Heart and Lungs Week 3 Flashcards
Describe a cardiac muscle ?
- Cardiac muscle is one of the three types of muscle in the body. The others being skeletal muscle and smooth muscle.
- involuntary ( you cannot control) , striated muscle
- branched
-contain many mitochondria
- the individual cardiac muscle cells are joined together by intercalated discs and encased by collagen fibers and other substances that form the extracellular matrix.
- each myocyte contains a single centrally located nucleus and is surrounded by a cell membrane known as the sarcolemma.
- intercalated discs important for signaling and conductance
Close up a cardiac myocyte
Close up image allows you to see branching
- you can see gap junctions more clearly
- Desmosome - critical adhesion structures in cardiac myocytes
- Gap junctions - are membrane channels that mediate cell to cell movement of ions and small metabolites
In the heart gap junctions play an important role in impulse conduction
z line to z line sacromeres
What are sacromeres ?
Cardiac muscle is made up of fibers called MYOFIRILS which in turn are made up of many repeating units called SACROMERES.
SACROMERE -> MYOFIBRILS -> CARDIAC MUSCLE
Understand the striation pattern of sacromeres
Myofibrils are made up of many short units called sarcomeres, which are made up of two types of myofilament: myosin and actin. Myosin is a thick myofilament and appears as a dark band (called the A band) under the microscope. Actin is a thin myofilament and appears as a light band (called the I band) under the microscope. At the end of each sarcomere is a Z-line. Sarcomeres are joined together lengthways at the Z-line. Right in the middle of the sarcomere is a region called the M-line. The H-zone refers to the portion of the A-band which only contains myosin filaments (and not the portions where actin overlaps with myosin).
Describe the sliding filament theory ?
When muscle fibres contract, the myosin and actin myofilaments move closer together by sliding over one another. This makes the sarcomere shorter and they contract. Remember that the actin and myosin myofilaments themselves don’t contract - they always stay the same length. As the muscle fibre relaxes, the myofilaments slide away from each other and move further apart, lengthening the sarcomere.
Myosin myofilaments possess head groups which contain bindings sites for actin and ATP. Myosin heads are a globular shape that are hinged, allowing them to move back and forth and enabling it to slide the actin filaments closer towards it. The region on actin where myosin binds is called the actin-myosin binding site. This binding site is blocked under resting conditions by two proteins called tropomyosin and troponin. When the muscle is not contracting, tropomysin covers the actin-myosin binding site and is held in place by troponin.
When an action potential (nerve impulse) arrives at a muscle fibre, a wave of depolarisation passes along the sarcolemma and down the T-tubules. This stimulates the sarcoplasmic reticulum to release calcium ions, which bind to troponin. Binding of calcium ions to troponin cause it to change shape, which pulls the tropomyosin out of the actin-myosin binding site. Now that the binding site is uncovered, the myosin head can bind to actin forming a bond called an actin-myosin cross bridge.
The release of calcium ions also activates the enzyme ATPase which catalyses the hydrolysis of ATP into ADP and inorganic phosphate. The energy released from ATP hydrolysis is used by the myosin head group to move backwards, pulling the actin filament closer towards it in a sort of rowing action which is referred to as a power-stroke. ATP hydrolysis also provides the energy to break the actin-myosin cross bridge. The myosin head can then reattach to a binding site further along the actin filament. The process is repeated, pulling the actin further and further towards the myosin filament. This shortens the sarcomere and results in muscle contraction.
When the muscle stops being stimulated, calcium ions move back into the sarcoplasmic reticulum by active transport, in a process which also requires ATP. The troponin molecules reform their original shape, pushing tropomyosin back into the actin-myosin binding site. Myosin can no longer bind to actin and the actin myofilaments slide back to their original position. The sarcomere lengthens and the muscle becomes relaxed.
What does Excitation - contraction coupling mean ?
A process where an action potential triggers a myocyte to contract.
- Influx of extracellular Ca+
- Ca+ activates the troponin complex
- At this point the muscle contracts
- The Ca+ has to be got rid of now to relax the muscle.
- The Ca+ leaves the cell through the Na-Ca exchanger.
Describe the autonomic control of the heart ?
- The vagus nerve has parasympathetic fibers. It starts at the dorsal horn of the medulla oblognata. And sends messages to the SAN and AVN.
Sympathetic chain ganglion ( cluster of nerve cell bodies, ganglia are 20,000 to 30,000 afferent and efferent nerve cell bodies that run along the side of the spinal cord.) on the sides of the vertebral column is the origin of the sympathetic cardiac nerve. Which also stimulates the SAN and AVN but causes the sympathetic effects.
Describe the mechanism of noradrenaline (aka norepinephrine) on SA Nodal cells ?
Norepinephrine released by sympathetic activation of the SA node binds to beta-adrenoceptors. This increases the rate of pacemaker firing
Describe the mechanism of acetylcholine on SA nodal cells ?
Acetylcholine (ACh) released on vagal stimulation reduces the heart rate by making K+ leave the cell conductance of pacemaker cells in the sinoatrial (S-A) node.
How does noradrenaline effect cardiac contractability ?
- Noradrenaline would normally bind to B1-adrenergic receptor
- When we use beta blockers they bind to the B1-adrenergic receptor instead so that noradrenaline can no longer bind to receptor and cause an increase in heart rate.
- This is how beta blockers slow down tachycardia.
Summarize the effects of sympathetic and parasympathetic stimulation?
- Sympathetic nerves - noradrenaline - B1 and B2 receptors
- Parasympathetic nerves - Acetylcholine - M2 receptor
Chronotropic effects : factors which affect the rate at which the cardiac muscle fibers contract
Inotropic effects: an agent which alters the force or energy of muscular contractions
Dromotropic: the rate of electrical impulses in the heart. Affects the conduction speed of the AV node
Lusitropy - the rate of myocardial relaxation.
Describe the action potential of the SAN and AV node ?
The action potential of SAN and AV node is similar.
resting potential: -70mv
Depolarisation: +10 mv
Hyperpolarization then back to resting potential
Describe the action potential in atria and ventricles ?
Resting potential -80mv
plateua
repolarization
How does a cardiac action potential work?
- the standard model used to understand cardiac action potential is that of ventricular myocyte
-Unlike the action potential in skeletal muscles, the cardiac action potential is not initiated by nervous activity.
- instead it arises from a group of cells known as pacemaker cells which are found in the SAN.
- the resting membrane potential of ventricular cells is about -90mv.
- the main ions found outside the cell are Na+ and Cl- whereas inside the cell is mainly K+.
- The action potential begins with the voltage becoming more positive. This is known as depolarization (negative to positive) and is mainly due to the opening of sodium channels that allow Na+ to flow into the cell.
- plateau phase: Release of calcium ions Ca (2+) from the sarcoplasmic reticulum via a process called calcium -calcium release is essential for the plateau phase of the action potential.
- The action potential terminates as potassium channels open allowing K+ to leave the cell and causing the membrane potential to turn negative, this is known as repolarization (positive to negative).
Outline the 5 phases of the ventricular myocyte action potential ?
Phase 4: occurs when cell is at rest is a period known as diastole. Voltage is usually -90mv.
Phase 0: Depolarisation stage. There is a net flow of Na+ into the cell.
Phase 1: rapid inactivation of Na+ channels reducing the movement of sodium into the cells.
Phase 2: plateau phase because the membrane potential remains
almost constant.
phase 3 : rapid repolarization stage. The L type Ca2+ channels close. The K+ channels open and potassium leaks out of the cell. Making the inside og the cell more negative
What does the sodium calcium exchanger do ?
3 Na+ come into the cell
1 Ca2+ leaves the cell
What does the sodium potassium pump do ?
For every ATP molecule the pump uses.
3 Na+ leave the cell
2 K+ enter the cell
What the conduction pathway for the heart ?
- The action potential begins at the SAN
- They are transferred through internodal pathways to the AVN
- Travels through the bundle of His
- The bundle branches
- To the purkinje fibers then we have ventricular contraction.
What is the cardiac cycle ?
- The cardiac cycle is the performance of the human heart from the beginning of one heartbeat to the beginning of the next.
What is Stroke volume ?
SV = EDV - ESV
What is cardiac output ?
CO = HR x SV
What is the Ejection Fraction ?
- Is a measurement expressed as a percentage of how much blood the left ventricle pumps out with each contraction
What is the relationship between calcium ions and tension generation in cardiac sarcomeres at different lengths ?
The more calcium ions (Ca2+) available - the shorter the sarcomere length, the stronger the contraction so the higher the tension.
What is the relationship between calcium ions and tension generation in cardiac sarcomeres at different lengths ?
The more calcium ions (Ca2+) available - the shorter the sarcomere length, the stronger the contraction so the higher the tension.
What is the Frank Starling Law / Relationship ?
- The frank starling law of the heart represents the relationship between stroke volume and end diastolic volume.
-The law states that the stroke volume of the heart increases in response to an increase in the volume of blood in the ventricles, before contraction (the end diastolic volume), when all other factors remain constant.
- As a larger volume of blood flows into the ventricle, the blood stretches cardiac muscle, leading to an increase in the force of contraction.
Describe the cardiac action potential ?
Recognize the action potential of different parts of the heart
What is automaticity ?
aka autorhythmicity
- Automaticity is the property of cardiac cells to generate spontaneous action potentials
- Automaticity can be normal and abnormal.
Describe the innervation of the heart ?
Chronotropic (timing): rate of contraction
Inotropic (force): how strong id the contraction.
What does the action potential in the SAN look like ?
First graph: shows SAN stimulated by normally The timing between each action potential is about 0.8 seconds.
Second graph: shows SAN stimulated by parasympathetic fibers. The timing between each action potential is 1.4 seconds. Which is why the heart rate is slower.
Fourth graph: shows stimulation by sympathetic fibers. The timing between each action potential is less than 0.6 seconds. So the heart rate ahs increased.
Key feature: no plateau in SAN action potential
Describe adrenaline ?
Positive chronotropic effect: increasing heart rate
Positive inotropic effect: greater force. Make heart muscle contractions stronger.
If you wanted to compete with adrenaline and decrease heart rate you can use beta blockers
Adrenaline gives faster heart rate and forceful contractions
Describe an ECG ?
ECG is an electrocardiogram.
- its a simple test that can be used to check your hearts rhythm and electrical activity.
What is the timing of the squares on ECG paper
The ECG paper set up.
Normally the big square is 0.2 sec
Little squares 0.04 sec
Explain different parts of an ECG ?
Rest - normally 60-100 action potentials per minute
P wave: atrial depolarization. Rush of Na+ ions into cell causes P wave.
What is the PR interval?
PR interval is the time onset of the p wave to the start of the QRS complex.
It suggests the time it takes for the electrical impulse to travel through the atria and across the atrioventricular node to the ventricles.
PR interval: There is a 100millisecond delay at the AV node
Q wave:
The beginning of ventricular depolarization
The impulse travels along the interventricular septum to the ventricle.
QRS complex: completion of ventricular depolarization.
The impulse is distributed by the purkinje fibers and relayed throughout the ventricular myocardium
T- wave: ventricular repolarization
Summary of the main components of an ECG ?
What is a 12 lead ECG ?
A 12-lead electrocardiogram (ECG) is a medical test that is recorded using leads, or nodes, attached to the body. Electrocardiograms, sometimes referred to as ECGs, capture the electrical activity of the heart and transfer it to graphed paper.
Electrode Placement Area
V1 Fourth intercostal space to the right of the sternum.
V2 Fourth intercostal space to the left of the sternum.
V3 Directly between leads V2 and V4.
V4 Fifth intercostal space at midclavicular line.
V5 Level with V4 at left anterior axillary line.
V6 Level with V5 at the midaxillary line. (Directly under the midpoint of the armpit)
The correct positioning of leads is essential to taking an accurate 12 lead resting ECG. Incorrect lead placement can cause a false diagnosis of infarction or negative changes on the ECG machine
What is cardiac axis ?
The cardiac axis refers to the net effect of all of the generated action potentials.
- leads aVR and II look at the heart from opposite directions. The normal wave of depolarization passes from 11 o’clock (aVR) to 5 o’clock (lead II).
- The average spread of depolarization passing through the ventricles (visualized from the front) is termed the cardiac axis. In different disease states, the axis can be shifted to the left or the right.
Describe a standard ECG ?
- A 12 lead resting ECG has 10 leads which each have a specific position:
- 4 leads are considered to be “limb leads” because they are placed on the arms and or legs of the individual. 1 on each arm and one on each leg. The following letters are symbols for which ecg positioned lead we are talking about.
R - Right arm (aVR)
L - Left arm (aVL)
F - Left leg (aVF)
N - Right leg (aVN)
- the other 6 leads are considered ‘precordial leads’ because they are placed on the torso (precordium: heart and chest area)
-The six precordial leads are called leads V1, V2, V3, V4, V5 and V6
What is right axis deviation ?
When the average wave of depolarisation is shifted to the right beyond +90º (aVF) it is termed right axis deviation.
- Right axis deviation (RAD) is commonly seen in association with pulmonary disease. This is because pulmonary disease can lead to increased pulmonary pressure, which increases the afterload that the right ventricular has to pump against. In doing so, the right ventricle undergoes hypertrophy and thus has more effect on the QRS complex.
Causes of RAD:
Chronic pulmonary disease
Right ventricular hypertrophy
Left posterior fascicular block
Acute pulmonary embolism
Lateral myocardial infarction
You can recognise RAD in an ECG if:
RAD: leads II, III and aVF are POSITIVE; Leads I and aVL are NEGATIVE
What is left axis devaition ?
When the average wave of depolarisation is shifted to the left beyond -30º (aVL) it is termed left axis deviation.
Left axis deviation (LAD) leads is commonly seen in clinical practice and usually indicates disease of the left ventricular conducting system (bundle branch, anterior fascicle). By itself, it usually non-specific. However, it may be a feature of more widespread conduction disease or associated with acute cardiac pathology so it is important to consider the clinical context.
Causes of LAD:
Left anterior fascicular block
Left bundle branch block
Left ventricular hypertrophy
Inferior myocardial infarction
You can recognize LAD if:
- Leads I and aVL are positive; leads II and aVF are negative
Describe rate on an ECG ?
R to R interval: you go from the top of one R (in a QRS) and go to the top of another R. Then divide this number by 300.
Describe the rhythm of an ECG ?
The rhythm of an ECG can be regular or irregular.
Describe p waves on an ECG ?
- Sometimes p waves are not present in the case of atrial depolarization such as atrial fibrillation
- The should have a normal amplitude of about 3-5 squares.
If it is enlarged it could suggest atrial enlargement, vascular resistance due to a pulmonary embolism or because of heart failure.
Describe QRS complex on an ECG ?
- We need to see how wide or narrow the QRS complex is.
- Normally its quite narrow less than 2 small squares.
- Wide QRs complex indicates poor ventricular conduction.
You need to check if each QRS complex is preceded a p wave. If it is not it could suggest there is a ventricular ectopic or heart block.
Describe the T waves on an ECG ?
- normally t waves are not that large.
- but it would be very large in someone who had hyperkaliemia. We use the phrase ‘ tall tented t waves’ to describe this.
- T - wave inversion is a sign of Ischemia ( where blood flow is reduced in parts of the body)
What is a bundle branch block ?
Be able to recognize a right bundle branch block ?
- A bundle branch block is either a complete or partial interruption of the electrical pathways inside the wall of the heart between the two lower chambers (ventricles).
- a bundle branch block is diagnosed with an electrocardiogram
- SAN releases wave of excitation
- The muscle fibers that carry the signal from the atrioventricular node go into the wall that divides the ventricles and then splits into two branches, the bundle branches.
- You can have a block in the right or left branch block.
- If there is a block in the right bundle branch, the signal (excitation) is not send to the right ventricle. The electrical signal cannot travel down this path the way it would normally. The signal still gets to the right ventricle, but it is slowed down, compared to the left bundle. Because of this, the right ventricle contracts a little later than it normally would. This can cause the heart to eject slightly less blood
- A block in the right bundle branch may cause an electrocardiogram to become distorted.
How we recognize a right bundle branch block: WiLLiaM
- First the QRS complex looks like a W
- Then it looks like a L
- Then it looks like a M
Be able to recognize a left bundle branch block ?
In normal cardiac conduction, impulses travel equally down the left and right bundles, with the septum activated from left to right and the formation of small Q waves in lateral leads
In LBBB, conduction delay means that impulses travel first via the right bundle branch to the RV, and then to the LV via the septum
The delay between activation of the RV and LV produces the characteristic “M-shaped” R wave seen in lateral leads
Delayed overall conduction time to the LV extends the QRS duration to > 120 ms
How we recognize a left bundle branch block: MaRRoW
- First looks like a M
- The looks like a very wide W
Describe Ischaemic changes in an ECG?
Indicators of ischaemic:
- ST elevation or depression
- T wave inversion
What is atrial fibrillation ?
Atrial fibrillation is a condition that causes an irregular and often fast heartbeat.
Symptoms of atrial fibrillation include heart palpitations, dizziness and shortness of breath.
Treatments for atrial fibrillation include medicines to control your heartbeat and thin your blood.
It’s not clear what causes atrial fibrillation, but it’s common in people with other heart conditions.
Atrial fibrillation increases an individuals risk of stroke by 4 to 6 times.
Describe atrial fibrillation on an ECG ?
- The R waves are irregular
- There’s no p waves
- There’s no F waves
How do we manage Atrial fibrillation ?
Digoxin is a treatment for Atrial Fibrillation. Describe how it works?
Why is digoxin no longer routinely used to manage atrial fibrillation ?
- Digoxin is no longer used to treat atrial fibrillation because it can cause arrythmia
What is Ventricular Ectopic ?
- Ventricular ectopic is a wide QRS complex which is not preceded by a P wave
Where are the aortic valves found ?
The tricuspid area is located at the lower left sternal border
The primary pulmonary area is located at the left second intercostal space adjacent to the left
sternal border.
The mitral area is located at the left fifth intercostal space in the left midclavicular line.
The aortic area is located at the right second intercostal space adjacent to the right sternal border
Which lymph nodes are related to the bifurcation of trachea ?
- The tracheobronchial lymph nodes are lymph nodes that are located around the division of trachea and main bronchi.
Paratracheal nodes are located on either side of the trachea.
Tracheobronchial nodes can be divided into three nodes including left and right superior tracheobronchial nodes, and the inferior trachiobronchial node. The two superior tracheobronchial nodes are located on either side of trachea just before its bifurcation. The inferior tracheobronchial node is located just below the bifurcation in the angle between the two bronchi.
Bronchopulmonary nodes situate in the hilum of each lung.
Pulmonary nodes are embedded the lung substance on the larger branches of the bronchi.
Where is the thoracic duct found ?
- Lies posterior to the oesophagus
- Between the descending thoracic aorta and the azygous vein.
What is the course of the left brachiocephalic vein ?
Brachiocephalic veins used to be called innominate veins
The left brachiocephalic veins is nearly always longer than the right.
The left brachiocephalic vein is approximately 6 cm long and runs a long, oblique course to the right through the superior mediastinum (above the heart) anterior to the branches of the aortic arch to unite with the right brachiocephalic vein posterior to the first sternocostal joint to form the superior vena cava.
Both of the brachiocephalic veins drain into the aorta.
It is formed by the union of the right and left brachiocephalic veins – which provide venous drainage of the head, neck, and upper limbs. At the level of T4, the superior vena cava receives the azygous vein, which drains the upper lumbar region and thoracic wall.
Working out if its LAD or RAD ?
