Cardiopulm Patho

Front 1

what are 8 things you do with a strip

Back 1

1. lable waves
2. p wave normal (upright, alike)
3. PR interval (3-5)
4. P: QRS
5. regularity (R-R distance)
6. QRS wave (<3)
7. symptoms
8. t-wave
9. st segment
10. rate
11. PVC

Front 2

What are the determinants of cardiac blood flow in healthy subjects? (3 factors)

Back 2

1. Mechanical factors (driving pressure or DBP, extravascular pressure, diastolic filling time)

2. metabolic factors (hypoxia)

3. neural influences (SNS, PNS)

Front 3

***What are the effects of atherosclerosis?***

Back 3

Decreased Driving pressure beyond lesion --> ischemia
Ischemic myocardium doesnt relax fully, leading to:
1. increased systole, decreased diastole
2. decreased left ventricle compliance
3. increased Left ventricle EDP
--> causes a further decrease in drving pressure --> increased ischemia

Front 4

ischemia causes the heart muscle to _______________ and typically leads to _______. thus increasing/decreasing _______ and _______

Back 4

work less efficiently
arrhythmias
decreasing
cardiac output and ejection fraction

Front 5

Effect of HTN on the failing heart

Back 5

Stresses the heart further by
Increasing afterload

If chronic HTN --> LV hypertrophy --> increasing demand OR need for oxygen

Front 6

Explain this diagram

Back 6

aaff

Front 7

List the four mechanisms of coronary artery obstruction

Back 7

1. complete obstruction by lesion
2. obstruction + thrombus = Total occlusion
3. obstruction + coronary aa spasm = pritzmetals angina
4. near total obstruction + high MVO2

Front 8

Obstruction + thrombus

Back 8

Occlusion of LAD, blood cant get downt to ant apex. necrosis. cells die and release chemical components into the blood stream. triggers and immune response. inflammation and wound healing. scar formation. cardiac cells die and they dont regenerate. filled with fibrous scar. takes 6-8 weeks to form.
after Heart attack dont want to give them a bunch of exercises because it increases pressure and work load on the heart.

Front 9

Complete obstruction by lesion

Back 9

arteries cut open. endothelial layer should be smooth. these are plaques that have formed. vessel shown had a complete obstruction

Front 10

***list the three types of clinical syndromes***

Back 10

1. stabile angina
2. unstable angina
3. myocardial infarction

Front 11

***Stable angina***

Back 11

typically occurs with activity, resolves with rest.

usually very predictable. at a set heart rate, set BP, know when its going to come on.

Front 12

***unstable angina***

Back 12

occurs at rest OR with activity below usual ischemic baseline ... Two types:
1.) angina at rest. more severe, more problematic. more dangerous if pt has pain at rest.
Unstable angina
2.) for a pt that has a hx of stable angina, now its coming on sooner, which means its worse. --- they know they have a hx of stable angina, make sure they have their perscription with them. know where it is. Technically they have to take the pill (under their tongue) by them selves. nitroglicerine is supposed to burn and if it doesnt it may be expired or deactivated. -> dialates the vessels, decreases pressure. they can take up to three doses (in 5 min intervals) and it still hasnt gotten better, call 911.

Defined as the presence of signs/symptoms of inadequate blood supply to the myocardium in the absence of demands that usually provoke this imblanace.

call 911 or initiate emergency procedures

Front 13

Myocardial infarction

Back 13

occurs with prolonged or unmanaged ischemia. different amounts of blockages to the coronary arteries. organization of a thrombus - body may try to reorganize but by the time it does the tissue distal to the thrombus is already dead.

true death of myocardial cells - once theyve had the infarct

occurs due to prolonged or unmanaged ischemia

Front 14

explain this diagram

Back 14

irritibility in area. dead tissue doesnt contract. not ejecting blood well --> drop in BP, not much is getting past the aortic valve -> poor coronary artery perfusion -> ischemia of the heart. mural (ventricular) thrombus = clot in one of the chambers of the heart --> embolism.

dead tissue (where is it located). if the papillary muscle dysfunction --> lose function of the mitral valve. if in the interventricular septum --> high enough pressure it could rupture = ventral septal defect (VSD) --> mixing of blood, typicall highly oxygenated blood in the. if located in the L circumflex --> L lateral wall became necrotic and died (trying to heal this area) --> this could rupture if there is enough of an increase in pressure --> blood leaking out of the heart into the pericardial sac --> cardiac tampanade --> heart suffocates itself because the fluid is pushing against it.

Front 15

Clinical courses

Back 15

sudden cardiac death - with one hour in the ER = #1 course

Chronic stable angina

unstable angina

Myocardial infarction yeilding cardiac mm dysfunction = death of some muscle, necrosis, part of the heart cant pump, and no longer has electricity running through it

Front 16

Sudden cardiac death

Back 16

in 20-25% of patients, sudden cardiac death (death within one hour) is the presenting symptom

cause of death is ventricular fibrillation, leading to cessation of cardiac output

bystander CPR and entry into the emergency medical system within 10 minutes provides the only hope for survival. - so impt that you know your CPR. in adults when they have this problem, the electrical wiring goes, really need a defibrillator

Front 17

***Angina pectoris***

Back 17

as a blood vessel becomes occluded by a plaque or mm spasm, supply is limited and unable to keep up with demand, often resulting in chest pain or a variety of associated sx referred to as anginal equivalents - i.e. as blood gets narrowed, supply and demand is off. start to see pain in some people. could also just be that you have low BP, not getting perfusion of the blood into all of the coronary arterries. patiet can be dehydrated

demand exceeds supply resulting in ischemia or death of the myocardium

also seen with HTN or blood loss

Front 18

***Location of typical anginal patterns***

Back 18

substernal chest is most common. and then down the L arm in the ulnar nerve distribution. pain in the jaw. or in between the shoulder blades

females tend to have more vague symptoms. heart attack - heart is failing to pump blood out. brain will turn on the SNS to try to get blood up to brain. Associated symptoms = naseua, vomitting, sweatting. females = feel sense of impending doom, really tired, really fatigued.

Front 19

***Levels of angina/ angina graded***

Back 19

higher the number = more severe = they have pain

Level I: initial perception of discomfort. reflects a minimum level of discomfort

Level II: initial discomfort has intensified over the same approximate body area, or presence of referred discomfort to another area

Level III: initial discomfort has become so severe that the pt stops whatever he/she is doing and seeks medicinal relief

Level IV: same severity of discomfort as that experienced during a heart attack

Front 20

***chronic stable angina***

Back 20

has a well established level of onset
can be reliably predected with a set level of myocardial demand
predictable level of physical or emotional stress
can be controlled with a reduction in intensity of activity or by taking nitroglycerin
location varies with individual
behavior or pain/discomfort: worse with activity, better with rest. not reproduced with palpation.

same diagram for pain. draw your pain. ask what brings on your pain - Aggs/eases. helps differentiate pain above the waist is highly suspicious. any time pt has pain above the waist you should screen the GI system and the cardio pulm system. check out their skin - shingles?.

worse with activity, better with rest, semi recumbant position.

Pt has and takes their nitroglycerine up to three doses. if the pain does not go away - 911

Front 21

***clinical cues for unstable angina***

Back 21

angina at rest
OR
occurrence of the pts typical angina at a significantly lower level of activity than usual

deterioration of a previously stable pattern i.e. angina occurring several times a day vs. several times a week.

evidence of loss of previously present myocardial reserve, such as a drop in BP or increase in HR with levels of activity previously well tolerated.

Front 22

***other sources of chest pain***

Back 22

MSK
pulmonary
integumentary
Chest pain of cardiac origin = medical emergency

Front 23

evolution of an myocardial infarction

Back 23

The process of infarction involves either a single event or a series of events through which the infarction progresses gradually

changes in the myocardial tissue begin within 15 mins. after the tissue becomes hypoxic

Front 24

site and extent of myocardial infarction depends on:

Back 24

1. anatomic distribution of aa
2. adequacy of collaterals (do they have adequate collaterals - if they worked out alot, they would have more collaterals formed. if they have a heart attack when theyre young the HA is more massive and more deadly. )
3. presence and extent of prior MI
4. amount of myocardial demand

Front 25

what are the stages of myocardial infarction

Back 25

stage 1: ischemic myocardium

stage 2: cells in the middle begin to die (dead tissue is non functional, and the surrounding cells supplied by collaterals are minimally functional

stage 3: the area of dead cells grows - some cells in the minimally functional area give in to prolonged mild ischemia. dead cells are eventually replaced by fibrous scar tissue, which further shrinks with time. Minimally functional area shrinks with better collateral function

Front 26

myocardial infarction and EKG

Back 26

on the EKG you will have inversion of the QRS upon the onset of ischemia.

with tissue injury, the ST segment changes.

also might see q wave become more prominent

Front 27

transmural myocardial infarction

Back 27

extends through the subendocardial tissue to the outer layer of the myocardium = full thickness.

Front 28

Subendocardial myocardial infarction

Back 28

subendocardial layers, weakness on inside but some part is still contracting

involves only the innermost layer of myocardium and sometimes portions of the middle layer - better prognosis than transmural MI

patients are more stable but if you progress their work load you could progress it towards a full thickness MI.

so make sure you dont over do the workload.

Front 29

***symptoms of myocardial infarction (8*)***

Back 29

Angina: central chest or substernal discomfort (may radiate to arm, scapula or jaw. May wax and wane, not relieved by NTG).

SOB
Diaphoresis - excessive sweating
Light headedness
nausea and vommiting
weakness
hypotension
tachycardia

20-25% are silent = no symptoms

Front 30

***What can a 12 lead EKG tell us***

Back 30

rate, rhtyhm, myocardial infarction. tell us area or vessel.

take home message, an EKG can tell you abou the location of an MI

Front 31

dominance

Back 31

occlusion of the R posterior coronary artery led to ischemia to the posteior wall of the L ventricle

Front 32

Looking at the ST segment

Back 32

ID the isoelectrical line between two consecutive PR intervals
find the J point = break point between the end of a QRS and the start of the ST segment.
from the QRS complex, move to the R 2 small boxes.
depression measured in mm - each small box is 1 mm
will tell you about myocardial ischemia

Front 33

ischemia on an EKG

injury on an EKG

infarction on EKG

Back 33

inversion of the T wave

elevated ST segment AND inverted T wave.

prominant Q wave, elevated ST segment, Inverted T wave

Front 34

subendocardial MI EKG

Transmural MI EKG

Back 34

new T wave inversion OR ST depression OR both that persist for >48 hours. NO changes in Q or R.

ST elevation associated with T wave inversion. Q wave. Increase or decrease in R wave

Front 35

Serum enzymes

Back 35

CK = creatine kinase = CPK
LDA = lactate dehydrogenase
Troponin
myoglobin

Front 36

"peak" times and CPK, LDH, torponin

Back 36

CPK = only present for 6 days after onset of chest pain. peaks at day 1
LDH: present for 14 days, peaks at day 4
Troponin: present for 14 days, peaks at day 2

all enzymes are above normal

Front 37

***Complications after myocardial infarction (8)***

Back 37

1. infarct extension (arrhythmias, bradycardia, SVT etc)
2. myocardial dysfunction
3. acute LV failure, hypotension, shock
4. mechanical rupture (rupture of papillary mms, VSD)
5. myocardial ruputre
6. LV aneurysm
7. pericarditis
8. mural thrombus

Front 38

ventricular aneurysm

Back 38

rupture
blood leaks into the pericardial space causing cardiac tamponade. trapped blood within the pericardial sacs restricts the hearts ability to pump.

Front 39

cardiogenic shock

Back 39

results from drastic decrease in CO.

ischemia mm is uncoordinated
systolic stretch - the dying mm bulges outward during systole due to increased pressure. this decreases pumping ability of the heart.

result - the heart is incapable of contracting with sufficient force to pump blood into the arterial tree, causing cardiac failure and death of peripheral tissues.

this almost always occurs when more than 40% of the LV is infarcted (MI). death occurs in 80%

RX: pressors, digoxin, IABP

Front 40

***pathophysiology of MI***

Back 40

healed infarcts (hypokinesis, akinesis, dyskinesis)

wall motion of a chamber:
Normal chamber: ventricle is larger in diastole, ventricle is smaller in systole.
HYPOKINESIS: space is smaller indicating under movement/under pumping. still having a contraction just not as strong

AKINESIS: part of the ventricle is not contracting

DYSKINESIS: dyscoordinated movment, part of the wall is splaying outward. Aka, paradoxical movement bc its movement in a different direction than what you would have expected

Front 41

CHF

Back 41

congestive heart failure - pump failure

since the heart is not able to continue pumpint the blood forward, it dams in the venous system of the lungs or systemic sirculation.

CHF can occur on either side of the heart or both.

Clinical presentation varies by the location

isolate problem or deficit and work circulation backwards to determine where the fluid will back up.

something wrong with aortic valve/mitral valve, start to back up towards the ___ . at first might hypertrophy, and then from there it will back up into the R atria. atria is very thin wall. at first will try to expand to except this new fluid. onver time it starts to back up into the vena cava. may see more fluid in the extremities, prominent jugular veins, fluid in the abodmen.

L sided problems back up into the pulmonary circulation = problems with breathing. can also cause the R side of the heart to fail. or a bunch of pulmonary diseases that raises the pulmonary pressure can also cause r sided heart failure

Front 42

Compensated heart failure

Back 42

if CHF - if the demand to move fluid through the system is in excess of what the heart can handle, there are compensatory mechanisms that exist to ease the demand on the heart:

1. SNS stimulation; increases CO to supply tissues - get faster HR and stronger contraction to better supply tissues.

2. sodium and water retention by the kidneys - decreased CO from failing hearth 'fools' kidneys into thinking there is not enough fluid volume, so the kidneys hang onto more fluid to increase plasma levels. kidneys thing the person is dehydrated so they start to hold onto fluid - fluid retention causes the heart to struggle even more

3. dilation of the cardiac mm to accommodate the increased volume. alters the length tension relationship; helpful at first but doesnt last very long

4. ventricluar hypertrophy

if compensatory measures work pt will be at risk only in situations of increased myocardial demand

Front 43

chronic heart failure

Back 43

with CHF; this develops gradually as the pt relies on compensatory mechanisms to assist the heart in keeping up with the demand.

with time, the chronic overuse of compensatory mechanisms may lead to end organ failure, as the organs (eg kidneys) fail due to chronic overuse. [usu see kidney dz and heart dz together]

the heart stretches over beyond optimum length, less cross bridges are formed and the contraction weakens. the heart is more bulbous. already stretched at rest. decreased contraction bc decreased number of cross bridges.

Front 44

uncompensated heart failure

Back 44

this occurs when, despite systemic attempts at compensation to ease the demand on the heart, the heart cannot maintain adequate cardiac output.

eventually the heart becomes so stretched in its attempt to keep up with he demand that it cannot pump any blood, and the pt dies.

basicallly, when compensations fail, can keep up anymore --> death or a heart transplant

Front 45

***Pathophysiology of L heart failure***

Back 45

1. intrinsic (ASHD, cardiomyopathy)
2. excessive workload (HTN, valve dz, congenital defect)
3. arrhythmia (bc they decrease cardiac output)
4. alcohol, drug toxicity, irradiation

occurs when the LV is u/a to overcome the pressures in the atrial system or stenosis of say the aortic or mitral valve.
--> blood/fluid backs up into the lungs, causing pulmonary edema.
the fluid doesnt get into the alveoli of the lungs, but causes swelling of the parenchymal tissues of the lungs, hence pulmonary edema

Front 46

pulmonary edema

Back 46

fluid leaks into the interstitial space. swelling of the lung tissue itself. shortness of breath.

occurs with L sided heart failure

Front 47

***Signs and symptoms of L sided CHF (14)***

Back 47

1. SOB
2. orthopnea (SOB when lying flat)
3. paroxysmal night dyspnea (sudden)
4. cough (non productive)
5. fatigue
6. rales (begins in lower lung fields and progress cranial
7. third heart sound
8. pleural effusion - fluid in the pleural space
9. increased RR/tachychardia
10. decreased urine output - kidneys hold onto fluid, but they are also given a diuretic drug to increase urine output.
11. pink, frothy, blood tinged sputum
12. LVH, EKG/cardiomegaly on CXR - EKG shows enlarged heart or on x ray
13. sudden weight gain (>3 lbs per day)
14. decreased exercise/activity tolerance.

Front 48

***Pathophysiology of R sided CHF***

Back 48

occurs when the R ventricle is u/a to produce enough force to overcome the pressures in the pulmonary system
--> the fluid from the R side of the heart backs up into the venous system

Front 49

***Signs and symptoms of r sided heart failure (12) ***

Back 49

1. abdominal pain
2. anorexia/nausea - not wanting to eat, feel too bloated, nausea may be due to SNS
3. bloating
4. fatigue
5. ankle swelling
5. distended jugular veins (JVD) - observed in 45º angle position, occurs when fluid backs up into venous system, increased pressure in the veins causes a visible pulse in the juguar veins
6. hepatomegaly/splenomegaly
7. ascites - fluid in abdominal cavity, shiny skin, hard/firm
8. elevated CVP, R atrial pressure
9. fourth heart sound
10. peripheral edema - pitting edema
11. decreased urine output
12. decreased exercise tolerance

Front 50

B type natriuretic peptide (BNP)

Back 50

released from cardiac ventricles in response to increase wall tension.
cut off point of 100pg/ml
rule out CHF with value of <100
used to differentiate cause of dyspnea
as BNP increases the likelihood and severity of CHF increases

Front 51

Ascites

Back 51

free fluid in the abdominal cavity. when too much fluid is backed up into the venous system, sometimes the body will dump fluid into the body cavities (also happens in the pleural cavities)

Front 52

Other possible causes of CHF (besides MI) (13)

Back 52

1. HTN
2. CAD
3. arrythmias
4. renal insuffiency
5. pericardial effusion
6. myocarditis
7. pulmonary embolism
8. valvular heart dz
9. pulmonary HTN
10. age
11. congenital
12. SCI
13. fluid overload

Front 53

causes of rhythm/conduction disturbances

Back 53

ischemia/cad
myocardial injury
metabolic/electrolyte imbalances
drugs

Front 54

diagnosis of rhythm/conduction disturbances

Back 54

ekg

Front 55

signs of rhythm/conduction disturbances

Back 55

1. perception of irregular beats varies widely
2. chest discomfort, lightheaded, weakness, fatigue, hypotension, syncope, dyspnea
3. sudden death

Front 56

cardiomyopathy (dilated, hypertorphic, restrictive)

Back 56

dilated: stretched ventricle results in marked systolic dysfunction. example: R atrial dilation possibly due to tricuspid regurgitation

hypertrophic: thickened ventricular myocardium takes up room inside ventricular cavity resulting in decreased filling during diastole. hypertrophy of the heart with exercise

restrictive: endocardial scarring of ventricles results in both decreased filling in diastole and decreased force during systole. scar tissue does not stretch during diastole or contract during systole

Front 57

pulmonary embolus

Back 57

when a clot travels from the body into the R heart and then to the pulmonary artery or branch, it cuts off blood flow to a portion of the lung. Size of infarct depends on size and location of the clot. the more proximal the more severe. Worse off increased afterload to R heart and decreased blood flow to the L heart.

Front 58

SCI and CHF

Back 58

CHF can occur in acute stages of SCI (esp higher SCI) because of unopposed parasympathetic nervous system outflow, as sympathetic nervous system input to the heart is interrupted by transection of the cord.

Front 59

Atrial /ventricular septal defect

Back 59

a hole in the septum between either the atrias or the ventricles results in flow of blood back and forth and a mixing of oxygenated and deoxygenated blood

Front 60

patent ductus arteriosus

Back 60

the shunt normal in fetal circulation, should could upon birth. failed closure results in blood flowing back into the R side of the heart.

Front 61

coarctaation of the arota

Back 61

congenital defect where narrowing results in high BP before the coarctation and low BP after.

often UE/upper body and LE/lower body have the differing BP. presentation: HTN, cold legs/feet, CHF

Front 62

Tetralogy of fallot

Back 62

BAD combo of defects causes increased right afterload, mixing of oxygenated and venous blood

Front 63

aging results (5)

Back 63

increased stiffness/fibrosis
decreased lean body mass
decrease response to SNS
increased time for repolarization of cardiac mm
heart is less efficient

Front 64

cardiovascular changes of CHF

Back 64

decreased pumping ability of heart yields systemic vascular constriction to attempt to increase cardiac output and stroke volume

Front 65

pulmonary changes of CHF

Back 65

pulm. edema leads to decreased gas exchange

Front 66

neurochemical changes of CHF

Back 66

reflex SNS stimulation eventually leads to desensitization to SNS neurotransmitters

Front 67

renal changes of CHF

Back 67

retains water to improve perfusion of the kidney which further increases workload for the failing heart

Front 68

hepatic changes of CHF

Back 68

potential cirrhosis from decreased perfusion of venous congestion

Front 69

Hematologic changes of CHF

Back 69

polycytemia and hemostatic abnormalitites from decreased O2 transport

Front 70

pancreatic changes of CHF

Back 70

potential decreased insulin secretion and glucose tolerance

Front 71

nutritional changes of CHF

Back 71

ascites causes anorexia and therefore decreases nutrition

Front 72

msk changes of CHF

Back 72

skeletal mm wasting and osteoporosis

Front 73

valvular stenosis

Back 73

due to the restricted valve opening, creates a pressure and volume load on the chamber preceding the abnormal valve. the chamber then develops compensatory hypertrophy.

leaflets get stuck together, narrow opening. not much blood can be pumped past this valve. creates increased afterload, increased workload, and hypertrophy of the preceding chamber

Front 74

valvular regurgitation

Back 74

chamber retrograde (behind) initially dilates, followed by hypertrophy because of increased volume

Front 75

valvular prolapse

Back 75

valve leaflet billows backward

ruptured chordae tendinae. a MI can also result in rupture of papillary mm. both can lead to prolapse. A blood clot can form as a result of the prolapse

Front 76

rheumatic disease

Back 76

age 5-15. after an untreated strep infection

MV 70%
AV 30%
TV and PV <5%

mitral valve disease, regurgitation complication = enlarged L atrium

Front 77

4 steps that lead to atherosclerotic heart disease

Back 77

1. injury (endothelial hypertenion, genenitcs, congenitial, virus
2. platelet aggrigation
3. LDL proliferation/ smooth muscle
4. calcium\

Front 78

types of valvular heart problems

Back 78

aortic stenosis
aortic regurgitation (acute and chronic)
mitral stenosis - increases P in LA, thin atrial walls.
mitral regurgitation (acute and chronic)
mitral valve prolapse - thin atrial wall can handle

Front 79

explain why some people get HA but dont have high BP

Back 79

o there could be inflammation. heart dz, inflammation, cancer... inflammation followed by wound healing. cells releasing inflammatory markers are cytokines. certain cells release different inflammatory markers. adipokines release and therefore people with alot of fat have chronic inflammation. then you release off inflammatory markers. how can you stimulate the turn off markers.. exercise. released from myokines. will see a dip in off myokines if you cease to exercise for two weeks.

Front 80

signs and symptoms of valve problems

Back 80

1. heart murmur - valve isnt closing smoothly, wooshing sound
2. thrill - palpable evidence of change in blood flow - fluid shloshes around bc it cant pass smoothly, palpable vibration
3. B rhales on auscultation - gurggling over lung fields
4. weight gain/peripheral edema
5. JVD
6. ascites
7. orthopnea
8. decrease activity tolerance
9. palpitations
10. dry hacking non productive cough
11. paroxysmal night dyspnea PND - sudden SOB awakening patient
12. SOB
13. lightheadedness - if AV or decrease CO - blood cant be pushed forward
14. angina - most often if MV involvement

Front 81

differential dx

Back 81

signs and symptoms of valve problems looks just like CHF. in fact, CHF is the most common complication of valve dysfunction. Either R, L or BL CHF will arise depending on which valve is problematic

Front 82

valve dysfunction treatment options

Back 82

valve replacement
valvuloplasty
valvulotmy
commissurotomy

Front 83

valve replacement

Back 83

2 types, mechanical or animal/tissue valve.
if it is a mechanical valve the pt will be on blood thinners for life (because its foreign). if it is a tissue valve they will start on blood thinners but not chronically.

tissue valve usually lasts longer than the mechanical valve

valves that arent functioning properly are removed and surgically replaced

Front 84

valvuloplasty

Back 84

balloon tip catheter is inflated to open the leaflet and relieve incompetence or stenosis

similar to angioplasty

more for people who wont tolerate surgery.

opens it up but doesnt close completely so you get regurgitation

to open a stenotic valve, may cause a leaky valve.

helps to un stick the valve. they dont leave it in. ideal thing is to replace the valve. ideally they would do a tissue valve. they leave this in for 15 seconds. acts to stretch the valve out to maybe stretch out the valve's adhesions.

if you dont change your lifestyle or diet you will reocclude.

Front 85

valvulotmy

Back 85

surgical incision through stenosed leaflet to relieve obstruction

clean up the valve. sometimes there are adhesions along the sides of the valve causing opening and closing to be more difficult, stenosis. they go in and cut the adhesions to make it open and close more easily.

Front 86

commissurotomy

Back 86

surgical incision to separte adhered leaflet

similar to a valvulotomy, different based on the extent to which they had to cut.

Front 87

complications to a valve replacement

Back 87

1. thrombosis (pt on blood thinners, does not prevent clots 100% and subsequent embolization)
2. infection (on or around, sometimes septic embolization)
3. structural failure (leaflets become stiff and calcify)
4. dehiscence (separation of the prosthetic valve suture from the heart, leads to paravalvular leakage)
5. disproportion (prosthetic valve not fitting well, blood flow is not optimal)

Front 88

infective endocarditis

Back 88

complication after valve replacement

some infection made its way to your heart and then it grows. can break free and cause clots down stream. go to your weakest link. so i fyou have a weak valve, they tend to grow on the valve.

infection ate right through the valve. can infect the cordae tendonae.

Front 89

pericarditis

Back 89

inflammation of the pericardium

can result in pericardial effusion and cardiac tampoade

fluid in the pleural space = pericardial effusion. if its blood in the space its called a cardiac tamponade

Front 90

serous pericarditis

Back 90

serous fluid in the pericardium

fibers throughout the pericardium - not going to be able to pump as well. can cause adhesions of the two layers. restrictive pericarditis. constricting the heart wont allow for good filling during diastole. if fiber gets thick enough, two layers can fuse.

Front 91

fibrinous pericarditis

Back 91

if serous pericarditis persists fibers can begin to develop and the two layers adhere to one another. this can cause a constrictive pericarditis which causes a diastolic dysfxn.

Front 92

constrictive pericarditis

Back 92

this can be treated surgically if recognized soon enough

constrictive percarditis - the pericardium fills with fibers and fuses/adhesions.

Front 93

prululent pericarditis

Back 93

pus in the pericardial sac

Front 94

hemopericardium

Back 94

this typically follows blunt chest trauma

coagulated blood in the pericardium

Front 95

Chest pain - differentiate, pain pattern, distributinon, aggs, eases.

stable angina.
unstable angina
pritzmetals = variant
pericarditis

will add -
lung diseases

medical screening -
GI (reflux disease) liver, diaphragm, referral patterns, integumentary system (shingles)

Back 95

?

Front 96

signs and symptoms of pericarditis

Back 96

1. chest pain (AGGs: anything that puts stretch on it. worse with SB or trunk rotation. worse with deep breaths, better with breath holding, EASES: better with kneeling on all fours, leaning forward, sitting upright)
2. difficulty swallowing - bc its an infection. typicall has a previous infection.
3. hx of fever, chills, malaise, previous heart dz

Front 97

treatment of pericarditis

Back 97

treat underlying cause (ie infection)
antiinflammatory drugs
pericardiocentesis as needed