Cardiovascular Physiology 1 (9/17b) [Biomedical Sciences 1] Flashcards
Path of RBC from vena cava to vena cava
Vena cava Right atrium -Tricuspid Valve Right Ventricle -Pulmonary Valve Pulmonary Circulation -Pulmonary artery → vein Left atrium -Mitral/Bicuspid Valve Left Ventricle -Aortic Valve Systemic circulation -Aorta → Vena Cava
Atrioventricular valves
tricuspid and mitral valves
Semilunar valves
aortic and pulmonary valves
When do arteries carry deoxygenated blood?
Pulmonary artery carries deoxygenated blood to the lungs to get oxygenated
Main functions of cardiovascular system
Deliver enough blood to satisfy metabolic needs
Deliver O2 and nutrients, remove waste
Redistribute cardiac output
Range of metabolic demand
measure respiration/oxygen consumption rate to understand metabolic demand
Resting = about 250 mL O2/min
Exercise = about 5000 mL O2/min
Cardiac Output (CO)
measure cardiac output (L/min) by Heart Rate (beats/min) x Stroke Volume (mL/beat)
CO = HR * SV
Cardiac output increases as heart rate does, but not enough to keep up with oxygen consumption. What is needed?
redistribution of blood
During heavy exercise, more of cardiac output will be directed to ___ ___ ___
active skeletal muscle
___-____ fold increase in blood flow to active muscle
20-30
Sodium-Potassium (Na+/K+) pump
sets up electrochemical gradients
Lots of K+ inside cell, little outside → pumped out
Lots of Na+ outside cell, little inside → pumped in
Creates an electrical potential of about -90 mV in a resting cardiac/muscle cell
An electric current is needed to depolarize the current → action potential
Na+/K+ pump creates an electrical potential of about ___ mV in a resting cardiac/muscle cell
-90 mV
Action Potential - Skeletal Muscle (Myocytes)
Threshold reached → Na+ channels open quickly and Na+ rushes in (upstroke)
Depolarizes the cell, brings it up a little past neutral
Na+ channels close → K+ channels open and K+ rushes out (downstroke)
All of this happens in about 1-2 milliseconds
Action Potential - Cardiac Muscle (Nodal Cells)
Slow calcium (Ca2+) channels open and calcium comes in while potassium is leaving → they oppose each other and makes it a slow process → creates a plateau
Calcium has positive charge, so it keeps depolarizing the membrane; but potassium leaving hyperpolarizes it
Once Ca2+ channels close → membrane potential brought back to -90 mV
Upstroke rapid influx of Na+, plateau is balanced influx of Ca2+ and efflux of K+, downstroke is efflux of K+
happens in about 300 milliseconds
Contraction Ability - Skeletal vs Cardiac Muscle
Skeletal muscle → needs innervation to cause contraction, some electrical stimulation needed
Cardiac muscle → could beat on its own without innervation, has sinus or AV nodal cells
Automaticity
Nodal cells have an unstable resting potential → creates automaticity (able to beat on its own)
Gradual inward current of Na+ creates funny current
Once threshold is reached → action potential spreads to other myocytes
Flow of Signal Conduction
Sinoatrial (SA) node (60-100 bpm)
Atrioventricular (AV) node (40-60 bpm)
Bundle of His (15-40 bpm)
Bundle branches
Purkinje fibers
Overdrive suppression
high intrinsic rate of SA node makes it the dominant pacemaker
Ectopic foci can become pacemakers in pathological states
AV node delay allows time for…
atrial contraction and ventricular filling
aka leads to coordinated heart beat
How do we evaluate the signal of the heart?
with an ECG
Normal sinus rhythm is defined by
Regular rhythm
rate between 60-100 bpm
normal shape of waveform (shape of P, QRS, T waves) (duration of PR, ST, and QT intervals)
What do P, QRS, and T segments of ECG correspond to in the heart?
P = atrial depolarization
QRS complex = ventricular depolarization (also partly atrial repolarization) (mitral valve closing)
T wave = ventricular repolarization
What parts of ECG correspond to ventricular systole and diastole?
Ventricular Systole → beginning QRS complex to end of T wave
Ventricular Diastole → end of T wave to beginning of next QRS complex
ECG abnormalities
Sinus tachycardia → fast rhythm
Sinus bradycardia → slow rhythm
Triplet Premature Ventricular Contraction → ectopic foci, wide bizarre signals
Ventricular fibrillation → wavy line with no distinct rhythm/shapes
Atrial fibrillation → lacks P wave
The signal that makes the heart beat
the depolarization of cardiac myocytes
How does the signal produce a heart beat?
Excitation-Contraction Coupling (E-C Coupling)
E-C Coupling - Contraction/Systole
Ca2+ influx during action potential triggers release of Ca2+ from sarcoplasmic reticulum (SR)
(Calcium-induced calcium release)
Ca2+ binds to troponin, causing it to shift, allowing myosin-actin interaction and contraction
E-C Coupling - Relaxation/Diastole
Ca2+ falls as it is transported
- Into SR via SERCA pump (requires ATP)
- Out of cell by membrane Ca2+ pump and Na+/Ca2+ exchanger
Fall in Ca2+ causes troponin to shift back, blocking actin-myosin interaction and contraction
Echocardiography
uses sound waves to image the heart and evaluate the beat
provides info about stroke volume and ejection fraction
Stroke Volume (SV)
the volume of blood ejected each beat
SV = End Diastolic Volume (EDV) - End Systolic Volume (ESV)
Ejection Fraction (EF)
the fraction of end diastolic volume ejected each beat
normal is about 50-70%
EF = SV/EDV
Issues with heart response
Valve disease (stenosis and regurgitation)
Decreased contractility during systole → systolic dysfunction
Decreased relaxation during diastole → diastolic dysfunction
Valve Disease - Stenosis
narrowing of valve opening
Valve Disease - Regurgitation
valve allows backflow of blood
Phases of Cardiac Cycle
Ventricular Systole (contraction)
- Isovolumetric contraction
- Ejection of blood into aorta
Ventricular Diastole (relaxation)
- Isovolumetric relaxation
- Passive filling of ventricle
- Active filling of ventricle → atrial systole (“atrial kick”)
How can the autonomic nervous system charge heart rate?
The sympathetic and parasympathetic systems change the slope of the resting membrane potential by changing Na+/K+ levels, impacting the funny current
Cardiac Regulation - Sympathetic
Positive Chronotropic effect → increases slope
Norepinephrine acts on beta-1 receptors in SA node to increase HR
Cardiac Regulation - Parasympathetic
Negative Chronotropic effect → decreases slope
Acetylcholine released from vagus nerve acts on muscarinic receptors to decrease HR
As HR increases (above ~150 bpm), diastole duration decreases, reduces time for ___ ___
ventricular filling
To increase cardiac output, increased HR is accompanied by increased ventricular filling, but how?
Venoconstriction by sympathetic nervous system
Muscle pump - muscles in our legs contract, squeeze veins, push blood back up to heart
Factors that affect stroke volume
Preload (increases)
Afterload (decreases)
Contractility (increases)
Preload
volume of blood in ventricles at the end of diastole
Directly correlated with SV → increased preload = increased SV
Increased preload → increased stretch on myocyte → stronger contraction → increased stroke volume
Length-tension relationship (Frank-Starling Curve)
Venous return and duration of diastole affect preload
Afterload
resistance the ventricle must overcome to eject blood
The left ventricle must overcome aortic pressure
Inversely correlated with SV → increased afterload = decreased SV
Hypertension and aortic stenosis increase afterload, hypotension decreases afterload
Contractility
strength of myocardial contraction, calcium dependent
Directly related with SV → increased contractility = increased SV
Inotropy (+/-)affects calcium concentration in myocyte
Positive (+) Inotropy
Positive inotropy → increased calcium concentration → stronger contraction → increased stroke volume
SNS → norepinephrine acts on β-1 receptors to increase calcium concentration
Cardiac glycosides (digitalis) also increases calcium concentration
Negative (-) Inotropy
Negative inotropy → decreased calcium concentration → weaker contraction → decreased stroke volume
Calcium channel blockers (diltiazem) decrease calcium concentration
At the beginning of ___ ___, mitral (on left) and tricuspid (on right) valves close
isovolumetric contraction
At the beginning of ___ ___, the aortic valve closes when ventricular pressure falls below aortic pressure
isovolumetric relaxation
