Cardiac Flashcards
Cardiac muscle contraction
Heart muscle is stimulated by nerves and is self-excitable. (automaticity)
Contracts as a unit has a long
absolute refractory period.
Autorhythmic cell function
- Initiate action potentials
- Have unstable resting potentials called pacemaker potentials.
- Use calcium influx (rather than sodium) for rising phase of the action potential.
Electrical activity of the heart
- SA node and AP spreads throughout right and left atria.
- Simultaneously, impulse goes down internodal pathway to excite the AV node.
- Impulse passes from atria into ventricles through the AV node ( the point of electrical contact for the chambers). Fibrous ring separates chambers.
First two components to cardiac excitation
SA node - generates impulses 75x/pm
AV node - delays impulse 0.1 sec
SA nodal rise to threshold and AP
- Rising phase of the action potential is due mainly to slow Ca2+ channels (L)
- Many voltage-sensitive Na+ channels would be in an inactivated state due to the node’s depolarized state.
Ventricular muscle action potential
Phase 0. fast Na+ channels, like skeletal
1. fast Na+ channels inactivated, ( Gated- Cl- increase, while gated K+ decrease)
- Slow Ca2+ channels or Na+-Ca2+ channels. (slower to open and stay open for 200 msec), decrease in G-K+ so repolarization is not as fast.
- When Ca2+ channels close, G-K+ increases
- Resting state
Excitation-contraction coupling in cardiac contractile cells
Sequence of excitation
- Impulse passes from atria to ventricles via atrioventricular bundle
(Bundle of His)
AV bundle splits into two pathways in the interventricular septum (bundle branches)
- Bundle Branches - carry the impulse toward the apex of the heart.
- Perkinje Fibers - carry the impulse to the heart apex and ventricular walls.
Spiral arrangement of cardiac muscle
Arranged spirally around the ventricles. They “wring” blood from the apex to the base where the major arteries exit.
ECG components
- P wave - atrial depolarization
- PR segment - AV node delay
- QRS complex - ventricular depolarization - simultaneous atrial repolarization
- ST segment - Ventricular contraction and emptying
- T wave - ventricular repolarization
- TP interval - ventricles are relaxing and filling.
Cardiac cycle part I
Filling of ventricles
- 1st 1/3 of vent. diastole - period of rapid filling - blood from atria rushes into vent.
- 2nd 1/3 of diastole - diastasis - only blood coming back to the heart goes from the atria to the ventricles.
- 3rd 1/3 of diastole - atria contract: dump 20-30% of final ventricular volume into ventricle.
(the heart can operate without this 20-30% in most cases. Has 300-400% more capacity to pump than required at rest. )
Cardiac cycle - part II
Period of isovolumic (isometric) contraction- leads to ventricle emptying during systole.
As ventricular contraction begins, ventricular pressure increases greatly causing AV closure. Before vent. P is sufficient to push open semilunar valves open, both entrance and exit valves are closed and contracting.
(no change in overall volume or length)
Cardiac Cycle III
Period of ejection - vent P sufficient to push open semilunar valves -
- Period of rapid ejection - 1st 1/3- 70% of emptying
- Period of slow ejection - 2nd 2/3 - 30% of emptying
- Period of isovolumic (isometric) relexation- no volume change
Drop in intraventricular pressure back to low diastolic values and AV valves open to fill again.
HR abnomalities
- Tachycardia - Rapid rate of more than 100 beats per minute.
- Bradycardia - slow rate of fewer than 60 beats per minute.
Cardiac Rhythm abnormalities
Arrhythmia - variation from normal rhythm and/or sequence of excitation of the heart.
ex. Atrial flutter - 200-350 bpm
Afib - random, uncoordinated excitation and contraction
Ventricular fibrillation - “bag of worms”
Heart block
block somewhere in the excitatory and conducting pathway - AV is common. (pacemaker might be required)
Ectopic focus
PVCs
PSVT
paroxysmal supraventricular tachycardia
Damage to the heart muscle
- Myocardial Ischemia - inadequate delivery of oxygenated blood to heart tissue.
- Necrosis - death of heart muscle cells.
- Acute myocardial infarction - heart attack, occurs when blood vessel supply becomes blocked.
When HR increases…
Diastole shortens, SV is less, CO output is less and less O2 to tissues.
Isovolumetric contraction
All four heart valves closed.
Factors affecting S1 - part I
- Long PR -
longer diastolic filling - LV P gradually increases - mitral valve leaflets slowly drift together and there is a smaller distance between leaflets. (soft s1) - Very short PR -
(ventricle and atrial systole coincide with each other) Mitral leaflets are farther apart at the onset of ventricular systole - closes with a high velocity. (Loud S1)
Factors affecting S1 - part II
- Increased myocardial contractility increases rate of LV pressure ( loud S1, exercise_
- Decreased contractility - (MI, myocarditis) Soft S1
Factors affecting S1 - part III
- Heart Rate - Tachycardia - Loud S1 - shorter PR interval -
– wide open valves due to short diastole and increased myocardial contractility.
Factors affecting S1 - part IV
1.Transmission characteristics of thoracic cavity and chest wall.
[obesity, emphysema, pericardial effusion decrease the intensity of ausculatory events. ]
A thin chest wall increases intensity
S4 presentation
Ususally associated with a stiffened ventricle and is therefore heard in patients with ventricular hypertrophy and myocardial ischemia.
[Ameloidosis,sarcoidosis]
Rubs
1.Pericardial rub - pericarditis
(velcro sound heard throughout the cardiac cycle)
- Pericarditis - upper resp. tract infection; chest pain that is better with leaning forward and worse with laying down.
** IV- NSAIDs
Timing and frequency of S1
Frequency - 50-60 Hz
Time - 0.15 sec.
Timing and frequency of S2
Frequency - 80-90 Hz
Time - 0.12 sec.
(short and sharp)
Timing and frequency of S3
Frequency - 20-30 Hz
Time - 0.1 sec
Occurs beginning of middle third of diastole. rush of blood from atria to ventricle during rapid filling phase of cardiac cycle, causes vibration in blood.
