x HR
70 x 75
= 5250ml/min
5.25L/min
preload
degree of stretch of the heart before it contracts
(how much space can it make)
contractility
force of contraction
afterload
pressure that must be exceeded in order for the ejection to occur
regulation of stroke volume by
preload
contractiltiy
afterload
frank-stirling law =
greater preload, and therefore the volume, the greater the force of contraction (in a healthy heart)
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
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
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
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
blood pressure =
systolic / diastolic
e.g. 120/80mmHg
mean arterial pressure
MAP
diastolic pressure + 1/3 pulse pressure
MAP = average systemic BP
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
Blood vessels macrostructure
layers
tunica intima
tunica media
tunica externa
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
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
tunica externa
contains a variety of nerves
also vasa vasrum (vessels to vessels)
this tissue anchors the vessel to surrounding tissues
blood vessel flow
equation
Poiseuille
Flow Rate = π (Pressure x Radius4 ) / 8 (Viscosity x Length of tube)
5 types of blood vessels
arteries
arterioles
capillaries
venules
veins
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
arterioles
regulate blood flow into the capillaries
causes resistance between the vessel walls and the blood itself
capillaries
involved in the microcirculation where exchanges are carried out between blood and interstitium
1 cell thick + basement structure
venules
receieve blood from the capillaries and begin flow back toward the heart
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
cardiovascular disease risk factors
irreversible
- age
- sex
- family history
reversible
- smoking
- obesity
- diet
- exercise
- hypertension
- hyperlipidaemia
- diabetes
- stress
CV disease risk modification by
information
belief
motivation
behavioural change
primary prevention of CV disease
exercise
diet
stop smoking
risk assessment (tx if high risk)
secondary prevention of CV disease
medical tx to reduce risk factors
antiplatelet drugs e.g.
-grel
- aspirin
- clopidogrel
- dipyridamole
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
clopidogrel
inhibit ADP induce platelet aggregation
dipyridamole
inhibits platelet phophdiesterase
oral anticoagulant e.g.
warfarin
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
New Oral Anticoagulants e.g.
NOACs (-an)
Rivaroxiban
Apixaban
Dabigatran
activated factor X inhibitors
NOACs
rivaroxiban
apixaban
direct thrombin inhibitors dTi
NOACs
dabigatran
statins e.g.
simvastatin, atrovastatin, rosuvastatin (-in)
inhibit cholesterol synthesis in liver
interact with antifungals
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
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
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
short acting nitrate e.g.
glycerly trinitrate spray (sublingual)
emergency management of angina pectoris
long acting nitrate e.g.
isosorbide mononitrate - prevention of angina pectoris
(transdermal and IV)
calcium channel blockers e.g.
nifedipine
amolodipine
verapamil
N.B Gingival Hyperplasia (also seen with Cyclosporin and Phenytoin)
nifidipine and amlodipine
Ca channel blockers
peripheral BVs
relax and vasodilate
verapamil
Ca channel blocker
cardiac muscle, slow conduction of pacing impulses
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
angiotensin II blockers e.g.
-artan
losartan
inhibit same system but different mechanism as ACE inhibitors
2 types of acute coronary syndromes
BV narrowing
BV occlusion
BV narrowing
poor O2 delivery, cramp in affected tissue/muscle
BV occlusion
No O2 delivery, severe pain, loss of tissue function
Dx of acute coronary syndromes
history
ECG findings
STEMI (ST elevation MI or NSTEMI)
biomarkers - troponin
CVS major issues
7
artherosclerosis
atheroma
thrombosis
embolism
aneurysm
ischaemia
infarction
artherosclerosis
fatty streak -> fibrolipid plaque -> complicated plaque
precursor to more serious CV disease
atheroma
fat in tunic intimi
synonymous with artherosclerosis
thrombosis
solid mass of blood constituents formed within vascular system during life
Virchow’s triad
- surface of BV
- pattern of blood flow
- blood constituents
embolism
mass of material floating free in vascular system able to lodge into a vessel to block its lumen
often thrombotic or atheromatous debris
aneurysm
permanent vasodilation causing a bulge in the vessel wall ballooning
ischaemia
inappropriate reduction of blood supply to organ or tissue
infarction
death of tissue due to ischamia
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)
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
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.)
ischeamia -> infarction
- Atheroma in vessels
- ulcerated plaques with platelet aggregates
- thrombosis on the surface
- Thrombosis can enlarge rapidly to block vessel
- Plaque surface/ platelets detach travel downstream and BLOCK vessels
- no blood flow to that area - infarction
Infarction tends to occur in
➡Heart- Coronary Artery Atheroma
➡Limb- Femoral and Popliteal arteries
➡Brain- Carotid Arteries
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
spontaneous MI
primary coronary event
plaque fissure/rupture
MI secondary to ischaemia due to
imbalance in supply and demand
2 tx modes for MI
aspirin
thrombolysis
MI on ECG
ST elevation (can vary in position)
Q waves - indicate previous MI
hypertension is
raised BP
systolic - > 140mmHg
diastolic - > 90mmHg
taken as 3 separate measurements whilst sitting
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
aetiology of hypertension
None usually
Rarely : Renal Artery Stenosis, Endocrine Tumours- Phaeochromocytoma (Adrenaline) Conn’s Syndrome (Aldosterone) Cushing’s syndrome (Cortisol)
investigations for hypertension
urinalysis
serum biochemistry (electrolytes, urea and creatinine)
serum lipids
ECG
occasionally renal ultrasound, renal angiography, hormone estimations
tx hypertension
- single daily drug dose (compliance)
- thiazide diuretic (gout)
- beta blocker (COPD and asthma)
- calicum channel antagonist
- ACE inhibitor (PVD)
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
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
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
2 e.g. valve diseases
valve stenosis
bicuspid aortic valve
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
bicuspid aortic valve
normally tricuspid
can lead to aortic or valve stenosis
dilation of the ascending aorta
valve infection
2 types of valve replacments
porcine - well acccepted by body, but shorter lifespan
mechanical - longer lasting but need lifelong antibiotic prophylaxis
5 congental heart defects
tetralogy of fallot
ventricular septal defect
artrial septal defect
co-artication of the aorta
patent ductus arteriosus
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
ventricular septal defect
cause a mixing of oxygented and deoxygenated blood
artrial septal defect
can cause pulmonary hypertension
co-artication of aorta
narrowing in aorta in the region of the ligamentum arteriosus
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
noraml sinus rhytm
ventricular fibrilation
atrial fibrilation
ventricular tachycardia
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
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
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
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
