Cardiovascular/CAD/PAD/Pulmonnary Flashcards
Flash cards for exam 3
Blood flows from the RA thru the __ valve
Tricuspid
Blood flows from the LA thru the __ valve
Mitral
Blood flows from the RV thru the __ valve
Pulmonary
Blood flows from the LV thru the __ valve
Aortic
Heart valves in order of flow:
Tricuspid
Pulmonary
Mitral
Aortic
Average stroke volume:
70mL/Beat
Cardiac output is determined by:
SV X BPM
Ability of the heart muscle to pump effectively!
Cantractility
Volume of blood in ventricles before contraction
Preload
Pulmonary vascular Resistance
RV afterload
Systemic vascular resistance
LV afterload
RV afterload can cause
right sided heart failure
LV after load can be too high due to:
HTN or atherosclerosis/arteriosclerosis
RV afterload can be caused by
atherosclerosis/arteriosclerosis of pulmonary vessels; stiff, noncompliant lung tissue
Normal preload value:
~4-6 L/min
Blood flow back to the heart
venous return
Most venous disorders occur in:
the legs
CVI
chronic venous insufficiency
DVT
deep vein thrombosis
CVI & DVT are usually related to problems pertaining to:
maintaining forward flow
AKA “valve incompetence”
Venous insufficiency
Pooling of blood due to venous insufficiency
venous congestion
Factors contributing to venous congestion
Gravity (standing for long periods)
Valve incompetence
Worn out, “floppy” valves in leg veins
Venous insufficiency
Blood pooling due to worn out, floppy leg vein valves
Venous stasis
Venous stasis causes an increase in:
hydrostatic pressure
Increased hydrostatic pressure can result in:
fluid shifting into the legs > edema
Mini concept map for Venous stasis ulcers
Venous stasis > increased hydro. pressure > fluid shift into tissue > edema > improperly functioning skin cells due to pressure > skin breaks easily > venous stasis ulcers
Another possible sequela to Venous insufficiency caused by increased hydrostatic pressure
Varicose veins
Contributing factors to CVI
Aging Genetics Obesity Pregnancy Job functions (standing) Immobility
Pathologic clot that forms in walls of veins, especially in veins of thighs & calves
deep vein thrombosis
Inflamed tissue around a DVT
thrombophlebitis
S/S of DVT
SHEP
Usually occurs unilaterally
May be extreme or discrete
May have no S/S
Risk factors of DVT are called:
Virchow’s Triad
Virchow’s triad consists of:
Injury to venous endothelium
Stasis of blood flow (due to immobility or venous insufficiency)
States of hyper-coagulability (dehydration, individual tendencies to clot easily)
Individual tendency to clot easily is called
coagulopathy
Potentially deadly sequela of DVT
Pulmonary embolism
Mini concept map of PE
DVT > thrombus or part breaks loose & travels > embolus > embolus travels to/thru the heart > embolism lodges into pulmonary arterioles
Oxygenated blood blocked from entering the pulmonary capillaries due to an embolism can cause:
SOB, chest pain
Hemoptysis as a S/S of PE is caused by:
inflammation of alveolar tissue causing leakage of blood/fluids into the alveolar space
S/S of PE include:
SOB, chest pain, shock, hemoptysis, death
Treatment/prevention of PE includes:
Encouraging mobility & hydration
Elevating feet & legs
Monitor skin for breakdown & stasis ulcers
Anticoagulants
Ability of arteries to work efficiently is determined by
vasomotor tone
State of the lumen
__ can be determined by vasomotor tone
BP
Normal, healthy arterial lumens should be
smooth and patent (free of any sort of blockage)
Delivery of O2 & nutrients to tissue beds via the arterial system
perfusion
Good perfusion results in:
adequate delivery of O2 & nutrients
Normal pulses & BP
Normal cap refill
Normal organ function
Strength & quality of pulses are indicative of:
state of the lumen & vasomotor tone
AKA “arterial disease”
arterial insufficiency
Common to all arterial disorders is:
ischemia
Arterial dz is almost always due to
athero/arteriosclerosis
Atherosclerosis=
stiffening of arteries & buildup of fat & other substances in arterial walls
Chronic dz of arterial system usually related to aging, where arterial walls become thick & hard
arteriosclerosis
Etiology of arteriosclerosis is caused by vessel damage from:
HTN smoking diabetes infection high cholesterol aging genetics free radicals
Mini concept map of arteriosclerosis
tunica intima microscopically damage > collagen fibers enter vessel wall > stiffening of vessel wall > decreased elasticity & arterial compliance
Atherosclerosis develops from:
atherous involvement of arteriosclerosis
“fatty deposits”
Athero
Atherosclerotic walls have deposits of:
collagen as well as LDLs
Fatty deposits in arterial walls cause:
irritation
inflammatory & coagulation responses
Formation of a fibrous capsule with a fatty middle section
Plaque
Formation of plaque is caused by:
stiff arteries, fat deposits, and inflammatory & clotting responses
Sequela of plaque growing & protruding into the lumen
Ischemia
Buildup of blockage in/along arterial walls results in:
loss of vasomotor tone and non-patent lumen
If arterial pathology exists in one area…
it is usually occurring system-wide
Narrowed, stiff, atheromatous arteries often result in:
compromised perfusion > ischemia
Characteristics of ischemic pain:
increased with exacerbation
decreases with rest
present in tissue distal to the plaque or narrowed arteries
S/S of ischemia seen in the periphery
diminished/absent pulses
delayed cap refill
pale, cool skin/mucous membranes
delayed healing
Specific S/S of ischemia in the heart
Altered function
decreased cardiac output
Specific S/S of ischemia in the brain
Altered LOC
Specific S/S of ischemia in the kidneys
Decreased urine output
Non-modifiable risk factors of arterial dz
Family HX (tendency to atherosclerosis &hypercholesterolemia) Advanced age > stiffer arteries
Modifiable risk factors for arterial dz
Diet, obesity, sedentary lifestyle
Alcohol consumption
DM2
Cigarettes/nicotine
Characteristic of DM2, increased circulating LDLs
lipodystrophy
Nicotine is a powerful ___
vasoconstrictor
Cardiovascular dz can be described as ___
atherosclerosis of coronary arteries
Venous insufficiency is often due to ___ and results in ___
bad valves in leg veins; venous congestion & peripheral edema
Arterial insufficiency is almost always due to ___ and results in ___
atherosclerosis; ischemia
PAD =
Peripheral artery disease
PAD is a dz of ___
any arterial vessels outside the heart, but most commonly refers to arterial problems of the legs
PAD usually manifests as __ due to __
problems of ischemia; narrowed peripheral arteries
S/S of PAD
Intermittent claudication Cool, pale feet Diminished pulses & delayed cap refill No hair growth on legs (shiny skin) Ischemic skin ulcers
5 Ps of PAD
Pain Pallor Paresthesias Pulselessness Poikilothermia
Poikilothermia =
cold, pale feet
Arterial thrombi form where __
flow is sluggish, and/or where there is narrowing/injury to vessel walls
Veinous thrombi block blood flow ___, causing ___
to the heart; congestion distal to the blockage
Arterial blockage results in ___
ischemia to distal tissue
If narrowing/injury/atherosclerosis occurs at an arterial bifurcation:
a thrombus might form
Emoboli of a bifurcation thrombus would travel to:
distal arteries &arterioles
Hypertension is ___
consistent elevation of systemic arterial BP over 140/90
2 categories of HTN
primary & secondary
Secondary HTN is caused by ___
altered hemodynamics associated with a dz process
Primary HTN, AKA ___, is caused by ___
Essential HTN; a complex set of factors
__% of hypertensives have primary HTN
92-95
Non-modifiable Risk factors of HTN
Family HX (inherited tendency) advanced agin
Modifiable risk factors of HTN
Diet, obesity, sedentary lifestyle
Heavy alcohol consumption
DM2
Cigarette smoking/nicotine intake
Certain conditions usually present in HTN to come degree:
Atherosclerosis
Overactivity of SNS & RAAS
Atherosclerosis contributes to HTN due to __
decreased elasticity of vessels
__ is consistently released by intracardiac nerve fibers, causing over stimulation of ___ to increase __ & __
Epinephrine
beta receptors
HR & contractility
Mini concept map of increased HR & contractility due to SNS overactivity
greater cardiac output & ejection pressure > pathologically larger volume of blood & pressure > sustained increase in BP
RAAS is usually a ___ triggered by ___
compensatory mechanism; drop in BP
For unknown reasons the RAAS sometimes becomes ___ causing ___
chronically activated; chronically high BP & blood volume
Vicious cycle of chronic HTN
arterial walls stimulated to strengthen via hypertrophy & hyperplasia > decreased lumen size > HTNn increases even more
Chronic HTN damages the __
tunica intima
S/S of HTN are often __
secondary to years of vascular damage
3 systems most often affected by HTN
Neuro
Renal
Cardiovascular
Neurological effects of HTN on the brain
Strokes due to ischemia from narrowed vessels
Effects of HTN on the eyes
ischemia & infarcts of parts of retina, vision changes
Effects of HTN on the renal system
High pressures & vessel damage can cause spilling of blood & protein into urine > eventually kidney failure
Effects of HTN on the cardiovascular system
increased workload ejecting blood against narrowed, stiff arteries;
Multiple problems including MI
Local dilation or out pouching of arterial vessel walls
Aneurysms
Pathology of aneurysms
Atherosclerosis & HTN cause weakness in arterial walls which can cause bulges in certain areas;
Minute injuries to intimal lining accumulate & allow blood to seep into muscle & tissue layers of arteries, which increase the size & chances of rupture
Areas of typical aneurysms
brain & aorta
The aorta is susceptible to aneurysms due to:
constant stress, especially from higher pressure of HTN
S/S of AAA
pulsatile, palpable mass inn abdomen; abdominal pain
S/S of thoracic aortic aneurysm
S/S usually resemble that of MI (chest pain, diminished pulses unilaterally)
Educational aspects of nursing implications for managing HTN
managing stress, smoking cessation, moderation of alcohol intake
Dietary aspects of managing HTN
low LDL intake; high intake of HDL & omega-3 fats
Desired daily intake of HDL:
40 mg/dL
Medicinal approaches for overactivity of SNS
beta & Ca channel blockers
Medicinal approaches for overactivity or RAAS
ACE inhibitors or angiotensin receptor blockers
Symbolizes ventricular repolarization on an EKG
T wave
Symbolizes ventricular depolarization on an EKG
QRS complex
Consistent, regular pattern or PQRST
sinus rhythm
Good CO is linked with ___
S/S of good perfusion
S/S of good perfusion
normal BP, pulses, cap refill, mentation, and skin color/ and warmth
SV is affected by:
contractility
preload
afterload
CO can improve or deteriorate based on:
changes in HR/rhythm; changes in SV
Definition: how well cardiomyocytes responds to electrical impulses
contractility
The effect of different factors on contractility
Inotropic
Some thing that enhances contractility
Positive inotropic effect
Something that decreases contractility
Negative inotropic effect
Amount or volume of blood in the ventricles before contraction
Preload
Any form of resistance to ejection of blood from any heart chamber
afterload
Normal after load exists when the receiving arteries have:
good vasomotor tone; smooth, patent lumens
Normal RV after load is called:
pulmonary vascular resistance
Normal LV after load is called:
systemic vascular resistance
HR >100BPM
tachycardia