RAT #5a Flashcards
Sequence of blood flow through the heart
Oxygen poor:
Vena Cave (superior/inferior), Right atrium, Tricuspid valve, Right ventricle, Pulmonary valve, pulmonary artery, pulmonary (arterioles, capillaries, venules, veins)
Oxygen rich
Left Atrium, Bicuspid valve, Left ventricle, Aortic valve, Aorta, Arteries (arterioles, capillaries, venules, veins) *repeat starting at superior vena cava
Where does oxygen poor blood return to
Right atrium
-Blood from upper body returns to superior vena cava
-Blood from lower body returns to inferior vena cava
then heads off to the right atrium etc.
Where does oxygen rich blood from the lungs return to
Left atrium then goes on to the bicuspid valve, L ventricle etc.
Action potential in an autorhythmic cell
- After hyperpolarization causes a sodium leak through channels causing a GP (aka pacemaker potential)
- Slow voltage gated calcium channels also open towards end in order to help bring the membrane to threshold - Rapid depolarization due to opening of voltage gated calcium channels (rapid influx of calcium)
- Very briefly depolarized from calcium entry
- Repolarization and after hyperpolarization due to opening of voltage gated potassium channels (repolarization) and closing of voltage gated calcium channels
Action potential in a myocardial cell
- No graded depolarization, AP arrives directly through gap junctions so no GP needed
- Rapid depolarization due to opening of Voltage-gated sodium channels leading to Na+ entry
- Depolarization plateau due to opening of slow voltage gated calcium channels and closing of voltage gated sodium channels
- Repolarization due to closing of voltage gated calcium channels and opening of voltage gated potassium channels
What are autorhythmic cells responsible for?
Heart rate
What are myocardial pumping cells responsible for
Stroke Volume
What is the point of the long refractory period in a pumping cell
To allow the heart to have time to relax preventing tetanus
Effect of ANS on the SA node (HR) - Sympathetic
EPI/NE
3 main things happen:
1. Less hyperpolarization (less neg membrane potential)
2. Steeper rise to threshold (doesnt take as long)
3. More beats per minute
Summary:
When EPI and NE bind with receptors on autorhythmic cells they cause an increase is sodium leak - faster depolarizing. Also increase in permeability of calcium ions causes quicker depolarization.
Effect of ANS on SA node (HR) - parasympathetic
Ach
3 main things happen:
1. More hyperpolarizaed (more neg membrane potential)
2. Slower rise to threshold (takes longer)
3. Fewer beats/min
Summary:
When Ach binds with muscarinic cholinergic R’s on SA node there is a decreased permeability to calcium ions, increased permeability to potassium, and decreased conduction velocity through heart
Main factors that cause peripheral vasodilation
- increased concentration of bad stuff (co2, k+, and other organic acids)
- Decreased good stuff (oxygen, glucose)
- Sympathetic activation of beta-adrenergic receptors on blood vessels that supply skeletal muscle, liver, heart (bigger blood blast)
- Increased Atrial natriuretic peptide (ANP -makes u pee)
- Increased nitric oxide
- Increased histamine (too much can cause anaphylactic shock and constriction)
Factors causing peripheral vasoconstriction
- Sympathetic activation at alpha-adrenergic receptors
- Antidiuretic hormone
- Anglotensin II
Blood flow to a tissue will increase if the:
- level of oxygen at the tissue increases
- Level of co2 at the tissue decreases
- pH decreases
- level of adenosine decreases
pH decreases (makes blood more acidic = bad)
When Ach is present at the sinoatrial node, the threshold level of depolarization to generate action potentials occurs _____ frequently, due to _____ in the membranes permeability to _____.
- more; a decrease; calcium ions
- more; an increase; sodium ions
- less; an increase; calcium ions
- less; an increase; potassium ions
less; an increase; potassium ions
An antagonist of adrenergic receptors applied to the heart would
- increase heart rate
- decrease heart rate
- increase force of contraction
- have no effect
- increase cardiac output
Decrease heart rate
