Flashcards in how does the heart work? Deck (30):
At the level of the myocyte and myofibril, _____ are key determinants of contractile performance
calcium handling and calcium sensitivity
How do we think about cardiac muscle physiology?
1. Force – calcium relationships
2. Frank-Starling relationships
3. PV loops
Integrated cardiac performance
1. calcium relationships
2. Highlights calcium regulation and biochemistry
1. Intact muscle physiology
2. Highlights length tension relationships
Integrated cardiac performance
Mechanisms by which the heart moderates its performance
throughout the day include:
1. Length dependent activation (Frank-Starling effects)
2. Enhanced contractility,
3. enhanced chronotropy.
The effect of increasing preload on force of contraction:
1. the greater the volume of blood entering the heart during diastole (end-diastolic volume),
2. the greater the volume of blood ejected during systolic contraction (stroke volume) and vice versa.
So, how does increasing preload affect cardiac performance?
1. This is the basis of the Frank-Starling law of the heart.
2. The Frank-Starling law of the heart describes the effect of increasing preload on the force of contraction.
3. the greater the volume of blood entering the heart during diastole, the greater the volume of blood ejected during contraction.
4. due to increase the fiber length, the force of contraction for a given stimulus is increased.
phosphorylation of Ca channels (SA node cells) will cause
1. ↑ Heart rate
2. Improved CO
Phosphorylation of Ca channels
1. ↑ Ca entry
2. ↑ Force of contraction
3. improved ejection fraction (+ inotropy)
Phosphorylation of Na pump
1. ↑ Ca efflux (via Na-Ca exchange)
2. enhanced relaxation and diastolic filling
Phosphorylation of Phospholamban
1. Disinhibition of SR calcium pump (SERCA2)
2. Increased SR calcium load
3. improved diastolic filling
Phosphorylation of FKB
1. Enhances Ryr receptor mediated calcium release
3. enhanced contractility
Phosphorylation of troponin I
will result in
1. ↓ Ca affinity for TnC
2. enhanced relaxation
How do we get through the day?!?!
1. postural accomodation
2. isotonic (exercise: cardio)
3. isometric (weight training)
1. Venous pump: skeletal musculature
2. Increase venous return
3. Increased EDV → increased SV
1. Decrease peripheral vascular resistance
2. Increase venous return (Frank-Starling)
3. Increase heart rate
4. Increase inotropy
Isometric (weight training)
1. Increased peripheral vascular resistance (maintain blood flow to exercising muscle group)
2. Increased HR
3. No increase (or decrease) in CO
What happens acutely during a heart attack?
1. Loss of functional myocardium
2. Increased catecholamine surge
3. Increased inotropy to maintain CO despite increase BP (afterload)
4. Heterogeneous cellular environment
Increased catecholamine surge symptoms are
Sweating, tachycardia, ± hypertension
Heterogeneous cellular environment symptoms are
1. Local /regional changes in pH
2. change in membrane potential
3. secondary effect on cytosolic calcium
Ca regulated by
phospholamban and serca 2a pump.
1. typically inhibitits the pump
2. Ryanodine receptor is how ca gets out.
3. A little leaks out then a lot flows out of the SR
which part of myosin has ATPase activity?
head of myosin
muscle shortening is an ATP dependent process
no interaction between actin and myosin
interaction between actin and myosin
Regulation between actin and myosin is by
Calcium C on troponin C and phophosrylation of troponin molecules
Factors that influence EC50 (calcium sensitivity) include
3. sarcomere length
4. contractile protein phosphorylation
PKA effect on pCa
1. causes an increase in velocity,
2. Force calcium relationship shifts to the Left.
3. Ca sensitivity increase,
4. this is the positive inotrope.