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Patho Week 8 Key Points
Terms in this set (64)
volume of blood flowing through either the systemic or pulmonary circuit in liters per minute (3.5-8)
max percentage of increase in cardiac output that can be achieved above the normal resting level (300-400%)
- ability to make increase depends on preload, afterload, cardiac contractility, and heart rate
what is preload?
the work imposed on the heart before contraction occurs
- pressure generated in the ventricle at the end of diastole
- represents the amount of blood the heart will pump with each beat
how is preload determined?
by how much blood returns to the heart and how much the muscle fibers stretch
what is the Frank-starling mechanism (law)?
the heart can adjust its pumping ability to accommodate various levels of venous return
- increased muscle stretching (EDV) = increased contractility = higher stroke volume
what factors influence preload?
venous bl volume, body position (horizontal = inc venous return, muscular pumping action, venous tone, intrathoracic pressure, intrapericardial pressure
what is afterload?
resistance to ejection of blood, pressure the heart must work against to move blood into the aorta or pulmonary artery
what causes rt ventricular afterload?
pulmonary vascular resistance (pressure in pulmonary artery)
what cause left ventricular afterload?
systemic arterial BP (aortic systolic pressure)
what determines the force of contraction?
- changes in the stretching of the ventricular myocardium
- oxygen and carbon dioxide levels in coronary artery
- inotropic influence
effect of positive inotropic agents
sympathetic stimulation (E and NE) increase force of contraction which results in an increased HR
effect of negative inotropic agents
decreased force of contraction such as hypoxia and ischemia which interferes with the generation of ATP
chronotropic effects on HR
- cardiovascular centers in medulla (excitatory and inhibitory)
- neural reflexes (baroreceptor reflexes)
- atrial (bainbridge) receptors (distention results in inc HR)
- hormones and biochemicals (thyroid hormone, NE, etc)
properties of arteries
- elastic and muscular
- vasocontriction and vasodilation alters the lumen of the vessel and bl volume
properties of veins
- thin, large diameter
- skeletal muscle pump maintains venous return
what affects bl flow
pressure and resistance
- force exerted on a liquid per unit area
- high pressure in arteries
- low pressure in veins
- opposition to force
- diameter and length of the bl vessel contribute to resistance
resistance to blood flow is secondary to length of the tube, viscosity of the fluid, and the radius of the tube lumen
what is short term regulation of BP?
changes in BP over minutes to hours resulting from changes in exercise or body position
things that affect BP short term: neural stimulation
neural control of total peripheral resistance
- vagal stimulation (parasympathetic) - vasodilation and slow heart rate
- sympathetic stimulation- speeds heart, vasocontriction, inc contractility
things that affect BP short term: extrinsic factors
cold and pain inc blood pressure
things that affect BP short term: baroreceptors
pressure sensitive receptors located in the blood vessels (carotid sinus and aorta) and heart respond to changes in vessel stretch
- fall in BP = decrease in stretch = increase HR
things that affect BP short term: arterial chemoreceptors
reacts to changes in O2 (mainly), CO2, and H+ content
- inc O2 = inc BP
- inc CO2 = dec BP
things that affect BP short term: humoral mechanism
RAAS system responds to dec bl volume and pressure
- angiotensin II inc BP b vasoconstriction
- aldosterone retains water and Na
long term reg of BP
kidneys regulate the ECF volume
- inc fluid volume will inc BP
- dec fluid volume will dec BP
formula for BP
CO x PVR
what determines systolic BP?
- stroke volume
- velocity of ejection
- elastic properties of the aorta (dec in older adults)
what determines diastolic BP?
- closure of the aortic valve
what is needed to maintain diastolic BP?
- BP falls when resistance decreases
what causes varicose veins?
trauma or gradual venous distension due to incompetent valves (inc venous intraluminal and hydrostatic pressure)
- pools goes forward and backward, or pools in veins
S&S of varicose veins
engorged palpable superficial veins
aching in lower extremities
how to prevent VV
avoid standing for long times
weight loss if obese
treatment for VV
what is chronic venous insufficiency? what is the most common cause?
inadequate venous return over a long period due to varicose veins or valvular incompetence
- DVT is the most common cause
S&S of CVI
tissue congestion, edema, impairment of tissue nutrition
what can CVI lead to?
stasis dermatitis - skin pigmentation changes (thin, shiny, bluish brown)
development of stasis ulcers (usually on medial maleolus)
what is superficial venous thrombosis (thrombophlebitis)?
thrombus in a vein and the accompanying inflammation response in the vessel wall
what is DVT?
obstruction of venous flow in deep veins and increased venous pressure - can lead to incompetent valves
** people with DVT are at a high risk for a pulmonary embolism
what is Virchow's traid?
3 things that contribute to thrombosis...
- venous stasis (bedrest, immobilization)
- venous endothelial damage (trauma, surgery)
- hypercoagulable state- inc in clotting factors
clinical manifestations of DVT
- often asymptomatic
- pain, swelling, deep muscle tenderness, fever, high WBC and ESR, positive Homan's sign
how do you diagnose and treat DVT?
US, ascending venography, anticoagulant therapy
how can DVT be prevented?
- early ambulation after birth
- avoid poor body position
- support stockings
- exercise legs
- antiembolism stockings
- pneumatic compression devices, alternating pressure (SCD)
what is primary hypertension? what causes it?
- essential or idiopathic hypertension without an identifiable cause
- combined systolic and diastolic hypertension
- caused by genetic or environmental causes
- affects 90-95% of people with hypertension
manifestations of primary hypertension
- usually asymptomatic
- risk for cardiovascular disease (heart failure, stoke, CAD, PAD)
risk factors for primary HTN
- family history of HTN
- race (black)
lifestyle factors associated with primary HTN
- high sodium intake
- excessive calorie intake/obesity
- lack of physical activity?
- excessive alcohol consumption
- oral contraceptives
Dx of primary HTN
based on average of 2+ BP readings taken at each of 2+ visits after initial screening visit
Tx for primary HTN
- control the HTN
- modify lifestyle
meds for primary HTN (and what they do)
- beta blockers (decrease HR, CO, and renin release from kidneys)
- ACE inhibitors (reduces effect of angiotensin and aldosterone, intrarenal bl flow and GFR)
- Ca channel blockers (dec PVR)
what is pulmonary hypertension?
high bl pressure in the pulmonary arteries, MAP 5-10 mm Hg above normal
primary (idiopathic) pulmonary htn
rare, may be hereditary, poor prognosis (death within 5 years of Dx)
secondary pulmonary htn
associated with other chronic pulmonary or cardiac disease
causes of 2nd pulmonary htn
- elevated of pulmonary venous pressrure (mitral valve stenosis, left heart failure)
- increased pulmonary blood flow (left to right shunt)
- pulmonary vascular obstruction (PE, COPD)
- hypoxemia (vessel constriction due to high CO2 levels)
S&S of pulm htn
dyspnea and fatigue
Dx of pulm htn
precise measurements of pulm pressures obtained with heart catheter
- doppler or echo can help diagnosis
Tx for pulm htn
primary- lung transplant
secondary- treat underlying cause (O2, digoxin, diuretics, vasodilators, anticoagulants)
what is orthostatic htn and why does it happen?
sudden decrease in syst and diast bp upon standing due to lack of normal bl pressure compensation in response to gravitational changes in the circulation
manifestations of OH
blood pools in lower extremities = dec preload
dec bl flow to brain = dizziness, syncope
cause of OH
reduced bl volume from diuretics or V/D
drug induced (most common)
how to check for OH
take BP when pt is supine, immediately after they are upright in a seated position, and 2-3 min after standing up
Tx for OH
treat cause, alter position slowly, lean forward
what is an aneurysm?
local dilation or outpouching of a vessel wall or cardaic chamber secondary to weakening of the vessel wall
- can be caused by congenital defect, trauma, infections, atherosclerosis
manifestations of OH
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