Cardio-vascular physiology Flashcards
Structure of heart muscle
Cell structure is of branching fibres ~100um
Generally 1 nucleus in each fibre
The myofilaments are organised into myofibrils producing a striated structure
Fibres are interwoven into bundles so they can contract in all directions
Muscle tissue is highly vascular
The cells contain many mitochondria
Beneficial heart muscle properties
Heart muscle cells are smaller in diameter than skeletal muscle
This gives a very short diffusion distance for the oxygen molecules to travel from the blood capillaries to the mitochondria
The mitochondrial density of the heart is very high
The mitochondria use oxygen to metabolise carbohydrate and fat to produce ATP
Contractile protein makes up ~60% of cell volume
Heart cells produce very little lactate despite being very metabolically active.
They can receive and consume oxygen, without getting fatigued
The heart has very little tolerance of oxygen deprivation i.e. Heart attack
ATP production in the heart muscle
Cardiac muscle produces very little ATP via anaerobic respiration, it relies on aerobic respiration in its mitochondria.
The oxygen needed comes from the coronary circulation and can also be released from myoglobin in the muscle itself
About 60% of the hearts ATP at rest, comes from the oxidation of fatty acids and ~35% from glucose, the remainder from other fuels such as lactic acid.
During exercise the heart uses lactic acid produced by actively contracting skeletal muscle cells
Regeneration of heart muscle
The heart of a heart attack survivor will have regions of dead
heart muscle, this is overtime replaced with fibrous scar tissue
our heart is not able to regenerate the muscle tissue lost, you do not see active mitosis in mature cardiac tissue.
There is some evidence that this may not always be the case as recent research from transplants indicates that some of the cells in the transplanted heart become replaced by the recipients own cells over time, this would indicate there is the potential for heart cells to regenerate?
Evidence from a recent papers has confirmed that myocytes can regenerate albeit at a very slow rate, we replace ~ ½ of them over a life-time!
Right side of the heart, oxygenated or deoxygenated?
Deoxygenated
Left side of the heart, oxygenated or deoxygenated?
Oxygenated
Membrane potentials and ion movement in cardiac contractile cells
Resting phase- -80mV in atria, -90mV in ventricles
When stimulated by action potential, voltage-gated channels rapidly open
Depolarisation- to +30mV then Na+ channels close- this lasts 3-5ms
Plateau phase- membrane potential decreases relatively slowly as Ca2+ channels in are open slow and a few K+ are open out- lasts 175ms
Once membrane potential reaches zero, Ca2+ close and K+ open to release and this depolarisation lasts 75ms back to starting potential
Overall process lasts 250-300ms
Cardiac excitation
Cardiac excitation begins at the sinoatrial (SA) node
located on the right atrial wall. The SA node cells do not
have a stable resting potential, they spontaneously
depolarise at a threshold potential, called the
pacemaker potential.
Each action potential from the SA node propagates
through both atria via gap junctions in the intercalated
discs of the atrial muscle fibres.
Following the action potential the atria contract
Activation of the AV node and the ventricles contraction cycle
By conduction of the action potential goes along the atrial muscle fibres, the action potential reaches the atrioventricular (AV)node located in the septum between the R&L atria.
From the AV node the action potential enters the AV bundle (the bundle of His), this bundle is the only site where the action potentials can conduct from the atria to the ventricles, elsewhere the heart is electrically insulated. The AV bundle branches to the right and left finally terminating at the large diameter Purkinje fibres, these rapidly conduct the action potential from the apex of the heart rapidly upwards to the remainder of the ventricular myocardium. The ventricles contract–pushing blood upwards towards the semilunar valves.
The sinoatrial node
The auto-rythmic fibres of the SA node would initiate an action potential about every 0.6 seconds ~ 100 times per minute
This rate is faster than the other auto-rythmic fibres in the heart
The action potentials from the SA node spread through the system and stimulate the other areas before they enable an action potential of their own.
In this way the SA nose acts as the hearts pacemaker
The atrioventricular node
AV node has an important property called decremental conduction in which the more frequently the AV node is stimulated the slower it will conduct. Thus preventing rapid conduction to the ventricle which could lead to rapid atrial rhythms which could lead to atrial fibrillation (irregular heart beat)
The cardiac cycle: Atria systole
Lasts about 0.1 s
During the atrial systole the atria are contracting
At the same time the ventricles are relaxed
The blood is forced through the AV valves into the ventricles
The atrial systole contributes about 25 mL of blood to the volume of blood already in each ventricle (105 mL) so there is ~130 mL of blood in the ventricles at the end of its relaxation period (diastole)
This blood volume is called the end-diastolic volume (EDV)
The depolarisation of the SA node causes atrial depolarisation on and ECG it is marked by the P wave
The onset of ventricular depolarisation is marked by the QRS Complex on ECG
Cardiac cycle: Relaxation period
This lasts about 0.4s at rest as the heart beats faster so
the relaxation period will decrease
The atria and ventricles are both relaxed
Ventricular repolarisation causes ventricular diastole as
they relax pressure in the chambers falls, blood in the
aorta and pulmonary trunk flows back into the ventricles,
as it does so the valve cusps are caught in the flow and the SL valves close this produces the dicrotic wave in the aortic pressure curve
For a brief period all four valves are closed
Electrocardiogram
As action potentials propagate through the heart they
generate electrical currents. These conduct to the surface of the body where they can be detected by electrodes placed on the skin
The ECG is a record of the action potentials produced by the heart during each heart beat
The ECG can be compared to a normal trace to give valuable diagnostic information
Factors affecting heart rate
The Autonomic nervous system (ANS) and hormones can modulate heart rate.
The cardiovascular centre of the brain situated in the medulla oblongata in the brain stem receives sensory inputs from the body and higher brain functions (e.g. fear response), then alters the frequency of nerve impulses both in the sympathetic and parasympathetic ANS
Hormones epinephrine and norepinephrine enhance the hearts pumping effectiveness, excessive thyroid hormone can increase heart rate.
Imbalances in cations Na+, K+, Ca2+ can as you would expect have dramatic effects on heart function.
Excess Na+ can block Ca2+, decreasing the force of contraction, excess K+ blocks the generation of action potentials and excess Ca2+ speeds up heart rate and strengthens beat.
