Cardiovascular System Flashcards
Serous Pericardium
Double layered membrane surrounding the heart muscle with an outer parietal layer and inner visceral layer.
-Visceral layer is continuous with the epicardium
-Contains a pericardial cavity between the 2 layers
Epicardium
Outer muscle layer of the heart continuous with the visceral serous pericardium
Myocardium
Percent cell composition
Middle layer of heart muscle composed of 1% pacemaker cells and 99% contractile cardiac muscle cells.
Cardiac Skeleton
Criss crossing of connective tissue to anchor cardiac muscle fibers, support large vessels, and limit the spread of action potential to specific paths.
Functional syncytium
Synchronized contractions of myocardial muscle cells due to the presence of intercalated discs (desmosomes and gap junctions) for communication
Endocardium
Lining of heart chambers and valves continuous with blood vessels. Made of endothelium and connective tissue
Septums of the heart
-Interatrial: Membranous and separates the 2 atria
-Interventricular: Mostly muscular and separates the 2 ventricles
Role of valves in atrial systole
- Blood returning to the heart fills the atria pressing against the AV valves until the pressure forces it open
- As ventricles fill, AV valves flap hang limply into ventricles
- Atria contract forcing remaining blood into ventricle
Role of AV valves during ventricular systole
- Ventricles contract forcing blood against the AV valve cusps
- AV valves close
- Papillary muscles contract and chordae tendinea tighten to prevent valve flaps from everting into atria
Path of electrical signal of the heart
-Sinoatrial node
-Atrioventricular node
-Bundle of His
-Right and Left bundle branches
-Purkinje fibers
Cardiac pacemaker cells potential
- Unstable RMP
- Funny channels open to allow Na and K influx for a constant depolarization
- Fast Ca channels open to cause fast depolarization
- Once an MP of 20+ mV is reached, Ca channels close and K channels open to efflux K from cell
Phases of cardiac action potential
- Depolarization: Na influx for rapid depolarization
- Plateau phase: Ca influx trough slow Ca channels to keep cell depolarized
- Repolarization: Ca channels inactivate and K channels open for K efflux to bring back to resting voltage
P Wave
Depolarization of SA node & atria
QRS complex
Depolarization of ventricles & repolarization of atria
T wave
Ventricular repolarization
P-R Segment
Delay of impulse at AV node following atrial depolarization
S-T segment
Ventricular depolarization complete
Q-T interval
Ventricular depolarization to repolarization
End diastolic volume
Volume in each ventricle at the end of ventricular diastole
Iso-volumetric contraction phase
After atrial systole as the ventricles begin to depolarize/contract. Volume of blood is maintained in ventricles as both valves are closed causing a pressure increase that leads to opening of semilunar valves
Process of Ventricular Ejection
-Pressure in ventricle is larger than the pressure in the artery causing the semilunar valve to open.
-Rapid ejection followed by reduced ejection
-Lasts for entirety of the plateau phase of myocardial action potential
End systolic volume (ESV)
Remaining volume following ventricular ejection
Stroke volume (SV)
Volume of blood ejected during ventricular ejection (~70 mL)
-EDV-ESV
Ejection fraction
(Stroke volume/End Diastolic Volume)=~54% (Usually)
End diastolic volume
Amount of blood the ventricles can hold following diastole (The relaxation phase where they are being filled)
Isovolumic relaxation
-Early ventricular diastole: ventricles relax & expand
-Atria are relaxed and filling
-Blood in arteries close SL valve
-Pressure of atria increases
-AV valve will eventually open from pressure
Cardiac output
Heart Rate (BPM) x Stroke Volume
Normal cardiac output, heart rate, and SV
5.25 Liters/Minute
-HR: 75 BPM
-SV: 70 ml/beat
Maximal Cardiac output
-4 to 5 times the resting cardiac output
-Up to 35 L/min for athletes
Cardiac reserve
Difference between resting and maximal cardiac output
Preload
Degree of stretch of cardiac muscle cells before they contract, aka end diastolic pressure
Frank-Starling law of heart
Within physiological limits, the heart pumps all the blood that returns to it.
Venous return
Amount of blood returning to the heart
Contractility
Contractile strength –> dependent on factors that make the muscles more responsive to stimulus
Afterload
Pressure ventricles must overcome to eject blood
Pressure gradient
Tendency to move from areas of high pressure to low pressure
Impact of positive chronotropic factors
Increased heart rate
Impact of negative chronotropic factors
Decreased heart rate
Impact of positive inotropic factors
Increased stroke volume
Impact of negative inotropic factors
Decreased stroke volume
Impact of sympathetic nervous system on heart
Increases HR
Impact of parasympathetic nervous system on heart
Decreased HR
Impact of Sympathetic nervous system on HR
-Release of epinepherine
-B1 receptors of SA node cause influx of Na and Ca
-Repolarization limited
-Increased HR
Impact of ParaSympathetic nervous system on HR
-Vagus nerve stimulates acetylcholine release that binds to M2 receptors on SA node
-Opens K+ channels and Closes Ca2+ channels
-Hyper-polarization occurs
-Extended pacemaker potential of cells
-Decreased HR
Hypocalcemia affect on HR
Depresses HR
Hypercalcemia affect on HR
Increased HR and contractility
Hyperkalemia impact on HR
Hyperpolarization, cardiac arrest in diastole
Hypokalemia impact
-K+ diffuses out of the cardiomyocytes
-No repolarization –> Feeble heartbeat, arrythmia, and cardiac arrest in systole
Epinepherine
Increases heart rate and contractility
Tachycardia
Abnormally fast heart rate (>100 BPM)
Lumen
Central space containing and carrying blood
Tunica intima
Endothelium lines lumen of all vessels and basement membrane
Tunica Media
-Smooth muscle and elastin
-Autonomic nerve system –> vasoconstriction and vasodilation
Tunica Adventitia/Externa
Collagen fibers in fibrous tissue
Elastic (Conducting) arteries
-Large lumen
-Large springy thick-walled (Elastin not muscular)
-Pressure reservoir of systemic circulation
-Aorta and its major branches
Muscular (distributing) arteries
-Distal
-Thick tunica media with more smooth muscle
-Active in vasoconstriction
Arterioles
-Lead to capillary beds
-Control flow into capillary beds via vasodilation and vasoconstriction
Capillary
-Exchange of gases, nutrients, wastes, hormones, etc.
-Diapedesis, immune response, cells to blood flow
Continuous capillaries
-Most common with complete endothelium and basement membranes
-Leaky junctions
-Located in BBB, skeletal/smooth muscle, and lungs
Fenestrated capillaries
-“Windows” and basement membranes for the exchange of large molecules
-Small intestine, kidneys, choroid plexus (CSF), hypothalamus
Sinusoid Capillaries
-Extensive intercellular gaps and incomplete B<
-Exchange of plasma proteins and even cells
-Incredibly rare: found in liver, spleen, red bone marrow, and lymph nodes
Movement of blood in arteries
-Pumped by heart
-Aided by gravity in some cases
Movement of blood in veins
-Skeletal muscle pump
-Respiratory pump
-One way valves
Response to increase body temp
-Hypothalamus signal
-Warm blood flushes into superficial capillary bed
-Heat radiates from skin
-Lower body temp
Brandykinin
Signaling molecule that signals for vasodilation to occur from sweat in order to evaporate sweat
Response of lowering body temp
-As temps decrease blood is shunted to deeper vital organs
-Maintains optimal temperature for sustained metabolic reactions.
Blood pressure
Force per unit exerted on wall of blood vessels
-Measured by millimeter of mercury
Mean arterial pressure
-Maintenance required for adequate perfusion (Blood flow) of organs (minus lungs)
-Proportional to cardiac output and total peripheral resistance
Regulation of peripheral resistance in arterioles
-Baroreceptors
-Sympathetic nervous system
Blood flow
-Volume of blood flowing over a period of time
-Q=ΔP/R
-ΔP: change in BP between 2 points
-R: Resistance
Resistance
Friction with vessel walls
Main sources of resistance
-Blood viscosity
-Total blood vessel length
-Blood vessel diameter
Causes of increased contractility
-Sympathetic stimulation causing increased calcium influx and more cross bridging
Causes of decreased contractility
Ca2+ channel blockers
Hyperpolarization
Moving of membrane potential to more negative values
