Electrical properties of the heart Flashcards
excitation-contraction coupling.
actin myosin fillaments overlap - cross bridges oull closer together. sarcolemma is membrane surrounding whole muscle.
t - tubule deviations rul down tubule (transferse)
sarcoplasmic reticulum acts as calcium store.
Why does cardiac muscle have a longer depolarisation time than skeletal muscle?
To allow for regulation of the amount of calcium getting into the cell, the calcium released inside the cell and so the strength of contraction
What does cardiac muscle form to allow it to function as a unit?
A functional syncytium
*A syncytium is a mass of cells that have merged together. The muscle cells in the cardiac syncytium are derived from the mesoderm. *
What allows the functional syncytium to work?
Gap junctions - electrical connections
Desmosomes - physical connections
What is the cardiac output of the heart?
5l / minute
CO = SV x HR
sarcoplasmic reticulum acts as__
calcium store
in skeletal muscle how would the sarcoplasmic reticulum get activated
sat at -90mv; activated by motor neuron releasing acetylcholine and binds to nicotinic receptors at end plate;
depolarises cell = evoke an action potential in muscle membrane
action potential will travel along being self-propagated by voltage-gated sodium channels
all along membrane then down t tubules and through interaction with sarcoplasmic reticulum which release calcium inside cells = calcium binds to troponin
Why does cardiac muscle have a longer action potential period than skeletal muscle regarding a long refractory period?
Stops the cardiac muscle from exhibiting tetanus
(twitch contraction which creates sustained contraction tetanus if you wish to keep a muscle contracted) skeletal good for holding things and avoiding dropping
QRS in chest leads v1 and v2 are usually
negative.
When venous return decreases there is a corresponding decrease in .
cardiac output
is the type of penicillin used for prophylaxis against rheumatic fever and rheumatic heart disease.
Benzathine penicillin G
Infants with (dextro-transposition of the great vessels/levo-transposition of the great vessels) might not show symptoms at birth, but will eventually develop heart failure later in life.
(dextro-transposition of the great vessels/levo-transposition of the great vessels) levo-transposition of the great vessels
Infantile coarctation of the aorta is associated with both patent ductus arteriosus and (chromosomal anomaly) syndrome.
Turner syndrome.
There is a ____ to ____ shunt between the atria in hypoplastic left heart syndrome.
left to right shunt
The normal axis of the heart points downward and to the patient’s
left
__is the imaging test of choice to diagnose deep venous thrombosis.
Compression ultrasound with doppler
What are capillaries made up like
Exchange vessels
Very narrow lumen and thin wall
BP very low
What are veins made up like
Low resistance so blood can get back to the heart
Wide lumen
2/3 of blood stored in veins = capacitance vessels
What is MAP determined by
Cardiac output and total peripheral resistance
end-diastolic volume -
the left ventricle is filled with the maximum volume of blood,
Preload -
amount blood left in left ventricle before contraction (determined by end diastolic pressure) = volume work of heart
Stroke volume -
blood vol(l) pumped by heart per contraction - determined by blood filling ventricle, compliance of ventricular myocardium.
Cardiac output-
blood pumped by heart per minute (co=svxhr)
MAP -
is the average arterial pressure throughout one cardiac cycle, systole, and diastole. influenced by co and systemic vascular resistance
can be used for reversing witnessed ventricular fibrillation in the absence of defibrillators.
Precordial thump
What is a functional syncytium?
A group of cells that are synchronised electrically in an action potential
How is arteriolar resistance controlled
Extrinsic neural control
Extrinsic hormonal control
Intrinsic control - individual tissue
how long is the action potential of cardiac muscle
how long action potential for skeletal muscle
cardiac 250msec
skeletal 2 msec
basic electrophysiology cell heart non-pacemaker what makes it depolarise?
the neighbouring cells depolarising (syncytium)
0 - rapid depolarisation - rapid sodium influx
1 - early repolarisation - efflux potassium
2 - plateau - the slow influx of calcium
3 - final repolarisation - efflux of potassium
4 restoration of ionic concentration ions - resting potential restored by na+/k+atpase. slow entry of na+ into the cell until a threshold for new action potential
ECG explain 1st-degree block
delayed p - q interval
the atrioventricular node is a delay box slowing the conduction of action potential to
ventricles this can slow/ stop so no depolarisation from the atrium to the ventricle. delay
normal interval p wave to start QRS complex should be less than 0.18 seconds. one large square is 0.2s
2nd degree block ECG
some depolarisations don’t get through at all. the increasing delay between Q to QRS interval and sometimes no QRS
3rd-degree heart block ECG
no transmission between atria and ventricles
depolarising from another place (not coordinating with atrium) hence inverted t wave
atrial flutter (conduction disorder) ECG
normal P QRS t sequence but each depolarising occurring quicker than should so superventricular tachycardia.
atrial flutter
atria and pacemaker isn’t depolarising spread of a wave of depolarisation across the atria. individual cells depolarising causing AF
ventricular fibrillation ECG
Lethan uncoordinated depolarisation in ventricles.
defibrillator - to depolarise all cells same time = enters a refractory period
pacemaker cells able to try to start rhythm again
standard ecg box
augmented limb leads aVR aVL aVF
are derived from the same three electrodes as leads I, II, and III, but they use Goldberger’s central terminal as their negative pole.
precordial/ chest leads
labelled v1-v6
