Chapter 19: Heart Flashcards
Sinoatrial Node
- specialized cardiac muscle cell
- does not control
- job=pacemaker cells
- exhibit autorhythmicity
How Action potential travels from SA Node through the heart:
- Initiated in Sinoatrial node
- Through gap junctions of cardiac atria
- Action potential is slowed down by the
Atrioventricular node - Bundle of HIS (AV bundle) & Purkinje fibers all
have a larger diameter than cardiac muscle
cells.*Action potential travels faster through the
fibers than cardiac muscle cells - Contraction of the ventricles start at the apex
of the heart
Pacemaker of the heart:
Sinoatrial Node
Autorhythmicity
Spontaneously depolarize & depolarize at regular intervels
Create a heart beat every .6 seconds =100 beats per minute
Vagal Tone
Slowing of heart rate
Normal resting heart rate is:
Constant signal through parasympathetic pathway to slow the heart
Resting Membrane Potential
*(Pumps/voltage gated channels)
Na/k pump, Na leak, k leak
1) slow voltage gated Na channels
* open slowly
* narrow channel (Na flows slowly)
2) fast voltage gated calcium channels
3) voltage gated k channel
EKG or ECG
Place electrodes on wrist, ankle, chest
Measures the electrical change in heart rate
P Wave (pulse)
Atrial Depolarization
QRS complex
Due to ventricular depolarization but also atrial repolarization
T Wave
Ventricular repolarization
PQ Segment
Atrial plateau
ST segment
Ventricular plateau
Cardiac cycle describes:
Order of events in turn of contraction, relaxation, valves opening/closing, & blood flow
Diastole
Relaxation
Systole
Contraction
Valves open when:
Pressure in preceding (prior) chamber or vessel is greater than pressure in proceeding hollowing chamber or vessel.
Pressure keeps valve open/closed
Cardiac cycle-1st stage
Heart completely relaxed after ventricular contraction
- start–> complete diastolic (at rest)
- after ventricular contraction blood flows into the right atrium from vena cavas
- blood flows into the left atrium from pulmonary veins
*left/right AV valves open because ventricles emptied;
pressure in filling atria > just contracted ventricles
- blood is flowing passively into ventricles because of open AV valve (no result of contraction)
- 70% of blood gets into ventricles through passive filling in AV Valve
- semilunar valves: closed because of pressure in ventricles is < the pressure in arteriol trunk (aorta & pulmonary arteries)
Step 2: Atrial Systole
- during contraction of the atria (right after AP is Initiated in SA node)
- forcing blood into ventricles (vent almost full) through open AV valves
- semilunar valves still closed
- end of atrial systole; we have maximum amount of blood in ventricles (30% result of atrial contraction)
–most of us have around 130 ml of blood–
End Diastolic Volume (EDV)
Maximum amount of blood in ventricles
Step 3: Early Ventricular Systole
- Beginning of ventricular contraction-right after AP is initiated in the AV node
- travels into Purkinje fibers
- As soon as ventricles start contracting, some blood enters atria forcing AV valves to shut
- Semilunar valves are closed:
- -> because not generating enough pressure in ventricles to overcome the pressures in the arterial trunk
Isovolumetric Contraction is happening in ventricles
Isovolumetric Contraction:
All valves are closed & no movement of blood during early ventricular systole
Step 3: Late Ventricular Systole
- contraction of ventricles nearing end
- contracting ventricle created enough force to overcome pressure in arterial trunks
- semilunar valves open causing ventricular ejection
- AV valves remain closed. Pressure in Atria is < than contracting ventricles
- Blood leaves ventricles to the arterial trunks
Stroke volume
Amount of blood in ventricular ejection
*about 70 ml
End Systolic Volume
Blood left over
SV-EDV=ESV
130 ml-70ml=60 ml
Step 4: Early Ventricular Diastole
- After contraction of ventricles,beginning of relaxation of ventricles
- AV valves closed
- Pressure in atria is < than pressure in ventricles
- Semilunar valves closed
- -> because pressure outside of semilunar > than that in ventricles
Step 5: Late Ventricular Diastole
(Almost like step 1)
- After contraction of ventricles
- AV valves open. Pressure of the atria > than the pressure in ventricles
- semilunar valve closed
END OF CARDIAC CYCLE!
Cardiac Output is measured by:
How efficient the heart is @ it’s job of perfusion.
*Perfusion: describes the amount of blood needed in certain areas of the body per minute
Cardiac Output is described as:
The amount of blood that is ejected from ventricles per minute
Cardiac Output Is determined by:
*SV (stroke volume) x HR (heart rate)
Example of a person at rest:
HR= 75 beats per min
SV= 70 mL per beat
70 mL x 75 beats per min = 5.2 L per minute
*CO explains why:
- babies need faster resting HR because smaller heart.
- Athletes have lower HR, heart more efficient
Chronotropic Agents
Anything that affects HR
Sympathetic stimulation of nodal cells (SA node):
1)NE releases from the medulla oblongota or
adrenal glands
2) Your nodal cells have adrenergic receptors
3) NE binds to adrenergic receptor on nodal cells
4) Activate enzyme called adenylate cyclase
5)Adenylate cyclase speeds up: turning ATP into
cAMP
6)cAMP is cofactor for protein kinase c (PKC)
7)PKC adds phosphate to volume gated Ca
channels in nodal cells
8)Volume gated Ca channels open—> more Ca
inside = faster AP generation
Positive Chronotropic Agents:
- speed up HR
- NE
- caffeine (prevents breakdown of cAMP)
*thyroid hormone: increase# of adrenergic
receptors on nodal cells
*cocaine (prevents breakdown of NE)
Parasympathetic innervation:
*decrease rate of autorhymicity of nodal cells
(SA nodes)
- medulla oblongota during rest releases Ach
- Ach binds to volume gated potassium channel
- nodal cells even more–hyper polarized
Negative Chronotropic Agents:
*Ach
*Beta blockers (prevents stimulation of
adrenergic receptors)
Factors that effect Stroke Volume:
1) Venous Return
2) Inotropic Agents
3) Afterload
Venous Return:
Filling of the atria
A) Frank-Starling Law: as more blood fills the
heart, more & more cross bridges formed
during contraction
(stronger contraction–>more ventricular ejectory–>longer stroke volume)
B) During Exercise:
1.HR increases to improve cardiac output
2.skeletal muscles contracting bringing more
blood to the heart
C) Lower heart rate:
1. Allows more time to fill atria/ventricles
—more venous return= more stroke volume
Frank-Starling law:
Frank-Starling Law: as more blood fills the
heart, more & more cross bridges formed
during contraction
(stronger contraction–>more ventricular ejectory–>longer stroke volume)
Inotropic Agents
(Hormones/chemical drugs that affect stroke volume)
Positive Inotropic agents:
Increase calcium inside cardiac muscle cells
1) release of NE & E from the sympathetic
response
Negative inotropic Agents:
Decrease calcium inside cardiac muscle cells
1) electrolyte imbalances
2) some drugs
Chronotropic vs. Inotropic cells
Chronotropic = nodal cells
Inotropic = cardiac muscle cells
Afterload:
Resistance in arteries to incoming blood
- age
- atherosclerosis
