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140 Cards in this Set
- Front
- Back
Circulatory System: two systems
|
• Cardiovascular
•Lymphatic system |
|
Cardiovascular – 3 basic components
|
– Heart – establish pressure gradient
• Dual pump ( right/left systems) • Atria and ventricles – Blood vessels – passageway, regulation of distribution – Blood – transport medium |
|
Cardiovascular subdivisions
|
• Pulmonary circulation –heart/lungs
• Systemic circulation – heart/other systems • Functional differences? • Anatomical differences? |
|
Lymphatic system
|
– accessory route
– unidirectional vessels |
|
Cardiac system Anatomy
|
• Position - between sternum and
vertebrate • Gross anatomy – base, apex, pericardial sac – atria atop ventricles, septum – Right/ left sides =two separate pumps |
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Atrioventricular (AV) valves
|
– Prevent backflow \from ventricles into atria
– Right AV/tricuspid valve – Left AV valve (bicuspid/mitral) – Chordae tendinae • Fibrous cords prevent valve eversion • Papillary muscles |
|
Semilunar valves
|
– Aortic and pulmonary valves
– Lie at juncture where major arteries leave ventricles |
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Cardiac Layers
|
– Endothelium – thin/inner, lies entire CV
– Myocardium – middle/muscle • myocytes - autonomic innervation • intercalated discs (gap junctions and desmosomes) – Epicardium – thin/external • squamous mesothelium/basal lamina • blood/nerve supply within CT network |
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Pericardium
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– fluid filled sac
– Fibrous outer layer – Inner secretory lining – pericardial fluid |
|
tunica intima
(inner layer) |
– endothelial lining with basement membrane
– some connective tissue (CT) |
|
tunica media
(middle) |
– variable muscular elements – regulate diameter
– variable elastin – “elastic lamina” |
|
tunica adventitia
or externa (outer) |
– variable connective tissue
– extensive blood and nerve supply |
|
Cardiac muscle
|
• Similar to skeletal
muscles – sarcomeres – actin/ myosin • Differences from skeletal muscle – mononucleated – branched – connect through intercalated disks (gap junctions, desmosomes) |
|
Cardiac muscle fibers
|
• Interconnected by intercalated discs, form functional
syncytia • Within discs – two kinds of membrane junctions – Desmosomes – Gap junctions |
|
T-tubules
|
larger than
in skeletal muscle, are aligned with Z-disks (one per sarcomere)` |
|
SR is juxtaposed with
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T-tubules at very small
terminal bulbs, rather than large cisternae. |
|
SR structure/size
|
thin and lacy, with
much smaller volume than skeletal SR |
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Contractile cells
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(99% cardiac cells)
• Do mechanical work of pumping • Normally do not initiate own APs |
|
Autorhythmic cells
|
• Send electrical signals to the contractile cells
• Specialized for initiating and conducting action potentials responsible for contraction of working cells • Locations: – Sinoatrial node (SA node) – Atrioventricular node (AV node) – Bundle of His (atrioventricular bundle) – Purkinje fibers |
|
SA node
|
– right atrial wall near superior vena cava
– Pacemaker of the heart |
|
AV node
|
– base right atrium
– only connection to ventricles |
|
Bundle of His
(AV bundle) |
– at AV node towards interventricular septum
– Form R and L bundle branches down septum |
|
Purkinje fibers
|
extend
from Bundle of His through ventricles |
|
Cardiac APs originate
|
at SA
node – spread through atria |
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APs to AV node
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– only point of electrical contact
between chambers – delay ensures atrial contraction precedes ventricular contraction (allow complete filling |
|
APs down interventricular
septum |
via bundle of His
|
|
Disperses via
|
Purkinje fibers,
spread via gap junctions |
|
Pacemaker cells
|
• Pacemaker potential
– small Na+ leak (If) -"funny" channels – open at Vm more negative than ~ -50 mV – plus some T- Ca2+ channels) • Threshold – depolarization at ~ -40 mV – L - Ca channels open , • Repolarization – Slow K+ channels open – close Ca2+ channels |
|
Electrical Conduction – Contractile cells
|
• No pacemaker potentials
–driven by pacemaker cells • Threshold/depolarization -classic fast Na+ channels • Plateau phase – elevated L-type Ca2+ channels (dihydropyridines) • Repolarization - Slow ("delayed rectifier") K+ channels open/ close Ca+channels; close to restart cycle. |
|
Electrical Activity of Heart
|
• Long refractory period with prolonged plateau phase
– limits summation/tetanus of cardiac muscle – Ensures alternate periods of contraction/relaxation |
|
Modulation of Cardiac Excitation/
Contraction |
• Epi/NE – sympathetic - Depolarize V
mat baseline, increases “funny” current • Ach – parasympathetic – Hyperpolarize Vm, decreases “funny” |
|
Epinephrine
|
sympathetic
–beta 1/increase cAMP – increase Ca 2+ channel Conductance (permeability) |
|
Ach
|
parasympathetic
– Muscarinic – decrease cAMP – decreasing Ca2+ entry |
|
Electrocardiogram (ECG)
|
• Record of overall spread of electrical activity through heart
– part of activity in body fluids by APs that reaches body surface – not direct cardiac recording • Overall spread throughout heart during depolarization and repolarization/not single Aps • Comparing V differences on body surface – not actual potential – no potential recorded with heart completely depolarized/ repolarized |
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P wave
|
atrial depolarization
|
|
PR segment
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AV nodal delay
|
|
QRS complex
|
ventricular depolarization (atria repolarizing simultaneously)
|
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ST segment
|
time during which ventricles are contracting and emptying
|
|
T wave
|
ventricular repolarization
|
|
TP interval
|
time during which ventricles are relaxing and filling
|
|
Heart rate
|
Normal ~
70 beats/min (SA note similar) – Tachycardia >100 bpm – Bradycardia < 60 bpm |
|
Rhythm –
regularity/spacing |
– “sinus” –(SA node) P
same direction/ before QRS – Normal intervals • PR - 0.20 sec • QRS - 0.08 – 0.10 sec • QT- 450 ms in men, 460 ms in women |
|
Electrical Abnormalities
|
• Arrhythmia - Variation from normal rhythm
and abnormal sequence of excitation – Atrial flutter (200-300 BPM) vs fibrillation (irregular) – Ventricular fibrillation – Premature Ventricular Contraction (PVC) – Heart block • 1 st degree – PR fixed > 0.2 sec • 2 nd degree (two types) – PR gradually lengthened, then drop QRS – PR fixed, drop QRS randomly - 3rddegree block - PR and QRS dissociated |
|
Mechanical
Events |
• Systole = period of contraction
• Diastole = period of relaxation • Cardiac Cycle = alternating periods of systole and diastole |
|
Phase of Cardiac Cycle
|
1. Rest
(atria/ventricles in diastole – filling with low pressures) 2. Atrial Systole – completes ventricular filling 3.Isovolumetric Ventricular Contraction – Increased pressure in the ventricles causes the AV valves to close… why? (1st heart sound) – Atria go back to diastole – No blood flow as semilunar valves are closed as well 4. Ventricular Ejection – interventricular > aortic pressure (semilumar valves open) 5. Isovolumetric Ventricular Relaxation - interventricular < aortic pressure (Semilunar values close – 2 nd heart sound) |
|
Cardiac Output
|
• Volume of blood ejected by
each ventricle each minute • Cardiac output = heart rate (HR) x stroke volume (SV) – SV ~ 70 ml – HR ~ 70 beats/min – Output about 5 L/min at rest – Increase to 30-40 L/min during high intensity exercise |
|
Stroke volume
|
Determined by extent of venous return
and by contractility/afterload |
|
Venous return
|
end-diastolic volume (EDV)
– Increases “pre-load” • Amount of stretch within myocardium (‘load’ prior to contraction) • Length-tension patterns (Frank-Starling Law) – Determinants • Skeletal muscle pump • Respiratory pump • Cardiac “Suction |
|
Contractility
|
contributes to ESV
– Stronger contraction = larger stroke volume – “inotropic agents” (epinephrine/NE; Ach is opposite) – Increased Ca2+ entry/modulation – more force per unit muscle/length |
|
Afterload
|
contributes to ES
– aortic pressure to overcome to open semilunar valves – Higher afterload - reduces ejection fraction (SV/EDV) ~ normal=52% – indirect relationship- Higher aortic pressure = lower stroke volume – Causes? • Elevated blood pressure • Loss of compliance in aorta (loss of elasticity) |
|
Cardiac Mechanics (Pressure/Volume Curve)
|
• Pressure/Volume relation often plotted to indicate
demands on cardiac tissue – Start at (a) diastole, (b)-(c) systole, (d)-(a) diastole – Curve runs counter-clockwise |
|
LEFT VENTRICULAR
PRESSURE/VOLUME CURVE |
A. mitral valve opens
– Heart relaxation – vent P < atrial P B. diastole (filling) – increase volume in ventricle – Low pressure-chamber expanding C. start of systole – Mitral valve closes (vent P > atrial P) – Rapid increase in pressure (no change in volume no valves open) |
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LEFT VENTRICULAR
PRESSURE/VOLUME CURVE |
D. aortic valve opens
– Vent P > aortic P – Blood starts to be ejected E. systole (cont) – Decreased vent volume with blood ejection – Maintaining high pressures F. start of diastole – Aortic valve closes (vent P < aortic P) – Rapid drop in pressure (no change in volume – no valves open) |
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Coronary Circulation
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• Supplies oxygen and nutrients to heart (blood received
during systole and diastole) • Coronary blood flow keep pace with oxygen needs |
|
Coronary Arterial Disease (CAD)
|
– Primary cause of mortality in US
– Can cause myocardial ischemia or infarction (3 mechanisms) • Vascular spasm of coronary arteries • Formation of atherosclerotic plaques • Thromboembolism – Angina Pectoris • Controlled w/ exertion • Uncontrolled – vasospasm ? |
|
Outcomes Post-Myocardial Infarction
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1. Immediate death
2. Delayed complications/death 3. Full recovery 4. Recovery with impaired function |
|
Immediate death
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– heart ineffective in pump function
– fatal ventricular fibrillation 2⁰ damage conducting tissues |
|
Delayed complications/death
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– Fatal rupture of dead/degenerating
cardiac wall – Progressive heart failure |
|
Full recovery
|
– Replacement of damaged wall with
scar – Enlargement, compensation of remaining contractile tissue |
|
Recovery with impaired function
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– Permanent functional defects
– bradycardia, conduction blocks |
|
Blood Vessels Function
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– Route for transport (arteries – away, veins – towards)
– Exchange (capillaries) – Control/regulate blood pressure |
|
Structure allows function
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– Aorta – absorb pulse pressure (SBP - DBP)
– Large arteries- conduct/distribute blood to specific regions – Arterioles – regulate flow and mean arterial pressure (MAP) – Capillaries – exchange – Venules – collect/direct blood to veins – Veins – return blood to heart/reservoir |
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Arterial system
|
away from heart
– Large elastic arteries (little resistance to flow – Systolic Blood Pressure ~120 mmHg at brachial artery – Diastolic Blood Pressure – with aortic recoil/closure of aortic semilunar valves (~80 mmHg at brachial artery) – Pulse Pressure – SBP - DBP – Mean Arterial Pressure (MAP) • MAP = DP + 1/3 Pulse Pressure • Evaluates general health of CV system |
|
Blood Pressure
|
Measured indirectly using
sphygmomanometer • Korotkoff sounds – Sounds heard when determining blood pressure – Sounds are distinct from heart sounds associated with valve closure |
|
Measured indirectly using sphygmomanometer
|
1. Cuff pressure > SBP -No sound.
2. The first sound is heard at peak SBP. 3. Sounds are heard while cuff pressure < SBP but > DBP 4. Sound disappears when cuff pressure < DBP |
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Flow dynamics (CO, MAP, Resistance)
|
• Cardiac output = net flow throughout CV system
• MAP – mean hydrostatic pressure gradient driving fluid flow (depends on blood volume/vessel compliance) • Resistance – ease of flow through vessels, total peripheral resistance (TPR) proportional to MAP and CO – With increased resistance but similar CO, what happens to MAP? – With anaphalaxis, what happens to resistance, MAP, CO |
|
Blood Flow/reconditioning
|
• Blood constantly reconditioned
(composition relatively constant) • Reconditioning organs receive more blood than metabolic needs – Digestive organs, kidneys, skin – Adjust extra blood for homeostasis • Blood flow to other organs can be adjusted according to metabolic needs • Brain can least tolerate disrupted supply |
|
Arterioles
|
• Major resistance vessels
– Radius adjusted independently to distribute CO – Help regulate arterial blood pressure • Histology/function – Larger arterioles – reduced elastic fibers from arteries, increased muscle fibers – Smaller arterioles - relatively greater smooth muscle • Adjusting arteriolar resistance – Vasoconstriction - narrowing a vessel – Vasodilation – increase vessel radius – Alter smooth muscle contractions |
|
Smooth Muscle
Characteristics |
– Walls of hollow organs/tubes
– No striations (no sarcomeres/ myofibrils) – Spindle-shaped cells, single nucleus • Cells usually arranged in sheets within muscle • Have dense bodies containing same protein found in Z lines |
|
Filaments/structures
|
– myosin (thick) - Longer than those
in skeletal muscle – actin (thin) - Contain tropomyosin, no troponin – Intermediate - part of cytoskeleton, not directly related to contraction |
|
Activation of smooth muscle
|
– Ca
2+ dependent 2 nd messenger – Increased Ca2+ entry from ECF – Result in phosphorylation of myosin thick filament – Actin-myosin interaction |
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Multi-unit
|
– Neurogenic
– Discrete units that function independently of one another – Units must be separately stim ulated by nerves to contract – Locations (large blood vessels, large airways, vision (iris/lens), hair follicles |
|
Single-unit
|
– Self-excitable (does not always require PNS for contraction)
– Visceral smooth muscle – Fibers become excited and contract as single unit – gap junctions/desmosomes interconnecting - “functional syncytium” – Slow/energy-efficient contractions - distensible, hollow organs |
|
Opposition to blood flow in
arterioles |
– Resistance (R) directly
proportional to: • vessel length (L), • blood viscosity(η), • inversely proportional of radius (to the 4th power) R =Lη/r4 – L and η constant, so R = 1/r4 |
|
Vessel diameter controls
are local and systemic |
– Enables tissues to control
their own blood flow – Local controlling mechanisms include intrinsic and extrinsic |
|
Intrinsic responses
|
1. myogenic responses
2. paracrine vasoconsrictors 3. paracrine vasodilators |
|
Myogenic responses
|
stretch with increased pressure (mech gated Ca2+ channels)
|
|
Paracrine vasoconstrictors
|
• Serotonin – activated platelets
• Endothelin – by endothelium |
|
Paracrine vasodilators
|
NO – by endothelium
• Bradykinin/histamine/prostaglandins (inflamm) • Adenosine – hypoxic cells •decrease O2, -increase CO2, -increase K+, -increase H+, -increase temp |
|
Extrinsic responses
|
-vasoconstrictors
-vasodilators |
|
Vasocontrictors
|
• NE – sympathetic postganglionic
• Vasopressin (ADH) – post pituitary (CNS release with low BP) • NE – sympathetic postganglionic • Vasopressin (ADH) – post pituitary (CNS release with low BP) |
|
Vasodilators
|
-beta 2 Epi (adrenal medulla) • Ach – parasymp postganglionic • ANP (atrial natriuretic peptide) – atrial myocaridum /brain • VIPs (vasoactive intestinal peptides) – from neurons |
|
Vascular Control of Blood Flow (hyperemia)
|
Hyperemia is locally mediated increases in blood
flow (active or reactive) |
|
Vasoconstriction/dilation
depending on demands |
– Rest
• Vasodilation – Ach release (parasymp) at GI/splanchnic • Vasoconstriction (no NE release, locally mediated – Exercise • Vasodilation – dominated by metabolic factors at local active muscle (active hyperemia) • Vasoconstriction – NE mediated |
|
Medullary Cardiovascular
Control Center |
– Receives inputs from carotid and aortic baroreceptors
– Outflow to ANS • Symp- SA & AV nodes, myocardium, arterioles/veins • Parasymp- SA Node Neural signals to **cardiovascular control center in medulla |
|
Cardiovascular Physiology
|
• Change in flow, velocity, pressures
, resistance throughout CV system • Flow constant, decrease in velocity with increased crosssectional area • Pressure drop with blood movement/friction along vessel length |
|
Capillaries
|
• Thin-walled, small-radius, extensively branched
• Sites of exchange |
|
What allows for exchange
|
– Slow velocity – adequate exchange time
– Passive exchanges (diffusion and bulk flow) • Diffusion (area, permeability, concentration gradient, diffusiondistance) – Water-filled gaps (pores – aquaporins selective for H20) – Some capillaries are more “leaky”, less with pericytes – Lipid-soluble right through |
|
Passive exchanges (diffusion and bulk flow)
|
• Hydrostatic Pressure (P) and Osmotic (oncotic)
Pressure |
|
Driving forces into blood
|
– hydrostatic interstitial pressure (PIF)
– osmotic blood pressure |
|
Driving forces out of blood
|
– hydrostatic blood pressure (PC)
– osmotic interstitial pressure (IF) |
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Lymphatic System: function
|
– Return of excess filtered fluid and protein
– Defense – nodes with lymphocyte aggregates – Transport of absorbed fat |
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Structures
|
– Blind-ending capillaries (overlapping endothelial
cells) throughout IF – Lymphatic vessels - drainage – Drainage between |
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Veins: structures
|
– Capillaries to venules, to small/large veins
– Mostly collagen/little elastin (“valves” in larger veins) – Variable muscular tissues – Leaky in venules (inflammatory cells) |
|
functions
|
– Large radius = little resistance
– “reservoir” – capacitance vessels |
|
Factors which affect/enhance
venous return |
– Gravity
– Initial blood pressure, cardiac “suction” – Venous vasoconstriction – Skeletal/respiratory muscle activity (venous valves) |
|
Blood pressure monitored/ regulated
|
– Provides adequate driving pressure (brain/organs)
– Prevents extra work |
|
Primary determinants
|
– Cardiac output
– Total peripheral resistance MAP = CO x TPR |
|
Mean Arterial Pressure
|
• Constantly monitored by baroreceptors (pressure
sensors) within circulatory system • Short-term control adjustments (secs) – Adjustments made by alterations in cardiac output and total peripheral resistance – Mediated by ANS influences on heart/vasculature • Long-term control adjustments (minutes/days) – adjusting total blood volume – restoring normal salt and water balance via thirst, renal system (aldosterone/ADH) |
|
Additional factors influencing CV function
|
• Left atrial receptors and hypothalamic osmoreceptors - longterm regulation of BP via plasma volume (ANP)
• Chemoreceptors (carotid/aortic bodies) are sensitive to low O2 or high acid levels in blood –increase respiratory activity • Associated with certain behaviors and emotions mediated through cerebral-hypothalamic pathway • Exercise modifies cardiac responses • Hypothalamus controls skin arterioles for temperatureregulation |
|
Cardiovascular Disease: Epidemiology:
|
• Over 300 risk factors associated with coronary heart disease, hypertension and stroke
• Approx. 75% CVD attributed to conventional risk factors • Developing countries: 2X risks (undernutrition, infections+ CVD) Major modifiable |
|
BP Abnormalities - Hypertension
|
• Definition: > 140/90 mm Hg
• Primary - Catch-all for increased BP by variety of unknown causes (vs single disease entity) – Defects in renal Na regulation/excessive Na intake – Diets low in K+ and Ca2+ – Plasma membrane abnormalities (defective Na+-K+ pumps) – Gene variation for angiotensinogen – Abnormalities in NO, endothelin, or other local-acting chemicals – Excess vasopressin • Secondary hypertension (10% cases) – renal, endocrine, neurogenic |
|
Hypertension - complications
|
• Cardiac failure
• Atherosclerosis (stroke, heart attack) • Spontaneous hemorrhage/aneurysm • Renal failure • Retinal damage |
|
Cardiac failure:
|
• adaptive mechanisms to compensate for altered physiology
• deleterious structural changes with increased compensation • Increased O2 demands of heart vs decreased blood supply • Mismatch leads to ischemia (may lead to angina) |
|
Congestive heart failure
|
• heart cannot pump or fill adequately
• division of circulation that requires most work usually the most affected • where does blood back up? • what could we expect from such a back-up?? |
|
Cardiac failure: causes
|
• Hypertension
• Myocardial infarction • Additional causes: |
|
Hypertension –
|
– Adaptive response to increased stretch (filling) and increased NE release/effects
– Both have immediate and long-lasting (trophic) effects on cardiac function |
|
Myocardial infarction:
|
– Impaired cardiac muscle function – decrease “pump” capacity
– Damaged, non-regenerative muscle – scar formation leads to loss of tissue distensibility |
|
Additional causes:
|
– Altered blood flow regulation (regurgitation)
• Valve incompetence • Oxygenated blood flow to deoxygenated blood sources – Valve stenosis |
|
Pathophysiology: cardiac failure
|
• Septal defects
– Atrial (ASD) – Ventricular (VSD) – Patent ductus arteriosus • Valvular diseases – Mitral valve prolapse – Aortic stenosis |
|
form of arteriosclerosis (‘hardening’)
|
– intimal wall thickening
– collagen deposition, loss of elastic tissue (think tissue healing and scar formation) |
|
formation of atheroma
|
– 1st stage - sub-endothelial accumulation of cholesterol (aka fatty streak)
– 2nd stage - smooth muscle migration, division, enlargement – 3rd stage - plaque formation, calcification |
|
Virchow’s triad
|
• Abnormality of vessel wall
(endothelium) • Abnormality of blood flow • Alterations in blood contents |
|
Atherosclerosis (cont.)
|
primary cause of mortality, major cause of
morbidity |
|
formation of thrombus
|
– roughened surface, damaged endothelium,
stagnant blood – breaking off of thrombus?? |
|
will occlude blood flow downstream
|
– stroke, heart attack, arterial insufficiency
– if have one disease, obvious predisposition for other |
|
with arterial damage
|
weakening can lead to aneurysm
– out-pouching, held together by elastic lamina, adventitia – rupture – potential for massive blood loss – other causes?? Genetic? Environmental? |
|
Endothelial injury (heart and arteries)
|
• Direct injury
– Trauma to cardiac valves – Hypertension (arteries) – Cigarette smoking – Hypercholesterolemia – Radiation • Abnormal flow – Turbulence (heart and arteries) – Stasis (veins) |
|
Hypotension
|
Low blood pressure (BP < 100/60 mm Hg)
– There is too little blood to fill the vessels – Heart is too weak to drive the blood |
|
Orthostatic (postural) hypotension
|
– Transient (typically)
– insufficient compensatory responses to gravitational shifts |
|
Circulatory shock – when BP falls
|
– BP falls, inadequate flow to tissues
– Hypovolemic, cardiogenic, vasogenic, neurogenic |
|
Venous insufficiency
|
• loss of valve integrity
• external dilations/ contortions of superficial veins • varicosites |
|
varicosites
|
– chronic – genetic component, manifest in legs
– esophagus, anal plexus – secondary to portal hypertension – hemorrhoids – pregnancy, constipation |
|
Sustained venous hypertension
|
venous ulceration
10% population with valvular incompetence, 0.2% with ulceration |
|
Clinical features
|
• Pitting edema - preceded ulceration, greater later in day
• Hemosiderin pigmentation • Lipodermatosclerosis – indurate, fibrotic subcutaneous tissue • Atrophic, sweat gland/hair follicle loss |
|
Atherosclerosis of peripheral
vasculature |
arterial ulceration
– Other causes: diabetes, thromboangitis, vasculitis – Resultant tissue hypoxia and damage |
|
VENOUS insufficiency/ulceration
|
-Hemodeserin (brown discoloration)
-lipodermatosclerosis |
|
Arterial insufficiency/ulceration
|
-Punch-out ulceration
-Champagne bottle deformity (can occur in either) |
|
Systemic and localized edema
|
Regulation of fluid via oncotic vs. hydrostatic
pressures |
|
Hydrostatic
|
Hydrostatic
• Increased BP • Fluid accumulation/backup – “Pump” failure – Drainage failure |
|
Oncotic
|
• altered plasma proteins
• albumin production |
|
Diuretics
|
increase Na excretion (thiazides)
|
|
Sympatholytic drugs
|
– blockers – vasodilation
– blockers – decrease HR and contractility |
|
Vasodilator drugs
|
(hydralazine, minoxidil)
|
|
Calcium antagonist drugs
|
– Verapamil and diltiazem act on heart and vessels to lower BP
– Nifedipine - lower BP only by vasodilation – also used to treat angina pectoris and cardiac arrhythmias |
|
ACE inhibitors
|
– inhibit formation of angiotensin II – less vasoconstriction
– decrease aldosterone release - decreased Na, H20 retention |
|
Nitrites and nitrates
|
amyl nitrate, nitroglycerin
– NO - potent vasodilator of all blood vessels – Raipdly decreases cardiac work, oxygen consumption – Decrease BP may cause reflex tachycardia, dizziness, hypotention |
|
Beta blockers
|
– decreases cardiac work, oxygen demands
– used prophylactically to prevent angina, – Blunted HR responses to exercsie |
|
Ca channel blockers
|
act on myocardium or vessels
|
|
CHF
|
• Digoxin and digitoxin
– Main effect: increase myocardial contractile force • inhibit Na/K ATP pump, more Na inside myocardial cells • Increased intracellular Na stimulates Na/Ca exchange, • more Ca entry increases contractility – Cardiac glycosides also decrease heart rate and atrioventricular conduction (vagal stimulation) • Also utilize diuretics, vasodilators to decrease work of heart |