cardiovascular function Flashcards
1
Q
decreased cardiac output
A
less than normal amount of blood being pumped by the heart
2
Q
clinical manifestations for cardiac output
A
results from the inability to maintain sufficient blood flow
- fatigue
- oliguria
- cyanosis
- fluid accumulation
- decrease peripheral pulses
3
Q
inflammatory and infectious disorders
A
- pericarditis
- endocarditis
- myocarditis
4
Q
pericarditis
A
inflammation of pericardium
- acute: viral/trama/heart attack
- chronic: autoimmune disease
5
Q
pericarditis etiology
A
viral infections
trauma
Mi
autoimmune disorders
6
Q
pathophysiology of pericarditis
A
- inflammation –> perixardial effusion=above 75ml
- ventrical filling reduced
- decreased cardiac output
- cant relax as much= blood cant come in
7
Q
endocarditis
A
inflammation of endocardium
- infective of bacterial endocarditis
8
Q
etiology of endocarditis
A
staphyloccus aureus and streptoccus entercoccus
9
Q
patho of endocarditis
A
- invading organism attaches to endocardium/ valve
- platelets and fibrin deposits lead to what are known as vegetative lesions
- vegetation grows–> damages valve leaflets
- vegetation may become embolic- clot dislodges from place of origin in blood stream
10
Q
risk factors of endocarditis
A
- immunocompromised
- artificial heart valve
- congenital or valvular heart disease
- iv drug use
- gingival gum disease
11
Q
myocarditis
A
inflammation of myocardium
12
Q
myocarditis etiology
A
poorly understood
- viral, bacterial, protozoal or fungal organisms
13
Q
patho of myocarditis
A
- inflammation of muscle leads to muscle destruction
- potential necrosis
- atrophy- long time of working harder
14
Q
valvular disorders
A
- discruption of blood flow
- congenital or acquired
values affected - mitral - aortic - tricupsid - pulmonary (first 2 most commonly affected, left side is more muscular/ works harder)
types of alterations
- stenosis
- regurgitation
15
Q
stenosis
A
- narrowed, valve does not open completely
- forward blood flow hindered
- decreases cardiac output
16
Q
regurgitation
A
- valve does not close completely
- blood flow backs up
17
Q
cardiomyopathy
A
enlargement of the heart muscle
etiology: acquired or inherited
18
Q
patho of cardiomyopathy
A
- myocardium becomes weakened
- less effective pumping mechanism
3 types
- dilated: heart not pumping effectively
- hypertrophic: septum and nventricle enlarged
- restrictive: not enlargement but stiffness/ridgity
19
Q
heart failure
A
heart fails to pump enough blood to meet bodys oxygen/ nutrient needs
20
Q
heart failure etiology
A
- coronary artery disease
- cardiomyopathy
- hypertension
- heart valve disorders
- myocardial infarction
21
Q
heart failure patho
A
- inability to fill
- ineffective contractility
- each ventricle pumps an equal amount of blood
- if more than either ventricle can handle, the heart not effective pump
- left ventricle typically weakens first
- failure of one leads to failure of other
22
Q
left- sided heart failure
A
- afterload: force generated by left ventricle to eject blood to the aorta through aortic valve
- peripheral vascular resistance: pressure within aorta/arteries
- pvr influences afterload
- hypertension major cause
- blood backs up from left ventricle into lungs into pulmonary circulation= flooded capillaries
- avelora edema
23
Q
right- sided heart failure
A
- left-sided heart failure major cause must continually pump blood against increased fluid in the pulmonary artery and lungs
- cor pulmonale: right ventricle hypertrophies and fails due to increased pulmonary pressures
- a backward buildup of blood systematic blood vessels
- peripheral edema results
- backs into body= edema, jugular vein distension
- body can attain a liter of fluid before showing signs: weigh pt.
24
Q
compensatory mechanisms
A
- designed to maintain cardic output
- contribute to the cycle of heart failure
maintain cardiac output when low
- sympathetic nervous system raises heart rate: increases cardiac oxygen needs
- chambers enlarge (dilation)
- muscle mass increases (hypertrophy): increases cardiac oxygen needs
25
ineffective tissue perfusion
- deprivation of oxygen and nutriens at cellular level
- leads to cellular ischemia
clinical manifestations
- pain
- skin color
- necorsis
26
aneurysms
bulging, ballooning, dilation
locations
- adominal/ aortic
- cerebral
types:
- fusiform:both sides
- saccular: one side
- dissecting: tear in first linning- blood seeps out into 2nd and 3rd layer
27
dyslipidemia
hyperlipidemia: increase of lips in blood
normal roles of lipids:
- formation of cell membrane
- storage of energy
- production of steroids
- carrying of vitamins
- protecting nerves/organs
- insulation of body
28
lipoprotiens
- low density lipoproteins
bad cholesterol
- high-density lipoproteins
good cholesterol
29
hypercholesterolemia
increase cholesterol
- common in us
leads to:
- atherosclerosis
- pvd
- cad
- htn
- stroke
30
atherosclerosis
thickening/ hardening of arterial walls from plaque formation
- may begin in childhood
31
patho of atherosclerosis
- injury to artery--> inflammation--> accumulation of lipids, platelets and clotting factors
- scar tissue replaces normal endothelial lining
- plaque leads to narrowing (stenosis)
32
non-modifiable risk factors
- age: 50+
- gender: male
- ethnicity: African Americans
- genetics
33
modifiable risk factors
```
diabetes
hypertension
smoking
obesity
sedentary lifestyle
increased serum homocysteine
increased serum iron levels
infection
depression
hyperlipidemia
excessive alcohol intake
stress
```
34
peripheral vascular disease pvd
narrowing of peripheral vessels
- arterial: perfusing fingers and toes
- venous: veins blood pools= edema
results in decrease blood flow
35
coronary artery disease (CAD)
obstruction of blood flow through coronary arteries typically caused by atherosclerosis
can cause:
- angina
- myocardial infarction
- sudden death
36
CAD prevention
- non-modifiable risk factors: age and family
modify risk factors
- tabacco use
- obesity
- inactivity
- stress
- dm
- hld
- htn
37
myocardial infarction
death of heart muscle
types
- non-st segment elevation myocardial infarction (NSTEMI)
- st segment elevation myocardial infarction (STEMI)
etiology
- atherosclerosis: narrowing of coronary arteries
- thrombus: embolism
- vasospasm: constriction
38
patho of MI
- coronary artery blockage
| - decreased cardiac blood supply
39
signs and symptoms of mi
- crushing viselike pain arm, shoulder, neck, jaw, back
- shortness of breath
- restlessness
- dizziness, fainting
- nauesea
- sweating
40
atypical signs of MI
- abscne of classic pain
- dyspena
- fatigue
- anxiety
- impending doom
- chest cramps
- abdominal pain
- indigestion
- restlessness
- falling
41
prehospital MI
"time is muscle"
- asprin
- call 911 of 5 min of chest pain
- do not drive
42
hospital MI
Morphine
Oxygen
Nitroglycerin
Aspirin
43
hypertension
persistently high blood pressure
- systolic BP > 130 mmhg
- diastolic bp > 80 mmhg
- average of two or more readings on different dates: two weeks apart
44
etiology
unkown
two types:
- primary- essential hypertension which is a chronic elevation of bp from an unknown cause
```
- secondary
known cause
- acute stress
- excessive alcohol intake
- sickle cell disease
- renal disorders
- endocrine disorders
- neurologic
```
45
risk factors
non modifiable
- age
- gender
- ethnicity
- family history
modifiable
- alcohol
- cigarette smoking
- diabetes
- obesity
- stress
- elevated serum lipids
- excess dietary sodim
- decreased kidney function
46
signs/ symptoms of HTN
silent killer
rare:
- headache
- dizziness
- blurred vision
- angina
- fatigue
- dyspena
47
hypertensive urgency
- sever bp elevation without target organ dysfunction progression
- relatively asymptomatic
- oral medication
48
hypertensive emergency
- sbp> 180 mm hg systolic
- dbp > 120 mm hg systolic
- risk for progression for target organ dysfunction
- immediate gradual reduction of bp to protect target organs
