Cardiovascular\Respiratory Flashcards
1
Q
Contraction of a Cardiac Muscle Cell
A
- Vagus nerve transmits impulses to heart muscle, Na+ diffuses into cardiac cells.
- Electrochemical impulse travels along the sarcolemma of the cells.
- Impulse triggers Ca+2 outside the sell to diffuse in which then causes sarcoplasmic reticulum to release Ca+2
- Ca+2 interacts with contractile proteins causing the cell to contract and shrink in size.
2
Q
Cardiac Cycle
A
- SA node depolarizes
- Wave of depolarization spreads through atria, atria contract = ATRIAL SYSTOLE, AV valves are open, blood is forced into ventricles
- Atria repolarize and relax = ATRIAL DIASTOLE, wave of depolarization hits AV node, delay at AV node allows ventricles to fill with blood
- After delay AV node depolarizes and impulse travels through the rest of the conduction system (bundle of his, r/l bundle branches, and purkinje fibers), ventricles contract = VENTRICULAR SYSTOLE, blood is pumped into aorta and pulmonary trunk, AV valves close, SL valves are open
- Ventricles repolarize and relax = VENTRICULAR DIASTOLE, SL valves close, blood returns back to atria from the body
3
Q
Frank-Starling Law
A
States that the force of the cardiac muscle contraction is proportional to the of stretch on the fibers.
4
Q
Sinus Bradycardia
A
Slower than normal HR,
5
Q
Sinus Tachycardia
A
Faster than normal HR, b/w 100-180bpm, normal under strenuous exercise.
6
Q
Preload
A
Amount of stretch on the cardiac muscle fibers d/t returning blood.
7
Q
Afterload
A
Amount of force required to open SL valves.
8
Q
Sinus Arrhythmia
A
Speeds up/slows down, normal ECG but rate varies, normal esp. in children.
9
Q
Paroxysmal Atrial Tachycardia
A
B/w 180-250 bpm, atrial and cardiac efficiency decrease, usually due to drug use etc.
10
Q
Atrial Flutter
A
B/w 250-350bpm, atria contracting rapidly, ventricles keep at their normal pace due to refractory period of AV node, saw-tooth P waves.
11
Q
Atrial Fibrillation
A
> 350bpm, atria are spazming, most common heart arrhythmia, loss of organized signal from SA to AV, no distinct P waves.
12
Q
Ventricular Tachycardia
A
Ventricles are contracting rapidly which disables them from filling with sufficient amounts of blood per pump, poor circulation, ex. scarring d/t prior MI, impulse has to move around scarred V cells which stimulates the purkinje fibers more rapidly.
13
Q
Ventricular Fibrillation
A
No blood getting to the body, no identifiable ECG waves, ventricles are spazming.
14
Q
First Degree Heart Block
A
Longer than normal P-R interval, longer delay at AV node, due to minor damage to the conduction system.
15
Q
Second Degree Heart Block
A
Occasional skipped beats, AV node cannot keep up to the sinus rhythm, ventricles don’t contract due to severe blockage of conduction system.
16
Q
Third Degree Heart Block
A
No signal from atria to ventricles, ventricles must set up their own slower rhythm of 40-60bpm.
17
Q
PAC
A
Ectopic focus in atria causing the atria to depolarize, not abnormal unless persistent.
18
Q
PVC
A
Ectopic focus in ventricles causing ventricles to contract before atria have the chance to, also not abnormal unless persistent.
19
Q
Bi/geminal
A
Every second beat is a PVC
20
Q
Tri/geminal
A
Every third beat is a PVC
21
Q
Cardiac Center-BP Too High
A
Stretch (Baro) receptors in either the carotid sinus reflex or the aortic reflex detect and send and impulse via sensory neurons to the medulla oblongata’s cardioinhibitory center which sends motor impulses via the vagus (parasympathetic) nerve to the heart to slow the HR. Uses acetylcholine via cholergic fibers.
22
Q
Cardiac Center- BP Too Low
A
Stretch (Baro) receptors in either the carotid sinus reflex or the aortic reflex detect and send an impulse via sensory neurons to the medulla oblongata’s cardioacceleratory center which sends motor impulses via sympathetic nerves to the heart to increase HR. Uses norepinephrine via adrenergic fibers.
23
Q
Atrial Reflex
A
Stretch (Baro) receptors in the aortic reflex detect high BP due to high amounts of returning venous blood, info is sent to the cardiac center to increase HR so that more blood is pumped out of the heart.
24
Q
Ischemic Heart Disease
A
When the cardiac cells are receiving insufficient amounts of oxygen due to partial blockage of the coronary arteries as a result of atherosclerosis.
25
Atherosclerosis
Due to atheroma- plaque like structure forms on arterial walls in damaged endothelium, damage can be a result of hypertension.
26
Plaque
Mainly lipid (fatty) in nature but deposits of calcium salts follow (causes hardening of arteries=arteriosclerosis), may involves cell proliferation from artery wall.
27
Thrombosis
Stationary clot, partial blockage causing ischemia. May result in MI.
28
Embolism
Moving clot from heart may get caught downstream in coronary arteries. May result in MI.
29
Chronic Ischemic Heart Disease
Heart muscle is not getting sufficient O2, angina pectoris (chest pain upon exertion), contributing factor is hyperlipidemia ( high blood lipid levels)
30
HDL's and VLDL's
Good cholesterol, travelling to liver to be broken down.
31
LDL's
Bad cholesterol, travelling to cells, may eventually form plaque on damaged endothelium and result in atherosclerosis.
32
Congestive Heart Failure
Not enough CO to respond to tissue demand, therefore preload and afterload increases= congestion, causes edema (not enough force to pump blood back to the heart, results in excess fluid in tissues.)
33
Causes of Congestive Heart Failure
Myocardial weakness (aging, ischemia, MI's), valve problems, lung disease, hypertension.
34
Blood Flow %'s
```
Heart and Lungs=100%
Brain=15%
Digestive Organs=varies
Kidneys=20%
Muscles= at rest:20% active:75%
Storage Areas=5%
```
35
Pre Capillary Sphincters
Shunt blood from one area to maximize flow to another.
36
What does BP do further away from the heart?
Drops due to an increase in the total cross sectional area.
37
Venous Blood Return
Aided by skeletal muscle contractions and one way valves.
38
Phlebitis
Inflammation of veins causing roughened endothelium where clots can form. Results in thrombophlebitis. Further along causes deep vein thrombosis where clot can dislodge resulting in a pulmonary embolism.
39
Predisposing Factors of a Pulmonary Embolism
1. Pooling of venous blood (Static blood clots more easily due to muscle inactivity)
2. Endothelial damage
3. Varicose veins (Valvular incompetence= swelling in veins)
40
Determining Factors of BP
1. Volume of blood
| 2. Resistance of vessel walls against flow
41
Factors that Effect BP
1. Elasticity of arterial walls
2. Viscosity
3. Peripheral resistance=Vasomotor Center
4. Kidneys
42
Viscosity
Thickness of the blood, polycythemia=increases RBC count means thicker blood which is harder to pump, erythropoietin is a kidney hormone that controls RBC synthesis, at high altitudes kidney detects low O2 levels which causes it to release EPO which causes red bone marrow to undergo RBC synthesis= acclimatization.
43
Elasticity of Arterial Walls
blood is pumped at high pressure into the aorta, arterial walls expand (dampening effect) then recoil to somewhat re-pressurize the system. Arterial walls lose elasticity due to age and atherosclerosis= high BP.
44
Peripheral Resistance
Control of arteriolar diameter, vasoconstriction increases BP and vasodilation decreases BP.
45
Vasomotor Center-BP Too High
Stretch (Baro) receptors in carotid sinus reflex, aortic reflex or vasomotor center itself detect and send an impulse via sensory neurons to vasomotor center of medulla oblongata which sends less sympathetic nerve impulses which then decreases vasoconstriction (vasodilation) = lower BP.
46
Vasomotor Center- BP Too Low
Stretch (Baro) receptors in carotid sinus reflex, aortic reflex or vasomotor center itself detect and send an impulse via sensory neurons to vasomotor center of medulla oblongata which sends more sympathetic nerve impulses which then increases vasoconstriction = higher BP.
47
Renin-Angiotensin System
Kidneys detect a drop in BP which causes the JGA (juxtaglomerular apparatus) to release renin. Angiotensinogen (blood protein from the liver which is inactive) interacts with renin and changes to angiotensin I which is also inactive, ACE (angiotensin converting enzyme) converts angiotensin I to angiotensin II which is active.
48
Effects of Angiotensin II
1. Directly vasoconstricts the efferent arteriole which increases BP
2. Detected by adrenal cortex which releases aldosterone which increases the kidney's retention of Na+ therefore water follows therefore increased BP
3. Causes the post pit to release ADH which directly increases the kidneys retention of water therefore increasing BP
49
Hypertension
If persistent, 140/90bpm
50
Renal Hypertension
When a kidney's renal artery is partially blocked by a fatty plaque the kidney detects low BP and responds accordingly by releasing renin which overall causes BP to increase. This results in a drastic increase in BP in the rest of the body.
51
Fetal Circulation
Lungs are not yet functional so...
1. Ductus Arteriosus: Shunts blood from pulmonary trunk to aorta.
2. Foramen Ovale: Shunts blood from right atrium to left atrium.
Patent ductus and patent foramen: When the holes remain open.
52
Functions of Blood
1. Transports gas (O2 from lungs to tissues and CO2 from tissues to lungs).
2. Waste transport (Urea which is filtered into the kidney and urinated out)
3. Transport of immune system components (ex. leukocytes, antibodies etc.)
4. Nutrient transport (amino acids and glucose etc.)
5. Distribution of hormones (ex. renin, angiotensin, adrenaline, ADH etc.)
6. H2O storage (92% plasma is water, fluid reservoir)
53
Hematocrit
Packed RBC volume.
54
Erythrocytes
Bi-concave disk, lack nucleus when mature
55
Hemoglobin
Heme= Fe+2 plus pigment Globin= Protien (2alpha and 2beta)
56
RBC Production
Red bone marrow is the site of RBC synthesis controlled by EPO when kidney detects low pO2.
Stem cell undergos mitosis and creates rubriblasts which differentiate into erythroblasts which then differentiate into reticulocytes which finally differentiate into erythrocytes and release their nucleus. RUB-ER-RET-ER
57
RBC Recycling Process
Breakdown occurs in the liver and spleen.
1. Hemoglobin breaks into heme and globin
HEME: 1. breaks down into Fe+2 which gets stored in the liver and 2. pigment (biliverden) which the liver converts into bilirubin which is used in bile production and excreted in feces.
GLOBIN (protein): Broken down into amino acids which then are metabolized and reused.
58
Anemia
Low hemoglobin and RBC count, any condition involving impaired O2 carrying capacity of blood.
59
Iron Deficient Anemia
- Dietary source of Fe+2 is not keeping pace with usage.
- Metabolic problems associated with Fe+2
- Eat leafy greens and liver
60
Pernicious Anemia
- Low vitamin B12
- malabsorbtion due to lack of stomach produced Intrinsic Factor (IF) which attaches to B12 and helps it through the small intestine and into the blood.
61
Hemolytic Anemia
- Breakdown rate of RBC's too high for bone marrow to keep up
- usually results in spenectomy
62
Hemorrhagic Anemia
-Chronic loss of blood (nose bleeds, severe menstrual periods)
63
Aplastic Anemia
- Not enough types of blood cells
- Production of RBC and other types of blood cells in bone marrow very low
- Leukemia causes overcrowding of dysfunctional cells
64
Polycythemia
High RBC counts=opposite of anemia
High altitudes=acclimatization
Exogenous EPO=performance enhancing drug
65
Leukocytes=5 Kinds
Granulocytes:
1. Neutrophils
2. Eosinophils
3. Basophils
Agranulocytes:
4. Lymphocyes
5. Monocytes
66
Neutrophils
- Pale pink granules
- 3/4 lobed nucleus
- 54-60% of WBC's
- Function: Phagocytosis
67
Eosinophils
- Large red granules
- bilobed nucleus
- 2-4% of WBC's
- Function: Antiviral/anti-worm
68
Basophils
- Large blue granules
- indistinct nucleus
- 1% of WBC's
- Function: histamine and heparin production
69
Lymphocytes
- Nucleus fills cytoplasm
- 30% of WBC's
- Function: B cells and T cells for immune systems specific immunity
70
Monocytes --> Macrophages
- Largest WBC
- 10% of WBC's
- Function: Phagocytosis/immune system
71
Thrombocytes
Platelets which are anuclear cell fragments produced in red bone marrow from stem cells. IMPORTANT in hemostasis=blood clotting.
72
Hemostasis
1. Trauma induces circulatory leak
2. Transient vasospasm w/ vasoconstriction slows initial blood loss
3. Platelets attach to sticky CT then form a platelet plug
4. Platelets release serotonin which locally vasoconstricts. Prothrombin activator is present.
73
Hemostasis Details
Prothrombin (normal blood plasma protein from liver) is changed to thrombin by prothrombin activator. Thrombin changes fibrinogen (from liver) into fibrin (active) which forms a lattice-like meshwork clot.
74
Blood Plasma
-92% water
-8%:
1. Electrolytes (Na, K, H, etc)
2. Wastes (urea, uric acid etc)
3. Semi dissolved lipids
4. Glucose, amino acids
5. Hormones
6. Vitamins
7, Gases (O2 and CO2)
8. Plasma Proteins
75
Plasma Proteins
1. Albumins: maintain blood volume, create OP
2. Fibrinogens: changes to fibrin in the presence of thrombin for clotting.
3. Globulins: a) alpha (prothrombin) b) beta (lipid carriers) c) gamma (antibodies)
76
Functions of the Lymphatic System
1. Drains tissues of interstitial fluid
2. Houses immunes system
3. Transports fat
77
Pericardium
Parietal pericardium, pericardial cavity (serous fluid), and visceral pericardium
78
Epicardium
- corresponds to visceral pericardium
- Function: outer protective layer
- serous membrane consists of loose areolar CT covered by simple squamous
- includes blood capillaries, lymph capillaries and nerve fibers
79
Myocardium
- relatively thick
- consists of cardiac muscle tissue and amid fibrous skeleton for pumping blood
- muscle fibers arranged in planes separated by CT richly supplied with blood capillaries and nerve fibers.
80
Endocardium
-consists of epithelial tissue and CT mainly elastic and collagen fibers
CT contains blood vessels and purkinje fibers
lines all heart chambers and covers the four heart valves
-continuous with inner lining of blood vessels=endothelium
81
Trabeculae carneae
muscular interior ridges of ventricles
82
Chordae Tendineae
collagen rich CT hear strings run from AV valves to hearts walls to prevent valves from inverting
83
Papillary muscles
Muscular protrusions from ventricle walls, connect to chordae tendineae
84
Biscuspid Aortic Valve
Aortic SL valve has two cusps instead of three. Usually go undiagnosed until person calcific aortic stenosis
85
Rheumatic Heart Disease
Autoimmune disorder from childhood acute rheumatic fever (bacterial infection), scarring of valves (typically mitral valve) later in life, may require valve replacement.
86
Pathway of Circulation
Simultaneous pulmonary circuit to the lungs and systemic circuit to the body= double pump
87
Lymphatic Power
PHP-strongest pressure out of the capillary.
PCOP- second strongest power but going in, due to albumins.
ICOP-third strongest but going out of the capillary
IHP-smallest force but going in capillary
88
Lymph Node
Made of reticular CT, has phagocytes inside them.
89
How is lymph moved?
1. Intrinsically by contractions of the lymphatic vessels.
| 2. Extrinsically by compression of lymphatic vessels d/t contractions of skeletal muscle (like in venous system)
90
Major Lymph Nodes
1. Deep cervical: drains head
2. Submandibular: drains nose, face, etc
3. Axillary: armpits, drains upper torso,arms, etc.
4. Inguinal: drains legs, lower torso
91
Edema
Swollen tissues due to excess interstitial fluid due to congestive heart failure, liver/kidney problems (albumins) and starvation.
92
Lymphatic System and Cancer
Lymphatic vessels carry cancerous cells from their site of origin (primary tumor) to other parts of the body-this is called metastasis. Lymph nodes along the way can trap cancer cells and if they cannot destroy them, the nodes may become the secondary tumors,
93
Resp. System
Function: to filter, humidify, warm and transport air into and out of the body to allow gas exchange.
94
Upper Respiratory Tract
above thoracic cavity, usually colonized
95
Lower Respiratory Tract
within thoracic cavity, normally sterile
96
Pathway of Air Flow
External nares, nasal cavity, pharynx, larynx, trachea, bronchi, bronchioles, alveoli
97
Respiratory Tree Includes
Trachea, primary bronchi, secondary bronchi, segmental bronchioles, terminal and respiratory bronchioles, alveoli
98
Bronchial Tree
Primary bronchi, secondary bronchi, segmental bronchioles, terminal and respiratory bronchioles.
99
Pleura
Visceral and parietal, serous membranes.
- Covers lungs lines thoracic cavity
- lubricates and simplifies lung expansion
100
Concentrations of Inspired Air=Requires ATP
21% O2
79% N2
0.04% CO2
101
Concentrations of Expired Air= elastic
14% O2
80% N2
5.5% CO2
102
[Blood Gas]
measures as pO2 and pCO2= partial pressure
103
Where does gas exchange take place?
across the pulmonary membrane
104
Breathing Mechanism
1. When pCO2 levels rise in the blood, the med obls respiratory center detects and sends out motor impulses to the diaphragm and external intercostals
2. The dome shape diaphragm flattens as it contracts. The contracting external intercostal muscles move the rib cage up and out (elevation) increasing the volume of the thoracic cavity.
3. The lungs expand sticking to the pleural membrane creating negative pressure inside the lungs relative to outside the lungs. Air rushes into the lungs (INSPIRATION) which is the active phase= ATP required.
4. Stretch receptors in the alveoli are stimulated during inspiration and send inhibitory impulses to the med obls respiratory via sensory neurons to stop further inspiration (Hering-Breuer Reflex)-protective.
5. Diaphragm relaxes and the intercostals also relax allowing the ribcage to move down and in (depression) decreasing volume in the thoracic cavity.
6. Elastic lungs recoil creating positive pressure in the lungs compared to outside of the lungs, air rushes out from higher pressure to lower pressure (EXPIRATION) which is the passive phase of breathing meaning no ATP involved.
105
Respirometry
Measurement of lung capacities: anatomical dead space, IRV, TV, ERV, residual volume, VC and TLC
106
Intercalated discs between cardiac muscle cells allow the heart to behave like this.
Functional Syncytium
