In terms of action potentials, in what type of muscle are slow Ca++ channels found?
Slow Ca++ channels are found in cardiac muscle, not skeletal muscle. These open during a cardiac action potential to allow Ca++ from the extracellular fluid, not just the sarcoplasmic reticulum, as is the case with skeletal muscle. The slow Ca++ channels are responsible for the "plateau" phase in the action potential. They take much longer to open than Na+ channels & they stay open much longer. They are contrasted against the "fast Na+ channels" in cardiac muscle, open & close very quickly.
In the context of a cardiac action potential, when does a heart-muscle contraction reach its peak strength?
In the late plateau phase, as the calcium concentrations are just starting to drop inside the cell (repolarisation beginning). Contractile strength decreases during the repolarisation phase of each action potential.
The mitral valve is the valve between the X and Y and its closure marks the Z of the ventricular systole.
X = left atrium Y = left ventricle Z = beginning The mitral valve is the valve between the left atrium and left ventricle and its closure marks the end of the ventricular systole.
The two heart sounds, lub-dub, are associated with the closure of the AV valves, the X & the Y. The sounds is not actually due to the closure of the leaflets of the valves, but the sound of momentary backflow of blood from the A to the B at the C of ventricular systole.
X= mitral - left Y= tricuspid - right A = ventricles B = atria C = beginning
Cardiac Output is equal to:
Stroke Volume X Heart Rate CO = SV x HR
The second heart sound is associated with closure of the aortic valve on the left side of the heart and the pulmonic valve on the right side of the heart. Is it longer or shorter, louder or quieter than the first heart sound? Why?
It is shorter, sharper & higher-pitched than the first heart sound because it is the reverberation caused when the momentary backflow into the ventricles is suddenly stopped by the closure of the valves.
What exactly is Stroke Volume, besides SV = Cardiac Output / Heart Rate
Stroke volume is end-diastolic volume minus end-systolic volume ie., the total amount of blood that fills the ventricles during diastole minus the total that's left over at the end of systole.
Does greater end-diastolic ventricular volume increase or decrease the force of contraction, all else being equal? What is the effect on stroke volume?
Increases. This is because the muscle fibres are placed in a "more favourable geometry for the ejection of blood during the next systole", and stretching the ventricular muscle fibres during diastole causes a greater amount of calcium to be released from the SR during subsequent systolic contraction (like a rubber band). Increases or decreases from normal ventricular end-diastolic volume result in approximately proportional increases or decreases in stroke volume.
What do you call the pressure within a ventricle during diastolic filling?
End-diastolic ventricular volume is determined by pre-load, but also by x and y.
x = Ventricular COMPLIANCE - a measure of the ease with which the ventricular walls stretch to accommodate incoming blood during diastole. Also, compliance = change in volume/change in pressure. y = Diastolic filling time
An increase in contractility brings about an increase in stroke volume without requiring an increase in end-diastolic volume. True or False?
True. More contractility means there's more complete emptying of the ventricles, so end-diastolic volume decreases.
How can contractility be increased?
Sympathetic nerve activity: neurotransmitter norepinephrine binds beta receptors on ventricular muscle, causing increased influx of extracellular Ca++ during action potential, resulting in stronger contractions that are faster and shorter. Epinephrine & norepinephrine produced in adrenal medulla, beta-receptor agonists such as epinephrine & isoproterenol, & cardiac glycosides such as digitalis can all increase cardiac contractility - ie., inotropic.
What are beta-receptor antagonists used most often to DECREASE heart contractility?
Beta blockers propranolol & atenolol. There are also Ca++ channel blockers.
What is another name for arterial pressure?
If CO = SV x HR, why is it that doubling the heart rate doesn't double the cardiac output?
When HR increase, diastolic-filling time decreases, so end-diastolic volume is reduced, and this reduces SV, because SV is: SV = end-diastolic volume - end-systolic volume In fact, when heart rates increase so much eg., beyond 160 bpm, SV decreases so much that CO actually DECLINES! However, there usually is some increase in CO, especially when heart rate increases due to exercise, but this is because SV also increases.
Why is it that cardiac output increases with increased heart rate brought on by exercise but not when heart rate is increased experimentally by a pacemaker, for example?
CO increases with exercise because the HR during exercise is stimulated by the sympathetic nervous system, specifically neurotransmitter norepinephrine that binds to beta-adrenergic receptors on heart muscle cells. The effect of adrenergic stimulation is not only increased heart rate, but ALSO increased contractility, which increases STROKE VOLUME! ALSO, very importantly, the sympathetic stimulation causes the systole to be shorter, preserving the diastolic filling time. When HR is increased without sympathetic/adrenergic stimulation, there is no inotropic effect, so the heart doesn't contract harder and end-systolic volume doesn't decrease. Instead, diastolic filling time decreases as the heart beats faster, so end-diastolic volume decreases instead. Since SV = end-diastolic volume - end systolic volume, then SV becomes smaller, and so can CO.
What is patent ductus arteriosus?
PDA is the persistence of the ductus arteriosus, a foetal circulatory shunt, after birth. The ductus arteriosus in the foetus shunts mixed (oxygenated & deoxygenated) coming from the right ventricle into the aorta, diverting it away from the pulmonary artery and the deflated lungs. In the adult, some blood destined for the general circulation via the aorta is diverted into the pulmonary artery due to the high pressure differential between the aorta & the pulmonary artery. This can lead to reduced blood pressure or even cyanosis as not enough oxygenated blood reaches the peripheral vascular system.
How does a patent ductus arteriosus lead to both left & right ventricular hypertrophy?
The left ventricle ends up pumping a normal amount of oxygenated blood through the aorta but also pumps 2-3 times that amount through the PDA (because it's lost from the aorta). The blood that enters the PDA goes into the pulmonary artery back into the lungs, so the pressure in the pulmonary artery is high. This higher-pressure blood returns to the left ventricle, causing the left ventricle to pump with greater force. This greater force results in hypertrophy. On the right side, a normal amount of deoxygenated blood enters the right ventricle, but now that right ventricle has to pump harder to get that blood into the pulmonary artery, where the pressure has increased due to the PDA. This increase in work results in hypertrophy. Exercise intolerance ensues as the heart can't pump enough blood out to the muscles. Sometimes, the volume of blood carried through the pulmonary artery is four times normal! This increase in pulmonary arterial pressure can lead to pulmonary oedema.
What are the only two factors that determine mean arterial blood pressure (blood pressure)?
Cardiac output (CO) & Total Peripheral Resistance (TPR) MAP = CO x TPR
Endothelin-1 (ET-1) is released from endothelial cells in response to a variety of mechanical or chemical stimuli, especially trauma to the endothelium (eg., laceration, bruise). What is the effect of ET-1 on vascular (blood-vessel) smooth muscle?
ET-1 causes vascular smooth muscle to contract, therefore causing vasoconstriction & increased vascular resistance ie., decreased blood flow to an area. This is important, for example, in wound-healing. It is a paracrine chemical signal.
Nitric Oxide, like endothelin-1, is a paracrine chemical signal released by endothelial cells. What is its effect on vascular smooth muscle? What is a stimulus for NO release from endothelial cells?
Also a paracrine chemical signal, NO has the opposite effect of ET-1. It relaxes vascular smooth muscle, and thus causes vasodilation, increasing blood flow to surrounding tissue. This is important in an infection, to bring WBCs such as neutrophils and eosinophils to a site of infection, but for this reason it is also considered a pro-inflammatory chemokine. One stimulus for NO is an increase in blood-flow velocity across the vascular endothelium. In genital erectile tissue, parasympathetic nerve endings release BOTH Ach & NO. The Ach stimulates endothelial cells to release more NO, & the NO dilates local blood vessels, resulting in engorgement & therefore erection.
Thromboxane (TXA2) & prostacyclin (PGI2) are paracrine chemical signals important in haemostasis & the inflammatory response of the immune system.
In terms of their effect on vascular smooth-muscle, they have antagonistic effects that balance each other out under normal conditions.
Which is the vasoconstrictor & which is the vasodilator?
How are they synthesized?
TXA2 is the vasoconstrictor and PGI2 is the vasodilator.
Thromboxane signals platelets
Both are eicanosoids aka prostanoids that are synthesized from arachidonic acid in cell's lipid membrane, triggered by mechanical trauma & cytokines, broken down by phosphlipase & catalysed by cyclooxygenase (COX) enzymes.
Histamine, released by degranulated mast cells and other granulocytes, is a paracrine signal that does what?
Vasodilates, increases vascular permeability to proteins, so proteins leave the bloodstream, accumulating in the interstitial fluid (tissue), drawing water from plasma with it.
As a result of both vasodilation and increased oncotic pressure in the interstitial fluid, filtration of liquid out of plasma increases.
What is bradykinin? How is it formed? What effect does it have on vascular smooth muscle?
Bradykinin is a paracrine signal formed from globulin proteins in plasma or interstitial (tissue) fluid. The proteolytic enzyme kallikrein catalyses that formation of bradykinin from globulin.
Bradykinin can also be formed in sweat glands when activated by ACh released from SYMPATHETIC nerve endings.
Like histamine, bradykinin causes vasodilation of skin blood vessels, increases evaporation of sweat & promotes heat loss. Both of these paracrine signalling factors also stimulate formation of NO by endothelial cells.
What CVS structures can be seen in a radiograph?
A. Multiple intrathoracic structures simultaneously
B. Pulmonary parenchyma & vasculature simultaneously
C. Shows presence of pulmonary congestion & oedema.
D. Soft tissue vs. fluid
E. Enlarged right atrium vs. normal left atrium
A, B & C only.
X-ray is good at providing view of several structures in the thorax at the same time. It also allows view of lung parenchyma and the blood vessels (pulmonary arteries & veins) at the same time. It can also show the presence of pulmonary congestion & oedema from fluid accumulation.
However, it cannot show distinctions between soft tissue & fluid, nor can it distinguish between enlarged heart chambers as they are superimposed on a radiograph.
What is another name for echocardiograph?
How does it work?
Sound waves reflected back to a transducer by target structures. 3D image of the subject’s organs, tissue formed from speed-of-reflection data.
What is Doppler Echocardiography?
Same idea as regular echocardiography (ultrasound), but enables measurement of velocity & direction of blood flow, displayed with spectral Doppler used for accurate quantification of direction & colour
Useful for examining wide are in short time.
Echocardiography (ultrasound) is used to detect:
- Anatomic lesions
- Hypertrophy patterns
- Abnormalities of motion, eg., myocardial, valvular
- Abnormalities of timing of events in the cardiac cycle
- Can distinguish soft tissue from fluid, therefore can see individual chambers & their internal margins
- Can distinguish pericardial effusion from hypertrophy
- Can determine movement
- can derive functional measurements
- Can get real-time images of heart
- Quantify movement
- With Doppler ultrasound, we can
show blood flow at known points in cardiac cycle
What are disadvantages of echocardiograph?
Can’t see through lung, thus unable to investigate pulmonary vasculature or determine extent or severity of left-sided heart failure.