Cardiovascular Physiology (heart) Flashcards
ECG Diagnostic issues
- Heart rate,
- heart rhythm: irregularities arrhythmia, atrial fibrillation
- Are all waves present P, R, T?
- For each P-wave is there a QRS complex? - heart block if no P-wave present
Cardiac cycle systole & diastole
- Late diastole
- Atrial systole
- Isovolumetric ventricular contraction (1st sound)
- Ventricular ejection
- Isovolumetric relaxation (2nd sound)
Late diastole
Step one:
superior and inferior vena cava & pulmonary veins Fill atria in heart, causing high pressure, and by gravity and pressure starts to fill ventricles (about 80%)
*AV valves open
Atrial systole
Step 2: atria contracts last 20% of blood goes into ventricle.
(End diastolic volume) : volume of blood in ventricles at the end of diastolic phase
Isovolumetric ventricular contraction
Step 3: increase of ventricular pressure causes, AV valve to shut (AV and SL are both shut) * s1, 1st heart sound (Lup)
High pressure is create volume is same
[when the av node delays the signal in the conduction cycle]
atrial repolarization before QRS
Ventricular ejection
Step 4 : Increases in ventricular pressure causes SL valves to open, blood goes into aorta and pulmonary arteries
( end systolic volume ) : blood remaining in ventricles after contraction
* ventricular contraction
Isovolumetric relaxation
Step 5: ventricular diastole begins; high pressure in aorta and pulmonary arteries close the SL valves (causing the s2 heart sound ‘dub’)
Pwave
Atria depolarization
QRS complex
Ventricular depolarization and contraction. (Ventricular systole and atrial repolarization)
T wave
Ventricular repolarization (relaxation of ventricles)
EDV
End diastolic volume is the maximum amount of blood in the ventricles before contraction *during atrial systole End (finished) Diastolic (relaxation) [low pressure high volume]
ESV
End systolic volume: blood remaining in ventricles after contraction. During the ventricular ejection phase of the cardiac cycle
[high pressure low volume]
Pressure volume curve
X axis : left ventricle volume (ml)
Y axis : left ventricle pressure (mmhg)
A= (late diastole) (ESV) ~65ml
1. A-A1: passive filling ventricle
2. A1-B: aorta contracts (EDV) ~135ml
3. B-C: isovolumetric ventricular contraction (pressure building)
4. C-D: ventricular ejection (stroke volume)
5. D-A: isovolumetric ventricular relaxation. (ESV)
Stroke volume = EDV-ESV
135ml-65ml= 70 ml
- practice on whiteboard
Ways to modulate heart variables
Heart rate (BPM) x stroke volume (ml/beat) [EDV-ESV] = cardiac out put (ml/min)
To meet metabolic needs
Increase or decrease HR and/or increase or decrease in stroke volume is controlled by ANS control and neurohormones (epi/ne)
Modulating stroke volume
- Length of sarcomere cells at beginning of contraction (effects preload) [starlings curve]
- Contractility of cells (more calcium = stronger HB)
- After load (refers to resistance of arterial system)
Stroke volume
Stroke volume= force of contraction
^force=^stroke volume
Starlings curve
*length of sarcomere
As stretch^ [preload EDV{ml}]= ^force [rubber band] = ^ stroke volume.
More blood in heart = more blood pumped out “Frank’s starling law of the heart”
Stretch is a function of EDV and function of venous return.
- white board
Modulating stroke volume:
Contractility of cells ca2+
^ca2+= ^ force of contraction
Altered by Structures:
•altered by ECF entry ; SR release / reuptake/ storage
• chemicals that have an effect of contractility:
- Inotropic agents : positive (E,NE) & negative
- Phospholambin: protein that ^ ca2+atpase activity
Epi/NE catecholamines increase of cardiac contraction
Epi/NE bind to B1 (adrenergic) receptors>
activates cAMP 2nd messenger system>
1.Voltage gated Ca2+ channels: open time increases> ^ca2+ entry from ECF> *on both ^ ca2+ stores in SR, ^ ca2+ released[more forceful contraction]
- phospholamban> ^ ca2+ atpase on SR: ca2+ removed from cytosol faster > shortens ca-troponin binding time [ shorter duration of contraction]
Afterload
The resistance or pressure exerted of the arterial system.
^ afterload resistance = less stroke volume
Lower compliance = ^ afterload (heart must work harder)
^ work= ^ muscle hypertrophy = enlarged heart
Explain mechanistic level how sympathetic nervous system influences EDV and cardiac output
** 20 point question **
Cardiac output : HRxSV
..
Sympathetic nervous system on EDV
Sympathetic(Epi) ^ causes venous construction = greater venous return = ^EDV = ^ force of contraction = larger stroke volume (ml/beat)
[which affects cardiac output]
How does the sympathetic nervous system affect HR, therefore cardiac output?
ANS (sympathetic) controls rate of depolarization of autorythmic cells NE
Increases HR and cardiac output
Where does blood go after aorta
To arteries, arterials, capillaries
>
Venules, Veins, vena cava
Heart circulation
Superior and inferior vena cava to R atrium, R ventricle, pulmonary vein , into lungs (gas exchange co2-o2) left atrium through pulmonary vein , left ventricle, aorta and pulmonary artery
What are the three pathways Of blood?
Systemic circuit, pulmonary circuit, portal system(bypasses the systemic circuit example hepatic, renal nephron)
Cardiac muscle
Called Myocardium, is made of myocytes cells. The two types are contractile Cells and autorythmic cell
Perfusion carries
Oxygen, carbon dioxide, proteins, ions, nutrients, waste to tissues and organs from the transportation of blood.
Differences of contractile myocytes from skeleton muscle fibers
- Smaller/shorter,
- mono nuclear/one nucleus per myocyte,
- branched structure connected to one another via intercalated discs
Intercalated discs
Forms coordinated network of cells that share their cytoplasm through gap Junction and Desmosomes
Name 4 similarities in the process of contraction in cardiac muscles as skeleton muscles
- Calcium is primarily ion involved
- Calcium Stored SR
- Action potential influx of sodium travels down the t tubules to initiate the calcium signal ( not same mech.)
- Sodium potassium ATPase pump maintains RMP
Name the four differences in the contraction process of cardiac muscle in comparison to skeleton myself
- Voltage gated Calcium L type channels in t tube initiate the ligand gated a calcium spark from the SR ( calcium inducible, Calcium release)
-  calcium Sparks Summit intracellularly to build a strong enough calcium signal to cause contraction (graded contraction)
-  calcium is removed from cytoplasm by two pumps NCX and ca atpase pump
- Cardiac muscles do not have motor units because Intercalated discs act as one big motor unit
(variation of tension comes from altering the calcium signal strength) 
How does calcium concentration affect force of contraction
More calcium causes more cross bridges which causes higher tension
What are the different types of channels involved in cardiac contraction compared to skeletal
- Fast and slow K+ channels (contractile cells)
- ca2+ channels (plateau) - Na & K+ If (funny) leak channels (auto rhythmic) (cause pacemaker potential)
- ca2+ channels (depolarization)
Name the steps of contractile cell action potential
- Cell is at resting potential -90 mV
- Depolarization occurs when signal received from a neighboring myocyte.
- Na channel open (influx) reaches +20mV. Na close, fast K begin open. - Initial repolarization begins as fast K channels are fully open (k efflux)
- Repolarization Plateau occurs as Calcium channels open (ca influx) and fast k close.
- Rapid repolarization occurs as calcium channels close and slow potassium channels open (K efflux)
What are the unique characteristics of a contractile cell action potential’s
- Resting membrane potential is -90mv
- Action potential are triggered by auto rhythmic cells
- Action potential plateaus during repolarization (caused by Ca)
- Action potential lasts about 200 ms due to plateau
Why is the plateau important in contractile cell action potential
It prevents tetanus in myocardium which would be fatal. Because the action potential lasts about as long as the contraction, the longer refractory period prevents summation
List the steps of auto rhythmic cell action potential‘s
- pacemaker potential around -60 mV
- Open IF channels allow Na influx mainly and Drift potential towards threshold -40mv
- As membrane potential nears threshold if channels close and some calcium channels open CA influx pushing membrane toward threshold
- At threshold many channels Ca open causing depolarization (ca influx) -20mV
- Rapid repolarization begins when CA channels close and K channels open (K efflux) bringing membrane potential back down to pacemaker potential -60mv
Autorythmic cell action potential unique characteristics
- Resting membrane potential is unstable and fluctuating (pacemaker potential )
- Action potential‘s initiate on their own through iF channels and then opening of calcium channels
- Rising phase of depolarization is caused by influx of calcium (compared to contractile and skeletal are Na )
- Action potential duration is variable generally 150 ms
How can heart rate the modulated
By altering ion permeability of auto rhythmic cells through autonomic nervous system and or hormonal imput
HR modulation in autorythmic cells example
Increase or decrease duration of pacemaker potential
causes
increase or decrease rate of action potential
which causes
increased or decreased rate of contractions
which causes
increased or decreased heart rate
How do the 2 ANS divisions control heart rate
*antagonistic
Parasympathetic signal decrease heart rate.
Sympathetic signal increases heart rate

The signal to increase or decrease heart rate initiates where
In the cardiovascular center in the medulla oblongata
How does the parasympathetic signal continuously and put tonic control on the heart rate
SA node (hearts pacemaker) Autorythmic cells have a basal rate at 90 to 100 bpm. Average heart rate is 70 bpm, meaning that parasympathetic signals normally have a continuous input and allow fine-tuning to decrease or increase heart rate
Mechanisms of parasympathetic control
- ACh released by parasympathetic neurons from ANS in the CVCC medulla oblangata
- Stimulation of auto rhythmic cell muscarinic cholinergics receptor
- ^ k+ efflux, decrease ca influx
- Lowers depolarization (hyperpolarization )
- Decreases HR
What sets the pace for contractile cell contraction
The depolarization of auto rhythmic cells, that are normally led by the cells in the SA node
Trace the pathway through the heart of the cardiac conduction system
- Sa node ( right atrium, initiate the pace of depolarization)
- Internodal pathway (conducting non contractile)
- Av node (slows down signal)
- Av septum (AV bundle and RL bundle branches)
- Purkinje fibers (smaller branches ) contract ventricles
What are two important functional characteristics of the conduction Pathway
- Atria contracts first and the ventricles due to AV node delay. If this didn’t happen the atria and ventricles were to contract at the same time and blood wouldn’t flow properly
- Ventricles contract from Apex to base direction due to location of fibers and direction of signal conduction. This allows blood to be pushed down from the atria to the ventricles and up from the ventricles into the aorta/pulmonary trunk
ECG waves, segments, and intervals
Waves: departure from baseline
Segments: regions between waves
Intervals: consisting of both waves and segments
What does the cardiac cycle describe
The mechanical events of the heart namely diastole (relaxation of cardiac muscles) and systole (contraction of cardiac muscles)
How does blood flow
From areas of high pressure to low pressure
Contractility
The hearts ability of cardiac fibers to contract at any given length and is affected by calcium levels (determines force some contraction)
