Physio - Cardio Muscle Contraction Flashcards
What are the 6 important characteristics of Myocardial Cell Structure & Function?
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Latticework of fibers (no skeletal attachment)
- Function over wide range of length & angles
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Sarcomeres (similar to skeletal muscle)
- Similar cross-bridge cycle mechanism of contraction
- Similar length-tension & force velocity relationship
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Intercalated disks (gap junctions)
- Low resistances btw cells
- Allows heart to function as one unit
- functional syncytium
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Large T-tubules
- High propagation velocity of APs
-
SR forms close connection w/ SL & T-tubules
- Extracellular & intracellular Ca2+ affect contraction
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Cardiac isoforms of actin, myosin, troponin, tropomyosin
- Cardiac specific regulation
- ↑ muscle length = ↑ Ca sensitivity of cTnC
- (P) of cTnI ↓ Ca sensitivity
- Cardiac specific regulation
Explain Excitation Contraction Coupling
Basics:
- More Ca = more contraction
- Extracellular Ca is related to intracellular Ca
Magnitude of tension:
-
Proportional to INTRACELLULAR [Ca2+]
- AKA: Contractility or Inotropy
-
Regulated by INWARD Ca2+ current
- Inotropy = affected by plasma [Ca2+]
-
At resting HR, cardiac contraction = submaximal
- amt of Ca2+ in myoplasm ONLY reacts w/ some troponin C
- room for positive and negative ionotropic effects
[Ca]e and [Ca]i connection:
- Example: Lack of sunlight & tiredness
- Hypocalcemia = ↓ Ca Influx during AP = ↓ Inotropic state = ↓ SV (heart)
What causes Myocardial Relaxation?
Myocardial Relaxation
- due to ↓ intracellular [Ca] caused by Ca-ATPase & Na/Ca exchangers in sarcolemma
- factors that affect Na gradient affect contractility
- 3Na into cell / 1 Ca out
- factors that affect Na gradient affect contractility
What is the main difference between Cardiac AP and skeletal Twitch?
Cardiac muscle:
- CANNOT change strength of contraction
- Plateau
Skeletal muscle:
- CAN change strength of contraction
- No plateau
What are the Mechanisms for Force Gradation?
Basics:
- Functional syncytium of heart muscles = neccessary to prevent tetanus
- also removes possibility of recruitment of motor units
Heart muscle contractions are influenced by:
-
Mechanisms independent of length:
- Altering inward Ca2+ current
- Sympathetics/ parasympathetics
- Contraction frequency
- Altering SR Ca2+ stores
- Other agents (e.g. hormones, pH, O2, drugs, etc)
-
Mechanisms dependent of length:
- Stretch
What happens after altering inward Ca2+ current?
Influence cardiac muscle contraction
-
Example: Hypocalcemia
- ↓ Ca influx during AP = ↓ Inotropic state
- Heart muscle = ↓ peak force, shortening velocity
- Heart: ↓ SV
- ↓ Ca influx during AP = ↓ Inotropic state
Note:
- Less Ca = Less contraction
Explain the Influence of Sympathetic (Parasympathetic) on Cardiac Contraction
Sympathetic (NE infusion)
- beta1 receptor –> G protein –> cAMP –> protein kinases –> (P)
- of Ca2+ channels –> ↑ trigger Ca2+
- of phospholamban –> ↑ SR Ca-ATPase activity –> more Ca for next beat
- overall = leads to ↑ contraction & ↑ SV
Parasympathetic (ACh infusion)
- ↓in Ica –> ↓ trigger Ca2+
- And ↑ in Ik-Ach –> shorter AP
- overall = leads to slight ↓ contraction & ↓ SV
Note:
-
Major effects of parasympathetic are on the HR & conduction velocity
- only minor effect on inotropy
How does Contraction frequency influence cardiac contraction?
Basics:
-
HR & contractility = DIRECTLY proportional
- ↑ HR = ↑ contractility & vice versa
- Effects mediated by ↑ & ↓ trigger Ca
- Intracellular Ca = DIRECTLY proportional to strength of contractility
Treppe = Staircase Phenomenon
- Intrinsic property:
- present in the transplanted heart
- Physiological meaning:
- compensation for ↓ filling time with ↑ HR
Postextrasystolic Potentiation
- Pause augments the force of next beat
- Ex: Compensatory pause in PVCs
How does Altering SR Ca2+ stores influence cardiac contractility?
Increasing Ca stores = INCREASE contractility
-
Can be caused by:
- Caffeine
- Catecholamines
- Thyroxin
- Digitalis
Example Pathway
- Digitalis –>
- Blocks Na/K pump –>
- ↓ Na pumped from cell –>
- ↑ Intracellular Na –>
- ↓ Gradient [Na]out to [Na]in –>
- ↓ Energy driving Na/Ca countertransport –>
- ↓ extrusion of Ca –>
- Intracellular Ca ↑ –>
-
Contractility ↑ (positive inotropic)
- ↑ SV
Note:
- Cardiac glycosides = help for failing heart
- Digitalis (Foxglove plant) = used to treat CHF & arrhythmias
Decreasing Ca stores = DECREASE contractility
-
Can be caused by:
- Severe hypoxia
- Hypercapnea
- Decreased pH
How does Stretch influence cardiac contractility?
Basics:
- There is an optimal length for optimal tension
- Stretch = caused by MORE volume (EDV)
Similar to skeletal muscle, contractile force depends on..
- Degree of overlap of thick & think filaments
- Muscle length ↑ increases the Ca sensitivity of troponin C
- Muscle length ↑ increases Ca release from SR
How do SV, EF, and CO impact stretch?
Stroke Volume: SV = EDV - ESV
- Volume ejected on one beat (50-70ml)
- EDV = volume in ventricle BEFORE ejection
- ESV = volume in ventricle AFTER ejection
Ejection Fraction: EF = (SV/EDV) x 100
- Fraction of EDV that is ejected per SV (~55%)
- Indicator of contractility
Cardiac Output: CO = SV x HR
- volume of blood ejected from heart per min
- 5-6 L per minute (normal, healthy adult)
- ~8% of body wt per min
Notes:
-
Sympathetic:
- HR↑, SV↑ (via contractility↑)
-
Exercise:
- HR↑, SV↑ (via contractility & via skeletal muscles squeezing on veins increasing venous return)
What is the Frank Starling Mechanism?
Basics:
- ↑ venous return to heart = stretches the ventricle
- results in more FORCEFUL ejection at next heart beat
- Matches venous return to CO
Example:
- Hypocalcemia –> ↓ Ca Influx during AP –> ↓ Inotropic state –> ↓ Stroke Volume (Heart)
- For next venous return,,,
- ↑ ESV
- ↑ EDV
- Frank-Starling = EDV ↑ –> SV ↑
Note:
- In the end, SV is ↓ , but not as much as it would have been at the onset of hypocalcemia
What is Preload? What effects it?
Basics:
- Preload = EDV (volume BEFORE ejection)
Depends on End-Diastolic Pressure:
- Regurgitant aortic valve = ↑ preload
- Pulmonary HTN = ↑ preload
- Stenotic mitral valve = ↓ preload
Depends on Blood Volume:
- Hemorrhage leads to ↓ preload & ↓ CO
Depends on Ventricular Compliance:
- Heart disease may ↑ stiffness (↓ compliance)
- Same preload can result in shorter fiber length & ↓ force of
contraction
- Same preload can result in shorter fiber length & ↓ force of
What is Afterload? What effects it?
Defintions:
- Force against which the ventricle must contract to eject blood
- Tension produced by chamber of heart in order to contract
- Pressure that the chamber has to generate in order to eject blood out of the chamber
Depends on Aortic Blood Pressure:
- pressure in the ventricle > blood pressure in the aorta
- cause aortic valve to open
- also depends on TPR
Depends on Ventricular Systolic Pressure:
- Stenotic aortic valce = ↑ afterload
What is the Force Velocity Relationship?
Force Velocity Relationship & Preload Changes
- Comparable to skeletal muscle
-
Increasing preload increases…
- Velocity of shortening at given afterload
- Fmax w/out changing Vmax
-
Cardiac Ventricle
- Velocity of ejection (mL/s)
- Pressure (mmHg)
Force Velocity Relationship & Inotropic Changes:
- Specific to cardiac muscle
- Vmax can be changed at ZERO AFTERLOAD
-
Increasing inotropy increases…
- Velocity of shortening & given afterload
- Fmax & Vmax
Notes:
- Velocity = maximal when afterload = ZERO
- Velocity ↓ by ↑ afterload
