Circulatory System - Hemodynamics And blood vessels Flashcards
What is hemodynamics
Hemodynamics is the study of blood flow and the forces involved in circulation.
Are the basic parameters associated with cardiovascular function which facilitate blood flow during each cardiac cycle.
Blood pressure
Blood flow : volume of blood flowing through the vessels of the body ( given period; mL/min)
- circulation time ( Rt atrium to Rt atrium) =~ 1 min
- velocity : speed a volume of blood flows through a tissue ( slow at branching, eg capillary networks, fast in large vessels eg aorta)
Responsible for blood movement via flow from high to low pressure
- 2 measures: systolic pressure and diastolic pressure
-120/75 ( difference = pulse pressure:45)
Mean Arterial pressure (MAP) - average blood pressure between systolic and diastolic pressure in the aorta
- Map = cardiac output (Q) x peripheral resistance (PR)
- BP of 120/75. MAP = 75+45/3 which 90mm Hg
Atherosclerosis
Ageing = less distensible (arteriosclerosis)
Atherosclerosis is the growth of lipid deposits in the arterial walls
Cardiac output
Volume of blood pumped from the heart per minute
Q= HR x SV
Heart Rate (HR) - number of times the heart beats per minute (bpm)
Stroke Volume (S) - volume of blood pumped per heartbeat (cardiac cycle)
Eg. Q = 75 bpm x 70 ml per beat
Q = 5,250 ml min-1 / 5.25 L min-1
Cardiac output varies with levels of activity - vigorous exercise increases Q to as much as 35 L/min (maximum Q) (elite athletes)
Cardiac reserve = maximum Q - resting Q ( measures heart output in response to exercise)
Determining cardiac output- fick equation
Q=
O2 consumption (ml min-1)
Over
a-VO, difference (mI per 100ml blood) X100
Oxygen consumption is measured via expired gases
a-VO, difference is the difference between oxygen content of arterial and mixed venous blood and oxygen uptake in 1 minute
Stroke volume- preload
EDV = end diastolic volume
ESV = end systolic volume
SV= EDV - ESV
Governed by
Preload -Preload
- Volume coming Into ventricles (end diastolic pressure)
- Increased in: Hypervolemia
Regurgitation of cardiac values
-Preload- the amount of tension in ventricular myocardium immediately before it begins to contract
• exercise increases venous return and stretches myocardium
• cardiomyocytes generates more tension during contraction
Contractility
How hard the myocardium contracts for a given preload
1. Positive inotropic agents increase contractility:
• Hypercalcemia: cause strong, prolonged contractions and even cardiac arrest in systole
• Catecholamines: (adrenaline)increase calcium levels
• Glucagon: stimulates cAMP production
•Digitalis: raises intracellular calcium levels and contraction strength
- Negative inotropic decrease contractility:
Hyperkalemia: has a negative inotrophic effect, reduce force of heart contraction
Hypokalemia: has little effect on contractility
After load
The blood pressure in the aorta and pulmonary trunk immediately distal to the semilunar valves
• Opposes the opening of these valves
• Limits stroke volume
Hypertension increases afterload and opposes ventricular ejection ( high blood pressure heart has to work harder)
Anything that impedes arterial circulation can also increase afterload (scar tissue e.g emphysema)
Ventricular hypertrophy and heart failure
Stroke volume
Governed by -
• Preload
• Contractility.
• Afterload
Heart rate
Heart Rate
Pulse: surge of pressure produced by each heartbeat that can be felt by palpating a superficial artery with the fingertips
• Infants have HR of 120 bpm or more
• Young adult females average 72 to 80 bpm
• Young adult males average 64 to 72 bpm
• Heart rate rises again in the elderly
- Tachycardia-resting adult heart rate above 100 bpm( high heart rate)
- Bradycardia-resting adult heart rate of less than 60 bpm ( lower heart)
- Positive chronotropic agents- factors that raise the heart rate
- Negative chronotropic agents- factors that lower heart rate
Chronotopic effect on heart rate
Nervous System
• Cardiac centers in the medulla oblongata initiate autonomic output to the heart
- Cardiostimulatory effect: some neurons of the cardiac center transmit signals to the heart by way of sympathetic pathways
- Cardioinhibitory effect- others transmit parasympathetic signals by way of the vagus nerve
• Feedback from receptors to medulla oblongata provides information regarding a need for change in heart rate
- Proprioceptors
- Baroreceptors
- Chemoreceptors: looking for changes in oxygen ph etc
Chronotopic Effects on Heart Rate
Chemicals
• Affect heart rate as well as NTs from cardiac nerves
Drugs that stimulate heart
• Nicotine
• Thyroid hormone
• Caffeine
Electrolytes
• K+ has greatest chronotropic effect high levels slows down heart rate
• Ca2+ increase heart rate of levels are high
Blood vessels
General Anatomy of Blood Vessels
Arteries carry blood away from heart
Veins carry blood back to heart
Capillaries connect smallest arteries to veins
General Anatomy of Blood Vessels
- Tunica interna (intama)
• lines inside of the vessel exposed to blood,
• Simple squamous epithelium (endothelium)
• continuous with endocardium of the heart - Tunica media
• Middle layer typically thickest
• Smooth muscle, collagen and elastic tissue at places
• Strengthen and regulates vessels diameter because of smooth muscle that is able to contract - Tunica externa (adventitia)
• Outermost layer of loose connective tissue
• Providing an anchor for the vessel to connect to surrounding tissue
Arteries
‘Arteries
. ‘Resistance vessels’ due to relatively strong, resilient tissue structure that resists
high blood pressure
- Large elastic or conducting arteries eg aorta or carotid
- Medium muscular or distributing artieries.
Distribute blood to specific organs. Eg branc