CVS Flashcards
Why is CV research important
The ageing population:
Baby boomers make up a large proportion of the population and are heading into the age where CVD mortality risk increases
What are some recent trends in CVD
Acute coronary events have been declining due to treating risk factors. However, there has been an increase in heart failure (preventative measures?)
What are the 2 main functions of the CVS
Function as a distribution system (nutrients/water/gases, hormones, immune, waste, heat)
Maintain homeostasis
Name all the heart valves and where they are located
Tricuspid valve - right AV
Bicuspid valve - left AV
Aortic semilunar - left V to Aorta
Pulmonary semilunar - right V to Pulmonary arteries
What are the functions of the AV and semilunar valves
AV - Prevent back flow into the atria during ventricular contraction
Semilunar - Prevent back flow into the ventricle during ventricular relaxation
Features of myocardial muscle cells
Branched, single nuclei, connected by specialised junctions called intercalated disks
Features of intercalated disks
Contain desmosomes which transfer force from cell to cell. Contain gap junctions which allow electrical signals to pass rapidly from cell to cell
2 types of cardiac cells and their differences
Contractile cells - striated fibres organised into sarcomeres
Auto-rhythmic (pacemaker) cells - Signal for contraction, smaller and fewer contraction fibres, not organised into sarcomeres
Discuss the major events in the cardiac contractile cycle as it relates to left ventricular and aortic pressures, and valve sounds
1 - Ventricular diastole (fast and slow filling) causes pressure to drop close to 0mmHg
2 - AV valves close (HS 1) when ventricular pressure exceeds atrial pressure, and a ventricular isometric contraction causes ventricular pressure to rapidly rise
3a - Aortic semilunar valve opens when ventricular pressure exceeds aortic blood pressure. This causes rapid ejection of blood into the aorta, increasing pressure.
3b - Ejection of blood slows as ventricular capacity is depleted, causing pressure to flatten.
4 - Isometric relaxation of the left ventricle causes pressure to drop rapidly. When ventricular pressure falls below aortic pressure, the aortic semilunar valves close (HS 2), preventing a drop in aortic blood pressure.
5 - As left ventricular pressure falls below left aortic pressure, AV valves open and the ventricle begins filling with blood again.
Discuss blood volume and pressure changes throughout the CVS
Blood flows down a pressure gradient. Pressure is greatest in the aorta and drops in an S-shaped manner until it is lowest in the vena cava. Distribution of blood volume is inversely proportional to this - least blood volume in the systemic arteries while most blood volume in the systemic veins.
What is flow rate?
The volume of blood that passes a given point per unit of time (mL/min)
Vasoconstriction vs vasodilation?
Vasoconstriction is a decrease in blood vessel diameter which decreases blood flow.
Vasodilation is an increase in blood vessel diameter which increases blood flow.
Flow though a tube is inversely proportional to resistance
Flow =
change in pressure/resistance (R)
Total blood volume
~5L
What is diastole and systole?
Diastole is cardiac muscle relaxation
Systole is cardiac muscle contraction
What is auscultation?
Listening to the heart through the chest wall using a stethoscope
What is the major parameter controlled by the CVS?
Systemic mean arterial pressure
What happens when BP is too high or low?
Too high = hypertension (can lead to organ damage)
Too low = shock
What feedback loops act to regulate MAP?
Short term via neural pathways
Long term via the vasculature and kidneys
Formula for MAP?
MAP = CO (SV x HR) x TPR
Formula for SV?
SV = EDV - ESV
Average SV and CO
CO = 5L/min SV = 70mL
What are some challenges to BP regulation?
Posture (lying to standing) Dehydration Haemorrhage Surgery, wounds, burns Exercise Abnormal hormonal regulation
What are baroreceptors and how do they work?
Mechanical receptors in the carotid sinus and aortic arch which detect changes in BP
Increased firing triggers efferent pathways to decrease SNS and increase PSNS activity (decreases HR and hence BP). Few blood vessels innervated
Decreased firing triggers efferent pathways to increase SNS and decrease PSNS activity. Increases HR, contractile strength and hence BP. Also has impact on arterioles (vasoconstriction increases TPR) and veins (vasoconstriction increases venous return and hence SV, CO and BP)
Describe the effects of long-term regulation on the CVS
Regulation of ECF volume major pathway for long term regulation of MAP. ECF volume impacted by changes in input and output. Kidneys predominant organ
Describe the response to decreased MAP in order of increasing severity
Arterial baroreceptor reflex Autonomic response Renin-angiotensin system Aldosterone release Vasopressin release Increased erythropoietin release
What is the Frank-Starling law?
Increased venous return stretches the ventricle and makes the next contraction stronger (i.e. the more blood that comes back to the heart [increasing EDV] the more blood the heart will eject)
What impacts venous return?
Skeletal muscle pump
Respiratory pump - inhalation increases blood flow into thoracic veins; exhalation increases blood flow into the heart and abdominal veins
Sympathetic innervation of veins (vasoconstriction)
What is inotropy?
Inotropes are chemicals which increase contractility and hence increase SV (e.g. epinepherine, norepinepherine, digitalis)
What is lusitropy?
Lusitropes are chemicals which decrease contractility and hence decrease SV
Describe the factors which integrate to control CO
CO is a function of HR and SV
HR determined by depolarisation in auto-rhythmic cells. Decreases due to parasympathetic innervation. Increases die to sympathetic innervation and epinephrine
SV is determined by force of contraction in ventricular myocardium. This force is influenced by contractility (sympathetic innervation and epinephrine increases this) and end-diastolic volume. EDV varies with venous return influences by the skeletal muscle pump, respiratory pump and venous constriction.
How does the action potential of the auto-rhythmic cells differ to that in normal contractile cells?
In auto-rhythmic cells slow inward depolarising Na+ currents (“funny” currents) lead to spontaneous depolarisation (no stimulus required)
Provides stimulus for contractile cells to depolarise
How does the action potential spread throughout the conduction system?
Why is this important for optimal filling/ejection from the heart?
- Action potential originates at SA node in auto-rhythmic cells
- AP spreads throughout right and left atria
- AP can only pass from atria into ventricles via AV node, after a brief delay (due to slower conduction signals through node)
a. Allows atrial contraction to complete ventricular filling before ventricular contraction begins - AP travels rapidly down interventricular septum via Bundle of His (AV bundle), left and right bundle branches, then rapidly throughout the myocardium through Purkinje fibres
a. Ventricle begins contracting from base upward - Remainder of ventricular cells activated by APs moving through gap junctions
Important for optimal filling so the heart contracts from the base upwards, allowing all blood to be ejected from the ventricles during systole
If the SA node is not functioning normally, how does the heart respond?
Atrioventricular (AV) node (50bpm) and Purkinje fibres (25-45bpm) can act as pacemakers under some conditions
SA node = 70bpm
Sympathetic and parasympathetic effect on auto-rhythmic depolarisation?
Parasympathetic = hyperpolarizes the membrane potential and slows depolarisation, slowing HR
Sympathetic & epinephrine = depolarises the membrane potential & speeds up pacemaker potential (funny current), increasing HR
Steps in cardiac contractile cell action potential
- Na+ channels open
- Na+ channels close
- Ca2+ channels open; fadt 3. K+ channels close
Ca2+ channels close; slow K+ channels open - Resting potential
Plateau results from decreased K+ and increased Ca2+ (required for contraction). Plateau ends when flux is reversed
What is the difference between an action potential and an ECG?
Action potential = change in membrane potential
ECG = average electrical changes across two electrodes. PQRST waves allow us to monitor rate rhythm, intervals, pathology
Events caused by P wave, QRS complex and T wave
P = depolarisation of the atria
P-R segment = conduction through AV node and AV bundle (pause that occurs which allows AV node to block conduction, allowing atria to empty into ventricle)
QRS complex = wave of ventricular depolarisation
T = repolarisation of the ventricle
Atrial repolarisation part of the QRS (lost in larger wave)
Conclusions from EMG?
HR = time between 2 P waves or 2 Q waves
Rhythm = regular pattern
Wave analysis = presence and shape
Segment length constant
Describe the excitation-contraction coupling process
- Action potential starts with the heart pacemaker cells
- Voltage-gated L-type Ca2+ channels in the cell membrane open and Ca2+ enters the cell
- Ca2+ induces Ca2+ release through ryanodine receptors which open in the sarcoplasmic reticulum (SR)
- Calcium binds to troponin to initiate contraction via crossbridge cycle (as in skeletal muscle)
- Relaxation occurs when Ca2+ unbinds from troponin
- Calcium is removed from cytoplasm back into the SR for storage with Ca2+ ATPase, or out of the cell through the Na+-Ca2+ exchanger (NC)
- Na+ gradient is maintained by the Na-K-ATPase
What factors impact force of contraction
Force generated is proportional to number of active cross-bridges. This is determined by how much calcium is bound to troponin
Sarcomere length impacts force of contraction (filling the heart more increases force - Frank Starling Law)
