Lecture 2 CVS: the heart Flashcards
what is an electrocardiography
process of monitoring the electrical events of the heart over a given period
what is an electrocardiograph
a device that detects electrical currents generated by an transmitted through the heart
what is an electrocardiogram (ECG)
-a graphical representation of electrical changes that accompany each heartbeat
-obtained by placing electrodes at specific locations on body surface
-a composite of all APs
what do abnormal patterns of an ECG show
they are used to diagnose damage
cardiomegaly, defective cardiac conduction system, heart and chest injuries/pain etc.
what does an ECG show
there are three waves of each heart beat and intervals
what are the 5 steps shown on an ECG (slide 5&6)
- atrial depolarization, initiated by SA node which causes the P wave
- with atrial depolarization complete, the impulse is delayed at the AV node
- ventricular depolarization begins at the apex, causing the QRS complex and atrial repolarization occurs
- ventricular depolarization is complete
- ventricular repolarization begins at the apex, causing the T wave
- ventricular repolarization is complete
what does an enlarges P wave show
enlargement of the atria
what does an enlarged Q wave show
myocardial infarction (heart attack)
what does an enlarged R wave show
enlargement of ventricles
what is the P-Q interval
-start of P wave to start of QRS complex
-start of atrial excitation to start of ventricular excitation
what is the S-T segment
-end of S wave to the beginning of T wave
-depolarization of ventricular contractile fibers during plateau phase
what is the Q-T interval
-the start of the QRS complex to the end of the T wave
-from the start of ventricular depolarization to the end of ventricular repolarization
what does increased/ decreased P-Q interval show
CAD, rheumatic fever
what does increased/decreased S-T interval show
myocardial infarction
what does increased/decreased Q-T interval show
myocardial infarction, ischemia, defective cardiac conduction system
what is a summary of an ECG
tracks the electrical activity of the heart
-P wave: impulse across atria; atrial depolarization
-P-R interval: time taken for cardiac impulse to travel from the atria to the ventricles
-QRS complex: ventricular depolarization; spread of electrical impulses throughout the ventricles
-S-T segment: end of ventricular depolarization and the beginning of ventricular repolarization
-T wave: ventricular repolarization
what is the cardiac cycle
-period from the start of one heartbeat to the beginning of next
-one cardiac cycle consists of the contraction (systole) and relaxation (diastole) of both atria, rapidly followed by the systole and diastole of both ventricles
-blood pressure in each chamber: rises during systole, and drops during diastole
-blood flows from an area of higher pressure to one of lower pressure, it is controlled by timing of contraction, and directed by one-way valves
how many bpm does the heart do and how long does the cardiac cycle last
at 75 bpm, the cardiac cycle lasts ~800 msec (0.8 sec)
what are the two phases of the cardiac cycle
-systole: atrial and ventricular systole
-diastole: atrial and ventricular diastole
what happens to the cardiac cycle when heart rate increases
all phases of the cardiac cycle shorten, particularly diastole
what does atrial systole and diastole show
-atrial contraction begins, tricuspid and mitral valves are open
-atria eject blood into the ventricles
-atrial systole ends, and atrial diastole begins
-ventricles contain maximum blood volume known as end-diastole volume (EDV)
what does ventricle systole show
-ventricles contract and build pressure-> causes the AV valves to close, producing Isovolumetric Contraction
-ventricular pressure is greater then (>) arterial pressure, semilunar valves open, allowing blood to exit= ventricular ejection
-amount of blood ejected= stroke volume (70-80 ml of blood)
-as ventricular pressure falls: semilunar valves close, ventricles contain end-systolic volume (ESV)
what does ventricular diastole show
-isovolumetric relaxation occurs
-all heart valves are closed, ventricular pressure> atrial pressure, blood cannot flow into ventricles
-AV valves open; ventricles fill passively-> atrial pressure > ventricular pressure
atrial damage vs. ventricle damage
individuals can survive severe atrial damage, however, ventricular damage can lead to heart failure
what is dicrotic notch
-closure of aortic valve raises aortic pressure as backflow rebounds off closed valve cusps
-atria continue to fill during ventricular systole and when atrial pressure> ventricular pressure, AV valves open and the cycle begins again
how long do the atrial systole, ventricular systole and the quiescent period last for
-artial systole lasts ~0.1 seconds
-ventricular systole lasts ~0.3 seconds
-quiescent period (total heart relaxation) lasts ~0.4 seconds
what type of energy is used for cardiac contractions
-Aerobic energy
-from the mitochondrial breakdown of fatty acids and glucose
-oxygen is delivered by circulation
-cardiac contractile cells store oxygen in myoglobin
what are the different heart sounds and how do you detect them
-they are detected with a stethoscope
-S1 (lubb): loud sound as AV valves close, signals beginning of ventricular contraction
-S2 (dupp): loud sound as semilunar valves close, beginning of ventricular filling
-S3, S4: soft sounds that are hardly heard, blood flowing into ventricle and atrial contractionw
what is a heart murmur
sounds produced by regurgitation through the valves
where can you hear the different valves working
-Aortic valve: sounds heard in 2nd intercostal space at the right sternal margin
-Pulmonary valve: sounds heard in 2nd intercostal space at left sternal region
-Mitral valve: sounds heard over the heart apex (in the 5th intercostal space) in line with the middle of the clavicle
-Tricuspid valve: sounds typically heard in the right sternal margin of the 5th intercostal space
what is the cardiac output (CO)
volume pumped by the left or right ventricle in one minute into the aorta or pulmonary trunk
-CO (ml/min)= HR (beats/min) x SV (ml/beat)
what is the stroke volume
amount of blood pumped out by each ventricle with each heartbeat, correlates with force of contraction
what is the CO and HR at rest
HR= 75 beats/min, SV = 70ml
therefor, CO = 5250 ml/min =5.25 L/min
what is the regulation of heart pumping
-maximal CO is 4-5x resting CO in nonathletic people (20-25 L/min)
-maximal CO may reach 35 L?min in trained athletes
what is the cardiac reserve
the different between resting and maximal CO
-CO changes (increase/decrease) if either or both SV or HR is changed
cardiac output is affected by factors leading to what
regulation of stroke volume, and regulation of heart rates
what factors determine cardiac output (slide 22)
how do you calculate stroke volume (SV)
SV = EDV - ESV
EDV = end-diastolic volume: the amount of blood in each ventricle at end of ventricular diastole (~120 ml/beat)
ESV = end-systolic volume: amount of blood remaining in each ventricle at the end of ventricular systole (~50 ml/beat)
therefor: Normal SV = 120-50= 70ml/beat
what is the ejection fraction
the percentage of EDV ejected during contraction
what are the three factors affecting stroke volume
preload, contractility, and afterload
what is preload in the SV
-degree of stretch of heart muscle
-changes in preload cause changes in the stroke volume
-cardiac muscle exhibits a length-tension relationship
-at rest, cardiomyocytes are shorter than optimal length-> dramatic increase in contractile force
-most important factor in preload stretching of cardiac muscle is venous return (amount of blood returning to the heart), slow heart beat and exercise increase venous return, increased venous return distends (stretches) ventricles and increases contraction force
what is frank-starling law of the heart
in a normal heart, the higher the preload, the higher the SV
what is contractility in the stroke volume
-contractile strength at given muscle length, independent of muscle stretch and EDV
what is increased contractility (lowers ESV) caused by
-sympathetic epinephrine release stimulated increased Ca2+ influx-> more cross bridge formations
-positive inotropic agents- thyroxine, glucagon, epinepherine, digitalis, high extracellular Ca2+
what is contractility decreased by
-negative ionotropic agents
-acidosis (excess H+), increased extracellular K+, calcium channel blockers
what is afterload of the stroke volume
-back pressure exerted by atrial blood; it is the pressure ventricles must overcome to eject blood
-back pressure from arterial blood pushing on semilunar valves is a major pressure
-hypertension increases afterload-> increased ESV and reduced SV
what is the normal aortic and pulmonary trunk pressures in afterload
-aortic pressure is around 80 mm Hg
-pulmonary trunk pressure is around 10 mm Hg
what factors affect heart rate
autonomic innervation, chemical regulation, age, gender, exercise, and body temperature
what is autonomic innervation and how does it affect HR
-cardiac plexus innervates the heart
-Vagus nerve (CN X)- parasympathetic fibres to small ganglia in cardiac plexus
-cardiac centers of medulla oblongata
what does the cardioacceleratory center do
controls the sympathetic neurons that increase heart rate
what does the cardioinhibitory center do
controls parasympathetic neurons that slow heart rate
how does and which chemical/s regulation affect heart rate
-Hormones: heart rate is increased by catecholamine- epinephrine
(E) and norepinephrine (NE), thyroid hormone (T3)
-Ions: intra and extracellular ion concentrations (ex. Ca2+ and K+) must be maintained for normal heart function, imbalances are very dangerous to the heart
how does age affect HR
fetus has the fastest HR; declines with age
how does gender affect HR
females have a faster HR than males
how does exercise affect HR
it increases HR, trained athletes can have slow HR
how does body temp affect HR
HR increases with increased body temperature
how does hypocalcemia affect the heart
it depresses the heart
how does hypercalcemia affect the heart
it increases HR and contractility
how does hypokalemia affect the heart
it results in weak heart beat; arrhythmias, low levels of potassium
what is tachycardia
abnormally fast HR (>100 beats/min), if persistent may lead to fibrillation
what is bradycardia
heart rate is slower than 60 beats/min
-may result in grossly inadequate blood circulation in nonathletes
-may be a desirable result of endurance training
what is congestive heart failure (CHF)
is it a progressive condition: CO is so low that blood circulation is inadequate to meet tissue needs, reflecting weakened myocardium
what can weakened myocardium and CHF be caused by
-Coronary Atherosclerosis: clogged arteries caused by fat buildup; impairs oxygen delivery to cardiac cells, the heart becomes hypoxic (lacks O2) and contracts ineffectively
-Oersistnet HBP: aortic pressure> 90 mmHg causes myocardium to exert more force, chronic increased ESV causes myocardium hypertrophy and weakness
-Multiple Myocardial Infarctions: heart becomes weak as contractile cells are replaced with scar tissue
-DIlated Cardiomyopathy (DCM): ventricles stretch and become flabby and myocardium deteriorates, drug toxicity of chronic inflammation may play a role
what are three common types of congenital heart defects
ventricular septal defect, coarctation of the aorta, and tetralogy of Fallot
what is a ventricular septal defect
the superior part of the interventricular septum fails to form, allowing blood to mix between the two ventricles, more blood is shunted from the left to the right because the left ventricle is stronger
what is a coarctation of the aorta
a part if the aorta is narrowed, increasing the workload of the left ventricle
what is a Tetralogy of Fallot
multiple defects (tetra=4)
1. The pulmonary trunk is too narrow and the pulmonary valve stenosed, resulting in
2. hypertrophied right ventricle
3. ventricular septal defect
4. aorta receives blood from both ventricles
