Cardiology Flashcards
How are cardiomyocytes connected?
The cardiac syncytium is a network of cardiomyocytes connected by** intercalated discs** that enable the rapid transmission of** electrical impulses** through the network, enabling the syncytium to act in a coordinated contraction of the myocardium.
Striated, lots of mitochondria, involuntary
Syncytium:a single cell or cytoplasmic mass containing several nuclei, formed by fusion of cells or by division of nuclei. (Cardiomyocytes however do not have multiple nuclei).
What are “specialized” cardiomyocytes?
Pacemaker cells, Purkinje Fibers: generate/conduct electrical impulses.
What is different in cardiac muscle cells than regular skeletal muscel cells?
Adapted to the slower and more sustained single contraction! Also large t-tubules form a DYAD with SR. LOTS of Ca2+.
This can be see in the PLATEAU in the AP graph of cardaic muscle cells.
2 types of junctions at intercalated discs?
1-Mechanical (Fascia adherens anchors actin) & desmosomes (bind intermediate filaments of adjoining cells)
2-gap junctions (ion flow bt cells, propagate APs to neighboring cells.
Gap junctions: …
connexins
(connect cardiomyocytes)
Desmosomes:
Cadherins
(adhere actin to plasma membrane)
What is inclued in cardiac muscle cells? for graphing ap purposes
Atrial, Ventricular, AND perkinje fibers (perkinje fibers are not pacemakers!)
Describe Phase 0,1,2,3,4 and what channels/gates open.
-90 to +20
Refractory periods in skeletal vs cardiac muscle? Average time for cardiac?
Cardiac muscle cell in ventricle: 0.25-0.30
Cardiac muscle cell in **atrium: 0.15 **(much shorter than ventricle).
As shown by the graph, the refractory period is much longer in cardiac cells because they hold the contraction longer.
Relative refractory in heart?
0.05, can happen but only with strong stimulus. It can be see in the early “premature” contraction.
“Extra heartbeats”/skip a beat.
Mechanisms invovling excitation-contraction coupling and relaxation in cardiac muscle?
“Calcium-Induced Calcium Release (CICR)”, AP–>Ca2+–>T-tubule–>DHPR channel–>RyR–>Ca2+ release from the SR–> contraction.
Ca2+ reuptake during cardiac muscle relaxation?
**SERCA 2A: **Sarcoplasmic Endoplasm Reticulum Ca2+ ATPase with PLB phopholamban attached take up Ca into the SR. OR it goes out and across the sarcolemmal membrane via a Na+/Ca2+ exchange pump. This is secondary active transport bc the na will follow out of the cell kia a Na/K pump again.
What are the components of the EKG graph?
Please Quit Rusty Smoking Trinkets
Look and study this graph, in particular the AV valves closing/ ejection and how that relates across the board.
Isovolumic/Isometric Contraction
Ventricular contraction begins, pressure rises up, AV valves close quickly.
*Cardiac muscle tension is INC but length of muscle fiber remains constant.
What percentage of blood is ejected rapidly and slowly?
first 1/3rd= 70% fast
last 2/3rds= 30% fast.
What pressures do the right and left ventricles need to slightly surpass in order for ejection through the semilunar valves to happen?
80 mmHg for left ventricle (larger bc its pumping to rest of body) and 8 for right ventricle!
Isovolumic (Isometric) relaxation
Pressure in ventricles return back to normal, AV valves open again, and the cycle will start again.
What is the internodal pathways? Bachmann’s bundle?
Where electric impulses from the SA node will travel in the right atrium and the left atrium respectively
PR segment
Time delay between atrial and ventricular ACTIVATION (AV node related)
16 seconds
PR Interval
Time interval from onset of atrial activation to onset of ventricular activation.
ST Segment/interval
time between ventricular depolarization and repolarization
QT interval
Length of ventricular depolarization and repolarization
Average bp
120/60
Systole/Diastyole
Four phases of cardiac cycle
1.Inflow Phase
2.Isovolumetric Contraction
3.Outflow Phase
4.Isovolumetric Relaxation
Heart Pressures Systole/Dyastole
Heart Pumping= pulsatile, so the pressure goes from systolic to diastolic.
NOTE: Arterial Pressure 120/80 average, level of aorta. That’s the arteries in the rest of your body.
NOTE: Pulmonary Arterial pressure : ~16 mmHg
Stroke Volume Equation
SV= EDV-ESV
Usually SV is around ~70 mL blood
EDV: End Diastolic Volume; ESV: End Systolic Volume.
Usually SV: 70ml, EDV: 110-120, ESV: 40-50
Ejection Fraction
Usually around 60%
SV/EDV= %
Stroke Volume over the End diastolic volume
first and second heart beat sounds?
First sound: closing the AV valves, a bit softer
Second sound: closing of the aortic/pulmonary valves, rapid/harsh/cut quick
Sinodial Fiber aka pacemaker action potential vs cardiomyocyte?
Phase 4 (2 segments), Phase 0 (Depolarization), Phase 3 Repolarization. NO PHASE 1/2 in sinus nodes AP.
The depolarization varies becuase CALCIUM CA2+ causes depolariation in the SA /AV nodes
How long and why is there a delay from the AV node impulse conduction from the atria to the ventricles?
16 seconds, PR segement, allows time for atria to empty their blood into the ventricles before ventricular contraction begins.
Velocity of conduction in most atrial muscle is about…
0.3 m/sec
How long from when the cardiac impulse enters the bundle branches in spetum until it reaches Purkinje fibers?
0.03 seconds, very fast! high level of permeability of gap junctions at intercalacted discs.
Take a look at these times!
Parasympathetic nerves/ vagal stim
SA/ AV nodes, acetylcholine, increase K channel permeability, losers resting membrane potential making it harder to excite.
Sympathetic goes everywhere
NE–> beta 1 adrenergic receptors, increase Na and Ca ion permeability. Triples heart beat frequence and doubles contraction strength.
What is the normal pacemaker of the heart? What’s a normal heart rhythm?
Sinus Node:
between 60 and 100 beats per minute, which is generally considered a normal heart rate
AV: 40-60, Perkinje: 15-40
iii. Usually discharge rate of sinus node is considerably faster than the natural self-excitatory discharge rate of either AV node or Purkinje fibers so it is in control (because its impulse discharges their excitable membranes)
What cardiac cell is mainly responsible for synchronous contraction of ventricular muscle?
Perkinje Fiber, very fast, ventricles contract at same timeish.
Contraction follows what?
Depolarization. Act,react situation.
The monophasic action potential of ventricular muscle normally lasts between… seconds
0.25 and 0.35
Look at the EKG vs cardiac myocyte AP graph. Study it!
Function of capillaries?
to exchange fluid, nutrients, electrolytes, hormones, and other substances between the blood and the interstitial fluid
Total % of blood in heart, pulmonary system, and systemic circulation?
7%, 9%, and 84%!
Veins/Venules/Venous sinuses have 64% compared to areries 13%, arterioles/capillaries at 7%.
As the volume in something increases..
the pressure increases
Velocity is direct or indirect to cross-sectional area? Equation?
Velocity is indirect to cross-sectional area.
Velocity= Flow volume/ c-s area.
What type of vessel has biggest cross sectional and thus the slowest velocity?
Capillaries> Venules> Small veins> Arterioles> Small arteries> Venae Cavae> Aorta.
Cap is king, then usually veings over arteries, but rank them by size.
What is the pressure mmHg in systemic CAPILLARIES (arteriolar ends and venous ends)
35 mmHg–>10 mmHg
Functional pressure in most vascular beds: 17 mmHg.
Average pulmonary arterial pressure and capillary pressure?
16 mmHg.
25 systolic/8diastolic
Capillary: 7 mmHg
Ohm’s Law and blood pressure.
Laminar Flow
steady streamlined flow, center of vessel’s velocity is greater than outer edges due to adherence to wall.
Turbulent Flow
Flow in all directions, increase when blood flow increases too much. Eddy currents. Increase in resistane. Direct to velocity, diameter of vessel, and density of blood, but INDIRECT to blood viscosity (which if high will slow down the flow and decrease turbluence)
Reynold’s Number 200-400 trouble, but above 200 can even cause turbulence in straight,smooth vessels.
Factors that determine resistance/ Poiseuille’s Law
Pressure and Radius =direct with flow.
Viscosity and length= indirect with flow.
Adding more blood vessels does what to the total vascular resistance?
inc it
In series vs in parallel total peripheral resistance?
Rtotal=r1+r2+r3,
In parallel 1/rtotal= 1/r1+ 1/r2 etc
Vascular Compliance
Increase in volume/ increase in pressure.
total quantity of blood that can be stored in a given portion of circulation for each mmHg pressure rise; aka capacitance
What does sympathetic stimulation do to vascular compliance? Age? Disease like arteriosclerosis?
Increases pressure at each volume/decreases compliance; compliance decreases with age; cardio diseases decrease compliance.
What have higher compliance, veins or arteries?
Veins, 24x more.
Increases in Cardiac output= increase in compliance. The pressure in arteries in high so compliance is low. But in veins the pressure is not that high so more volume intake and raises compliance?
Not 100% sure this is right idea
Transmission of pressure pulse can be though of as…., like in the gi system.
peristalsis of the aorta. Progressive moments of distension and overcoming of block by presssure buildup.
● Transmission slows as blood travels to vessels with greater compliance and resistance (pulse pressure are dampened in smaller vessels)
What are the sounds hear when taking a bp reading?
Korotkoff Sounds. Systolic pressure heard first.
Pulse Pressure Equation
Systolic pressure- diastolic pressure
Equation to calculate Mean Arteriole Pressure
2(DBP)-(SBP) OVER 3
Another way to calculate mean arteriole pressure?
Pulse Pressure: SBP-DBP
MAP: DBP-(1/3)(PP)
Central Venous Pressure
a measure of pressure in the vena cava, can be used as an estimation of preload and right atrial pressure.
What is the hydrostatic/gravitational pressure effect on venous/arterial pressures?
Near the feet/at increasing distal levles, arterial and venous pressure increases.
Venous 0–>90 at feet
Arterial: 0–> 190 mmHg.
What happens if valves (which are support to pump venous blood back to heart) stop working?
Venous pressure in feet falls below ~20 mmHg, and fluid from varicose veins leaks to cause EDEMA.
Starling Forces!
Net Filtration Pressure = Out - In.
Out of the capillary (filtered) vs in the capillary (absorbed)
Hydrostatic or Pressure vs Colloid Osmotic Pressure.
Hydrostatic wants to give.
Colloid Osmotic Pressure is selfish wants to get stuff.
NFP= (Pc+πi) = (Pi + πc)
NFP: NEGATIVE= absorpbed.
If opposite, POSITIVE then itll be filtered.
c for capillary, i for interstitial fluid
What don’t sympathetics innervate?
Capillaries. They do innervate the heart, artery, and veins.
What do sympathetics do in small arteries/arterioles?
They increase resistance. And decrease rate of blood flow. In large vessels, they decrease the volume of vessels.
Sympathetics
Increase vasoconstrictoin and cardioacceleratory areas in vasomotor center to increase arterial pressure to keep up.
Where are baroreceptors found?
Carotid bifurcation and wall of aortic arch.
If there is high blood pressure, what will happen to the baroreceptors?
Above 50-60 mmHg pressure–stimulates–enter nucleus tractus solitarius of medulla and secondary signals INHIBIT VASOCONSTRICTOR center of medualla= excites vagal parasymp center.
CN XI goes to vasoinhibitors and CNX goes to vasodilators.
Carotid Sinus Reflec
The increase in blood pressure in carotid sinus will stimulate stretch receptors, which leads to reflex bradycardia and systemic vasodilatation. The baroreceptor reflex is also critical in maintaining heart rate and blood pressure during postural changes.
When going from lying. tostanding, what happens to the blood pressure in the uE?
It decreases. To compensate, baroreceptor reflec stimulates sympathetic nervous system to raise bp.
Norepinephrine> epinephinre in cardio system?
Vasoconstrictor
Angiotensin II
Vasoconstrictor–>increases peripheral resistance/ bp. It also DECREASES excretion of sodium/water.
Supplement:
Systemic Actions of Angiotensin II:
1. Vasoconstriction
2. Retention of Na+/H2O
3. Secretion of aldosterone from adrenal cortex
4. Release of ADH from posterior pituitary gland
5. Stimulation of SNS
6.** Stimulation of thirst**
As the arteries constrict, the resistance increases and as they dilate, resistance decreases. Resistance is tied with blood pressure.
Antidiuretic Hormone (ADH) aka Vasopressin
Increases water reabsorption/na reabsorption from renal system; Vasoconstrictor. Excreted from posterior pituitary gland.
Bradykinin
Vasodilator, causes increase in capillary permeability.
Kallikrein causes alpha-2-globulin to release kallidin, which is converted to bradykinin. Kallikrein is actived due to tissue inflammation, maceration of blood, other chemical/physical effects on blood/tissues.
Histamine
Vasodilators, increases capillary permeability/porosity. Mast cells/basophils. Respond to inflammation or allergic rxns.
How is Angiotensin 2 Formed?
RAAS Pathway
An inactive form of renin called “PRO-RENIN” in stored in the juxtagolmerular cells. Once arterial pressure falls, it’ll be released and coverts angiotensinogen from the liver into angiotensin I. Angiotensin I gets converted angiotensin II by angiotensin converting enzyme from the lungs. This vasoconstricts. If ANG-II goes to the adrenal gland, it’ll release Aldosterone which will help retain sodium/water.
How is Angiotensin 2 inactivated?
Angiotensinases.
Angiotensin 2 only lasts in the blood for 1-2 minutes or so.
Difference between ADH and Aldosterone?
Although very similar in outcome, ADH makes the tubules more permeable to** water** whereas aldosterone makes the tubules more permeable to **sodium **ions, increasing the water reabsorption by creating an osmotic pressure.
What else does angiotensin II do?
Angiotensin II also triggers (your adrenal glands to release aldosterone and) your posterior pituitary gland to release antidiuretic hormone (ADH, or vasopressin).
Relationship between Cardiac Output, Arterial Puressure, and Total peripheral Resistance?
CO is directly correlated with arterial pressure, but is inversely related to total peripheral resistance.
Good video: https://www.youtube.com/watch?v=VMJfiDsOgc8
Arterial pressure can be thought of as total peripheral resistance.
Cardiac output=
Stroke volume * heart rate
SV= EDV-ESV
What is peripheral resistance influenced by?
-diameter of vessels (indirect)
-length (direct)
-Viscosity or thickness due to RBC (direct)
Look at this.
When does compliance decrease?
Higher pressure and volume.
Where is ADH released from, Aldosterone?
ADH: Brain hypothalmaus/pit
Aldosterone: Adrenal Cortex
Blood Volume=
Intrathoracic (CBV) + Extrathoracic
What shifts the blood to/form extrathoracic blood volume?
A change in hydrostatic pressure, change in venous compliance.
What is central venous pressure?
Pressure in thoracic vena cava, near right atrium (reflects right atrial pressure)
Control of bP: Important Graph From Class Meeting
Determinants of MAP
Baroreceptor Reflex
Activity of Arterial BP/Barorectptors
Starling Force Diapgram
Once More
