CARDIOLOGY FOUNDATIONS Flashcards
Branches of the aorta
brachiocephalic
left common cartoid
left subclavian
Layers of the heart wall (inner to outer)
heart chamber
endocardium
myocardium
visceral pericardium
pericardial space
parietal pericardium
What is the fiborous skeleton
made from dense connective tissue
surrounds the valves of the heart and merges with the interventricular septum
prevents the spread of action potentials from the atria to ventricles
when is the bicuspid valve important
during systole
chordae tendineae close and open valves
Difference between the semilunar valves and bicuspid and mitral valves
No chordae tendinae
rely on pressure gradient for opening and closing
blood flow through the heart
RA deoxy
tricuspid valve
RA
pulm semi lunar valve
pulm trunk and pulm arteries
pulm caps, blood looses CO2 and gains O2
Pulm veins
LA
bicuspid
LV
aortic semilunar
aorta and systemic arteries
in systemic circulation
SVC,IVC, coronary sinus
where do the L and R side coronary arteries originate from
aortic root sinus
coronary artery supply to SA node
RCA 55% LCA 45%
CORONARY ARTERY SUPPLY AV NODE
RCA 90% LCA 10%
L VENTRICLE CORONARY SUPPLY
LAD 50%
RCA25%
CX 25%
TUNICA INTIMA MEDIA AND ADVENTITIA
intima- most internal. made from endotheliial cells, elastic, in contact with blood
media- thickest layer, smooth muscle, elastin, innervated by the sns
adventitia- external, elastic and collagen
PRESSURE IN VESSELS
- Aorta 100mmhg
- Arteries 100-40mmhg
- Arterioles 40-25mmhg
- Capillaries 25-12mmhg
- Venules 12-8mmhg
- Veins 10-5mmhg
- Vena cave 2mmhg
- R. atrium 0mmhg
Blood colloid oncotic pressure
the osmotic pressure exerted by large molecules, serves to hold water within the vascular space. It is normally created by plasma proteins, namely albumin, that do not diffuse readily across the capillary membrane
Interstitial Fluid Osmotic pressure
the (pulling) pressure that causes the reabsorption of fluids from the interstitial fluid back into the capillaries.
hydrostatic
pushing out from intravascular space
Net filtration pressure
=osmotic + hydrostatic pressure
two factors that affect resistance in perfusion
arteriolar radius
blood viscosity
preload
initial stretching of the cardiac myocytes (muscle cells) prior to contraction
factors that determine perfusion
HR
SV
Radius of vessels
blood viscosity
SV = HR X CO
CO X RESISTANCE = BP
Starling’s law (Frank–Starling law)
A law that states that the stroke volume of the heart increases in response to an increase in the volume of blood filling the heart (the end diastolic volume)
what does contractility rely on
calcium into the cytoplasm
SNS innvervation
afterload
The amount of pressure the LV has to contract against to push blood out of the aorta and into systemic circulation
where are baroreceptors found
aortic arch and cartoid sinus
how do baroreceptors work
stretch receptors
increase or decrease firing rate
send messages to cardiovascular control in medulla
sympathetic or parasympathetic activity sent to heart and blood vessels
SA NODE LOCATION
Epicardial surface
close to SVC
what is the bachmanns bundle
also called the interatrial bundle
conducts impulses from the right to left atrium
AV NODE LOCATION
lower right side of the interatrial septum
how long does av node delay impulses
0.1 sec
WHY does AV node delay
-less gap junctions (open channels that allow flow of iosn from one cell to another, less = slower conduction)
-small size of junctional conducting cells
-connective tissue interspersed among conducting cells (connective tissue is non conducting)
2 pathways from AV NODE + refractory periods
-slow pathway (w short refractory period)
-fast pathway (with long refractory period)
Bundle of HIS
Penetrates through fibrous skeletion and allows for conduction from the atria to ventricles
cardiomyocytes structure
striated
contain actin and myosin
contains lots of mitochondria
what is a desmosome
link myocytes together
what is a gap junction
intercalated discs join each cardiomyocyte together
Within the intercalated discs are gap junctions
-gap junctions are intercellular membranes which directly join the cytoplasm of two cardiomyocytes
- they permit the direct passage of ions from one myocyte to another, thereby allowing action potentials to spread quickly
- the result is the heart contracting as a unit, a type of ‘functional syncytium’
Ions outside vs inside the cell
outside - higher ca2++, Na+ and CI
inside- higher K+
Fast vs slow cardiac cells
Fast type myocardial action potentials
* Occurs in atrial and ventricular working contractile myocytes
* Stable resting membrane potential
* Upstroke of depolarisation and downstroke of repolarisation occurs faster
* Steep slopes
Slow type myocardial action potentials
* Occur in pacemaker/nodal cells (SA/AV nodes)
* Spontaneously depolarise between action potentials due to unstable resting potential = automaticity
* The upstroke of depolarisation and downstroke of repolarisation happens more slowly
* Gradual sloping
relative refractory period
around phase 3 if the signal is strong enough another action potential can be generated
excitation contraction coupling
= How electricity converts to contraction
* Calcium engages with sarcomeres to initiate contraction
* Calcium binds to troponin
* Actin and myosin binding = contraction
Parasympathetic and sympathetic effects on the AV node
HR is dependant on phase 4, if the slope is steeper our HR increases, if it is gradual our HR decreases
Which leads are bipolar and unipolar
- 3 standard limb leads (lead 1, lead 2 and lead 3) which are bipolar
- 3 augmented limb leads (aVR, aVL, aVF) which are unipolar
- 6 chest leads (precordial leads) which record electrical activity in the horizontal plane, these are unipolar
What is a vector
-represents the magnitude and direction of the electrical current generated by an individual myocyte
Atrial depolarisation
sequential
atrial repol
spreads in the same direction as depol
it would have a negative direction
depolarisation is moving towards a postive electrode = negative deflection on ECG
ventricular depol
proceeds from the endocardium (inner layer) to epicardium (outer). follows this order –> septal depol (L to R), apex depol, basal depol.
ventricular repol
follows the opposite direction to depol
epicardium (outer) to endo (inner)
starts with basal repol and moves to apex repol
Difference between ventricular endocardial cells and epicardial cells
epicardial cells - have shorter action potential duration, therefore they are depolarised last but repolarise first
Why is the t wave concordant with the QRS
2 negatives = a positive
since both the flow of ions AND the direction of the vector are opposite during repolarisation, the t wave will be in the SAME direction as the QRS complex
Summary of deflections and electrodes
- When depolarisation moves toward a positive electrode = positive deflection on the ECG
- When depolarisation moves away from a positive electrode = negative deflection on ECG
- When repolarisation moves toward a positive electrode = negative deflection on ECG
- When repolarisation moves away from a positive electrode = positive deflection on ECG
what is cardiac axis
reference to the QRS axis which is the average direction of all the vectors during ventricular depol
Normal cardiac axis
-30 and +90
ECG paper components
25mm/sec
1 small square = 1mm, 40ms (0.04s)
5 large squares = 5mm, 200ms (0.20s)
p wave
- Duration less than 0.12 seconds (3 small squares)
- Amplitudes less than 2.5mm in limb leads and less than 1.5mm in precordial leads
right atrial enlargement - p pulmonale
- Height >2.5mm
- Width remains unchanged (<0.12 seconds)
- In lead II and V1
- More peaked
left atrial enlargement p mitrale
- Height remains unchanged (<2.5mm)
- Width is longer (>0.12 seconds)
- Prolonged and delayed depol of left atrium, great muscle mass to depolarise
- In Lead II and V1
PR INT
The PR interval reflects the time from the start of atrial depolarisation to the start of ventricular depolarisation
Measured from the beginning of the p wave to the start of the QRS complex
Should be between 0.12-0.20 duration (3-5 small squares)
Narrow QRS
A narrow QRS(<0.12) means that the rhythm is supraventricular in origin
* SA node p wave (normal)
* Atria (abnormal p wave/flutter/fibrillatory wave)
* AV junction (abnormal p wave or no p wave)
* As long as its from the bundle of his or higher it will be narrow
BROAD QRS
A broad QRS complex >0.12 means that the rhythm is either
* Ventricular in origin (one ventricle to the other, sequential rather than simultaneous)
* Supraventricular in origin with
- Aberrant conduction due to a bundle branch block
- Presence of an accessory pathway causing preexcitation (delta wave or antidromic AVRT)
- Electrolyte disturbance (sodium/K+)
- Hypothermia
Low voltage QRS
Amplitude of all the QRS complexes in the limb leads are less than 5mm in height
OR
Amplitude of all the QRS complexes in the precordial leads are less than 10mm in height
Low QRS voltage causes
- Extra tissue between the heart and electrodes (fat, air or fluid)
- Infiltrative disease of the heart
- Loss of functional myocardium
Large QRS voltage
causes
- Ventricular hypertrophy (larger the heart muscle the larger the electrical current)
- Body habitus (taller slender individuals have a shorter distance between the heart and electrodes
Poor r wave progression causes
- Prior anterior myocardial infarct
- Left or right ventricular wall hypertrophy
- Misplacement of leads
- Dextrocardia (Heart sitting more rightwards)
- Congenital heart defects
t wave amplitude
<5mm in limb leads and <10mm in precordial leads
Causes of Left axis deviation
inferior MI
LAHB
LBBB
WPWS
obsesity
pregnancy
PPM
Causes of Right axis deviation
pulmonary hypertension
PE
dextrocardia
anterior/lateral MI
valve lesions
RV hypertrophy
COPD
when do triggered activity (after depolarisations) occur
An action potential itself may trigger an after depolarisation, which is a depolarisation occurring during or after the repolarisation phase (phase 3)
* Early after depolarisations: occur during repolarisation
* Delay after depolarisations occur after repolarisation
3 properties needed for a re entry circuit to occur
- There must be a path of electrically connected myocardium (cells must be able to conduct)
- Cells within the circuit must have varying ability to conduction an impulse (refractoriness)
- The circuit must surround a core of tissue that cannot be depolarised (e.g. scar tissue or valve)
anatomical re entry how and eg
- The central core consists of a distinct physical structure
- Creates a fixed circuit with constant location and velocity
- Eg- flutter (circulates around tricuspid valve in RA), AVNT, AVRNT, VT
Functional Re entry
- Due to electrophysiological heterogeneity (unclear the cause or why these exist sometimes) (variation in refractoriness and excitability)
- circus movement which is continously refractory
- If an impulse travels through such an area it may encounter a functional block and circulate around it. As it circulates it will emit impulses both outwards and inwards towards the core. The core will then be overwhelmed with impulses and essentially remain refractory
- They are often small, unstable circuits and may create additional re entry circuits (af/vf)
Flutter - where
macro re entry circuit around tricuspid valve
moves in an anticlockwise direction
flutter negative waves in which leads and why
negative flutter waves in inferior leads due to retorgrade conduction
Orthodromic vs antidromic AVRT
Orthodromic = regular narrow QRS, anterograde/forward conduction down the AV node and then back up accessory pathway
Antidromic = regular wide QRS (looks like VT), anterograde/ forward conduction down the accessory pathway and back towards av node = broad QRS
First degree av block
More a delay than true block
* PR int >200ms (0.2s)
* Reflects the conduction of the cardiac impulse through the atria, AV node, bundle of his, branches and purkinje
* This is usually due to a delay through the AV node
Second degree type 1 (wencke bach)
- Progressive prolongation of the PR interval until eventual dropped beat
- Reversible conduction block at the level of the AV node
- AV nodal cells gradually fatigue until they fail to conduct an impulse
second degree type 2
- Intermittent non conducted p waves
- PR interval remains constant (no progressive prolongation)
- Usually due to a block in the His purkinje system below the AV node
- 25% of cases, block is within the bundle of his, creating a narrow complex
- 75% of cases, block is below the bundle of his, creating a wide complex. Pts already have a BBB, with the 2nd degree AV block produced by an intermittent failure of the remaining bundle branch
- Often there is a pattern ie 3:2 conduction
sinatrial exit block
An outer layer of transitional cells which transmit the impulse to the right atrium. Failure of these cells to transmit the generated impulse = sinoatrial exit block
Sinus arrest
A central core of pacemaker cells which produce the impulse. Failure of these cells to produce the impulse.
more than 2 P-P intervals
ateriorsclerosis
- Hardening and thickening of vessel walls
- Smooth muscle cells and collagen fibres migrate into the tunica intima = hardening and thickening (weakening)
- Metabolism of lipids, cholesterol and phospholipids alters the tunica intima leading to hardening
4 stages of athersclerosis
- Endothelial injury
- Fatty streak
- Fibrous plaque
- Complication lesion/thrombus formation
endothelial injury causes
- Toxins – ciggies
- Hyperlipidaemia
- Mechanical stress – HTN
- More
functions of endothelium …. it regulates
- Vascular tone
- Platelet adhesion (endothelium releases nitric oxide which regulates platelet adhesion, so when it is injured it has a decreased ability to do this)
- Monocyte adhesion and inflammation
- Thrombus generation
- Lipid metabolism
- Cellular growth and vascular remodelling
UA
- Reversible myocardial ischemia
- New presentation type (at rest, or more often)
- Stable angina which has now changed new presentation
- Atherosclerotic plaque has now become complicated, transient episode of thrombotic vessel occlusion and vasoconstriction
Anaerobic metabolism in AMI
- Produces only 5% of required energy but critical for stunned myocardium to live
- Glycogenolysis occurs for a few min after the initial few seconds when creatine phosphate and ATP are burnt
- By-products accumulate secondary to anaerobic metabolism
- Lasts for 40-60 mins max
consequences of anaerobic metabolism in AMI
- Na-K pump fails (reduced contraction of the heart)
- Mg and calcium is also lost from inside the cell
- Accumulation of H+ and lactate
- Damage cells release enzymes such as creatine kinase and monocyte proteins such as troponin
- Cell oedema, membrane leak, contractile inhibition, depolarisation and conduction disturbance
causes of aneurysms
atherosclerosis, congenital, trauma, inflammation, cocaine use
Saccular aneurysms
80-90% cause on intracranial haemorrhage
most common cause for subarach
commonly due to congenital defect in tunica media
fusiform aneurysm
occurs due to diffuse atherosclerotic changes
false / dissecting anerurysm
considered false because it doesnt involve all layers
commonly seen in the thoracic aorta
Dresslers syndrome
onset of pericarditis secondary to inflammation and healing process of AMI
pericarditis ECG changes
PR segment depression, diffuse ST segment elevation
pericardial effusion
accumulation of fluid in the pericardial cavity
can lead to tamponade
cardiac tamponade
if the pressure is the same as diastoic pressure in the heart then artial filling will be impaired = right sided heart failure = reduced cardiac output
what is pulsus paradoxus
large decrease in systolic BP during inspiration. indicates low blood volume in all chambers
dilated cardiomyopathy
is due to ventricular dilatation and impaired systolic function
caused by IHD and valve dysfunction
ejection fraction equation
EF(%) = sv/edvx100
should be greater than 60%
hypertrophic cardiomyopathy
can be obstructive and non obstructive
enlargement of the inter ventricular septum and disorgansation of the cardiac myocytes and myofibrils
due to valve dysfunction, HT or genetics
restrictive cardiomyopathy
less common
reduction in stroke volume but normal thickness
impaired filling with reduced volume due to failure of the myocardium to relax during diastole
most common cause is R sided HF
types of valve dysfunction
stenosis (valve opening restricted, reduced blood flow, increased workload of the chamber behind to overcome the resistance) or
regurgitation/incompetence (valve doesn’t close properly, blood flows through in both directions, causes chamber dilation due to increased volume)
=dilation and hypertrophy of heart chambers
More common in valves on L side of heart
Aortic stenosis
causes
results in decreased SV and LV hypertrophy
mitral stenosis
LA dilatation and hypertrophy
aortic vs mitral regurgitation
LV receives blood from LA and then out aorta ->Increased EDV = increased stretch ->Ventricular dilation and hypertrophy
mitral
Blood flows from LV to LA
LV becomes dilated and hypertrophied to maintain CO
LA also becomes dilated causing valve to stretcher resulting in more regurg
= pulmonary HTN and R sided HF
mitral valve prolapse
Cusps of the valve prolapse upward into the atria during systole
Cusps are enlarged and thickened
Chordae tendineae become elongated allowing cusps to stretch
= mitral regurg
