Cardio Physio: Guyton Flashcards
What are the three types of cardiac muscle fibers?
- Atrial muscle
- Ventricular muscle
- Excitatory and conductive muscle fibers
Atrial and ventricular muscle fibers contract as skeletal muscle, but with longer duration of contraction
Excitatory and conductive fibers - exhibit automatic rhythmical electrical discharge as action potentials/ conduction of action potentials through the heart
How does cardiac muscle differ anatomically from skeletal muscle?
It is striated similarly to skeletal muscle, and has typically myofibrils that have actin and myosin filaments
They differ in the fact that they form a communicating uint called a syncytium
What are the components of a cardiac syncytium and the different types of cardiac syncytia?
Components:
Cardiac myocytes
Intercalated discs - cell membranes that separate individual cardiac muscle cells
Gap junctions - permeable, communicating junctions formed by intercalated discs fusing cells together (allows for rapid diffusion of action potentials along long axis)
Types:
Atrial syncytium - constitutes walls of atria
Ventricular syncytium.- walls of ventricles
***Atrial and ventricular syncytia are separated by a fibrous band around the AV valve openings allowing the atrial syncytium to contract a short time ahead of ventricular contraction
Review the phases of the cardiac muscle action potential
**The distinct plateau in the cardiac muscle action potential is caused by: 1) Cardiac muscle has both voltage activated fast NA+ channels (like in skeletal muscle) and L-type CA2+ channels (aka slow Ca2+ channels or Ca2+/Na+ channels) which remain open for a prolonged period of time allowing influx of Ca2+ after Na+ influx has stopped. 2) Cardiac muscle has a 5x fold decreased potassium permeability during depolarization (likely due to Ca2+ influx) and preventing early repolarization
Phase 0 = depolarization - fast Na channels open
— The cardiac cell is stimulated —-> the membrane potential is positive (+20 mV) —> voltage gated Na+ channels open —> Na+ rapidly flows into cell —> cell is depolarized
Phase 1 = initial repolarization/ fast Na channels close
—Na+ channels close —> cell begins to repolarize—> K+ leaves cell via open K+ channels
Phase 2 = plateau phase - Ca2+ channels open and fast K+ channels close
—Brief initial repolarization —> Plateaus due to increased calcium permeability and decreased potassium permeability
Phase 3 = rapid repolarization — Ca2+ channels close and slow K+ channels open
— K+ rapid exits the cell —> ends plateau phase and returns cell membrane to resting
Phase 4 - resting membrane potential (avg -90mV)
What is excitation- contraction coupling and how does it work in both skeletal and cardiac muscle?
Excitation contraction coupling - mechanism by which action potential causes myofibrils of the muscle to contract. In BOTH skeletal and cardiac muscle, an action potential is spread to the interior of muscle fibers along membranes of longitudinal transverse T tubules
Skeletal muscle - the arrival of an action potential results In a release of Ca2+ into the muscle sarcoplasm from the sarcoplasmic reticulum and results in sliding of actin and myosin filaments along each other (I.e. muscle contraction)
Cardiac muscle - the arrival of an action potential results in opening of voltage dependent Ca2+ channels in the T tubules , in turn activating Ca2+ release channels in the sarcoplasmic reticulum
**Cardiac myocytes are heavily dependent on voltage gated Ca2+ channels, as their sarcoplasmic reticulum is less well developed, meaning that cardiac muscle is highly dependent on the concentration of calcium in the ECF and would stop function in an environment devoid of calcium
Label the Wigger’s diagram
Cardiac cycle - Occurs from the beginning of one heart beat to the beginning of the next, and is initiated by spontaneous generation of an action potential in the sinus node, which then travels to both atria, the AV bundle and then both ventricles
The P wave occurs just prior to atrial contraction on an ECG, and the QRS occurs just prior to ventricular contraction and the T wave occurs at the end of ventricular contraction. There are three peaks in atrial pressure: a wave (atrial contraction), c wave (bulging of the AV valves during ventricular contraction), and v waves (passive filling of the atria)
**Wigger’s diagram = all has to do with ventricular contraction/relaxation or filling/ emptying ***
Diastolic phases -
Period of rapid filling of the ventricles - occurs when the AV valves open (as blood accumulates in the atria during ventricular contraction). Lasts for the first 1/3 of diastole. Passive blood flow from atria to ventricles - lasts middle 1/3 of diastole. Contraction of atria - lasts for last 1/3 of diastole, and accounts for 20% of ventricular filling
Systolic phases:
1. Isovolumetric/ isometric contraction - ventricular contraction without volume change (as pressure to open semilunar valves has not been met) - cardiac muscle tension is increasing but no shortening of muscle fibers is occurring.
2. Period of ejection - ventricular contraction where semilunar valves open and blood leaves the heart (LV pressure > 80 mmHg and RV pressure > 8mmHg).
Phases - 1) Period of rapid ejection - 70% flows out during the first 1/3
2) period of slow ejection - 30% empties during the last 2/3 of the period
- Isovolumetric/isometric relaxation - ventricular relaxation without volume change ( as pressure to close semilunar valves has not been reached)
Stroke volume = end diastolic volume - end systolic volume
Ejection fraction % = (EDV-ESV)/EDV = ~60%
Stroke volume can be increased by increasing cardiac contractility and increasing end diastolic volume (by increasing preload)
Describe the volume pressure diagram in regards to cardiac output
Phase 1 - ventricular filling - low end systolic volume and low diastolic. Venous blood flows from atria into ventricles. Ventricular volume and diastolic pressure increases.
Phase II - period of Isovolumetric contraction — volume of the ventricles does not change, all valves are closed, and pressure in the ventricles increase to equal that of the aorta
Phase III - period of ejection - systolic pressure rises even higher due to contraction of the ventricle —> aortic valve opens —> volume of the ventricle decreases as blood flows into the aorta
Phase IV - Isovolumetric relaxation = aortic valve closes —> ventricular pressure falls back to diastrolic pressure —> no change in volume and back to starting point of low volume and pressure.
Define preload and afterload
Preload - degree of tension on the muscle when it begins to contract (end diastolic pressure)
Afterload - load against which muscle exerts its contractile force (pressure in aorta leaving the ventricle)
What is the frank starling mechanism?
The greater the heart muscle is stretched during filling, the greater the force of contraction and the greater the quantity of blood pumped into the aorta (due to optimization of actin myosin overlap for contraction strength and to a lesser degree change in HR)
Name the components of the ECG wave form and what each of them represent
P wave - atrial depolarization (before atria contract)
QRS - ventricular depolarization (before ventricles contract)
T - repolarization of ventricles
PQ to PR interval - time between beginning of P wave and QRS complex/ interval between excitation of the atria and the ventricles
QT interval - time for contraction of the ventricles - lasts from the beginning of the q wave to end of T wave
Paper speeds -
25 mm/s = multiply R waves by 10 to get HR (30 big boxes = 150 mm or 6 seconds) — instant rate = 1500/tiny boxes between RR interval)
50 mm/s = multiply R waves x 20 get HR — instant rate = 3000/tiny boxes between R-R interval
What is the normal flow of current in the heart?
Negative to positive (primarily in the direction from the base of the heart towards the apex
What is mean electrical axis?
Average vector of depolarization (tends to deviate towards abnormalities)
Lead 1 = always - degrees (horizontal, points to the right)
Methods — Examine all leads and find the tallest R wave; MEA is within 15 degrees on either side
What defines first degree AVB?
Prolonged PR interval/ delay of conduction between atria and ventricles but not actual blockage of conduction
What is a mobitz type I AV block (aka Wenkebach)? How does it differ from type II?
Type 1 second degree AV block
Progressive PR prolongation until ventricular beat is dropped, which is then followed by resetting of the Pr interval and repeating of abnormal cycle
Almost always caused by AV node abnormality/ high vagal tone, benign
Pacemaker not needed
What is mobitz type II AVB?
Fixed number of nonconducted P waves for every QRS (e.g. 2:1 block, or 2 P waves for every QRS)
PR interval does NOT change before dropped beat, remains fixed
Caused by abnormality of His-Purkinje system
Pacemaker needed
Describe third degree AV block
Poor conduction in AV node/ bundle = severe problem - complete block of impulse from atria to ventricles
Ventricles spontaneously establish their own signal, usually originating in AV nodes or AV bundle distal to block.
P waves are dissociated from the QRST complexes (ventricular escape/ junctional escape beats)
Atrial and ventricular rates are not associated
Pacemaker is indicated
