Cardiovascular Flashcards
what layer does the cardiovascular system develop from in gastrulation
mesoderm
what forms in cardiac looping during embryonic development
2 bulges form; bulbus cordis and primordial ventricle
what are the 3 sources of blood flow to the embryonic heart
Vitelline Veins
Umbilical veins
Common cardinal veins
what are the 4 stages of cardiac septation in the atria
Septum primum forms and grows downwards
Foramen primum ‘space’ formed
Foramen secumdum forms in septum primum
Septum secundum begins to form
what is the foramen ovale
hole in the atrial septa that permits oxygen-rich blood to move from RA – LA (shunting)
what does the foramen ovale form in adults
fossa ovalis
what is a patent foramen ovale
Abnormal resorption of septum primum during formation of foramen secundum
Results in short septum primum and therefore foramen ovale is still open after birth
3 types of congenital heart defects
Transposition of the great arteries
Rare but very serious – pulmonary artery and aorta are swapped over
Truncus arteriosus
Rare but very serious – pulmonary artery and aorta don’t develop and remain as single vessel
Patent ductus arteriosus
Connection between pulmonary artery and aorta in the fetus – remains open after birth
what are the 3 layers of blood vessels
tunica intimida
tunica media
tunica adventitia
what are the 2 layers of the pericardium
Fibrous (outer layer)
serous (inner layer)
what are the functions of the pericardium
Fixation within mediastinum
Prevents over filling of heart
Lubrication (thin fluid film reduces friction)
Protection from infection
innervation of the pericardium
Phrenic nerve (C 3, 4 & 5)
what are the pericardial sinuses
Transverse pericardial sinus
Oblique pericardial sinus
what are the layers of the heart wall
- Endocardium
- Subendocardial Layer
- Myocardium
- Subepicardial Layer
- Epicardium (Visceral Pericardium)
the right atrium - anatomy
Receives blood from Superior & Inferior Vena Cavae, Coronary Veins • Right auricle • 2 distinct parts divided by Crista Terminalis • Coronary sinus (between IVC & right atrioventricular orifice)
the right ventricle - anatomy
Receives blood from RA • Pumps blood to pulmonary artery via pulmonary orifice • Triangular shape • Anterior heart border • Inflow and outflow portions • Separated by supraventricular crest
the left atrium - anatomy
Receives blood from pulmonary veins • Forms posterior border (base) of heart • Left auricle
the left ventricle - anatomy
- Receives blood from left atrium
- Forms apex of the heart
- Left & inferior heart borders
- Inflow & outflow portions
heart valves function
Ensure blood flow in one direction • Connective tissue & lined in endocardium • 4 heart valves - 2 atrioventricular 2 semilunar
atrioventricular valves
Close at start of systole (first heart sound) • Valves are supported by chordae tendineae - tricuspid - right side - mitral - left side
semi-lunar valves
Close at the start of diastole (second heart sound) • Found between ventricles & corresponding outflow tracts • Sinuses • Lunule (thickened free edge) • Nodule (widest area)
auscultating heart sounds
First heart sound - start of systole • Tricuspid valve • Mitral valve Second heart sound - START of diastole • Aortic valve • Pulmonary valve
coronary circulating - arteries
Vessels that supply & drain the heart • 2 main arteries - Right & left coronary arteries • Left coronary artery - Left anterior descending a. - Left marginal a. - Left circumflex a. • Right coronary artery - Right marginal a. - Posterior interventricular a. (85%)
Coronary Circulation – Venous drainage
Venous drainage of myocardium • 5 tributaries - Great cardiac v. - Small cardiac v. - Middle cardiac v. - Left marginal v. - Left posterior ventricular v. . Converge at coronary sinus • Drain into RA between atrioventricular orifice & orifice of IVC
the sequence of events with each heart beat
1) Flow into atria, continuous except when they
contract. Inflow leads to pressure rise.
2) Opening of A-V valves - Flow to ventricles.
3) Atrial systole - completes filling of ventricles.
4) Ventricular systole (atrial diastole). Pressure rise
closes A-V valves, opens aortic and pulmonary
valves.
5) Ventricular diastole – causes closure of aortic and
pulmonary valves.
cardiac output
Cardiac output is the volume blood pumped
per minute (by each ventricle).
Cardiac output = Heart rate x Stroke volume
At rest C.O. = 5 l/min
In exercise > 25 l/min as heart rate increases
2-3 fold and stroke volume increases 2 fold.
stroke volume dependant on
a) Contractility (the force of contraction).
e.g. adrenaline ↑force, ↑stroke volume.
b) End diastolic volume (volume of blood
in ventricle at the end of diastole).
Force is stronger the more muscle fibres are
stretched (within limits):
Frank - Starling Mechanism or Starling’s Law of the Heart
Stroke volume ∝ Diastolic Filling
Frank-Starling Mechanism
Also known as the Preload. Important in: a)ensuring the heart can deal with wide variations in venous return. b)balancing the outputs of the two sides of the heart
peripheral resistance - afterload
Resistance to blood flow away from the heart -
altered by dilation or constriction of blood
vessels (mainly pr-ecapillary resistance
arteries).
Cardiac Output = Blood pressure /
Peripheral Resistance
summary of excitation pathway
Sinus rhythm = heart rate controlled by S.A. node, rest rate approx. 72 beats/min (wide variation). • Action potential then activates atria. • Atrial A.P. activates A.-V. node. • A.V. node - small cells, slow conduction velocity - introduces delay of 0.1 sec. • A.V. node activates Bundle of His / Purkinje fibres. • Purkinje fibres activate ventricles.
cardiac muscle
‘myogenic’ – it generates its own action potentials.
Action potentials develop spontaneously at the
sino-atrial node.
SA node action potential
Pacemaker potential due to:↑gCa,↑gNa,↓gK Action potential upstroke due to: ↑gCa Repolarisation due to: ↑ gK, ↓ gCa Noradrenaline - ↑gCa Acetyl choline - ↑ gK, ↓ gCa
cardiac v skeletal muscle cells
1- neurogenic v myogenic
2-longer cardiac action potential (with plateau)
3-Action potential controls duration of contraction in heart.
4-Ion currents during action potential
– skeletal ‘simple’, cardiac complex
currents responsible for cardiac action potential
Depolarisation - large gNa Plateau - small gNa - increase gCa - decrease gK Repolarisation - decrease gCa - increase gK
source of Ca for contraction in cardiac muscle cells
Ca is released from the sarcoplasmic reticulum but
for heart cells Ca entry from outside is needed (‘Ca
induced Ca release’).
the mechanisms of ECG
Electrical impulse (wave of depolarisation) picked up by
placing electrodes on patient
The voltage change is sensed by measuring the current
change
If the electrical impulse travels towards the electrode
this results in a positive deflection
If the impulse travels away from the electrode this
results in a negative deflection
types of ecg leads
coronal plane (limb leads) -bipolar leads - I, II, III -unipolar leads - aVL, aVR, aVF transverse plane -chest leads , v1-v6
whats the paper speed in an ecg
25mm per second
Therefore one large box (5mm) corresponds to
0.2 seconds
causes of P QRS T ecg waves
P wave caused by atrial depolarization QRS complex caused by ventricular depolarization T wave results from ventricular repolarization
intervals between ecg waves
PR = 0.12-0.20sec QRS = <0.12s QTc = <0.440s (m), 0.460s (f)
what does the PR interval tell us
the time to conduct through AVN/His
what does the QRS interval tell us
time for ventricular depolarisation Patterns of conduction disease though Bundles RBBB, LBBB
what does the ST segment tell us
start of
ventricular repolarisation
(should be isoelectric)
ST elevation
acute infarction
Other things pericarditis,
repolarisation abnormalities
ST depression
Ischaemia, LV strain (LVH)what does the T wave tell us
ventricular depolarisation
right bundle branch block - RBBB
- RBBB in V1 no change in initial impulse travel small r wave impulse depolarizes LV by itself since RBBB (s wave) RV depolarized late by impulse thru muscle (r’ wave Hence RSR’ pattern (‘M’ shape) ‘MaRRoW’ pattern
left bundle branch block - LBBB
LBBB in V1 initial deflection altered since travels right to left now Q wave/ negative deflection RV depolarizes unopposed may produce small r wave travels across septum to depolarize LV deep S wave W pattern in V1 ‘WiLLiaM’ pattern ** note if patient has LBBB then ST segments is uninterpretable
calculating regular HR
Count the number of large squares between R waves (RR
interval)
Rate = 300 divided by number of large squares between R waves
Example: if RR interval = 4 large squares
Heart rate = 300/4 = 75 beats per minute
calculating irregular HR
Use rhythm strip at the bottom of 12-lead ECG
Rhythm strip is a 10 second recording of the heart
Therefore, Rate = number of QRS complexes multiplied by 6
Example: if number of QRS complexes = 13
Heart rate = 13 X 6 = 78 beats per minute
bradyarrhythmia
Any abnormality of cardiac rhythm resulting in a slow heart
rate (heart block, slow AF) (c.f. sinus brady)
HR < 60bpm
tachyarrhythmia
Any abnormality of cardiac rhythm resulting in a fast heart
rate (SVT, uncontrolled AF/ Flutter, VT) (c.f. sinus tachy)
HR > 100bpm
first degree AV block
- Regular Rhythm
- PR interval > .20 seconds and is CONSTANT
- Causes: IHD, conduction system disease, seen in healthy children or athletes
- Usually does not require treatment
second degree AV block / Mobitz I
Irregular Rhythm
• PR interval continues to lengthen until a QRS is missing (non-conducted sinus beat)
• PR interval is NOT CONSTANT
• Rhythm is usually benign unless associated with underlying pathology, (i.e. MI)
second degree AV block / Mobitz II
- Irregular Rhythm
- QRS complexes may be wide (greater than .12 seconds)
- Non-conducted sinus impulses appear at irregular intervals
- Rhythm is somewhat dangerous as the block is lower in the conduction system (BB level)
- May cause syncope or may deteriorate into complete heart block (3rd degree block)
- It’s appearance in the setting of an acute MI identifies a high risk patient
- Cause: IHD, fibrosis of the conduction system
- Treatment: pacemaker
3rd degree AV block (complete heart block)
Atria and ventricles beat independent of one another (AV dissociation)
• QRS’s have their own rhythm, P-waves have their own rhythm
• May be caused by inferior MI and it’s presence worsens the prognosis
• Treatment: usually requires pacemaker +/- temporary pacing/ isoprenaline
narrow complex tachycardia
(QRS duration <0.12 s)
Uncontrolled (ie “fast”) Atrial Fibrillation or Flutter
Atrial tachycardia
AVNRT/ AVRT
broad complex tachycardia
(QRS duration >0.12 s)
Ventricular tachycardia
Ventricular fibrillation
**Is rhythm from above AVN with BBB/aberrancy??
physiological causes of arrhythmia
automacity increase
re-entry
digoxin
INOTROPIC AGENT
used for Atrial fibrillation and heart failure
works on Na/K ATPase
increases ventricular contractibility
decreases conduction through AV node
side effect - anorexia, nausea, AV block,
visual problems,
atenolol
used for AF, hypertension, angina
beta-blocker (relatively beta 1 selective)
decrease sympathetic NS activity (B1) at heart
decrease conduction system
decrease ventricular response rate
side effects, lethargy, hypotension, bronchospasm
supraventricular tachycardia treatment
vagal stimulation - carotid massage, eyeball pressure…
drugs - adenosine (short acting purine), verapamil (calcium channel blocker)
ventricular tachycardia treatment
lidocaine (rarely used) - class I anti-arrhythmic blocks Na channels in excitable tissues, decreases excitability and cardiac conduction, effects CNS (drowsiness, confusions...)
amiodarone - class III anti-arrhythmic blocks K channels, prolong cardiac action potential, TOXICITY
biomarkers of myocardial injury
total creatine kinase myoglobin CK-MB lactate dehydrogenase (LDH) cardiac troponin - TnT, TnI
role of natriuretic peptides (BNP and ANP)
counter vasoconstriction
oppose renal salt and H2O retention
risk factors for thrombus
hyper coagulability
abnormal blood flow
endothelial injury
different types of thrombi
mural thrombi - on the walls of spacious cavities -eg aorta
arterial thrombi - may be mural or occlusive - eg in coronary, carotid, cerebral, femoral
venous thrombi - phlebothrombosis, - eg, pelvis and leg veins
what are lines of Zahn
in thrombi alternating pale(fibrin and platelets) and dark(RBC) lines
different types of embolism
arterial - away the heart
venous - towards from the heart
superficial - saphenous system
deep - may be asymptomatic until embolised in lungs
thrombus
A thrombus is a solidification of blood constituents that
forms within the vascular system during life
embolism
An embolus is a detached intravascular solid,
liquid, or gaseous mass that is carried by the
blood to a site distant from its point of origin
types of embolism
Pulmonary embolism • Systemic embolism • Amniotic fluid embolism • Air embolism • Fat embolism
paradoxical embolism
In the presence of an interatrial or interventricular
defect, embolisms may gain access to the systemic
circulation
systemic embolism
This term refers to emboli that travel through
the systemic arterial circulation
arise mostly from thrombi within the heart
almost always cause infarction in eg
-lower extremities
-the brain
infarct defintion
• Is an area of ischaemic necrosis caused by
occlusion of arterial supply or venous drainage in a
particular tissue
necrosis definition
Refers to a spectrum of morphological changes that
follow cell death in living tissue, largely resulting
from the progressive action of enzymes on the
lethally injured cells
causes of infarction
• Thrombosis and thromboembolism account for the vast majority • Other causes include: • Vasospasm • Expansion of atheroma • Compression of a vessel • Twisting of the vessels through torsion • Traumatic rupture
types of infarct
Red (haemorrhagic):
• Venous occlusion e.g. torsion
• Loose tissues
• Tissues with a dual circulation e.g. lung
White (anaemic):
• Arterial occlusions
• Solid organs e.g. heart, spleen
Septic
• Infected infarctswhat are the 2 blood circulations
pulmonary - low pressure
systemic - high pressure
primary systemic hypertension
idiopathic
Risk factors
• Genetic susceptibility
• High salt intake
• Chronic stress (excessive sympathetic activity)
• Abnormalities in renin/angiotensin-aldosterone
• Obesity
• Diabetes mellitussecondary systemic hypertension
Renal disease
• Chronic renal failure
• Polycystic kidneys
Endocrine causes
• Pituitary - ACTH
• Adrenal cortex - glucocorticoid; mineralocorticoid
• Adrenal medulla - catecholamines
Drug treatment e.g. steroids
Others e.g. coarctation of the aorta
Potentially treatable
• Careful clinical assessment
• Test the urine!systemic hypertension effects on the heart
Left ventricular hypertrophy • Fibrosis • Arrhythmias • Coronary artery atheroma • Ischaemic heart disease • Cardiac failure
systemic hypertension effects on the kidney
• Nephrosclerosis
• ‘Drop-out’ of nephrons due to vascular narrowing
• Proteinuria
• Chronic renal failure
• Malignant hypertension is associated with acute
renal failure
vascular changes in systemic hypertension
Benign hypertension • Acceleration of atherosclerosis • Intimal proliferation and hyalinisation of arteries and arterioles Malignant hypertension • Fibrinoid necrosis
ischaemic heart disease
Blood supply to the heart is insufficient for its metabolic demands • Deficient supply • Coronary artery disease (commonest) • Reduced coronary artery perfusion
coronary artery disease
Coronary blood flow is normally independent of
aortic pressure
• Initial response to narrowing is autoregulatory
compensation
• >75% occlusion leads to ischaemia
myocardial infarction
• An area of necrosis of heart muscle resulting
from reduction (usually sudden) in coronary
blood supply
• Due to
• Coronary artery thrombosis
• Haemorrhage into a coronary plaque
• Increase in demand in the presence of ischaemia
chronic ischaemic heart disease
Chronic angina
• Exercise-induced chest pain
• Heart failure
• Related to reduced myocardial function
• Usually widespread coronary artery atheroma
• Areas of fibrosis often present in the myocardium
cardiac failure
• Failure of the heart to pump sufficient blood to
satisfy metabolic demands
• Leads to underperfusion which causes fluid
retention and increased blood volume
• Two different, but linked, circulations
• Systemic
• Pulmonary
left ventricular failure general info
• Dominates hypertensive and ischaemic heart
failure
• Causes pulmonary oedema, with associated
symptoms
• Leads to pulmonary hypertension and,
eventually, right ventricular failure
• Combined left and right ventricular failure is
often called ‘congestive’ cardiac failure
right ventricular failure CAUSES
• Secondary to left ventricular failure
• Related to intrinsic lung disease – ‘cor’ pulmonale
e.g. chronic obstructive pulmonary disease (COPD)
