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Flashcards in Cardiovascular System Deck (35):


dual pump with valves
muscle cells connected by gap junctions


Conduction system

-non contractile cardiac cells that are use to initiate and distribute impulses throughout the heart
-self excitable
-dont need a stimulus, generate APs on their own at different rate.

1. sinoatrial node: in the right atrium
- 100 APs/min @rest 75 APs/min
- Pacemaker
2. atrioventricular node: in right atrium
- 50 APs/min
3. Bundle of His (AV Bundle)
- starts in AV node
- only way for the signals to get to the ventricles.
- Bundle Branches
30 APs/min
4. Purkinje Fibres
- 30 APs/min
- terminal fibres --> ventricular contraction starting at the apex.


Pathways of APs in the heart

*look at diagram, pg2)


APs of SA and AV nodes

non contractile cardiac muscle cells.
no RMP
threshold is -40 mV

1. Pacemaker potential
- Na slowly leaks out (Na Volt gates open) cause a depolarization towards the threshold.
- close at threshold of -40 mV
2. AP Depolarization
- Ca volt gates open and depol until +30 mV
3. AP repolarization
- K volt gates open and repolarization occurs
4. Na Channels open at -50mV
cycle occurs again.


APs in Ventricular Myocardium

Contractile cardiac cells
RMP = -90 mV
no relative refractory period or hyperpolarization

1. Depolarization
- Na channels open (fast) and depol till +30
2. Plateau
- Na channels close and there is a slight drop in MP, Ca (slow) volt gates open and maintain the MP.
3. repolarization
- K gates open and repol occurs.

Absolute refractory period is LONG
- Na channels are not activated until MP is -70mV


Excitation-Contraction Coupling in Myocardial Cells

1. Ca released from the plateau stage = small increase in cystolic Ca from the ECF, but this is not enough to create a contraction
2. opens chemically gated Ca channels on SR to increase cystolic Ca which binds to troponin
3. Contraction
- sliding filament mechanism
- happens after a few msec after AP.
- AP is 250 ms and twitch is 300 ms
- AP is done when twitch finishes therefore no summation or tetanus occurs.
- allows the heart to relax and refill.


3 components of the cardiac cycle

1. Electrical activity (ECG)
2. Mechanical activity
3. Blood Flow through the heart


3 components of the cardiac cycle (ECG)

small currents of depol and repol of the heart occurring in the salty body fluids
potential difference measured with an electrode lead pair
readings are seen as waves that show the overall electrical activity of all myocardial cells. (NOT APS)

- P wave: atrial depol. contraction
- QRS wave: vent depol and atrial repol contraction
- T wave: vent repol, relax

- PQ: atrtial con
- ST: vent con
- TP: heart at rest


Abnormalities of Heart beat

Tachycardia: resting HR more than 100 bpm
Brachycadia: resting HR less than 60 bpm
Heart block when signals take longer to pass through the PQ interval.
-ventricles may not contract


3 components of the cardiac cycle (Mechanical Activity)

1 heart beat = 1 dia and 1 sys of atria + 1 dia and 1 sys of vent
Diastole = relaxation
systole = contraction
- both events initiated by electrical activity

Timing of mechanical events
- Systole in the atria occurs for 0.1 sec, then diastole for 0.7
- systole in the ventricles occurs after systole in the atria (0.1 delay at AV node) is done and lasts for 0.3 secs. and dia for 0.5 secs.


3 components of the cardiac cycle (Blood flow through heart)

due to...
1. pressure changes
2. vavles
3. myocardial contractions (raises P)
- P is highest in ventricle sys
- lowest in ventricle dias.


Path of blood flow

*diagram pg 7*


during ventricular systole...

Higher P in ventricles than atria forces AV valves shut (LUB)
- QRS wave
P rises and is higher in the vents than in the pulm and aorta, semilunar valves are open, blood enters


During ventricular Diastole

P drops - becomes higher in the pulm trunk and aorta causes semi lunar valves to shut.
when P lower in the vent than atria, the AV valves open and blood goes through again.


Turbulent Flow

noisy due to turbulence when valves shut


Laminar Flow

no sound


sounds of kortokoff

turbulence heard from the brachial artery BP.
first sounds = sys
no sounds = dias


Cardiac Output

the volume of blood pumped out of one ventricle per minute.
CO = HR x SV

- CO (ml/min)
- HR is the number of beats/min
- SV is the amount of blood pumped out of one vent per beat. (ml/beat) SV = EDV - ESV


Control of CO (Heart Rate)

intrinsic controls. SA node pacemaker sets the pace.

extrinisic controls
1. Neural
- SNS (thoracic)
- opens Na volt gates wider so greater permeability. reaches threshold faster. steeper slope
-PSNS (Vagus)
- increase permeability of K. harder to reach threshold.
- keeps resting HR lower than the pace set by the SA node alone. (continuous impulses)

2. hormonal
- epi --> increases SNS therefore HR Vasocontriction
- thyroid hormone --> direct and slow takes days
- increases the number of epi receptors so more sensitive.

3. other factors
- increased K in the ISF
MP more + than usual, Na channels might not open, therefore no contraction occurs. also slows repol.
- decrease K in the ISF
membrane may change permeability and move Na, depolarizing the membrane and cause increase in HR, abnormal rhythms and feeble beat.
- fever
- age
- fitness


Control of CO (Stroke vol)

- Heart's built in ability to change SV to adjust to demands.
increase in venous return --> increase EDV --> increase heart muscle stretch --> increase force of contraction.
at rest cardiac fibers are not at optimal length, and by stretching, it is at optimal length and more cross bridges form. within physiological limits

Frank Sterling's Law of the Heart
- length of the ventricular contractile fibers is proportional to the ejection.

Extrinsic Controls
1. Neural
-SNS: increases force of contraction, increasing SV
- SNS increases the amount of Ca in the cytosol, causing more cross bridges.
- but SNS also increases HR which decreases EDV. but ESV also decreases.
- PSNS no sig effect.

2. hormones
EPi and thyroid

3. other
increase SV by...
- more external Ca
- digitalis
- verapamil blocks Ca channels
- acidosis
- increase external K


increased venous control due to

1. exercise
2. lower heart rate. --> longer time to fill


Blood Circulation

Blood flow: volume of blood passing through a tissue per min. (ml/Min)

F = P/R
P = pressure between two points. (decrease of p between the aorta and the large veins.
R - resistance, friction of blood against the vessel walls.
- arterioles
- depends on...
length, viscosity, and radius (main)


Blood flow to Organs are controlled by..

- decrease the radius of arteriole = increase in R
- P in artery increases, less blood to organ (low P)

- increase in radius
- P in artery decreases and blood to organ increases increases P as well.

local vasocon or dilation shows no big change in systemic BP. but if vasodil or con is systemic then the systemic BP will change.


Control of Vasoconstriction/dilation in the arteriolar radius

1. myogenic regulation
- when smooth muscle stretched it contracts
- ex. standing up
2. metabolic regulation
- monitoring blood gasses such as O2 and CO2.
- decrease in O2 = increase in CO2 endothelial cells will secrete nitric oxide (nt) to cause vasodilation
- increase in O2 = decrease in CO2 endothelial cells secrete endothelins (nt) vascon

1. SNS - arteriolar vasocon EXCEPT IN BRAIN (INTRINSIC ONLY)
2. Hormonal
- epi: vascon in skin and viscera (reinforce SNS), vasodil -heart, skel muscle, liver (Oppose SNS)
3. Other hormones
- angiotensin 2 and ADH - vasocon
- histamine - dilate


Blood Pressure

hydrostatic P exerted by blood on wall of vessel (arteries)

systolic P = pressure caused by VENTRICULAR contraction
diastolic P = pressure caused by the recoil of elastic art (vent relaxed)
Pulse Pressure = sys - dias
MAP: BP measured by our body.
- MAP = 1/3PP + dias


MAP regulated by...

1. TPR
2. SV
3. CO


Extrinsic Regulation of MAP

1. Neural control
Baroreceptor reflexes (SHORT term changes)
- ex standing
- stretch receptors monitor MAP in...
(a) carotid sinus (brain)
(b) aortic arch (systemic bp)

Chemoreceptor reflexes
- peripheral chemoreceptors (carotid and aortic bodies)
- used to monitor respiratory rate
- monitors blood gasses

2. Hormonal control
- Epi - Increases HR. therefore increase CO and MAP
- Renin angiotensin system
plasma angiotensinogen (protein) --> renin (enzyme +hormone) --> angiotensin 1 --> ACE (angiotensin converting enzyme) --> angiotensin 2.
causes vasocon, increase in aldo and ADH, increase thirst, increase blood vol, increase MAP.
-atrial natriuretic peptide (ANP)
inhibits ADH and Angiotensin 2
decreases blood vol, no constriction, increase urine prod.


capillary exhange

between blood and ISF

Solutes are moved by...
1. diffusion
- glucose, aa, ions, CO2, O2, hormones
- usually between endothelial cells
2. Vesicular transport
- bigger proteins such as antibodies
- transcytosis: endocytosis from blood to endothelial cell then exocytosis from endothelial cell to ISF.
3. mediated transport
- requires a membrane carrier protein.
- important in the brain

Fluid is moved by...
1. osmosis
2. bulk flow
- 4 pressures involved BOP, BHP, IFOP, IFHP
- BHP usually stays the same from the arteriolar end to the venous end of the capillary.


How much filtered fluid is reabsorbed to the blood?

90% because (-) in NFP = absorption


How much filtered fluid enters the lymph




when there is excess fluid in the tissues (ISF) swelling

due to...
- high BP
- leakage of proteins into the ISF which increases IFOP
- decrease of plasma proteins (malnutrition,burns) Decrease BOP
- obstruction of lymph vessels (elephantitis)


Circulatory Shock

Inadequate Blood Flow

1. hypovelmic shock
- blood volume is too low
-due to blood loss, burns, diarrhea, vomitting
2. vascular shock
- same blood vol, but vessels are enlarged.
- due to systemic vasodilation of blood vessels, decrease BP.
- ex: anaphylactic shock - allergic reaction
- lots of histamine released from mast cells
- ex: septic shock - due to bacteria
3. cardiogenic shock
- heart fails to pump


Stages of shock

1. compensatory
- body mechanisms are able to restore homeostasis by themselves
- involves baroreceptors, chemoreceptors and ischemia in the medulla. all trigger the SNS

2. progressive
- mechanisms inadequate, needs assistance
- decrease in CO = decrease bp = decrease in cardiac activity = decrease in blood to brain = decreased control.
- damage to viscera esp in kidneys.

3. irreversible
- decrease CO = too little blood to heart = decrease CO death.


Blood contains..

1. H20
- transport medium + carries heat
2. proteins
- albumin
- globulins
- fibrinogen
- buffers, a and b glob = transport, clotting, osmotic pressures (albumins), y glob antibodies
3. electrolytes
- buffers: HCO3
- membrane excitablility
4. other solutes
- gases, hormones, wastes, nutrients

Formed elements
RBC: no nucleus, no mitochondria, anaerobic
- transport O2 and CO2
- buffer: globin binds to H reversibly
- carbonix anhydrase - CO2 transport
- neutrophils: phagocytes, go to infected area first
- eosinophils: attack parasites, break down chemicals released in allergic reactions
- basophils: histamine and heparin: prevent local clotting
- monocytes: enter tissues and become macrophages
- lymphocytes
- T lymphocytes: helper T and cytotoxic
- B lymph: becomes plasma cells and secrete antibodies
- natural killer cells: directly attack foreign cells. (INNATE)
- cell fragments of megakaryocytes from the red marrow
- fucntions: form platelet plug, contains granules = coagulation factors



process of stopping bleeding
1. Vascular Spasm
- damaged blood vessel vasoconstricts
2. Platelet Plug formation
- platelets stick to damaged vessel +FB. --> release -chemical factors which cause more platelets to stick, healing, promote clotting.
- healthy endothelial cells secrete a chemical stopping spread of plug
- plug formation requires prostaglandin
3. Clot formation
- Prothrombin activator formed...
extrinsic: factors released from damaged tissues
intrinsic: from blood
requires Ca, tissue, platelet or plasma factors.
- prothrombin --> thrombin +fb stopped by plasma factors.
- factors come from diet, liver, damaged tissue, platelets, and we need VK.
4. retraction and repair
- blood vessel is pulled together, and fibroblasts form new CT, new endothelial cells repair lining
5. Fibrinolysis
- plasmin (Enzyme) is used to break fibrin down and macrophages come and eat the remaining material