260 midterm Flashcards
Coronary arteries on surface of heart
Prevent compression during contraction
Systole
Contraction and ejection
Diastole
Ventricular filling
Stenosis
Narrowing of the heart valve
Faulty opening, leading to decreased ejection
Murmurs heard when valve should be open
Regurgitation
Faulty closure, back-flow leads to decreased forward ejection
Murmurs heard when valve should be closed
Two types of myocardial cells
Auto rhythmic cells -> Pacemaker and conducting cells
Contractile cells -> 99%, mechanical work of contraction
Pacemaker action potential
Slow rise in membrane potential prior to AP
Initially just slow influx of Na+, then Ca++ and Na+, then regular repolarization of K+
Events are autorhythmic (self generated)
Contractile cells action potential
Three stages
Depolarization -> Na+ moves in
Plateau -> Ca++ moves in, stays depolarized
Repolarization -> K+ out
Myocardial contractile cells
LONG refractory period, to allow for filling
Sympathetic nervous system on HR
pacemaker cells become more depolarized, will reach threshold faster, increasing heart rate
Parasympathetic nervous system on HR
Hyperpolarizes pacemaker cells, will reach threshold slower, decreasing heart rate
ECG
different waves on an ECG correlate to specific electrical events
PQR -> Atria
RST -> ventricle
Each wave meaning
P -> Atrial depol, initiates atrial contraction
QRS -> ventricular depol and atrial repol, initiates ventricular contraction
T -> Ventricular repol, initiates ventricular relaxation
P-Wave initiation
in the SA node, delay of 100ms to allow ventricle contraction after atrial contraction and ventricular filling
Tachycardia
rapid HR of over 100 BPM,
Bradycardia
slow HR of less then 60 BPM
Arrhythmias
abnormalities in rhythm, can cause sudden death, fainting etc
Atrial Fibrillation
No P waves, can affect ventricular filling, risk of clotting, can be caused by caffeine, stress or genetics
Cardiac Cycle
4 Phases->
Diastolic filling, isovolumic contraction, ejection and isovolumic relaxation
Diastolic filling
LAP>LVP
Mitral valve open , aortic valve closed
Isovolumic contraction
QRS - LV contracts, both valves are closed
Ejection
once LVP>AP, aortic valve opens and blood is ejected
Isovolumic relaxation
T-wave, relaxation, once LVP>AP both valves close and there is no movement of blood
Average stroke volume
70ml per beat
Regulation of stroke volume
Preload - amount of myocardial stretching (greater = greater SV)
Contractility - amount of force produced during a contraction (greater = greater the SV)
Afterload - tension required to force open aortic valve (increase = decrease in SV)
Stroke volume
Venous return - amount of blood entering heard
End diastolic volume - affected by venous return and filling time
End systolic volume - amount of blood in chamber after a contraction
Frank-Starling Law
Stroke volume increases as end ventricular volume increases
Cardiac output
stroke volume x heart rate
average: 5L
Factors affecting heart rate
-Autonomic nervous system
Sympathetic -> increase HR
Parasympathetic -> decrease HR
-Age (older = higher hr)
-Gender (females faster HR)
-Physical fitness (low = higher HR)
-Body temp (increase temp = increase HR)
Exercise and HR
Higher demand for O2 -> more blood flow
More epinephrine, casual athletes can increase up to 5x 25L/min
Myocardial ischemia/infarction
Ischemia is heart attack, inadequate delivery of oxygenated blood to heart (plaques can cause this)
Infarction when blood vessel supplying heart gets ruptured (also permanent)
Cardiac aneurysm
Bulge of ventricular wall
Blood flow
Proportional to pressure gradient
Inversely proportional to vascular resistance
F=P^/R
Blood flow resistance factors
-Blood viscosity
-Vessel length
-Vessel radius
Effect of vessel radius
1/r^4
radius decrease by a factor of two would result in flow rate decreasing by 16
Effect of viscosity
Higher viscosity = lower blood flow
Variance in blood vessels
Arterioles - highest proportion of smooth muscle
Capillaries - single layer endothelium
Arteries - Reinforced with collagen and elasin
Arteries
High flow rate / High pressure
Collagen fibers for tensile strength
Elastin fibers for stretch/recoil
120/80 (sys/dia)
Atherosclerosis
Caused by buildup of cholesterol, can harden into plaques
restricts blood flow
Arterioles
Resistance vessels
Adjustable radius to distribute cardiac output, and regulate arterial blood pressure
Vasoconstriction and Vasodilation
Factors influencing vascular tone
Local (metabolic changes, histamine release and endothelial factors)
Local physical (hot/cold, myogenic response to stretch)
Extrinsic control of arterioles
Alpha 1 - norepinephrine, vasoconstrictor
Beta 2 - epinephrine, vasodilator
Angiotensin 2 - vasoconstrictor
Capilaries
Thin walled, small radius, large surface area
site of gas exchange, by diffusion
Capillary Bulk Flow
Hydrostatic (encourages flow into tissue)
Interstitial fluid hydrostatic pressure (opposes hydrostatic)
Plasma colloid osmotic pressure (encourages movement of fluid into capillary)
Interstitial fluid colloid osmotic pressure (opposes plasma)
Fluid exchange at Capillary
20L/day into tissue
17L/day into capillaries
3L through lymph
Lymphatic system
Network of open-ended vessels to drain
Similar structure to veins, has valves and are open ended
Function of lymphatic system
Return excess filtered fluid
Defence against disease
Transport absorbed fat
Edema
Swelling of tissue
Accumulation of interstitial fluid
Veins
Transports back to heart, low pressure / low resistance
60-70% of blood is stored in veins
Venous return
Decreased by venous compliance
Increased by
-cardiac contraction pressure
-skeletal muscle activity
-venous valves
-resp activity
etc
Strokes
Low blood supply to brain
Ischemic (87%), plaque blockage
Haemorrhagic (13%) bleeding/rupture
most strokes are preventable
Blood pressure
Determined by cardiac output x total peripheral resistance
Blood pressure control
Short term - Baroreceptors, cardiovascular system.
Long term - kidneys
Short term response to BP
Decrease in blood pressure, decrease in parasympathetic, increase in vaso/venoconstriction, increase sympathetic, which leads to increase in SV, Contractility, HR and BP
Long term response to BP
Direct/Indirect renal
Direct - increase in BP, increase filtration, increase urine, reducing BP
Indirect - Renin leads to angiotensin 1 decrease, which leads to angiotensin 2 decrease, which leads to decrease ADH and aldosterone, less water reabsorption, blood volume and BP
Hypertension
Blood pressure above 140/90mmHg
Two classes - primary and secondary
Primary - Excessive salt intake, poor kidney function, smoking, diet etc
Secondary - Secondary to other known problems, like endocrine and neurogenic hypertension
Bronchioles
Bronchoconstrict or dilate
Control airflow
Alveoli
Site of gas exchange, thin walled, large surface area for diffusion
Types of alveoli cells
Type 1 Alveolar -> Make up the wall
Type 2 Alveolar -> Secrete surfactant
Macrophages -> Immune funtion
Respiration
Ventilation, external/internal respiration
Muscles recruited in forced inspiration
-Scalenus
-Sternocleidomastoid
Muscles recruited in quiet inspiration
-Diaphragm and external intercostals
Muscles recruited in forced expiration
Abdominals and internal intercostals
Central chemoreceptors
-In medulla
-Monitors cerebrospinal fluid
-Sensitive to changes in H+, via CO2`
Peripheral chemoreceptors
-CO2 and H+ in BLOOD triggers peripheral receptors
Respiratory stimulants
CO2 most powerful, if arterial <60mmHG, it will also be a stimulant, as well as lactic acid
4 Physical factors of pulmonary ventilation
-Airway resistance
-Alveolar Surface tension
-Lung compliance
-Elastic recoil
Airway resistance equation
flow = pressure/resistance
Surfactant
Detergent like lipid, decrease surface tension of alveolar fluid
Lung compliance
increase by lung tissue and alveolar surface surfactant
diminished by fibrosis, reduced surfactant production and decreased flexibility of cage
Elastic recoil
How lungs rebound after being stretched
Depends on elastin/collagen, and alveolar surface tension
Lung volumes
Tidal: 500mL
Vital: 4L
Funct. Residual: 1200mL
External VS Internal Respiration
external is between alveoli and blood, internal is between blood and tissues
gas moves from higher partial pressure to lower partial pressure
Partial pressures
21% oxygen, 79% nitrogen
Ficks law of diffusion
k(diffusion constant) x A(area for gas exchange) x (difference in partial pressure)/diffusion distance
Respiration pressure numbers
Alveoli -> 100 O2 and 40 CO2
Arterial Blood -> 100 O2 and 40 CO2
Veinous Blood -> 40 O2 and 46 CO2
Tissue -> <40 O2 and >46CO2
O2 transport in blood
98% hemoglobin
2% dissolved in blood
(4 O2 per Hb)
CO2 transport
10 Dissolved in blood
30 bound to hemoglobin
60 as HCO3-
O2 unloading curve
30% to resting tissues, to 40 mmHg, 50% to exercise tissues to 20mmHg
Factors affecting unloading
pH, exercise and higher temp improve offloading speed
Hypoxia
Inadequate O2 delivery to tissues
Slow VS Fast diffusion of CO2
HCO3 is slow, H2CO3 bound in RBC is quick due to enzymes and Cl-
Blood makeup
45 RBC, 55 plasma, less then 1 WBC
Plasma
90-92% water, contains electrolytes and glucose and clotting factors
RBC
Need iron and B12, contain hemoglobin to carry oxygen
Anemia
Low oxygen carrying capacity, can cause fatigue
Polycythemia
High red blood cell count, causes dehydration, reduced plasma and high hCT
WBC
- Neutrophils (phagocytes, 60-70%)
- Monocytes (macrophages, 2-8%)
- Eosinophils (allergy resp, 1-4%)
- Basophils (histamine)
- Lymphocytes (20-30% of WBC)
Platelets
Allow clotting
Platelet plug
Exposure to collagen, activates other platelets
Surrounding healthy tissue inhibit platelets
Coagulation
Formation of fibrin threads, clotting factors required
Extrinsic pathway is initiated first
Blood type
Contain ANTIGEN for blood type, and antibodies for bloodtype you do NOT have
Virus VS Bacteria
Virus cannot replicate, DNA
Bacteria are small cells that rely on tissue for food
Antibiotics
Work on Bacteria, not viruses
Super-Bugs
antibiotic resistance bacteria, usually due to over-use of said antibiotics
Fungi
Plant-like organisms, usually an inflammation response
Specific VS Nonspecific resistance
Nonspecific -> Present at birth, include defence mechanisms against a wide range of pathogens
Specific -> involves lymphocyte activation that combat foreign substances
Non-specific
Quicker but weaker - External defence, inflammation, phagocytes
Specific
Slower but stronger - Acquired
T-cells -> kill infected cells
B-cells -> antibody response
Lines of defence
First -> External (skin mucous)
Second -> Phagocytes and inflammatory response (non-s)
Third -> Lymphocytes and antibodies (s)
Inflammatory
Increase blood flow and permeability to injury/infection site
B-cells
Attack free virus, an antibody reaction
Specific
T-Cells
Attack infected cells
Specific
Antibody response
Antibodies bind to antigens, mark them for destruction by phagocytes
Helper T-cells
secretes cytokines
mediates fever, increase B and T cells
Virus VS Bacteria response
Viruses will have active lymphocytes
Bacteria are more likely to have higher neurophils
