The Cardiovascular System (2) Flashcards
State the formula for cardiac output.
CO = SV X HR
SV = stroke volume
CO is always per minute.
State the formula for blood flow.
Flow = pressure gradient/resistance (of vessels)
Pressure gradient is the difference in pressure between the beginning and end of the blood vessel.
What is total peripheral resistance?
Total peripheral resistance (TPR) is the sum of all the peripheral vasculature in systemic circulation.
What is the pericardium? State its layers.
The heart is enclosed within the pericardium. The pericardium consists of a visceral layer, a parietal layer and the lubricating pericardial fluid between them, to reduce friction when beating.
State the layers of the myocardium (heart muscle).
Endocardium and myocardium
Label the diagram.
1=right coronary artery
2=anterior descending branch of left coronary artery
3=left coronary artery
4=left pulmonary veins
5=great cardiac vein
6=circumflex branch of left coronary artery
7=posterior descending branch of right coronary artery
8=right pulmonary veins
Intrinsic automaticity of the heart
The heart contracts rhythmically as a result of action potentials that it generates by itself. Contractile cells are 99% of the cardiac muscle cells. Autorhythmic cells: initiate and conduct the action potentials responsible for contraction of working cells. THERE IS NO REQUIREMENT FOR EXTERNAL NEURAL INPUT. There are specialized pacemaker areas of the heart, namely: the sinoatrial and atrioventricular nodes, bundle of His and Purkinje fibers.
However, the sympathetic and parasympathetic systems still effect on the heart for its rate and contractile strength.
State the innervation of the heart.
The vagus nerve innervates the SA and AV nodes. The sympathetic cardiac nerves of T1,2,3,4 innervate the SA and AV nodes and the ventricular myocardium.
Compare isotonic and isometric muscle contractions. What changes occur in the heart?
Isotonic contractions is where the muscle changes length while generating force. This leads to volume load and chamber dilation. Isometric contractions occur without any change in muscle length, maintaining a constant tension. This leads to pressure load and chamber hypertrophy.
Rest reverses these changes.
What type of hypertrophy is seen in: hypertension, infarction, diabetes, exercise?
Hypertension: concentric hypertrophy
Infarction: ECCENTRIC/concentric hypertrophy
Diabetes: eccentric/concentric hypertrophy
Exercise: eccentric hypertrophy
Describe the pacemaker activity of cardiac autorhythmic cells.
Beginning at -60mV, funny (f) channels open allowing Na+ influx while K+ permeability decreases. As the membrane depolarizes, transient-type (T) Ca²⁺ channels open, leading to a further influx of Ca²⁺. This gradual depolarization continues until the threshold potential (-40mV) is reached. At threshold, long-lasting Ca²⁺ channels open, causing a rapid influx of Ca²⁺ and thus the steep depolarization phase. At about 10mV, Ca²⁺ channels close. K+ channels open, leading to efflux of K+, restoring the membrane potential back toward -60 mV. This process repeats to support the regular beating of the heart.
How is the SA node connected to the left atrium?
Interatrial pathway
State the intrinsic rate of action potential production for each neural structure in the heart.
SA node: 75
AV node: 50
Bundle of His: 30
Purkinje fibers: 30
in AP/s
Describe the electrical conduction in the heart.
SA node depolarizes. Electrical activity goes rapidly to AV node via internodal pathways. Depolarization spreads more slowly across atria. Conduction slows through AV node. Depolarization moves rapidly through the ventricular conducting system (bundle of His and Purkinje fibers) to the apex of the heart. Depolarization waves spread up from the apex.
Describe the behaviour of action potentials in cardiac contractile cells and the respective contractile response.
RED: The membrane potential rises rapidly from -90 mV to 30 mV due to Na+ influx. Initial repolarization occurs in the form of a slight dip due to transient K+ efflux. L-type Ca channels open to balance the K+ and maintain the depolarized state. In repolarization, Ca channels close and the K+ efflux repolarizes the membrane potential to -90mV. This is then the resting membrane potential, ready for the next AP.
BLUE: The contraction develops slightly after depolarization. The peak contraction occurs during the plateau phase of the action potential. Relaxation occurs as repolarization progresses.
BLACK: This is the period within which another action potential cannot be initiated, preventing tetanus in cardiac muscle.
Describe the events of each segment.
P=atrial depolarization, blood is ejected from the atria through the valves, into the ventricles.
PR=AV nodal delay, preventing simultaneous atrioventricular contraction
QRS=ventricular depolarization to push blood into arteries. Atria repolarize simultaneously
ST=ventricles are contracting and emptying
T=ventricular repolarization
TP=ventricles are relaxing and filling
RR=heart rate
In what arrangement are ECG leads placed?
A total of 12 leads are placed, 4 on the limbs and others are placed on the 4th and 5th intercostal spaces.
Classify tachycardia.
> 100BPM
Classify bradycardia.
<60BPM, depending on patient
Identify extrasystole on an ECG.
Premature ventricular contraction
Identify ventricular fibrillation on an ECG.
Erratic changes in contractions. The heart is shaking. Electric shock by defibrillator is needed.
Identify complete heart block on an ECG.
Atria and ventricles beat independently. P waves bear no consistent relationship to QRS complexes.
Identify myocardial infarction on an ECG.
ST segment elevation is seen. Reciprocal ST depression and hyperacute T waves are seen in turn.
Describe the cardiac cycle.
The cardiac cycle is all the events associated with the flow of blood through the heart during a single complete heartbeat. It repeats approximately once every second. In late diastole, both the atria and the ventricles are relaxed. Blood passively flows from the atria to the ventricles due to the pressure gradient. The AV valves are open, while the semilunar valves remain closed. In atrial systole, the atria contract, pushing additional blood into the ventricles. The ventricles are thus optimally filled. In isovolumic ventricular contraction, the ventricles begin to contract, increasing intraventricular pressure. The AV valves close, preventing backflow. Semilunar valves also remain closed as the arterial pressure requirement has not yet been met. In ventricular ejection, ventricular contraction furthers, further increasing intraventricular pressure, forcing the semilunar valves open. Blood is ejected into the pulmonary artery and aorta. AV valves remain closed, preventing regurgitation. In isovolumic ventricular relaxation, ventricles relax, decreasing pressure. Blood flows back to the heart, filling the cusps of the semilunar valves, causing them to close and preventing backflow. Once ventricular pressure drops below atrial pressure, the AV valves open again, and the cycle repeats.
What is EDV?
End-diastolic volume, volume of blood in the ventricle at the end of diastole
What is ESV?
End-systolic volume, volume of blood in the ventricle at the end of systole
What is SV?
Stroke volume, volume of blood ejected from the ventricle in each cycle. SV=EDV-ESV (0.13-0.07=0.06)
What is ejection fraction?
% EDV ejected with each stroke, about 60%
What is a Wiggers’ diagram?
A Wiggers’ diagram consists of y-axis values of electrical activity (ECG), pressure (of chambers and aorta) and (left) ventricular volume and an x-axis value of time (msec).
What is the dicrotic notch?
The dicrotic notch, at the end of the T wave (heart), marks the end of systole and the beginning of diastole in the artery (aorta).
What do the lub dub sounds produced by?
Lub - AV valve closure
Dub - semilunar valve closure
By how much does cardiac output increase during exercise?
Up to 5 fold
What is cardiac index?
Cardiac index is the CO per m^2 of body surface area (BSA).
State the average CO.
5 L/min
Explain the control of SV.
SV is influenced by three major factors: preload, contractility, and afterload. Preload, an intrinsic mechanism, refers to the ventricular filling pressure and volume; an increase in EDV leads to cardiac muscle stretch, increasing contractility and SV. Contractility, influenced by both intrinsic and extrinsic factors, is affected by inotropic agents such as sympathetic stimulation, which increases intracellular Ca 2+ concentration, thereby increasing contractile force and SV. Afterload, an extrinsic mechanism, is the resistance the left ventricle must overcome to eject blood, primarily determined by aortic pressure; increased afterload opposes ejection, reducing SV.
What is the Frank-Starling law?
As EDV increases, the myocardium becomes increasingly stretched and contracts more forcefully. Therefore, an increase in preload (EDV) enhances contractility, which in turn increases SV.
What is ventricular contractility?
The force of contraction achieved from a given initial fiber length.
How does the sympathetic nervous system affect ventricular contractility?
It stimulates Beta 1 adrenoceptors on ventricular myocytes.
What intracellular pathway is activated by Beta 1 adrenoceptor stimulation?
β₁-adrenoceptor stimulation → g-protein activation → increase in cAMP → activation of protein kinase A (PKA) → opening of L-type Ca²⁺ channels → increased Ca²⁺ influx
How does increased calcium affect contractility?
Ca2+ that enters the cell increases calcium-induced calcium release. This Ca2+ acts in the actin-myosin cross-bridge cycle, causing increased contractile force on ventricular myocytes and increased SV.
At what ejection fraction is a heart said to be failing?
<30%
In what condition is the heart’s contractility weakened?
Heart failure
How does sympathetic stimulation try and reduce the effects of heart failure?
The blood volume is increased by the kidneys, increasing SV.
Which vessels are the least thin-walled?
Arteries and arterioles
What is the mean BP?
93 mmHg
Which vessels provide the most resistance and how?
Arterioles, by their large sympathetic input and high degree of smooth muscle
What is the distinguishing feature of a capillary?
Absence of smooth muscle
What is the continuity of the blood vessels as it crosses a capillary bed.
Arteriole, metarteriole, pre-capillary sphincter, throughfare channel (capillary), venule
What is the function of pre-capillary sphincters?
Local metabolic control, in order to completely seal a vessel
What is the difference between the way differently soluble materials diffuse into or out of capillaries?
Water-soluble substances pass through pores. Lipid-soluble substances pass through the capillary wall. Plasma proteins cannot cross. Exchangeable proteins are transported via vesicles.
What is the major characteristic of the BBB?
The tight junctions between endothelial cells that line cerebral blood vessels
What is the function of capacitance veins?
To store blood
What are the Starling forces?
The Starling forces are the ways in which substances are moved relative to capillaries. They are: capillary hydrostatic pressure, interstitial fluid hydrostatic pressure, plasma colloid oncotic pressure, interstitial fluid colloid oncotic pressure.
What are the functions of lymph vessels?
Tissue drainage, returning leaked plasma proteins, absorption of digested lipids, defence
What is oedema?
Oedema is a build-up of fluid in the interstitium.
What are the ways in which oedema arises?
Reduced plasma proteins, increased capillary permeability, increased venous pressure, lymph blockage (surgery/parasitic infection)
What is the study of the forces generated by the heart and the motion of the blood through the cardiovascular system called?
Haemodynamics
State the formula for pulse pressure.
Systolic pressure - diastolic pressure
State an alternative formula for the mean arterial blood pressure (MAP).
MAP = diastolic + 1/3 pulse pressure
State Poiseuille’s law.
(eta is interchangeable with myu)
This law describes the behaviour of a perfect fluid in a rigid tube.
How does the length of a vessel affect its resistance to blood flow?
The longer the vessel, the greater the resistance to flow.
State Laplace’s law.
wall tension = (pressure x radius) / wall thickness
What is haematocrit?
Haematocrit is the % by volume of RBCs in blood.
How does haematocrit affect blood viscosity?
The greater the haematocrit, the greater the blood viscosity.
Where do RBCs tend to flow in the stream of blood through vessels?
Centre stream
Name the phenomenon whereby the discharge hematocrit is lower than feed hematocrit, naturally occurring in capillaries with Poiseuille flow
Plasma skimming
Differentiate between the laminar and turbulent flow of blood.
Laminar flow is streamlined, it is fast centrally and slower at the surface. It is more likely in small tubes at slow velocities. It is silent. Turbulent flow is irregular. It is more likely in large tubes at high velocities, with a low blood viscosity. It is audible and is used in BP measurements.
What sympathetic stimulation results in vasoconstriction?
Endothelin, vasopressin (ADH), angiotensin II
What sympathetic stimulation results in vasodilation?
Histamine
Why does the sympathetic stimulation to vessel radius not affect those vessels that are found in the brain?
Absence of alpha 1 receptors
What is the exception to the absence of parasympathetic innervation in arterioles?
Genitalia
What are the main catecholamines?
Dopamine, epinephrine, norepinephrine
What is hyperaemia?
Hyperaemia is an excess of blood in vessels.
What is EDRF?
Endothelium-derived relaxing factor is a vasodilator. It is primarily NO. So it induces active hyperaemia.
What is the usual result of tissue hypoxia?
Reactive hyperaemia
How does histamine affect capillary permeability?
Increases it
Where is histamine derived from in the body?
Histamine is derived from connective tissue mast cells and circulating basophils.
Describe the autoregulation of blood flow.
Autoregulation of blood flow is an intrinsic mechanism that ensures stable perfusion despite fluctuations in MAP, primarily utilizing the myogenic mechanism. This is an inherent property of arteriolar smooth muscle, where an increase in pressure initially raises blood flow and stretches the vessel. In response, the smooth muscle contracts compensatorily, limiting the increase in blood flow and preventing excessive perfusion. This provides a defense against changes in MAP, maintaining steady perfusion. However, autoregulation can be overridden when essential increases in blood pressure are required, such as during active hyperaemia or exercise, where metabolic demand necessitates greater perfusion.
Describe renal circulation.
Renal blood flow (RBF) indirectly determines glomerular filtration rate (GFR). The kidneys receive a high resting blood flow, so active hyperaemia is not required. Blood flow regulation is primarily achieved through tubuloglomerular feedback. When GFR increases, the macula densa detects elevated tubular fluid flow and signals afferent arteriole constriction, thereby reducing GFR to maintain balance. The kidneys have a high sympathetic innervation, allowing for blood flow limitation during conditions requiring high MAPs, such as exercise. This ensures blood pressure control while still maintaining filtration processes.
What is perfusion pressure?
MAP - venous pressure or intercranial pressure (in the brain)
Describe cerebral circulation.
The brain is sensitive to changes in arterial pCO2 and pO2. An increase in pCO2 leads to vasodilation, while a decrease in pCO2 results in vasoconstriction, as seen in hyperventilation, where rapid breathing lowers pCO2 and causes light-headedness. When pO2 falls below 50 mmHg, cerebral blood flow increases to supply more oxygen.
Autoregulation fails at around 50 mmHg of CPP, below this, reduced perfusion can lead to fainting. For example, sudden postural changes, such as moving from a supine to an upright position, can cause a drop in MAP, triggering a reduction in CBF. Similarly, conditions like excessive peripheral vasodilation (high ambient temperature) or stress-induced vasovagal responses (decreased heart rate, cardiac output, and MAP) can compromise cerebral autoregulation, leading to dizziness or fainting. Upright CBP is about 77 mmHg.
Describe dermal circulation.
The skin requires about 250 ml/min of blood flow. It is influenced by sympathetic innervation controlled by the hypothalamus. In the cold, the body aims to conserve heat, so the sympathetic nervous system constricts the arteriovenous anastomoses, reducing blood flow to the skin and limiting heat loss. This is noradrenergic, meaning it involves the release of norepinephrine to constrict blood vessels. When the body is overheated, the sympathetic nervous system also stimulates sweat glands through preganglionic cholinergic fibres, leading to sweating to aid in cooling the body. Bradykinin, a vasodilator, is released during this process. Bradykinin induces pseudo-active hyperaemia, which increases blood flow to the skin in response to local tissue activity (such as sweating). This achieves thermoregulation.
How does blood flow to organs change during physical activity?
It decreases, sympathetic arteriolar vasoconstriction
Describe splanchnic circulation.
Blood flow to splanchnic organs is adaptive, meaning it can change based on its needs. When cardiac output is low, in states of reduced circulatory demand or shock, splanchnic blood flow can be drastically reduced to less than 10 mL/min/100 g. In contrast, after eating, the blood flow to the digestive organs can surge up to 250 mL/min/100 g to support digestion, nutrient absorption, and transport of nutrients to the liver via the portal vein.
Sympathetic innervation plays a key role in regulating blood flow, especially when there is an elevated MAP, like in exercise. During this, blood flow to splanchnic organs is reduced to prioritize perfusion to critical organs like the heart and muscles. There is a degree of active hyperaemia during digestion, which means that blood flow increases locally in response to the metabolic needs of the digestive system during the process of nutrient absorption and digestion.
Describe coronary circulation.
Coronary circulation exhibits phasic flow, with blood flow to the heart being influenced by both systolic compression and diastolic dilation. During systole, coronary vessels are compressed, reducing blood flow, while in diastole, the vessels dilate. Therefore, coronary flow is primarily diastolic, as the heart receives the majority of its O2 supply during this phase.
The coronary circulation also relies on active hyperaemia. In response to reduced oxygen levels in the heart, there is adenosine release, a vasodilator that increases blood flow to supply O2 to myocardium. This mechanism ensures that the heart receives adequate oxygen, especially during periods of increased workload.
While the heart rate can affect the time available for coronary perfusion (since shorter diastolic periods at higher heart rates can reduce coronary blood flow), this is often overridden by metabolic active hyperaemia. The heart can prioritize its own metabolic needs, ensuring adequate blood supply to meet the increased demands, even if sympathetic influences, such as changes in heart rate, might otherwise reduce the available time for coronary perfusion.
