Nursing 2005: Cardiovascular Disorders: (part 1) Disorders of Blood Flow and Oxygenation Flashcards
Systolic phase (S1)
- one contraction
- ventricle contraction
- mitral and tricuspid valves close
Stroke volume
.- amount of blood pumped out during systole
- 70 cc average
Ejection fraction
- ejects 66% of blood
- Estimated by echocardiography
- stroke vol/end- diastolic vol
Diastole (S2)
- ventricles fill = relax
- aortic and pulmonary valves close
- end of diastole
- atrial contract
- most supply goes to the heart because its relaxed
Frank-Starling Law
- length tension of preload to myocardial contractility
- contraction of heart increases if muscle fibers are stretched
- increase contractility if ventricles fill
- generated by vol
- over stretched = fatigue of muscles overtime
- inc contractility if inc in ventricle filling
Laplace law
- dilation = ?
- amount of tension in the wall that the ventricle produces depends on its size
- dilation = decreases ability to eject blood and to contract
Cardiac output
- amount of blood pumped out of the heart in 1 minute
- CO = HR x Stroke volume
- normal heart rate 70-80 beats/min
- 5-6 liters/min
What are the factors affecting cardiac output?
- Preload
- After load
- Heart rate
- Contractility
- Preload
- determined by
- inc preload
- pressure generated in left ventricle at the end of diastole = end diastole pressure
- more blood in ventricles = higher the preload
- increase preload =
- increase force of contraction = increase cardiac output
- inc force of contraction = inc cardiac output
- High preload is good for a healthy heart, but not for people with heart disease d/t weak heart
- determined by:
- amount of venous return entering ventricle after diastole
- blood left in ventricle after systole
- Afterload
- inc
- dec
- resistance that the left ventricle has to pump blood to eject it
- after contraction
- decrease after load = heart pumps easily
- inc in after load= harder for heart to pump because it has to work harder
- Heart rate
- autonomic nervous sys
- average 70 beats/min
- slight increase in HR = increase cardiac output
- as HR increases = stroke vol decreases –> decreases cardiac output
- Contractility
- heart changes force of contraction
Inotropic agents
- affects force of contraction
+ = inc contractility
Ex: epinephrine
Anatropic agents
- = dec force of contraction
Ex: meds that the heart has to work hard , use of alcohol
Arteriole blood Pressure
- measure of pressure exerted by blood against arterial system
- SBP (systolic blood pressure) = ventricles contract
- DBP (diastolic blood pressure) = ventricles relax
How do you calculate blood pressure?
SBP/DBP
What is normal bp?
120/70
Pulse pressure
- difference between SBP and DBP
- normal 1/3 of SBP
Ex: what is the pulse pressure of 120/80
120/1/3= 40
- high = arteriosclerosis
- low = heart failure
Mean Arteriole Pressure (MAP)
Average pressure in arteries throughout cardiac cycle
- MAP = DBP + 1/3 Pulse Pressure
What are the main factors that influence BP?
- Cardiac output
- Systemic vascular resistance (SVR)
- force opposing the movement of blood in small arteries and arterioles
What are the mechanisms that regulate BP?
- Nervous system
- Baroreceptors
- hormones
- Renal system
- Endocrine system
- Nervous system
A. Baroreceptors
B. hormones
A. Baroreceptors
- stim NS
- specialized nerve ells in arch of aorta and arteries
- sensitive to pressure and stretching
- shut down sympathetic = enhance
- parasympathetic = dec BP
B. hormones
- stimulate NS
- dec in BP = parasympathetic = inc BP
- Renal system
- no Na excretion and ECF
- renin -> angiotensinogen -> angiotensin 1 -> angiotensin 2 -> aldosterone inc
- water and sodium tension is cause by aldosterone
- Endocrine
- ADH is released
- inc ECF vol -> inc BP
Hypertension
- Incidence
- d/t
- failure of a system = high BP
- sustained elevation of arterial BP
- SBP= > 140
- DBP = >90
- repeated readings when monitored = HTN
- inc afterload d/t pressure and constriction
- strains heart and blood vessels
- cardiovasc problems and organ failure
- no symptoms
- Incidence
- depends on ethnicity = blacks more susceptible
- men >60
- people with diabetes
What is the significance of HTN?
- heart works harder
- more strain on the heart and blood vessels
Primary HTN
- cause = unknown
- genetic of environmental factors
- 95% of cases
- ages 30-50
- diet:
- high in sodium
- low mag, low cal
- smoking
- stress
- alcohol
Secondary HTN
- caused by systemic disease process that inc systemic vascular resistance or cardiac output
ex: renal disease = d/t kidney failure, hormone problem, meds that inc bp
- can be treated and eliminated
Isolated Systolic HTN
- sustained in elevation SBP= >160 DBP= < 90 - diastolic pressure would be low or normal -seen in elderly d/t weakened vessels
What are the pathophysiology of HTN
- high pressure stim thickening and strengthening to handle stress
- smooth muscles grow larger = lumens narrow
- injury = imflam = inc permeability
- which substances can enter vessel walls
- causes more thickening, vasoconstriction, inc resistance
- changes lining of vessels to let calcium in d/t thickening
What are the long term clinical manifestations?
- heart
- failure d/t afterload
- CAD, angina, MI - brain
- aneurysm, stroke - kidneys
- renal faulure - retina
- lack of o2 = blind
- sclerosis
What are the types of treatment for HTN?
- lifestyle modification
- diet
- exercise
- weight reduction
- meds if treatments above don’t work
Aneurysm
- localized dialation or outpuching of vessel wall or chamber of heart
- caused by arteriosclerosis and HTN
- develop in diff parts of body
- weak blood vessles = dilation of vessel wal
- stretch of vessel d/t pressure in diff parts of the arter
What is the risk factor of aneurysm?
- busting due to high pressure
What are the common areas of aneurysm
- cerebral artery = hemorrhage in brain
What are the types of aneurysms?
- True
2. False
What are false aneurysms?
- not entire blood vessel, injury
- bleeding is contained
What what true aneurysm? What are the 2 types?
- all layers of artery have bulges
a. fusiform
- all around the artery that bulges out
b. saccular
- only one side is bulged
Aneurysms in the abdominal aorta
- 3/4 of aneurysms occur here
- no symptoms
- as it gets bigger = hard to breathe and swallow
- poor survival rate if detected late
Aneurysms in the cerebral
- stroke
- s/s:
- headaches
- vision problems
What can be used to treat aneurysms?
- meds to dec bp and vol to prevent bursting of vessels
- surgery if spotted early enough
- replace vessel with a graft to make a new blood vessel
Thrombus
- blood vessel attached to a vessel wall
- inc clotting in body d/t injury or trauma
- creates clots
Thrombus:
1. Arteries
- cause damage to lining of blood vessel = clot
- where it is loc it affects tissue
- causes askemia = dec blood flow
- Veins
- blood clot in legs or pelvic region = deep vein thrombosis
- pooling of blood = immobile people because lack of blood flow
- clots can break and travel through other parts of the body = bad
- Heart
- pooling of blood in heart d/t lack of pumping= clot because attached to valve
- clots can break and travel to other parts of the body
What are the treatments for thrombus?
- anticoagulants to prevent clots
- blood thinner
- prevent new ones from developing
ex: herparin, coumadin
Embolism
- obstruction of vessel by embolus = a clump of matter
- parts can break off and travel through circulation
- ex: air, fat, bacteria
When an emboli becomes lodged in a vessel what can happen?
- ischemia = dec blood supply
- infarction = death of tissue d/t obstruction
- life threatening:
- coronary = heart attack
- cerebral arteries = stroke
- lungs = pulmonary embolism
Atherosclerosis
- abnormal thickening and hardening of arteries
ex: in femoral and coronary arteries
What does it do to the artery walls?
- deposits of cholesterol, lipids, and fibrous tissue within wall of artery
Atherosclerosis Stages:
- fatty steak
- lipid filled smooth muscle cell
- worsens with age
- raised fibrous plaque
- d/t chronic injury that activates platelets
- release growth factor and thickening of artery wall
- fibrous plaque develops
- platelets accumulate= blood clot
- narrowing/occlusion
ex: high cholesterol, smoking, HTN
- Complicated lesion
- necrotic damage and fibrous tissue
- rigid, hard
- occlusion = slows blood flow
What are the clinical manifestations of atherosclerosis?
- ischemia (dec blood flow)- > infarction (tissue death)
- dec oxygen ->blood flow = ischemia
- inc bp = HTN
Coronary = MI Cerebral = stroke Systemic = HTN
What are the treatments for atherosclerosis?
- lifestyle changes
- diet exercise stop smoking
- all in order to increase ipids
Coronary Artery Disease (CAD)
- impairment of pumping heart
- main cause of death in US
What are the risk factors for CAD?
- Unmodifiable
- age
- over 65 years old - gender
- men are more susceptible - family history
- even healthy people can develop CAD
- Modifiable
- elevated serum lipid levels
- atherosclerosis, LDL (cholesterol) - HTN
- cigarette smoking.
- nicotine = vasoconstriction and inc bp - sedentary lifestyle
- exercise = higher HDL, lower LDL
- dec bp - obesity
- high LDL
Angina
- transient chest pain due to myocardial ischemia
- not enough blood flow to heart and oxgen
- short term= 3-5 min
Myocardial ischemia
- imbalance of need of o2 and the supply of oxygen = angina
Mayocardial ischemia:
A. decrease supply
- dec in BP
- dec in blood volume
- inc in HR
- shorter time diastole - inc in coronary vasc resist
B. Increase need
- inc in BP
- inc in HR
- inc in ventricular volume
Dilation of vessels with heart disease
- its fully dilated and can’t dilate anymore because it is already over stretched
What is the most common cause for mayocardial ischemia?
- exercise because the lack of oxygen and needing more of with with not enough supply
Types of Angina
- Stable
- most common
- chest pain intermittent
- same pattern of onset, duration and intensity.
- Pain relieved with med or rest
- Can be controlled
- Unstable
- progressive inc in frequency, duration and intensity of symptoms.
- Unpredictable, advanced ischemia.
- associated w/ inc stenosis of vessels.
- Can occur from exercise and rest
- causes a heart attack = myocardial infarction
- Prinzmetal
- cyclic short bursts of pain at rest
- Unpredictable, spasms of coronary arteries
- not blockage, it’s a spasm
- assoc w/ REM sleep d/t electrolyte issue
What are the clinical manifestations of myocardial ischemia?
- chest, leg, arm pain
- similar to MInfartion attack
- causes anxiety
- constrictive, squeezing, heavy, choking sensation
- severe indigestion or burning
How to diagnose MIschemia?
- EKG (Electrocardiogram)
- measure electrolyte production of heart
- angina shows depressed ST segment - exercise stress test
- on a bike or treadmill to diagnosing to see ST segment - nuclear imaging studies (thallium)
- injected with radio active isotope to scan heart - coronary angiogram: (x)
- femoral artery scan
- ingest a dye and scan to see
What kind of treatments are used for MIschemia?
- Meds = nitroglycerin
- to reduce myocardial oxygen requirements
- decreases BP = decrease HR
Myocardial Infarction
- heart attack
- irreversible hypoxia and cell death because of prolonged ischemia
- destroyed d/t lack of blood flow
- ischemia can happen for 20 min in heart, if longer causes cell injury
What is the patho for MInfarction?
- cell injury
a. anaerobic
b. electrolytes
c. catecholamine release
- lack of oxygen
A. anaerobic metabolism:
- lack of o2 to heart
- not produce enough energy for heart
- lactic acid builds and affects heart
B. electrolytes
- potassium controls contractility and it is effected
C. catecholamine release
- epinephrine and norepinephrine and causes imbalance
- irregular heart rate
- Cell death
- irreversible hypoxia, enzymes
- releases enzymes into circulation when it dies
- can be measured
- Structural and func changes
- depends on area and size
- Repair
- cell death = inflammatory response = scar tissue
- scar tissues doesn’t let the heart pump as efficiently
What are the clinical manifestations of MInfarction?
- pain - severe and not relieved w/ nitroglycerin
- last for more than 20 min - Nausea, vomit (n/v)
- cool, pale clammy skin
- fever
- d/t inflam response - Cardiovascular (cv)
- weakness of heart, it’s output
- effect perfusion
What are the complications of MInfarction?
- dysrhythmias- abnormal heart rate
2. heart failure- dec output
What are the types of diagnostic tests for MInfarction?
- EKG
- inc ST waves - echocardiogram
- ultrasound - cardiac enzyme levels
- released enzymes can be measured - troponin
What are the types of treatments for MIfarction?
- EKG monitoring.
- O2
- aspirin
- prevent platelets for clumping - pain relief = morphine
- anticoagulants
- stop clotting - meds to decrease work of heart
- vasodilators to dec bp
