Physiology 2 + 3 Flashcards
What is striation of cardiac muscle caused by?
Regular arrangement of contractile protein
Why are there no neuromuscular junctions in cardiac muscle?
Heart capable of generating its own action potentials
How are myocytes electrically coupled?
Gap junctions
What are gap junctions?
Protein channels that form electrical communication pathways between myocytes
What is the all-or-none law of the heart?
Gap junctions ensure electrical excitation reaches all the cardiac myocytes
Where are desmosomes and gap junctions located?
Within intercalated discs
What are desmosomes?
Provide mechanical adhesion between myocytes ensuring tension developed by one cell is transmitted to the next
What are the contractile units of muscle?
Myofibrils (found in each muscle cell)
What are myofibrils made up of?
- Thin (actin) filaments which cause lighter appearance
* Thick (myosin) filaments which cause darker appearance
Within each myofibril, what are actin and myosin arranged into?
Sacromeres (functional unit of the muscle)
How is muscle tension produced?
Sliding of actin filaments on myosin filaments
What does force generation depend on?
ATP-dependent interaction between myosin and actin filaments i.e. cross bridge formation
What do both contraction and relaxation require?
ATP
When will interaction of actin and myosin not occur even when ATP is present?
In the absence of calcium
Why is calcium required for formation of cross bridge in addition to ATP?
- When muscle relaxed, myosin binding sites on actin are covered with regulatory proteins like tropomyosin and troponin
- Calcium binds to troponin, removing troponin-tropomyosin complex and allowing binding of myosin
How does action potential switch on cardiac muscle contraction?
Ca+ released from sarcoplasmic reticulum
What is release of Ca+ from SR dependent on in cardiac muscle?
Presence of extra-cellular Ca+
Explain the process of contraction from action potential in cardiac muscle (3)
- Phase 2: Ca+ influx through L-type Ca+ channels
- Ca+-induced Ca+ release from SR
- Increased intra-cellular calcium stimulates formation of cross bridges by removal of troponin-tropomyosin complex
How does heart muscle relax once action potential has passed? (2)
- Ca+ influx ceases
* Ca+ re-sequestered in SR by Ca+ ATPase
What is the importance of a long refractory period to normal cardiac function?
Prevents generation of tetanic contraction
What is the refractory period?
Period following an action potential where it is not possible to produce another action potential
What are the components of the long refractory period?
- Plateau phase: Na+ channels are in closed state
* Descending phase: K+ channels are open so membrane cannot be depolarised
What is stroke volume?
Volume of blood ejected by each ventricle per heart beat
Equation for stroke volume?
SV = end diastolic volume (EDV) - end systolic volume (ESV)
How is stroke volume regulated? (2)
- Intrinsic mechanisms: within heart muscle itself
* Extrinsic mechanisms: nervous and hormonal control
What is end systolic volume?
Volume of blood in ventricle at the end of contraction
What is intrinsic control of stroke volume?
Changes in SV caused by changes in diastolic length of myocardial fibres
What is diastolic length of myocardial fibers determined by?
End diastolic volume
What is end diastolic volume?
Volume of blood in ventricle at end of diastole
What determines the cardiac preload?
End diastolic volume
What is cardiac preload?
How much of heart is loaded with blood before it contracts
What is end diastolic volume determined by?
Venous return to heart i.e. the higher the venous return, the higher the EDV
What is the Frank-Starling Mechanism or Starling’s law of the Heart?
The more blood ventricle is filled with during diastole (EDV), the greater the volume of ejected blood during systole (stroke volume)
What does stretch of myocardial fibres also do?
Increases affinity of troponin for Ca+
When do skeletal muscles reach optimum fibre length?
Under resting conditions
When do cardiac muscles reach optimal fibre length?
Stretching the muscle (Frank-Starling Mechanism)
How does Starling’s Law match the stroke volume of RV and LV?
- If venous return to right atrium increases, EDV of right ventricle increases so increased SV into pulmonary artery
- Increased venous return to left atrium from pulmonary vein increases, EDV of left ventricle increases so increased SV into aorta
What is afterload?
Resistance into which heart is pumping
How does Frank-Sterling mechanism partially compensate for decreased SV caused by increased afterload?
- If afterload increases, heart unable to eject full SV so EDV increases
- Force of contraction increased by Frank-Sterling mechanism
What happens if increased afterload continues to exist e.g. in untreated hypertension?
Ventricular hypertrophy to overcome resistance
What is extrinsic control of SV?
Involves nerves and hormones
What effect does stimulation of sympathetic nerves have on force of contraction?
Increases force of contraction
What is anything that increases force of contraction the heart known as?
Positive inotropic effect
How does sympathetic stimulation increase force of contraction?
Activation of Ca+ channels - greater Ca+ influx
What happens to peak ventricular pressure during sympathetic stimulation?
Rises
How does sympathetic stimulation reduce the duration of systole?
Rate of pressure change (dP/dt) during systole increases
How does sympathetic stimulation reduce the duration of diastole?
Rate of ventricular relaxation increases (increased rate of Ca++ pumping)
What is the effect of peak ventricular pressure rising?
Contractility of heart at given EDV rises
What happens to Frank-Sterling curve in sympathetic nerve stimulation?
Shifted to left
What will a negative inotropic effect (e.g. heart failure) do to Frank-Sterling curve?
Shift to right
What is the effect of parasympathetic innervation on force of contraction?
- Very little direct effect on SV
* Vagal stimulation has major influence on rate, not force of contraction
What is the effect of adrenaline and noradrenaline released from ADRENAL MEDULLA (not neurotransmitters) on the heart?
Positive Inotropic and chronotropic effect
Cardiac output?
Volume of blood pumped by each ventricle per minute
Equation for cardiac output
CO = SV x HR
What is resting CO in a healthy adult?
5 litres per minute
How is cardiac output regulated?
Regulating heart rate and stroke volume
When do heart valves produce sound?
When they shut
What is cardiac cycle?
All events that occur from beginning of one heart beat to beginning of next
What is ventricular diastole?
Heart ventricles are relaxed and fill with blood
What is ventricular systole?
Heart ventricles contract and pump blood into aorta/pulmonary artery
At a heart rate of 75 bpm what is the length of ventricular systole and diastole? (2)
- Systole: 0.3 sec
* Diastole: 0.5 sec
What are the events of the cardiac cycle? (5)
1) Passive Filling
2) Atrial Contraction
3) Isovolumetric ventricular Contraction
4) Ventricular Ejection
5) Isovolumetric ventricular Relaxation
What is passive filling?
- Pressure in atria and ventricles almost 0 but atrial pressure slightly higher than ventricular pressure
- AV valves open so venous return flows into ventricles via pressure gradient
What is aortic pressure during passive filling? Is aortic valve closed or open?
~80 mmHg
Closed
What percentage of ventricles are filled by passive filling?
80%
At what point on an ECG do the atria contract?
Between P-wave and QRS
What completes the end diastolic volume?
Atrial contraction (20%)
What is EDV in normal resting adult?
~130 ml
At what point on ECG do ventricles contract?
After QRS
What happens when ventricular pressure exceeds atrial pressure?
AV valves shut producing first heart sound (LUB)
What is isovolumatric ventricular contraction?
- Ventricular pressure rises and AV valves shut
- Aortic valve/pulmonary valve still shut
- There is a closed volume as no blood can enter or leave the ventricle
What happens in ventricular ejection? (2)
- Ventricular pressure exceeds aorta/pulmonary artery pressure causing aortic/pulmonary valves to open
- SV is ejected by each ventricle leaving behind the ESV
Explain the vents of ventricular repolarisation (2)
- Ventricles relax and ventricular pressure falls
- When ventricular pressure falls below aortic/pulmonary pressure aortic/pulmonary valves shut, producing second heart sound (DUB)
What are LUB and DUB heart sounds produced by?
- LUB - AV valve closure
* DUB - Aortic/pulmonary valve closure
What does valve vibration produce?
Dicrotic notch in aortic pressure curve
What marks the start of isovolumetric relaxation?
Closure of aortic/pulmonary valves
Explain the events of isovolumetric relaxation (3)
- Tension falls around a closed volume as AV valves and pulmonary/aortic valves are shut
- When ventricular pressure falls below atrial pressure, AV valves open and new cardiac cycle begins
What does first heart sound (S1) herald the beginning of? S2?
S1 - systole
S2 - diastole
What valves are auscultated in a cardiac exam?
In order of position: All - Aortic Physicians - Pulmonary Take - Tricuspid Money - Mitral
Why does arterial pressure not fall to zero during diastole?
Elastic recoil of elastic arteries
When does jugular venous pulse (JVP) occur?
After right atrial pressure waves
What is a, c and v in the following diagram? (3)
- a - atrial contraction
- c - bulging of tricuspid valve into atrium during ventricular contraction
- v - rise of atrial pressure during atrial filling (release once AV valves open)
What do pressure changes in JVP reflect?
Pressure changes in the right atrium
