Cardiovascular Physiology Flashcards
What is a heart contraction?
Electrical impulse that triggers contractile cells
Is a heart contraction intrinsic or extrinsic?
intrinsic (arises from within the heart)
nervous system NOT required
What are the nodes?
clusters of conducting ells that initiate AP in the heart
they have an unstable resting potential (leaky to Na+)
What is the name for the gradual depolarization of nodal cells
prepotential
what happens when threshold is met in the nodal cells?
the voltage gated Ca2+ channels open and a spontaneous AP occurs
List the steps of a conducting cell AP
1) Na+ enters through leak ch. (slow influx)
2) cell develops a prepotential
3) v. gated ca2+ channels open @ threshold
4) rapid influx of ca2+ causes depolarization which causes an AP
5) ca2+ channels close and voltage gated K+ channels open
6) depolarization occurs
How do the AP’s spread beyond the nodal cells to the contractile cells?
gap junctions @ intercalated discs
How are the cells connected?
via desmosomes an anchoring protein which prevents separation
explain and list the electrical pathway that the impulse spreads
1) Sinoatrial (SA) node -In posterior wall of R. Atrium
* goes across internal pathway
2) Atrioventricular (AV) node - floor of R. Atrium
* AP delayed here to allow time for atria to contract
* impuse transmitted to…
3) AV bundle (in the intertribal septum)
4) L + R Bundle branches (in the inter ventricular septum)
5) Purkinje fibers (walls of ventricles)
* Ventricles contract
what is the contraction rate established by the SA node?
100 bpm
so if the SA node wants the heart to beet 100bpm… why doesn’t it?
the parasympathetic system innervates the node - Acetylcholine slows the heart
what happens if the sympathetic system innervates the nodes?
norepinephrine speeds the heart
What would happen if the SA node stopped working
the AV node would fire on its own 40-60bpm
Special aspects of cardiac cell anatomy
- Gap junctions: allow ions to move from cell to cell
- Desmosomes: prevent separation
- Mitochondria: are very fatigue resistant
- Myofibrils: Branch
- NO Terminal cisternae: T tubules release Ca2+ from sarcoplasmic reticulum
Describe the spread of AP to contractile cells
1) Na+ leaks in
2) V. Gated ca2+ ch. open in nodal cells
3) Action potential across nodal cells
4) Cations (+) diffuse into adjacent contractile cells via intercalated discs which house gap junctions
5) this depolarization causes fast v. gated na+ Ch and slow ca2+ channels to open in contractile cells
why are AP slower and more prolonged than in skeletal muscle
-V. gated Na+ channels close quickly
-V. Gated K+ Ch = open
**Repolarization is delayed because voltage gated ca2+ channels in the cell membrane are still open and Ca2+ comes in from the ECF
**This influx also opens ca2+ gated ca2+ channels (like a ligand) in the sarcoplasmic reticulum
**So there is a plateau in membrane potential as ca2+ moves in while K+ moves out
(AP is 30x slower)
Explain the steps of the cardiac muscle cell AP
1) Na+ & ca2+ influx through voltage gated ch.
2) na+ ch. close, k+ ch. open
3) ca2+ influx from ECF & SR and K+ influx -plateau
4) Ca2+ ch. close
5) K+ outflow continues
6) v. Gated K+ ch close (repolarized)
What does it mean that contraction of cardiac muscle cells is coupled to excitation
- Ca2+ enters from SR + ECF
- Ca2+ binds troponin causing tropomyosin to shift
- This allows the cross bridge to form (Myosin binds actin)
- the filaments slide which causes a contraction
- The ca2+ ch are slow to close so the contraction is prolonged
- eventually the ca2+ pumps will put all the Ca2+ back where it came from and outflux of K+ will repolarize the cell
What is meant by a cardiac cycle?
1 complete contraction & relaxation
What is systole
contraction phase (blood pushed out of chamber)
what is diastole
Relaxation phase (chamber fills with blood)
What does an electrocardiogram do?
Records electrical currents (AP’s) during the cardiac cycle
DOES NOT measure muscle contractions: just the electrical events that trigger it
what causes the p wave
atria depolarization then atrial systole occurs in space after
What causes QRS Complex
Ventricles depolarize then after the ventricular systole occurs
(@ same time atria is repolarizing and atrial diastole)
What is causes the T wave
ventricles repolarize then ventricular diastole occurs
What is happening at atrial systole
SA node depolarizes to AV node
both atria contract
both AV valves are forced open
the blood is pushed into the ventricles
What is happening at ventricular systole
The electrical impulse to AV bundle to R +L Bundle branches to purkinje fibers
-The isovolumetric contraction phase occurs
as pressure rises the SL valves open
the ejection phase
What is the isovolumetric contraction phase
both ventricles contract but blood has not been ejected yet
what is the stroke volume
amount ejected from left ventricle
what is the end systolic volume
the amount of blood remaining in ventricles after systole
What is happening at ventricular diastole
- Semilunar valves close
- isovolumentric relaxation phase (only the ESV is in ventricle)
- passive filling
- active filling
What is passive filling
low pressure pulls blood from atria through av valve
the ventricles fill 70%
w/o the atria even contracting
What is active filling
The atria contract and push 30% more blood in
the av valves close
What is end diastolic volume
blood in ventricles @ max
what is happening during atrial diastole
- Passive filling of atrial as the relax
- occurs during ventricular systole and diastole
What are the muscles doing @ P wave
passive ventricular filling & atrial contraction
what are the muscles doing @QRS complex
isovolumetric contraction
What happens just after QRS complex
ventricular ejection phase
what happens in muscles at T wave
isovolumetric relaxation
What is the equation for cardiac output
HR X SV
Explain the regulation of heart rate
Intrinsic contraction rate is altered by the ANS
ANS fibers innervate nodal cells (adjust pacemaker activity) by altering ion permeability
Explain what the cardio accelerator centers do
- Sympathetic
- Increase heart rate
- Norepinephrine binds to beta 1 receptors
Explain what the cardio inhibitory enters do
- parasympathetic
- vagus nerve
- decrease heart rate
- Acetylcholine binds to M2 recepters
What is the dominant influence on regulation of heart rate
Parasympathetic
The vagus nerve fibers release ACH which opens K+ ch in conducting cells to decrease HR
Steps of parasympathetic regulation of HR
1) cardio inhibitory center
2) Vagus nerve
3) ach. decrease hr on SA+AV node
steps of sympathetic regulation of HR
1) cardioacceleratory center
2) sympathetic chain ganglion
3) sympathetic cardiac nerve
- NE increase HR & Contractile force
4) can go to the nodes and the muscle cells
Equation for stroke volume
SV = EDV - ESV
what is ejection fraction
fraction of blood ejected from ventricles with each contraction
equation for ejection fraction
SV / EDV x 100
What are the 3 factors affecting stoke volume
1) Preload
2) Contractility
3) Afterload
Explain preload
Amount the ventricles are stretched by contained blood
Increased preload causes harder heart contractions
*Increased stretch increases sarcomere length, more cross bridges can form between actin & Myosin
*Factor that increase venous return will increase preload
*Hr will also increase in response to venous return (atrial reflex)
Explain the atrial reflex
Strech receptors in all or right atrium detect pressure and increase HR to get blood out of the heart
Explain contractility
Increase in contractile force
- Decreased ESV and increased SV
- regulated by hormones
- NE, THYROXINE, EPINEPHRINE
- increase Ca2+ entry into cardiac cells
Explain after load
pressure exerted bu arterial blood on SL valves
must overcome to eject blood into systemic circulation
ventricles must over come this resistance to circulate blood
