Cardiovascular System Flashcards
Function of the Heart
Meet metabolic needs of the body and is achieved by ensuring adequate exchange of fluids dependent on vessel integrity and sufficient pressure and output
Impulse conduction of the heart
- SA node activity and atrial contraction begins
- Stimulus spreads across atrial surface and reaches AV node
- 100msec delay at AV node. Atrial contraction begins
- Impulse travels along interventricular septum within AV bundle and bundles of branches to Purkinje fibers and by moderator band, to papillary muscles of right ventricle
- Impulse distributed by Purkinje fibers and relayed throughout ventricular myocardium. Atrial contraction completed and ventricular contraction begins
Pacemaker cells
Sinoatrial node, Atrioventricular Node, bundle of his, Purkinje fibers
Pacemaker ability
Action potential in heart =/= Action potential in NS
Rate of AP generation
- SA node: 70 - 80 AP/min
- AV node: 40 - 60 AP/min
- Bundle of His and Purkinje: 20 - 40 AP/min
SA node is the fastest and sets the pace
Electrical activity of the heart
Done by specialized myocardial fibers; not motor neurons
- Contractile cells: 99% of cells do pumping
- Autorhythmic cells: Initiate and conduct AP generation for contraction of working cells
How is heart rate controlled
Controlled by autonomous nervous system
- increased sympathetic stimulus = increased HR
- increased parasympathetic stimulus = decreased HR
- both are active but one will dominate based on certain condition
Cardiovascular Control Centre
- affected by pain, chemoreceptor, baroreceptor, respiratory center
Control SA node
- affected by epinephrine and temperature
- acts only on SA node; not ANS
Interpret ECG
P wave: atrial depolarization (SA node fires)
PR segment: AV node delay
QRS complex: Ventricular depolarization and atrial repolarizing simultaneously
ST segment: Ventricules contracting and emptying
T wave: Ventricular repolarization
TP segment: ventricules relaxing and refiling
When is there no electrical activity recorded?
AV node delay (PR segment)
Ventricules completely depolarized and cardiac cells undergo plateau phase (ST segment)
Heart muscles relaxed and ventricules filling (TP segment)
What makes SA node weird in ECG
SA node firing is not detected as it does not create sufficient electrical activity to reach body surface and not recorded
Impulse spreading through atria is recorded
Define cardiac ouput
Volume of blood pumped out by each ventricle per min
Factors of cardiac ouput
Heart rate: beats per min
Stroke volume: volume of blood pumped per beat
CO = HR x SV
Ejection fraction
Fraction of blood ejected from ventricle per heartbeat
Measured by echocardiography
Measure of cardiac contractility and definite measurement by cardiac catherisation
EF = SV/EDV x 100% (Normal range = 55 - 75%)
Parasympathetic effects on Heart rate
Decrease contractility and weaken contraction of atrial muscles
Decrease excitability and increase AV node delay
Decrease rate of depolarization to threshold of SA node
No effect
- ventricular conduction pathway
- ventricular muscles
- adrenal medulla (endocrine gland)
- veins
Sympathetic effects on heart rate
Increased rate of depolarization to threshold of SA node
Increased excitability and decrease in AV node delay
Increased contractility of atrial and ventricular muscles
Increased conduction through bundle of His and Purkinje fibers of ventricular conduction pathway
Increased venous return and increased cardiac contraction via intrinsic control of veins
Increased epinephrine secretion
What is EDV
End diastolic volume
Frank Starling Law of the heart
Intrinsic relationship between EDV and SV
- ↑ diastolic filling = ↑ EDV = ↑ stretching of heart = ↑ length of cardiac muscle fibers = ↑ cardiac contraction = ↑ stroke volume
- basically ↑ EDV = ↑ SV
- sympathetic stimulus = ↑ heart contraction
What are the factors of Stroke volume
Determined by extent of venous return and by sympathetic activity
SV = EDV - ESV
Intrinsic control = extent of venous return
Extrinsic control = sympathetic stimulus of heart
Stroke volume and cardiac output factors
Strength of cardiac muscle contraction
- Extrinsic control - varies extent of sympathetic stimulus
- Intrinsic control - varies initial length of muscle fibers dependent on ventricular filling
↑ Sympathetic stimulus = ↑ cardiac output by ↑ SV and HR
Define Cardiac output
Volume of blood pumped out by each ventricle per min
Factors of cardiac output
Preload (volume of filling)
Heart (contractility and heartrate)
Afterload (peripheral resistance)
Define cardiac failure
Occurs when cardiac output is insufficient to meet metabolic requirements of tissues
Causes of cardiac failure
Congestion in pulmonary and or systemic circulations
Compensatory measure for heart failure
Sympathetic stimulation and retention of salt and water by kidneys to ↑ blood volume
What supplies blood to heart
Coronary circulation during diastole flows to heart and adjusts to changing requirements such as ↑ O2 demands
Explain process of more O2 rich blood entering heart
- ↑ metabolic demand of cardiac muscle cells
- ↑ adenosine
- vasodilation of coronary vessels
- ↑ blood flow to cardiac muscle cells
- ↑ O2 available
Types of coronary heart disease
Angina Pectoris
- Myocardial ischemia causes chest pain (usually epigastric region such as neck and shoulder)
- Common symptom
Acute myocardial Infarction
- Heart disease
- Irreversible death (necrosis) of part of heart muscle secondary to ischemia
Causes of Coronary Heart Disease
Thrombus - abnormal clot in vessel wall
Embolus - abnormal particle floating in blood vessel
Thromboembolism - obstruction of blood vessel by blood clot dislodged from another site
Atherosclerosis - progressive degenerative arterial disease which causes occlusion of affected blood vessels and low blood flow
Treatment methods of Coronary Heart Disease
Coronary Artery Bypass Grafting (CABP)
Percutaneous Transluminal Coronary Angioplasty (PTCA)
Why is AV node delay called as such
PR interval is 0.12 - 0.20s (Average 0.16s)
Time for signal to travel from SA to AV node, AV node delay, out to bundle of His. Bulk of time is AV node delay hence the name
Difference between AP in Autorhythmic cells and AP in Cardiac contractile cells
Purpose
- Autorhythmic cells responsible for autogeneration of AP (impulses) whereas cardiac contractile cells is responsible for contracting upon receiving the impulses
Related to
- autorhythmic cells related to rate and rhythm of heartbeat whereas cardiac contractile cells are related to contraction
Ca2+
- autorhythmic cells necessary for self-induction of AP compared to Nervous system
- cytosolic Ca2+ directly involved for contraction
Plateau phase
- autorhythmic cells do not have this; only cardiac contractile cells have
Similarity between AP in autorhythmic cells and cardiac contractile cells
All ions (Na+, K+, Ca2+) are important to occur
Process of Autorhythmic cells to cardiac contractile cells
Autogeneration of impulses in autorhythmic cells > impulse spreads > AP in cardiac contractile cells > ↑ cytosolic Ca2+ in cardiac contractile cells > contraction
When does atrial systole and atrial diastole start and end
Atrial systole - 0msec to 100msec
Atrial diastole - 100msec to 800msec
Ventricular systole - 100msec to 370msec
Ventricular diastole - 370msec to 100msec
Process of atrial and ventricular systole and diastole
- Atrial contraction - forces small amount of additional blood into relaxed ventricles (atrial systole)
- Atrial systole ends, atrial diastole starts - atria relaxes after contraction
- Ventricular systole - ventricular contraction pushes AV valves closed but not create enough pressure to open semilunar valves. As ventricular pressure ↑ and > pressures in arteries, semilunar valves open and blood is ejected
- Ventricular diastole - As ventricles relax, pressure in ventricles decreases, blood flows against cusps of semilunar valves and forces them closed. Blood flows into relaxed atria and
4 phases of heart blood flow
- Passive filling and atrial contraction
- Ventricular contraction
- Ventricular depolarization and diastole
- Ventricular refilling
Explain passive filling and atrial contraction
- Atrial P >Ventricular P
- Blood flows into ventricles
- Ventricular volume ↑
- SA node fires and impulse spreads through atria
- Ventricular volume ↑ = Ventricular pressure ↑
- Atrial contraction ends
- End diastolic volume = 135 mL
Explain ventricular contraction
- impulse spreads through AV node
- occurs at QRS complex of ECG
- Ventricular P increases sharply
- AV valve closes (1st Heart sound)
- Isovolumetric ventricular contraction
- Ventricular P > Aortic P; Aortic valves open and blood is ejected
- aortic pressure ↑ as blood is pumped into aorta faster than blood can drain off
- ventricular P decreases
Explain ventricular depolarization and diastole
- End systolic volume = blood not pumped out
- ventricular repolarization (T wave)
- Ventricular P < Aortic P so aortic valve closes and created notch on aortic pressure curve called “dicrotic notch”
- all valves closed, no changes to chamber volume
Explain ventricular refilling
- ventricular P < atrial P (AV valves open)
- atrial P ↑ due to constant blood flow from veins
- Pool of blood in atria rush into ventricles when AV valves open
- Filling of blood slows down
- SA node fires and cardiac cycle repeats
What does extracellular fluid consist of
Interstital fluid + plasma
