Reading...
Play button
Play button
Use LEFT and RIGHT arrow keys to navigate between flashcards;
Use UP and DOWN arrow keys to flip the card;
H to show hint;
A reads text to speech;
88 Cards in this Set
- Front
- Back
|
Systole |
phase of contraction
|
|
|
Diastole
|
Phase of relaxation
|
|
|
Atrial Systole and Diastole
|
-Atrial systole occurs during the end of ventricular diastole
-Atrial diastole (relaxation) occurs during ventricular systole (contraction) |
|
|
End diastolic volume
|
total volume of blood in the ventricles at the end of diastole.
- final 20% of blood in the atria is squeezed into the ventricles when atria squeezes |
|
|
End systolic volume
|
total volume of blood in the Ventricles at the end of systole
-about 1/3 of blood remains at the end of systole, 2/3 ejected during systole |
|
|
1. Isovolumetric contraction
|
-Ventricles begin contraction, pressure increases
-AV valve snaps shut (first heart sound -Ventricles are neither being filled with blood nor ejecting blood (pressure not high enough to open the semi-lunar valves |
|
|
2. ejection
|
-pressure in the left ventricle becomes greater than the pressure in the aorta
-semi-lunar valves open -ventricular volume decreases |
|
|
3. isovolumetric relaxation
|
-pressure in the ventricles falls below the pressure in the arteries
-causes semilunar valves to close -second heart sound -AV and semilunar valves closed |
|
|
4. rapid filling
|
-pressure in the ventricles falls below pressure in the atria
-AV valves open |
|
|
5. atrial contraction (atrial systole)
|
-contraction of the atria delivers the final 20% of blood into the ventricles
|
|
|
5 heart stages
|
1. Isovolumetric contraction
2. ejection 3. isovolumetric relaxation 4. rapid filling 5. atrial contraction (atrial systole) |
|
|
pulmonary circulation
|
-blood enriched in oxygen that returns to left atrium from the lungs
-Low Oxygen content in arteries -High oxygen content in veins Right Ventricle>Lungs>Left Atrium |
|
|
systemic circulation
|
-oxygen enriched blood is pumped from the left ventricle into the aorta, supplying oxygen
-High oxygen content in arteries -Low oxygen content in veins |
|
|
tricuspid valve
|
the AV valve between the right atrium and right ventricle
|
|
|
mitral valve
|
the AV valve between the left atrium and left ventricle
|
|
|
"Lub"
|
-First heart sounds
-produced by closing of the AV valves during isovolumetric contraction of the ventricles -beginning of ventricular systole |
|
|
"Dub"
|
-second sound
-produced during the closing of the semilunar valves when the pressure in the ventricles falls below the pressure in the arteries -beginning of ventricular diastole |
|
|
mitral stenosis
|
the mitral valve becomes thickened and calcified
|
|
|
valve incompetence
|
-cannot close properly
-the tension in the cordae tendineae may not be sufficient to prevent the valve from everting as pressure rises during systole |
|
|
causes of heart murmurs
|
-rheumatic endocarditis: damage by antibodies produced in response to strep bacteria
-mitral stenosis: thickened and calcified mitral valve -septal defects: holes in the septum between sides of heart |
|
|
myocardium
|
the entire mass of cells interconnected by gap junctions
|
|
|
myocardial cells
|
-short branched
-interconnected by gap junctions (electrical synapses) |
|
|
automaticity
|
automatic nature of the heartbeat
|
|
|
four regions that can spontaneously generate action potentials in heart or carry electric current
|
1. SA Node (pacemaker of heart)
2. AV Node 3. Atrioventricular bundle (bundle of hiss) 4. Purkinje fibers |
|
|
pacemaker potential
|
-during the period of diastole, the SA node exhibits a slow spontaneous depolarization (-60 to -40)
-bottom of curve |
|
|
Action potential in the SA Node
|
-hyperpolarization cause by previous AP open HCN Channels
-Inward diffusion of Na+ cause by opening of HCN -Threshold causes opening of voltage gated CA2+ -CA2+ produces myocardial cell contraction -repolarization produced by opening of voltage gated K+ channels and outward diffusion of K+ -Sympathetic release ACh causes opening of K+ channels thereby slowing rate of diastolic depolarization |
|
|
diastolic depolarization
|
the spontaneous, automatic depolarization of the pacemaker occurs during diastole
|
|
|
funny current
|
-hyperpolarization triggers action potential
-NA+ gradient greater than K+, triggers AP similar to how chemically gated channels produce EPSP |
|
|
Epi and Norepi and diastolic depolarization
|
-faster in response to
-B1 beta adrenergic receptors cause stimulation of cAMP within pacemaker cells -cAMP keeps the HCN channels open (hyper-polarization activated cyclic nucleotide-gated channels) -faster rate of diastolic depolarization |
|
|
Ectopic pacemarker
|
-a pacemaker other than the SA node
-slower -AV Node (slight delay, slow conduction) -AV Bundles (left and right bundle branches) -purkinje fibers (stimulate contraction of ventricles) |
|
|
Myocardial AP
|
-Stimulated by SA Node AP
-Voltage Gated NA+ channels open (fast NA channels) -Plateau repolarization +slow inward diffusion of CA through slow channels +slow channels balances slow outward diffusion of K+ -Rapid repolarization resumes by opening of voltage gated K+ channels |
|
|
Refractory period of the heart
|
-Action potential lasts about 250 msec
-has refractory period similar to AP -Cannot be stimulated again until relaxed -relative refractory begins shortly after re-polarization of myocardial cells begins (downslope of contraction curve) |
|
|
Electrocardiogram
|
A recording of electrical activity of the heart conducted thru ions in body to surgace.
|
|
|
Bi-polar leads
|
-record voltage between electrodes placed on wrists and legs (right leg is grounded)
Leads: 1. - right and left arm 2. right arm and left leg 3. left arm and left leg |
|
|
Unipolar leads
|
-record voltage between a single electrode placed on body and ground built into ECG machine
Limb leads: AVR - right arm AVL - left arm AVF - left leg 6 chest leads placed around the heart left to right |
|
|
3 Waves produced by cardiac cycle
|
P Wave - Caused by atrial depolarization and contract
QRS Complex - caused by ventricular depolarization and contract T wave - results from ventricular re-polarization and relaxation |
|
|
Heart sounds and ECG
|
Lub (S1) - comes immediately after QRS wave as AV valves close
Dub (S2) - comes as T wave begins and semilunar valves close S3 - Sloshing, not good in adults. S4- stiffening of ventricle walls |
|
|
Endothelium
|
-innermost layer of all vessles
-capillaries are made of only endothelial cells |
|
|
Three layers of Arteries and Veins
|
Tunica Externa - connective tissue
Media - mostly smooth muscle Interna - endothelium, basement membrane, elastin Take home: Arteries and veins are quite different |
|
|
Arteries
|
-Large arteries are muscular and elastic
-Contain lots of elastin -Expand during systole and recoil during diastole ^ This helps maintain smooth blood flow during diastole. |
|
|
Small arteries and arterioles
|
-Are muscular
-Provide most resistance in circulatory system -Arterioles cause greatest pressure drop -Mostly connect to capillary beds -Some connect directly to veins which form ateriovenous anastomoses |
|
|
Capillaries
|
-Provide surface area for exchange
-Blood flow through capillary bed is determined by precapillary sphincters of arteriole supplying it |
|
|
Continuous Capillaries
|
Present in Muscle, Lungs, Adipose
-tightly joined endothelial cells -narrow intercellular channels that permit molecules smaller than proteins |
|
|
Fenestrated Capillaries
|
Present in kidneys, endocrine glands, intestines
-very permeable -wide intercellular pores |
|
|
Discontinuous Capillaries
|
Present in liver, spleen, bone marrow
-Are large and leaky -large gaps in endothelium |
|
|
Veins
|
-Contain majority of blood in circulatory system
-Expand readily (compliant) -Very low pressure ^Insufficient to return blood to heart |
|
|
Movement of blood through veins
|
-Moved toward heart by contraction of skeletal muscle pump
-Also pressure drops in chest during breathing - 1-way venous valves ensure blood moves only toward heart |
|
|
Atherosclerosis
|
-Most common form of Arteriosclerosis
^Accounts for 50% of deaths in US -Localized plaques (atheromas) reduce flow in an artery ^Act as site for thrombus clots -High blood cholesterol is associated with risk of atherosclerosis |
|
|
Thrombus clots
|
-Plaques begin at sites of damage to endothelium
-Causes: hypertension, smoking, high cholesterol, diabetes |
|
|
LDLs and HDLs
|
Produced in the liver, cholesterol are carried in blood attached to:
Low Density Lipoproteins - Oxidized in cells - can injure endothelial cells facilitating plaque formation. High Density Lipoproteins - Not atherosclerotic, arteries do not have receptors for HDL. |
|
|
Ischemic heart disease
|
-Commonly due to atherosclerosis in coronary arteries
-Often accompanied by chest pain (angina pectoris) -Detectable by changes in S-T segment of ECG (negative dip between S-T segment. |
|
|
Ischemia
|
-Occurs when blood supply to tissue is deficient
-Causes increased lactic acid from anaerobic metabolism |
|
|
Myocardial Infarction
|
-Heart attack, usually caused by block of coronary artery
-Heart muscles die -Diagnosed by high creatine and lactate (CPK and LDH) -Presence of Troponin T and I from damaged muscle. -Damaged cells are replaced by noncontractile scar tissue |
|
|
Arrhythmias
|
-Abnormal heart rhythms
<60/min is bradycardia; >100/min is tachycardia |
|
|
Arrythmic flutter
|
-Contraction rates can be 200-300/min
|
|
|
Arrythmic fibrillation
|
Uncoordinated myocardial cell contraction - no pumping
Ventricular fib - life threatening Electrical fib - resynchronizes heart by depolarizing all at once |
|
|
AV Node Block (damaged)
|
First Degree: long PR interval, slow conduction
Second degree: when only 1 out of 2-4 can pass to ventricles (P wave with no QRS) Third Degree: no atrial activity passes to ventricles. Ventricles are then driven slowly by bundle of His or Purkinjes |
|
|
Lymphatic system 3 functions
|
-Transport interstitial fluid (lymph) back to blood
-Transport absorbed fat from small intestine to blood -Help provide immunological defense against pathogens |
|
|
Lymphatic capillaries
|
-Closed-end tubes that form vast networks in inter-cellular spaces
-Porous - absorb proteins, microorganisms, fat -Lymph capillaries > lymph ducts > lymph nodes |
|
|
Lymph nodes
|
-Filter lymph before returning it into veins via Thoracic Duct and Right Lymphatic duct
-Make lymphocytes and contain phagocytic cells that remove pathogens -Lymphocytes also made in tonsils, spleen, thymus |
|
|
Skeletal muscle excitation-contraction coupling
|
-Sarcolemma is excitable - conduct APs like axons
-Release of ACh at NMJ causes end plate potentials -APs spread through sarcolemma and down into muscles via T tubules as extension of sarcolemma - |
|
|
Blood composition
|
-Five liters
-Plasma is water, ions, metabolites, hormones, antibodies -RBCs comprise most formed elements |
|
|
Hematocrit
|
-Percentage of red blood cells in centrifuged blood sample
-36% to 46% in women; 41%-53% in men |
|
|
Plasma proteins
|
- 7 to 9% of plasma
Albumin: creates colloid osmotic pressure, draws H20 from interstitial fluid into cappilaries Globulins: carry lipids (gamma are antibodies) Fibrinogen: serves as clotting factor, converted to fibrin |
|
|
Serum
|
Fluid left when blood clots
|
|
|
Formed elements- Red Blood Cells (RBCs)
|
-Flattened biconcave discs
-Shape provides increase surface area for diffusion -Lack nuclei and mitochondria -Hemoglobin sacks - 300 billion RBC produced each day |
|
|
Formed elements - Leukocytes (WBCs)
|
-Nucleus, Mitochondria, amoeboid ability
-Can squeeze through capillary walls (diapedesis) |
|
|
Granular Leukocytes
|
-Detoxify foreign substances and release heparin
Eosinophils, Basophils, Neutrophils (the phils) |
|
|
Agranular Leukocytes
|
-Phagocytic and produce antibodies
Lymphocytes and Monocytes |
|
|
Platelets
|
-Smallest of formed elements - no nucleus
-Are amoeboid framents of megakaryocytes from bone marrow -constitute most of mass of blood clots -Release serotonin to vasoconstrict and reduce blood flow to clot area -Secrete growth factors to maintain integrity of blood vessel wall |
|
|
Hematopoiesis
|
-Formation of blood cells from stem cells in bone marrow (myeloid tissue) and lymphoid tissue
|
|
|
Erythropoiesis
|
Formationof RBCs
Stimpulated by EPO from KIDNEY |
|
|
Leukopoesis
|
Formation of WBCs
-Stimulated by cytokines, which are autocrine regulators secreted by the immune system |
|
|
Type A Blood
|
Has only A antigens
|
|
|
Type B Blood
|
Has only B antigens
Makes antibodies to type A |
|
|
Type AB Blood
|
Has A and B antigens
No A or B antibodies UNIVERSAL RECIPIENT |
|
|
Type O Blood
|
Has neither A or B antigens
Makes antibodies to both Type A and B UNIVERSAL DONOR |
|
|
Agglutination
|
When different blood types are mixes
Caused by antibodies |
|
|
Hemostasis
|
Cessation of bleeding
1 Vasoconstriction restricts blood flow 2 Platelet plug form 3 Plug and surroundings are infiltrated by web of fibrin |
|
|
Platelets role in Clotting
|
-Damaged endothelium allows platelets to bind
|
|
|
von Willebrand factor
|
-Increases platelet/collagen bond by binding both collagen and platelets
|
|
|
Platelet release reaction
|
Platelets stick to collagen and release:
-ADP - causes other platelets to become sticky -Serotonin - stimulates vasoconst -Thromboxane A2 - stimulates vasoconst, cause other platelets to become sticky |
|
|
Role of Fibrin
|
-Platelet plug becomes infiltrated by meshwork of fibrin
-Clot now contains platelets, fibrin and trapped RBCs ^Then undergoes plug contraction to form more compact plug |
|
|
Fibrinogen to Fibrin
|
Intrinsic pathway: Initiated by exposure of blood to negative charged cutting thing or vessel callogen.
-Factor XII initiated > CA2+ convert pro to thrombin then fibrinogen to fibrin Extrinsic pathway: damage outside vessles release thromboplastin that triggers clotting shortcut. Skips whole Factor XII process in the middle |
|
|
Eosinophilia
|
High eosinophil count usually in response to allergic reaction of parasite.
Diagnosed with a complete CBC count |
|
|
Clot dissolution
|
-When damage is repaired
Factor XII activates Kallikrein -Plasminogen is converted to plasmin, plasmin digests fibring thereby dissolving clot |
|
|
Anticoagulants
|
Calcium Chelators - Sodium Citrate, EDTA
Heparin - Activated antithrombin III which blocks thrombin Coumarin - inhibits activation of vitamin k which reduces CA2+ availability |
|
|
Excitation contraction coupling
|
-Depolarization of myocardial cells opens V-gated CA channels
-Opens more VG CA channels and CA channels in Sarcoplasmic riticulum -CA binds to troponin and stimulates contraction -Calcium pumped back into SR during repolarization |
