8: Heart Flashcards
Describe the external structure and characteristics of the heart
- cone-shaped
- muscular organ
typically 12-14cm long, 9cm wide
weighs 250-350 g
approx the size of fist
Location of the heart
mediastinum= the cavity between the two pleural cavities and rests on the superior surface if the diaphragm.
Describe the position of the heart
To the patient’s left of the midline.
Describe the base of the heart
most superior and wide part of the heart.
Posterior to the cartilage of the 2nd and 3rd ribs.
Attachment point for many major arteries.
Describe the position of the apex
most inferior part of the heart located in 5th intercostal space, 12-14cm below base.
Covering of the heart- Pericardium
The double walled sac covering the heart.
parietal pericardium
- has a fibrous attachment to diaphragm
Coverings of the heart
Parietal pericardium
pericardial cavity
Epicardium
- the parietal pericardium meets large blood vessels at the base of the heart and turns to cover the heart itself, forming the epicardium
Pericardium fluid in the pericardial cavity prevents friction during heartbeat to prevent damage to the tissue.
List the three components of the heart wall and any structural features
Epicardium (or viceral pericardium)
- outermost layer of epithelial tissue.
Myocardium
- middle layer, cardiac muscle cells + muscle and nerves
Endocardium
- inner layer of endothelial cells (flattened epithelial cells)
Explain epithelial cells name change
change to endothelial when associated with the heart.
- still, outer covering cells that form smooth lining, cover valves, line inner surfaces of blood vessels, reduce friction.
Explain an auricle
the superior surface of the atrium that can expand slightly to increase capacity and therefore ability of the atrium.
Explain the trabecular carneae
the unsmooth muscular lining of the ventricles. Though to prevent suction of each side of the heart from occurring.
Explain what prevents the valves from inverting
Chordae tendineae= fibrous tendons that anchor heart valves and are attached to
Papillary muscles= connect chordae tendineae to the heart wall.
Papillary muscles contract to
make chordae tendineae tense to prevent eversion.
Relate the structural thickness of the walls to the function.
thick intraventricular septum and left ventricle wall to pump 4-6 times more pressure to get blood around the body through the systemic circuit compared to the right side that sends to the pulmonary circuit.
The circuit that supplies blood to the body
Systemic circuit
The circuit that supplies blood to the myocardium
Pulmonary circuit
Describe the function of atrioventricular valve
function= stop blood from moving backward- allowing the heart to effectively pump
Explain when the AV valves open and close
AV valves open= when artial pressure is greater then ventricular pressure
AV valves close when= atrial pressure is less then ventricular pressure.
Explain when the semilunar valves open and close
SL valves open= ventricle pressure > arterial pressure (pulmonary artery)
SL valves close= ventricular pressure< arterial pressure
open when ventricle contracts (more ventricular pressure) and close when ventricle relaxes and arterial blood attempts to move back into the heart but is caught by cusps of valves.
What is the name of the wall separating the ventricules
Intraventricular septum (wall)
Which valves have chordae tendillie and papillary muscles and which don’t? and why?
Atrioventricular= do
Semilunar valves= do not- they are flipped upwards meaning the pressure of backflow pushes them together preventing them from opening.
Describe the anatomical position of the coronary arteries
Arise from the base of the aorta and encircle the heart in the coronary sulcus
What is the coronary sulcus
the external grove that separates atriums from ventricles
Explain the path of blood through the coronary arteries
after exiting at the base of the aorta when ventricles relax, blood flows into the right and left coronary arteries. The Left coronary artery exists the coronary sulcus and gives rise to the anterior intraventricular artery. The right coronary artery gives rise to the posterior interventricular artery.
Name to two coronary veins and their position and function
Great cardiac vein= drains deoxygenated blood from the anterior ventricles
Middle cardiac vein= drains the posterior ventricles
What is CAD and how does it occur
Coronary artery disease
CAD= coronary arteries become narrowed and hardened (less elastic)
causes= atherosclerosis (fatty plaques occluding the arteries)
- overtime this reduces blood flow and weakens the myocardium and contributed ti heart failure.
Name and describe the two types of CAD
- Angina pectoris
- temporary deficiency in myocardium blood supply during physical activity- damages myocardium
- pain in neck, jaw, shoulder, back
2,. Mycocarial infarction
- prolonged artery blockage- myocardial death
- Males= prolonged, intense chest pain and pain in jaw, back, and stomach.
- Females= extreme fatigue and nausea
death= depends on extent and location of dead myocardium.
myocardial scar tissue loses previous capabilities (stretch + strength) therefore increasing likely hood of a heart attack to occur again.
What are the two types of innovation of the heart
Intrinsic conduction system
- from the inside- able to stimulate its own contractions
Extrinsic innervation
- from the outside- autonomic nervous system- modifies the cardiac activity
Explain the Intrinsic conduction system
myocardium hold auto-rhythmic pacemaker cells which have unstable resting membrane potentials that continually depolarise to generate action potentials.
Each muscle cell has special electrical connections when a pacemaker cell which creates AP’s that can be conducted to adjacent muscle cells and so on. this allows the coordinated activity of the entire myocardium.
List the 5 pacemaker cells that form the intrinsic conduction system
1- sinoatrial node
2- atrioventricular node
3- Atrioventricular bundle/ bundle of HIS
4- Bundle branches
5- Purkinje fibers (subendothelial conducting network)
Outline the path of electrical innovation of the heart.
- Sinoatrial node= depolarises (creates action potential) 100x/min (fastest component)
- Atrioventricular node= depolarisation pauses (0.1sec) at the AV nose.
- AV node depolarises 40-60x/min. Told what do do by SA nose. Will take over is AV node is damaged - Atrioventricular bundle (AV bundle)= electrical connection between atria to ventricles
- Bundle of His
- travels Ap’s through intraventricular septum to apex of the heart. - Purkinje fibres
- penetrate ventricle wall, depolarise ventricular myocardium 30x/min.
Explain extrinsic innovation and where it is located
Controlled by the autonomic nervous system to prevent the heart from beating at 100bpm as it would if SA node was in charge.
location= medulla oblongata
Name the two cardiac centers in the medulla oblongata and their function.
1- Cardioacceleratory center (cardiostimulatory): increases heart rate and force of contraction
- sympathetic input via thoracic spinal cord (T1-T3) to SA + AV nodes, ventricular myocardium and coronary arteries (causing dilation)
2- Cardioinhibitory centre: decreases heart rate only
- parasympathetic input via vagus nerve (CN X) to SA + AV nodes (this is why it only effects heart rate- it only touches these). Will slow SA node to 75depolarisations/min at rest
ECG measures
electrical currents measured at the body’s surface.
- is a composed image of all action potential generated.
Explain the innovation occurring with relation to the PQRST complex
P= atrial depolarisation QRS= Ventricular depolarisation and atrial repolarisation (not shown as masked) T= ventricular repolarisation
Describe systole
period of contraction- increased pressure forces blood out of the chambers
Describe diastole
period of relaxation- decreased pressure allows chambers to refill
The cardiac cycle refers to
One complete heartbeat
- atrial diastole and systole
- ventricular disatole and systole
one ventricle won’t contract until the other finishes to ensure blood lows in one direction.
Explain the phases of the cardiac cycle
1- Ventricular filling (mid-late diastole)
Ventricular filling
Atrial contraction
2- ventricular systole (artiral diastole)
2a) Isovolumetric contraction phase
2b) Ventricular ejection phase
3- isovolumetric relaxation (early diastole)
Describe the heart sounds
S1= AV valve closure "Lubb" S2= SL valve closure "Dubb"
heard over 2nd intercostal space
Bi and Tricuspid valves heart over 5th intercostal spaces
Cardiac output (CO)=
stroke volume x heart rate
Volume of blood pumped into the systemic (or pulmonary) circuit per minutes (L/min)
a measure of peripheral blood flow
Heart rate (HR)=
number of beats per minute (bpm)
average heart rate 75BPM
Stroke volume (SV)=
volume of blood ejected from the left (or right) ventricle per beat (ml)
average stroke volume= 70ml/beat
Stroke volume (SV)= in terms of end values
SV= EDV- ESV
therefore, any condition that effects EDV and ESV will effect stroke volume and cardiac output.
Explain end diastolic volume
the volume of blood in a ventricle at the end of its diastole (just before contraction)- when the ventricle is full (approx. 120ml at rest)
Explain end systolic volume
the volume of blood remaining in a ventricle after it has contracted (approx -50ml)
What 2 factors effect EDV and how?
Venous return= amount of blood returning to the heart from systemic or pulmonary circuits
- depends on total blood volume and patterns of blood flow determined by muscle/organ, sympathetic activity and body position
Passive filling time= time both the artia and ventricles are in diastole (phase 1)
- decreases as HR increases ie during activity
EDV determines preload (define preload)
preload= degree the myocardium is stretched before it contracts
- determines the force of ventricular myocardial contraction which determines SV
MORE BLOOD IN = MORE BLOOD OUT
Factors affecting ESV
Afterload and contractility
How dies after load affect ESV (define it)
After load
- the pressure that the ventricles must overcome to open the SL valves to eject blood into the arteries.
- impacted by factors that restrict floe in the arteries e.g. arteriosclerosis (decreases compliance)
- think the water bottle analogy
The less time there is for blood ejection, thus increases after load and decreases stroke volume.
How does contractility affect ESV (define it)
What factors increase or decrease contractility?
contractility= the amount of force produced by myocardial contraction
increase contractility= higher SV (thus lower ESV)= high CO
Increasing factors Sympathetic stimulation - hormones (e.g. adrenaline, noradrenaline, thyroxine) - High levels of extracellular CA2+ - exercise (increase size of myocardium)
Decreasing factors
- acidosis
- increased extracellular k+ levels
Explain heart rates ability to control CO and BP
makes rapid alterations
- does this to meet the needs to tissues/organs
- can compensate for changes in SV (if myocardium is damaged or blood volume is low due to dehydration)
What is the normal range and average heart rate?
Normal range= 60 - 100 BPM
Average rate= 75 bpm
Factors affecting average/resting heart rate
- fitness= stronger myocardium and more efficient so lower - females= typically smaller heart so higher - age - gender - general health - physical fitness - Lesser average heart rate as you age - babies have very high resting heart rate
What are some factors that effect heart rate?
- ANS (sympathetic and parasympathetic response)
- Hormones
- Body temp
- Plasma electrolytes
- age
- gender
- general health
- physical fitness
Explain how the ANS affects heart rate.
Where doe sit attain information form?
Where is it sent to?
Cardiovascular centre in the medulla oblongata
receives info from=
- proprioceptors- monitor movement
- Chemoreceptors- monitor CO2, O2 and H+ levels
- Baroreceptors- monitor blood pressure
to deliver=
sympathetic stimulation from cardioaccelaratory centre
- NA binding B1 receptors which speeds up depolarisation of SA and AV nodes which increases heart rate.
Parasympathetic from the cardioinhibitory center which
- ACh binding muscarinic receptors which slows depolarisation of SA and AV does- decreaseHR
Slows depolarisation of SA node (pacemaker) from 100/min to 75/min
Explain how hormones and temperature affact HR
- Temp (colder slower)
- Plasma electrolytes (effect action potential generation)
increased NA= or K= changes the membrane potential - Age/Gender/general physical health/physical fitness
- Adrenaline and noraadrenaline= released from adrenal medulla and increase heart rate
Thyrocine= increase cellular metabolism therfore increasing heart rate
