Cardiovascular Flashcards
relaxation & filling
diastole
contraction & ejection of blood
systole
sounds made by turbulent BF
murmur
palpable murmur
thrill
rhythmical throbbing of arteries as BF through
against bony prominence
pulse
difference in rate between apical & radial/peripheral pulses
pulse deficit
sound made by closure of atrioventricular valves (mitral, tricuspid)
S1
S1 occurs when?
end of diastole
beginning of systole
sound made by closure of semilunar valves (aortic, pulmonic)
S2
S2 occurs when?
end of systole
beginning of diastole
explain cardiac cycle including events, valve closure, sounds
SYSTOLE
- atria relax
- AV valves close (S1) — SL valves open
- ventricles contract
- blood moves out into pulmonic & aortic arteries
DIASTOLE
- ventricles relax
- SL valves close (S2) — AV valves open
- atria contract
- blood moves into ventricles
inflammation/pain from inside joint
arthralgia
particle moving through vessels
embolus
blood clot in vessel
thrombus
moving blood clot
thromboembolus
cardiac output =
stroke volume x HR
pathway of electrical conduction through heart (5)
Sinoatrial node (SA) → atrioventricular node (AV) → bundle of HIS → L & R bundle branch → Purkinje fibers
A normal event becomes audible
abnormal heart sounds
3 potential causes of a murmur
- Increased volume - ex pregnancy
- Abnormal valve
- Abnormal flow b/t structures
why can pregnancy cause a murmur?
blood volume ↑ 45% during pregnancy
“kentucky”
S3
Ventricular gallop
when does S3 occur
early diastole (after S2)
etiology of S3
impact of incoming blood against a distended ventricle wall
(extra compliant ventricular wall)
How to hear S3
apex
bell
S3 can be normal in…
it is always pathological in…
children; pregnant women; athletes
>35yo
“tennessee”
S4
atrial gallop
when does S3 occur
late diastole
before S1
etiology of S4
atria contract to force blood into stiff ventricle
how to hear S4
apex
bell
S4 is associated with…
left ventricular hypertrophy
when does split S2 occur?
during inspiration
split S2 normal in…
most young people
how to hear split S2
over SL valves (2nd ICS, sternal borders)
diaphragm
pt semirecumbent, quiet inspiration
when is split S2 pathological?
when it is heard as pt holds their breath
etiology of split S2 (5)
pulmonary HTN
ASD
conduction disorder
right side HF
vascular disorder
Valve leaflets become stiffer, narrowing valve opening
valves neither open nor close well
smaller amt of blood can pass through
valvular stenosis
etiology of valvular stenosis (4)
congenital
infection
overuse
Ca+ accumulation
congenital condition causing aortic valvular stenosis
bileaflet aortic valves
(normally there are 3 leaflets)
r/f for valvular stenosis
older age
renal disease
CV disease
hx infections
IV drug use (infection)
CHD
s/s of valvular stenosis (7)
fatigue
wt loss
lack of wt gain (children)
palpitations
chest pain
dizziness
murmur
a child is not gaining weight and has palpitations…
valvular stenosis
complications of valvular stenosis (7)
HF
CVA
emboli
dysrhythmia
bleeding
infection
death
BF back through closed/closing valves
regurgitation
etiology of regurgitation
congenital
infection
overuse
trauma
r/f for regurgitation
older age
infection
congenital
s/s of regurgitation (6)
fatigue; dyspnea; chest pain
edema
emboli
CVA
enlargement of walls of LV
left ventricular hypertrophy
LVH etiology
uncontrolled HTN
valvular disease
congenital
LV has to work harder
s/s of LVH
dyspnea; chest pain
S4
palpitations
dizziness
activity intolerance
LVH can lead to…
HF
Inability to pump enough blood to body
↓ cardiac output
heart failure
systolic HF vs diastolic HF
pump failing
filling problem - not enough blood
why does infarction increase the heart’s workload?
the rest of the heart has to “carry” the dead piece
why does HTN lead to hypertrophy of heart?
why does this lead to HF?
must work harder to overcome pressure in peripheral system
less space in the LV, lower stroke volume
HF r/f (5)
HTN
CAD
valvular dysfunction
MI
medications
A-stage HF
at risk — pt with HTN, CAD, DM, family hx
B-stage HF
ejection fraction
asymptomatic HF — pt with previous MI, LV systolic dysfunction, asymptomatic valvular disease
ejection fraction <55%
C-stage HF
symptomatic HF — pt with known structural heart defect, SOB, fatigue, activity intolerance, orthopnea, LVH, enlargement
D-stage HF
refractory end-stage HF — pt with marked sx at rest despite maximal medical therapy - hospitalized & cannot be discharged w/o specialized interventions
New York Heart Association stages of HF
- Class I — no physical activity limitation
- Class II — slight limitation of physical activity; comfortable at rest
- Class III — marked limitation of physical activity; normal activity causes sx; comfortable at rest
- Class IV — severe limitation & discomfort with physical activity; sx even at rest
most common form of HF
left side
left sided HF vs right sided HF
where does blood back up into?
left - pulmonary circulation
right - body circulation
left side HF etiology (4)
HTN
CM
CAD
MI
complications of left side HF (2)
right side HF
pulmonary edema
“cor pulmonale”
right side HF
right side HF etiology (2)
etiology of isolated right side HF
left side HF
CAD
isolated: pulmonary disease
complication of right side HF
ascites/3rd spacing
t/f most patients have sx of either left side or right side HF
false
most pts have sx of both
Impulses that coordinate heart do not work properly
dysrhythmias/arrhythmias
etiology of dysrhthmias (5)
disruption of normal conduction system
misfiring of action potential
damage to nodes
excitation of myocardial cells
genetic
r/f for dysrhythmias (7)
HTN; DM; obesity
CAD
high fat diet/high cholesterol
stimulant drug use
excessive alcohol
s/s of dysrhythmias (5)
palpitations
dizziness
weakness
loss of consciousness
pulse deficit
complications of dysrhythmias (2)
thrombi formation
CVA
atrium acts weird
atrial fibrillation
complications of a-fib
CVA - blood sloshing around in atria causes thrombus formation
Cessation of electrical activity of heart
cardiac arrest
s/s of cardiac arrest (3)
asystole
pulselessness
sudden loss of consciousness
tx for cardiac arrest
CPR
AED
Arteries supplying heart harden & narrow due to plaque buildup
coronary artery disease (CAD)
most common form of heart disease
CAD
etiology of CAD
atherosclerosis
blood components stick to plaque
why does smoking ↑ risk for all kinds of CV problems?
increases blood viscosity
plaque deposits in vessels
r/f for CAD (8)
older age; family hx; smoking; DM; HLD; HTN; obesity
male
population most affected by CAD
older males
s/s of CAD (4)
dyspnea
angina (especially with activity)
numbness in jaw/arm
other referred pain
complication of CAD
progression to MI
populations an S3 may be normal in
pregnant women
athletes
children
population a split S2 may be normal in
younger people
populations most affected by valvular stenosis
older
IV drug users
cardiac-related chest pain
angina
etiology of angina
ischemia to heart muscle
(not yet infarction)
3 types of angina
- Stable - predictable - with activity
- Unstable - unpredictable
- Variant - even less predictable
r/f for angina (9)
older age; family hx; DM; HTN; HLD; obesity; smoking
lack of cardio exercise
stress
locations for referred angina
jaw
arm
abdomen
complication of angina
MI
interventions & tx for if a patient is having/thinks they are having a heart attack (5)
try to calm their anxiety & slow their breathing
O2
chewable sublingual aspirin 325 mg
morphine for anxiety
PO nitroglycerine (massive vasodilator)
EKG indication of MI
labs indication of MI
ST elevation
T & I troponins elevated
muscle cells die due to hypoxia
myocardial infarction
etiology of MI
coronary artery blockage
if someone has MI, they probably have….
(same disease process)
peripheral artery disease
r/f for MI (8)
older age; family hx; HTN; HLD; obesity; smoking; DM
male
populations most affected by MI
older males
s/s of MI (7)
angina
jaw pain, arm pain
diaphoresis
dyspnea
pallor
anxiety
n/v
3 infectious/inflammatory disease process related to cardio
rheumatic heart disease
infective endocarditis
pericarditis
Valves permanently damaged by rheumatic fever
rheumatic heart disease
what cardio condition can strep throat lead to if untreated?
rheumatic heart disease
etiology of rheumatic heart disease
untreated strep throat
r/f for rheumatic heart disease (4)
incomplete antibiotic (stopping prematurely)
poverty
overcrowding
↓ access to medical care
s/s of rheumatic heart disease
fever; dyspnea
arthralgia
rash
nodules
uncontrolled arm/leg movement
weakness
SX
fever
dyspnea
arthralgia
rash
nodules
uncontrolled arm/leg movement
rheumatic heart disease
complications of rheumatic heart disease (3)
HF
bacterial endocarditis
damaged valves
Infection in heart lining, valve, or vessel of heart
infective endocarditis
populations most affected by infective endocarditis
immunocompromised
IV drug users
artificial valves
r/f for infective endocarditis (5)
IV drug use
artificial valves
damaged valve
congenital defect
hx endocarditis
s/s of infective endocarditis (10)
fever; dyspnea
new murmur
myalgia
angina
night sweats
wt loss
hematuria
Osler’s nodes (raised red lesions on hands or feet)
petechial rash
Osler’s nodes indicate…
infective endocarditis
when a person has a new murmur, always do a(n) _________ assessment
integumentary
how to dx infective endocarditis
echocardiogram
ultrasound
tx for infective endocarditis
long term antibiotics
sometimes surgery
complications of infective endocarditis (6)
endocardial vegetations in right valves leading to emboli
abscess
HF
valvular dysfunction
seizure
aneurysm w/i heart
Inflammation of pericardium
third-spacing of fluid into pericardium
pericarditis
etiologies of pericarditis
idiopathic
viral
chronic
r/f for pericarditis (4)
infection
recent MI
trauma
autoimmune disorders
EKG indicator of pericarditis
ST elevation through all 12 leads
s/s of pericarditis (7)
fever; cough
chest pain on inspiration
orthopnea
palpitations
edema
flu-like sx
complications of pericarditis (2)
constrictive pericarditis
cardiac tamponade
permanent thickening, scarring, contraction of pericardium
constrictive pericarditis
pressure on heart when blood/fluid accumulates in pericardium, impairing ability to pump
cardiac tamponade
Beck’s triad
indicates…?
indicates cardiac tamponade
low arterial BP
distended neck veins
distant muffled heart sounds
cellular & tissue hypoxia due to ↓ O2 delivery, ↑ O2 consumption, inadequate O2 utilization, or combo
shock
3 etiologies of shock (with regards to O2)
↓ O2 delivery
↑ O2 consumption
inadequate O2 utilization
6 types of shock
distributive/vasogenic
cardiogenic
hypovolemic
obstructive
septic
anaphylactic
vasodilation secondary to loss of sympathetic/vasomotor tone resulting in shock
caused by pain and fear, spinal cord injury, hypoglycemia
distributive/vasogenic shock
decreased pumping capability resulting in shock
caused by MI of LV, arrhythmia, PE, cardiac tamponade
cardiogenic shock
loss of blood/plasma resulting in shock
caused by hemorrhage, burns, dehydration, peritonitis, pancreatitis
hypovolemic shock
3 stages of shock
- Pre-shock - compensation for ↓ tissue perfusion
- Shock - compensation overwhelmed
- End-stage shock - irreversible multiorgan failure
s/s of pre-shock (3)
tachycardia
modest BP change
mild to moderate hyperlactatemia
s/s of shock (middle stage between pre- and end-stage)
tachycardia
dyspnea
restlessness
diaphoresis
metabolic acidosis
hypotension
oliguria
cool/clammy skin
how does shock affect pH balance?
metabolic acidosis
s/s of end stage shock (7)
anuria/acute renal failure
acidemia
severe hypotension
hyperlactatemia worsens
restlessness
coma
death
Swollen, twisted, visible veins
varicose veins
etiology of varicose veins (2)
↑ BP in vein
weakened/damaged valves in veins
r/f for varicose veins (6)
obesity; family hx; older age
female
pregnancy
standing or sitting for long periods
populations most affected by varicose veins & chronic venous insufficiency
older women
pregnant women
s/s of varicose veins (4)
large, raised, swollen, blue/purple vein
achy heavy feeling
itching
palpable twisted, swollen vein
Blood in legs not able to return to heart effectively
chronic venous insufficiency
etiology of chronic venous insufficiency
damaged venous valves
r/f of chronic venous insufficiency
older age; family hx; obesity
female
pregnancy
standing or sitting for long periods
tallness
hx DVT
intervention for chronic venous insufficiency
ambulate pt
s/s of chronic venous insufficiency (4)
bilateral edema in legs, feet
itchy
intermittent claudication
skin changes (shinyness, loss of hair, darkening color)
chronic venous insufficiency uni/bilateral?
bilateral
why can chronic venous insufficiency lead to ulceration?
inability to carry waste products away
inflammation of vein wall
thrombophlebitis
DVT uni/bilateral?
unilateral
Blood clot in deep vein - usually in legs
deep vein thrombosis
r/f for DVT (10)
obesity; smoking
injury to vein
surgery
immobility/decreased mvmt/prolonged disuse
pregnancy & postpartum period
oral contraceptives
clotting disorder
cancer
HF
populations most affected by DVT
postsurgical pts
truckers/others who sit constantly
pregnant women/postpartum
s/s of DVT (4)
pain
erythema
warmth
unilateral edema in leg
effect of DVT on pulses
none
complications of DVT
PE
postphlebitic syndrome
how to dx a DVT
ultrasound
tx for DVT
meds to prevent other DVTs and enlargment of current clot
do not dissolve current clot
Elevated force of blood against walls of vessels
hypertension
normal BP
<120/80
HTN range
130/>80
stage 2 HTN range
>140/90
most common form of HTN
essential HTN
__% of blood goes to kidneys
45
decreased blood flow to kidney causes continuous stimulation of RAAS system
causes HTN
renal artery stenosis
how does an adrenal tumor cause HTN?
stimulates sympathetic NS
r/f for HTN (11)
older age; obesity; smoking; family hx; DM
too much alcohol
sedentary
OSA
stress
excessive Na
deficient K
electrolyte r/f for HTN
high Na+
low K+
“silent killer”
HTN
s/s of HTN
usually none
dyspnea
h/a
complications of HTN (6)
MI
HF
CVA
kidney damage
aneurysm
dementia
screenings for HTN
recommended for everybody
adults should have BP taken at least 1x/year
Narrowed arteries (due to plaque) - ↓ BF to limbs
peripheral artery disease
etiology of PAD
atherosclerosis
r/f for PAD (7)
older age; smoking; DM; HTN; HLD; obesity; family hx
s/s of PAD (9)
intermittent claudication
coldness
numbness
paleness
sores on toes
no hair
thin shiny skin
weak/absent pulse
ED
leg pain aggravated by activity & relieved by rest, associated with vascular diseases
intermittent claudication
Vessels become thick, stiff, hardened
restrict BF to organs, tissues
atherosclerosis
etiology of atherosclerosis
excessive lipids in bloodstream (especially LDL)
inner layer of vessel becomes injured
plaque (fatty cholesterol substance) builds up at injury site & hardens
narrows vessel
impedes vessel’s ability to stretch
r/f for atherosclerosis (6)
HTN; HLD; DM; smoking; family hx
fatty diet
tx for atherosclerosis
statins
Part of vessel wall becomes weak and balloons out
aneurysm
r/f for aneurysm (6)
older age; family hx; HTN; smoking
men
trauma
populations most affected by aneurysms
older men
dissection
small hole in AAA → rupture
empties blood volume quickly into peritoneum
low survival rate
Anything lodged in vessels
causes ischemia & death of tissue
embolism
LEFT OR RIGHT SIDE HF
air hunger
left
LEFT OR RIGHT SIDE HF
pulmonary congestion
left
LEFT OR RIGHT SIDE HF
paroxysmal nocturnal dyspnea
left
LEFT OR RIGHT SIDE HF
orthopnea
left
LEFT OR RIGHT SIDE HF
tachycardia
left
LEFT OR RIGHT SIDE HF
exertional dyspnea
left
LEFT OR RIGHT SIDE HF
cyanosis
left
LEFT OR RIGHT SIDE HF
rales
left
LEFT OR RIGHT SIDE HF
raised peripheral venous pressure
right
LEFT OR RIGHT SIDE HF
hepatosplenomegaly
right
LEFT OR RIGHT SIDE HF
DJV
right
LEFT OR RIGHT SIDE HF
anorexia
right
LEFT OR RIGHT SIDE HF
dependent edema
right
LEFT OR RIGHT SIDE HF
weight gain
right
LEFT OR RIGHT SIDE HF
weight gain
right
ejection fraction
systolic vs diastolic HF
systolic - low EF
diastolic - normal EF
