Cvs Flashcards
Cardiac muscle types
Atrial ventricular and excitatory muscles
Cardian synctium, types and contraction
Group of cardiac muscle cells that are separated by intercalated disc
Types are atrial and ventricular synctium
Division of synctium is so that atria contract little time ahead of ventricles
Movement of electric potential and delay in contraction of atria and ventricles
Electric potential starts at SA node(superior lateral wall next to superior vena cava) then contracts atria —> av node —> ventricles
Delay of 0.1seconds occurs between atria and ventricles
What is mEq
The milliequivalent (mEq) is the unit of measure often used for electrolytes. It indicates the chemical activity, or combining power, of an element relative to the activity of 1 mg of hydrogen. Thus, 1 mEq is represented by 1 mg of hydrogen (1 mole) or 23 mg of Na+, 39 mg of K+, etc.
Difference in opening and closing of Fast sodium and sodium calcium channels
Fast-Na channels open n close in one thousandth of second while Na-Ca channels are slow to open and remain open for several tenths of a second
What causes action potenial of cardiac miscles and plateu
2 reasons
First is that 2 types of channels cause action potential in cardiac muscles fast Na channels and Na-Ca channels and na-ca channels are slower
Second is because action potential in cardiac muscles decrease the permeability for k channels about 5 folds
When and how repolarization occur in cardiac cells
The cause of low permeability of k channels is high influx of ca by na-ca channels. After 0.2-0.3sec na-ca channels influx ceases and k ions moves out and repolarization occur.
Cardiac work
Oxygen consumption depends on what and which part of cardiac work requires more oxygen
CW = CO * aortic pressure
CO shows volumic work
Oxygen consumption is directly proportional to Cardiac work i-e = CO *Aortic pressure
Pressure work requires more oxygen bcz more contraction it has to do
PW needs more oxygen
What is ficks principle and what it shows and how ? Give example
Ficks principle states that more the oxygen consumed more will be the CO , it shows CO
CO=O2 consumption/ venous O2 content -arterial O2 content
If 50 ml 02 is added each time when it passes lungs eg 50 ml were added to 1L then how many litres consumed 250ml 02 …….i-e 5L hence co is 5L
Sv
CO
EDV
EF and what is shows
Sv is volume of blood ejected per beat
CO=SV*HR -> volume of blood ejected per minute
EF=SV/EDV -> fraction of diastolic volume ejected per systole
EF shows efficiency of heart
What are phases of p-v graph(left ventricular pressure and volume)
What this area subtended shows
When some of phases increase and when decrease
4 phases 1-2period of filling (left to right). 2-3 of IVC (bottom to top). 3-4period of ejection(right to left). 4-1period of IVR(top to bottom)
The area subtended shows the cardiac work output OR END-SYSTOLIC VOLUME(edv-sv)
1-2 î when preload î or venous return î
3-4 î when contractility î or sv î
Half distance beyond 1 to 2 and î 2-3 and 3 to half distance beyond and then again the same shows î afterload
Laplaces law
Laplace law states that
P=2tensionthickness/radius
Decreasing radius(ventrodilators and diuretics) increase pressure
Contractility
dP/dt
Rate of pressure development during isovolumic contraction
Depends on EF and adrenaline
Contractility î when dp/dt î ,î peak of LF pressure, î V of relaxation
In ischemic heart disease or any other disease heart needs gets less oxygen so what can we do
We can reduce oxygen demand of heart by leplaces law
Relationship of SV with preload, contractility and Afterload
SV@ preload*contractility
Sv@1/afterload
@(propotional)
Effect of potassium ions on heart
K ions block the transmission of electrical impulse from SA node to AV node .actually decreases the resting membrane potential( depolarize it ). Therefore high K level from 8-12 mEq/L
Preload
Afterload
Load on ventricles after contraction means at relaxation
Can be called as EDV
Load on muscles during contraction or load against which ventricles has to work
Depends on MAP
Heart get its chemical energy from
70% fatty acid metabolism
30% other nutrients(specially glucose and lactate)
whats the relation of oxygen consumption and tension Whats the tension of heart muscle according to laplaces law
Oxygen consumption is directly proportional to tension which is itself proportional to pressure times radius of ventricles
Heart beat is regulated by ??
1) intrinsic regulation i-e described by frank starling mechanism which states the grtr the stretch of ventricles grtr will be the contraction (to lesser extent grt atrial p î heart rate bcz of stretch of SA node which itself has direct effect on heart beat)
2) control by sympathetic and parasympathetic nervous system
Nerve which transmit parasympathetic stimulation to heart and where it is attached
Vagus nerve are mainly distributed to SA and AV node less to atria and very less to ventricles
Effect of temperature on heart
Heat increases the permeability of ions therefore î heart beat
Effect of load on cardiac output
When load î cardiac output does not decrease upto a limit i-e 160mmhg because î arterial pressure î venous return ….co is Lowest on 250
Which channels open when myocardial cells depolarise
and what they cause and how this causes diminishes
Voltage gates k and ca channels open. K goes out while ca comes in . This causes plateau. As time passes by (in plateau) k permeability î and ca permeability decrease therefore plateau diminishes and repolarization occur
Which electrical activity causes systole
Movement of ca from extracellular matrix and SR to cytosol causes contraction of actin and myosin and hence systole occur
Starling curve says that
Sv @ EDV
Or
Tension developed by myocardial cells @ initial stretch
How positive inotropy î contractility
It increases cross bridging by allow more ca influx
What’s the molecular level Effect of acetylcholine on cells
Ach î permeability of k —> k goes out —> cell becomes hyperpolarise and make them less excitable
Effect of digitalis on heart
It inhibits Na-k pump therefore inside remains depolarised and Na-ca exchange doesn’t work —> cross bridging remains…… it also acts on vagus which release acetyl choline that works on SA and Av node and blocks their transmission by increasing k permeability—> hyperpolarzAtion makes them less excitable
Sv is affected by
What decrease preload and afterload
Sv cap
Contractility afterload and preload
Vasodilators like nitroglycerin decrease preload
Arterial Vasodilators like hydrAlAzine decrease afterload
Pulse pressure=
Systolic blood pressure -diastolic blood pressure
Channels in sarcoplasmic reticulum
1) ca active transporters move ca from cytosol to inside SR by use of energy
2) ca sensitive ca channels become active when they come in contact with ca —> allow movement of ca from inside of SR to cytosol
How SNS î contractility
It binds with beta-adrenergic receptors which stimulate cyclic adenylate enzyme—>cAMP—>protein kinase A —> phosphosrylates 1) voltage gated ca channels of cm
2) activates a protein that î ca ATPase of SR
Hence ca level inside cell increases
When is the oxygen consumption highest in LV p-V graph and what causes an î in that area and thus oxygen consumption
Phase between 2-3 (IVC) is the time of most oxygen consumption and it î when afterload î and so does the oxygen
What causes action potenial of cardiac miscles and plateu
2 reasons
First is that 2 types of channels cause action potential in cardiac muscles fast Na channels and Na-Ca channels and na-ca channels are slower
Second is because action potential in cardiac muscles decrease the permeability for k channels about 5 folds
Sv
CO
EDV
EF and what is shows
Sv is volume of blood ejected per beat
CO=SV*HR -> volume of blood ejected per minute
EF=SV/EDV -> fraction of diastolic volume ejected per systole
EF shows efficiency of heart
Which chemicals are positive inotropes
What substances affect (î n !) venous return -> RAP->change sv/ co
What affect TPR
Digoxin , catecholamines, dobutamine, milrinone, exercise
Infusion and symapatgetic activity î
Acute Hemorrhagic and spinal anesthesia !
RAP—> right atrial pressure
Vasopressors î
Exercise !
When and how repolarization occur in cardiac cells
The cause of low permeability of k channels is high influx of ca by na-ca channels. After 0.2-0.3sec na-ca channels influx ceases and k ions moves out and repolarization occur.
What is ficks principle and what it shows and how ? Give example
Ficks principle states that more the oxygen consumed more will be the CO , it shows CO
CO=O2 consumption/ p venous O2 content -p arterial O2 content
If 50 ml 02 is added each time when it passes lungs eg 50 ml were added to 1L then how many litres consumed 250ml 02 …….i-e 5L hence co is 5L
Cardiac work
Oxygen consumption depends on what and which part of cardiac work requires more oxygen
CW = CO * aortic pressure
CO shows volumic work
Oxygen consumption is directly proportional to Cardiac work i-e = CO *Aortic pressure
Pressure work requires more oxygen bcz more contraction it has to do
PW needs more oxygen
Preload
Afterload
Load on ventricles after contraction means at relaxation
Can be called as EDV
Load on muscles during contraction or load against which ventricles has to work
Depends on MAP
Contractility
dP/dt
Rate of pressure development during isovolumic contraction
Depends on EF and adrenaline
Contractility î when dp/dt î ,î peak of LF pressure, î V of relaxation
In ischemic heart disease or any other disease heart needs gets less oxygen so what can we do
We can reduce oxygen demand of heart by leplaces law
Relationship of SV with preload, contractility and Afterload
SV@ preload*contractility
Sv@1/afterload
@(propotional)
What are phases of p-v graph(left ventricular pressure and volume)
What this area subtended shows
4 phases 1-period of filling (left to right). 2-period of IVC (bottom to top). 3-period of ejection(right to left). 4- period of IVR(top to bottom)
The area subtended shows the cardiac work output
Effect of temperature on heart
Heat increases the permeability of ions therefore î heart beat
Which electrical activity causes systole
Movement of ca from extracellular matrix and SR to cytosol causes contraction of actin and myosin and hence systole occur
Heart get its chemical energy from
70% fatty acid metabolism
30% other nutrients(specially glucose and lactate)
Channels in sarcoplasmic reticulum
1) ca active transporters move ca from cytosol to inside SR by use of energy
2) ca sensitive ca channels become active when they come in contact with ca —> allow movement of ca from inside of SR to cytosol
whats the relation of oxygen consumption and tension Whats the tension of heart muscle according to laplaces law
Oxygen consumption is directly proportional to tension which is itself proportional to pressure times radius of ventricles
Laplaces law
Laplace law states that
P=2tensionthickness/radius
Decreasing radius(ventrodilators and diuretics) increase pressure
Effect of load on cardiac output
When load î cardiac output does not decrease upto a limit i-e 160mmhg because î arterial pressure î venous return ….co is Lowest on 250
Effect of potassium ions on heart
K ions block the transmission of electrical impulse from SA node to AV node .actually decreases the resting membrane potential. Therefore high K level from 8-12 mEq/L
Nerve which transmit parasympathetic stimulation to heart and where it is attached
Vagus nerve are mainly distributed to atria
Which channels open when myocardial cells depolarise
and what they cause and how this causes diminishes
Voltage gates k and ca channels open. K goes out while ca comes in . This causes plateau. As time passes by (in plateau) k permeability î and ca permeability decrease therefore plateau diminishes and repolarization occur
Heart beat is regulated by ??
1) intrinsic regulation i-e described by frank starling mechanism which states the grtr the stretch of ventricles grtr will be the contraction (to lesser extent grt atrial p î heart rate bcz of stretch of SA node which itself has direct effect on heart beat)
2) control by sympathetic and parasympathetic nervous system
How positive inotropy î contractility
It increases cross bridging by allow more ca influx
How SNS î contractility
It binds with beta-adrenergic receptors which stimulate cyclic adenylate enzyme—>cAMP—>protein kinase A —> phosphosrylates 1) voltage gated ca channels of cm
2) ca ATPase of SR
Hence ca level inside cell increases
Extra systole will î or ! Pulse pressure and why
It will ! Pulse pressure because of ! Stroke volume
Value of EDV and SV
How to calculate CO
EDV is 140ml
Sv is 75 ml
Co= 75ml*72=5.4L/min
Effect of increased venous return on contractility
Î venous return will î mean atrial filling pressure and therefore CO so both will be steady on graph and hence no change on contractility
Rmp of pacemaker cell
How potential is continuously produced in pacemaker cells
What are the stages
RMP of pacemaker cells is -60mV
Whenever cell become -ve less than -40 funny channels open then voltage gated ca channels open and potential reaches threshold. Remember na channels are inactivated because of less negative potential
Pacemaker potential funny channels
Dep ca channels
Rep. K channels
Increase in which ion concentration makes heart dilated and weak
Excess potassium ions in the blood and extracellular fluid cause the heart to become dilated and flaccid as well as slowing the heart. This effect is important due to a more positive resting membrane potential in the cardiac muscle fibers. As the membrane potential becomes more positive, the intensity of the action potential decreases, which makes the contraction of the heart progressively weaker
Effect of sympathetic activity on sv and co
Sv ! But CO î because of îheart rate
Normal delay at av node plus bundle
0.13 seconds
Rmp and threshold values of SA node
- 55
- 40
What is the positive electrode for limb 2
Left leg
What is the Q-T interval
How to calculate heart rate from ECG
0.35 seconds
60/(R-R interval)
Cardiac arythmias
Deviation oh heart from normal cardiac rhythm
Changes in cardiac impulse generation or conduction
Tachyarythmias and types
Bradyarythmias and types
Simple tachycardia—> 100-150
Flutter—> 250-350 b/m
Fibrillation—> more than 350
Mild bradyarythmias—> 60-40
Moderate BA—> 40-20
Severe BA—> less than 20
3 main causes of cardiac arythmias and their causes
Î automaticity—>by catecholamines
Triggered automaticty—> by ischemic or injured cell which load cations
Phenomenon of re-entry(circadian movement)—> around scar tissue
What happens to heart rate during inspiration and expiration and why
Î during insp. Because of vagus in inhibited
! During exp. vagus is stimulated
Sinus tachycardia and causes and change in ecg
Sinus tachycardia is the increase in discharge of impulses from SA node, resulting in increase in heart rate.
Causes are exercise, fever, hyperthyroidism, hemorhagic shock, exercise
Ecg is normal but R-R interval !
Heart block and it’s types
Blockage of transmission of impulses generated from SA node
Types
1) SA block or AV nodal rythm
2) AV block
SA block , what happens in it, types
Block of transmission of impulse from SA to AV node hence AV node becomes the pacemaker and the heart starts beating with decreased rate of 40 to 60/minute.
Types
1– if upper part of AV node discharges impulse then P wave is inverted
2– if middle part of AV node discharge impulse than p wave is absent and all chambers contract simultaneously
3- if lower part becomes the pacemaker then qrs appear prior to p wave and ventricles contract before atria. It is called reversed heart block.
Cognitive stimuli such as reading , talking and problem solving increase cerebral blood flow , how?
By î co2, H+ ions and adenosine
