January 5, 2016 - Intro to Cardiac Physiology Flashcards
Systole and Diastole
The myocardium has two jobs…
To contract - systole
To relax - diastole
The two of these together is known as the cardiac cycle. Electical, biochemical, and mechanical events take place during the cardiac cycle.
Electrical Stimulation in the Heart
The sino-atrial (SA) node generates an electrical impulse
This impulse is conducted through the atria to the atrio-ventricular (AV) node
Then goes through into the ventricles
The impulse enters cell membranes and induces changes to ion channels, which cause the heart to contract.
Biochemical Events in the Heart
Voltage-gated ion channels change shape with a change in voltage or the arrival of an action potential.
Calcium channels open with depolarization.
Calcium enters the cell and stimulates ranodine receptors on the sarcoplasmic reticulum.
The sarcoplasmic reticulum releases even more stored calcium.
The cytoplasmic calcium is greatly increased.
Mechanical Elements in Heart Cells
Myosin contains the mechanically active myosin head
Actin has sites for the attachment of myosin
Tropomyosin covers up the active sites on actin
Toponin binds calcium and moves tropomyosin
Mechanical Role of Calcium Ions
Myosin binding sites are covered by tropomyosin.
Troponin binds calcium ions.
Myosin binding sites become exposed.
Myosin head, bound to ATP, binds actin.
ATP is hydrolyzed, and a power stroke occurs (contraction)
ADP and Pi are released
Myosin binds new ATP and releases from actin and resets myosin to the starting position (relaxation)
Troponins
Are specific to cardiac cells
When cardiac cells die, they break open
Troponin levels in the blood increase when there is cardiac cell death
Measurement of troponins is a key test for myocardial infarction
Relaxation - Biochemical Events
Is all about getting calcium ions out of the cytoplasm
Some calcium is pumped out of the cell
Others is pumped back into the sarcoplasmic reticulum via SERCA (sarco/endoplasmic reticulum calcium ATPase). SERCA is regulated by phospholamban (PLB).
Impact of Hypoxia on the Heart
Low amounts of ATP are produced due to the lack of oxygen and the lack of the cell’s ability to use the electron transport chain.
Low ATP reduces the actin-myosin uncoupling and resetting of the myosin head.
Lack of ATP leads to impaired contraction (systolic dysfunction) and impaired relaxation (diastolic dysfunction)
Valve Action
Valves have two jobs; to open and to close.
Valves open and close according to pressure differences.
Isovolumetric State
No change in volume
Occurs when both the “in” and the “out” valves are closed
Can occur with contraction and with relaxation
Steps in Systole
Systole starts when the mitral valve closes (both mitral and aortic valve are now closed)
This occurs with early ventricular contraction (raising pressure in ventricle)
Isovolumetric contraction occurs until the pressure increases such that the aortic valve opens
Ejection phase occurs when the aortic valve is open
Systole ends when the aortic valve closes (both valves are now closed)
Steps in Diastole
Diastole begins when the aortic valve closes (both the aortic and mitral valves are now closed)
Isovolumetric relaxation occurs until the pressure in the atrium increases such that the mitral valve opens
Diastole ends when the pressure becomes high enough in the ventricle that the mitral valve closes (both valves now closed)
Preload
The volume of blood inside the ventricle right before the ventricle contracts. This is called “end diastolic” volume (EDV). Often we are just concerned with the left ventricle, so the preload is termed LVEDV.
It occurs during muscle relaxation - in the heart, this is diastole.
Stretching the myocardium “primes” the muscle for contraction. Venous return (filling volume) is the preload.
Think of a spring. If you stretched it a little bit, it will snap back harder.
Frank-Starling Curve
The relationship between stroke volume and preload.
With too little stroke volume, there will not be enough blood in circulation for the body.
With too much preload volume, the tissue will swell and may be damaged.
Appreciate that in healthy people, there is a lot of buffer room for patients if they become dehydrated or their heart is stressed. In patients suffering from cardiac problems, there is very little room for error before the body does not get enough blood or the heart becomes swollen and damaged.
Jugular Venous Pressure
Estimates the filling pressure of the right atrium… which estimates the filling pressure of the right ventricle… which indirectly estimates the preload of the right ventricle… which very indirectly estimates the preload of the left ventricle.
Is the indirectly observed pressure over the venous system.
Afterload
Occurs during systole when blood is ejected from the heart.
Think of it as resistance to ventricular ejection.
When afterload is high, the aortic valve may not fully open and the ventricle must generated very high pressures to eject blood.
High Afterload
High afterload is not good.
This requires the heart to generate excessive work.
This can remodel the heart, can “burnout” the heart and can cause heart failure.
Contractility
Describes how “strongly” the heart contracts
By definition, contractility is independent of ventricular filling. Therefore, filling the heart does not increase contractility.
For example, giving someone an injection of adrenaline would increase the force of contraction (high contractility) whereas a myocardial ischemia can reduce contractility in the heart.
Cardiac Ca2+ Channel Blockers
Results in less calcium in the cell, therefore less muscle activity.
This reduces contractility.
Stroke Volume
The volume of blood pumped out of the ventricle in one heartbeat.
Stroke Volume = Diastolic Volume - Systolic Volume
Stroke Volume = End Diastolic Volume (EDV) - End Systolic Volume (ESV)
Under normal circumstances, the blood is only ejected forwards because of the valves.
Stroke Volume Formula
Stroke Volume = End Diastolic Volume - End Systolic Volume
♦ Three Determinants of SV ♦
Preload (higher usually produces larger SV)
Contractility (higher produces larger SV)
Afterload (higher produces lower SV)
♦ Cardiac Output ♦
CO = SV x HR
Measured as the volume of blood per minute
Cardiac output increases with activity and exercise so if cardiac output is limited, these activities cause symptoms like shortness of breath or fatigue.
♦ Blood Pressure ♦
BP = CO x SVR (systemic vascular resistance)
The fluid pressure inside the arteries, measured in mmHg. The more fluid in the arteries, the higher the pressure will be. The more the arteries constrict, the smaller the radius and the higher the pressure will be.
Resistance is inversely related to the radius to the power of 4. Because of this, vasoconstriction and vasodilation have big influences on SVR.
Warm and Pink Extremities
Indicates vasodilation
Vasodilation results in a bigger diameter, which lowers systemic resistance, which allows more blood to flow, and because blood is warm and red, therefore the extremities will be warm and pink.
♦ Vasodilation in the presence of low BP is pathological
Cool and Pale Extremities
Indicates vasoconstriction
Vasoconstriction results in smaller diameter blood vessels, which increases systemic vascular resistance, which allows less blood to flow, which causes the extremities to become cool and pale.
Hypertension Treatment
BP = CO x SVR
BP = (HR x SV) x SVR
To lower BP, you can reduce HR, stroke volume, or resistance.
Hypotension Treatment
BP = CO x SVR
BP = (HR x SV) x SVR
To increase BP, you can increase HR, stroke volume, or resistance
Stroke Volume Factors
1. Volume status (preload)
2. Contractility
3. Resistance to ejection (afterload)
4. Valve function
♦ 1, 2, and 3 can be fixed at the bedside.
Mean Arterial Pressure
The mean, or average, or area under the curve is what is referred to as the MAP.
The MAP is estimated to be 1/3 of the difference between the systolic and diastolic.
MAP = Diastolic Blood Pressure + 1/3 Pulse Pressure
MAP = DBP + 1/3 (SBP - DBP)
MAP Formula
MAP = DBP + 1/3 (SBP - DBP)
♦ Ejection Fraction ♦
Describes how much (%) of the blood that is inside the ventricle gets ejected with one contraction.
55-65% is normal
15-30% is very reduced (heart failure)
<10% is incompatible with life
If the ventricle contains 100mL of blood in diastole and at the end of systole it only contains 40mL, the ejection fraction is 60%
