Cardiac (Adult Health)

Front 1

SV

CO

Preload

Afterload

EF

Back 1

Hint 1

•Bicuspid & Tricuspid:atrioventricular valves that close at the beginning of ventricular contraction

•Pulmonic semilunar & Aortic semilunar: semilunar valves

• Epicardium: outermost layer of the heart.

• Myocardium: middle layer of the heart, the contracting muscle.

• Endocardium: innermost layer of the heart, lines the inner chambers & valves.

Front 2

Pulmonary circulation

Systemic circulation

Coronary circulation

Back 2

Pulmonary circulation: Deoxygenated blood is transported through the right side of the heart and into the lungs

Systemic circulation: The movement of oxygen rich blood from the heart to the rest of the body through the arteries, and back to the heart via the veins.Then back to the left side of the heart

Coronary circulation: Supplies oxygen rich blood to the myocardium (heart muscle) via the coronary arteries, deoxygenated blood is returned to right atrium via coronary veins

Front 3

cardiac enzymes

Back 3

ROMI panel:

reevaluated every 6-8 hours all three are tracked to evaluate the severity of MI basically to see if the heart is getting worse/better

Hint 3

▪︎troponin: 3-4 h after MI releaseremain detectable up to 10 days

▪︎myoglobin(benefit): 30 min after MI(early detection but it doesn't always mean MI)

▪︎CK-MB: 3-4 h after MIremain elevated 3-4 dayshelpful to detect reinfarction

▪︎ANP: response to the increase stretching of atrial wall due to increase atrial blood volume

▪︎BNP: gets released by heart & blood vessels as there's increased pressure within heart, BNP increases to open up blood vessels in body and take pressure off heart

Front 4

natriuretic peptide

Back 4

•︎ hormones secreted by cells of heart chambers due to damage to heart & they're used to determine if heart chambers is stretched out from highBP

• 2 types of natriuretic peptides:

▪︎BNP Brain Natriuretic Peptide: shows deterioration of ventricles

biggest indicator of HF

BNP over 100 pg/ml= Heart Failure

less than 100 is normal

increased BNP: high sodium diet, sedentary life style (no exercise), high cholesterol diet, renal failure

▪︎ANP Atrial Natriuretic Peptide : in atriums

ANP affects nephrones & creat opposit affect of aldosterone in response to increased Blood volume that stretches out & damages heart tissue because aldosterone hlods sodium & fluid in body (ANP blocks reabsorption of sodium in kidneys & increase filtration)

incresed ANP: acute HF, SVT, Hyperthyroidism, small cell lung cancer

decreased ANP: Chronic HF, Hypothyroidism

Hint 4

Front 5

ACS

Back 5

“acute coronary syndrome”

Angina - Stable “Safer”- relieved w/rest

Angina - Unstable “Unsafe” -Unrelieved

Front 6

Stable angina

Back 6

Stable angina is chest pain induced by any physical activity like: walking up stairs, working in the yard or even from sex.

Anything that causes exertion! (classic exertional Angina)

There is less oxygen being delivered to the heart muscles during the physical excretion resulting in pain that stops when the physical activity stops.

Front 7

unstable angina

Back 7

Pain at rest! This is a warning sign for an MI (heart attack). It is the more severe angina as it means more severe narrowing of the coronary arteries resulting in less oxygen to the heart muscles.

Front 8

Prinzmetal

Back 8

variant angina

Coronary vasospasm

Sudden spasm, temporary narrowing or tightening in a coronary artery.the heart doesn't get enough blood & oxygen - resulting in pain

Short-term factors that cause vasoconstriction:

- Stress

- Stimulants (caffeine, meth, cocaine)

- Smoking, cold weather

NOT from long-term narrowing of the arteries from plaque buildup, which is more typical in stable & unstable angina.

Front 9

angina pharmacology

Back 9

Front 10

stable angina nitroglycerin

Back 10

Hint 10

Front 11

unstable angina nitroglycerin

Back 11

Hint 11

Front 12

MI

Back 12

Myocardial Infarction (MI) the heart muscles DIE “necrosis” from lack of oxygen. This occurs when there is a blockage of the coronary arteries.

causes:

SODDA

S– Stress, Smoking, Stimulants (caffeine, amphetamines)

O–Obesity (BMI over 25)

D–Diabetes & HTN (over 140/90)

D–Diet (high cholesterol) animal fats

A–African American males & Age (over 50)

*Men more than women

Hint 12

heart cells dies & release troponin #1indicator of MI

Front 13

Ischemic heart disease progression

Back 13

CAM

C–CAD “coronary artery disease”

A–ACS “acute coronary syndrome”

Angina - Stable “Safer” relieved w/rest

Angina - Unstable“Unsafe”Unrelieved

M–MI (heart die)

Hint 13

Front 14

MI signs & symptoms

Back 14

PAIN: Jaw, left arm, mid back/shoulder pain, heartburn (epigastric), Substernal chest pain, Crushing or Radiating

Key words = priority:“Sudden” “Crushing” “radiating”"Heavy Pressure"

SOB “dyspnea” “labored breathing”

NAUSEA Vomiting “Abdominal pain”

SWEATING “Diaphoresis”

PALE COOL SKIN “dusky”

ANXIETY

Hint 14

silent MI: diabetic patients

Front 15

MI diagnostics

Back 15

NCLEX: ST Elevation & positive troponin over 0.5 indicates MI

any new chest pain always require an ECG first

ST ELEVATION = No O2 / hyperkalemia

ST DEPRESSION = Low O2

always confirm with troponin labs

when heart muscle cells die, they release troponin & K (hyperkalemia)

other labs CK, Ckmb, CRP

Front 16

MI Treatment

Back 16

(+) Positive Troponin = Heart Attack (MI) PRIORITY: REMOVE THE CLOT!

the goal is to unclog the coronary artery within 45mins

patients are taken to cath lab immediately to locate & fix the blockages

we can also use thrombolytics (clot busters) if surgery is not immediately available TPA / Streptokinase

they are not for first line therapy since they cause massive bleeding & should be given within 2-6 hours from initial MI

Front 17

MI treatment:

ABC of MI surgery

Back 17

Hint 17

(+) Positive Troponin = Heart Attack (MI) PRIORITY: REMOVE THE CLOT! within 45 minutes

Front 18

MI treatment

clot busters

Back 18

Hint 18

(+) Positive Troponin = Heart Attack (MI) PRIORITY: REMOVE THE CLOT!

Front 19

STRESS TEST

(-) Negative Troponin

Back 19

• Non MI (non priority)

• Spot the Narrowing

TREADMILL STRESS TEST

STOP test: chest pain & ST elevation

NUCLEAR PHARMACOLOGICAL STRESS TEST

24–48 hours BEFORE

NO Cigarettes, Caffeine (tea, soda, coffee) *NO DECAF

NO Meds: Nitro, Beta Blocker, Theophylline (stimulant)

NPO (nothing oral) 4 hrs before/after

Front 20

اقدامات اولیه

for any acute chest pain

Back 20

Hint 20

we don't know until we take an ECG & troponin

Front 21

MI treatment

Back 21

Hint 21

oxygen for perfusion

Aspirin prevent platelets from sticking together

Nitro dilate coronary arteries

Morphine relax the heart & decrease the work load

Front 22

Nitro

Back 22

in chronic angina patients if there's pain 5 minutes after the first dose of Nitro call 911

Hint 22

HA = Headache

Front 23

Morphine

Back 23

any pain after morphine indicates MI

more pain = more tissue death

Front 24

cath lab

Back 24

angioplasty means baloon or stent replacement & patients are usually awake & not under general anesthesia

before angioplasty NPO 6-12 hours

after angioplasty lie flat for several hours & encourage to drink to dilute contrast dye

bypass = open heart surgery

NO Heavy Lifting

NO baths or soaking the wound but shower is ok

Prevent infection, monitor for redness, warmth, swelling & drainage report to HCP immediately

Front 25

Back 25

Hint 25

Front 26

bleed risk patient education

Back 26

Front 27

complications after MI

Back 27

Hint 27

Front 28

MI patient education

Back 28

Hint 28

daily weight any rapid weight gain or new edema or dyspnea (orthopnea) call HCP because these are early signs of heart failure

high sodium food: chips,dressings,meets,catchup, cheese, anything that comes in a package

Front 29

MI TREATMENT

Back 29

Hint 29

Front 30

congestive hear failure

Back 30

Hint 30

• HF - Heart Failure (failure to pump blood forward)

• HF - Heavy Fluid (backs up in lungs / body)

Weight Gain = Water Gain

Rales that don't clear with a cough

JVD: jugular vein distention

Front 31

pulmonary edema priority interventions

Back 31

Front 32

4 common NCLEX Question for worsening HF

Back 32

1.how does the nurse know if the treatment is successful?

clearer lung sounds with decreased HR

2.always question:

any order that wants to give fluids even maintenance IV fluids

3.when you transferring a heart failure patient to another unit:

always reassess heart & lung sounds any patient transferring to another floor "worsening crackles in lungs"

4. sodium:

swells the body nothing from package like chips, package foods, salad dressing, sauce, meet, cheese nothing OTC cold/flu medicine, Tylenol (acetaminophen), antiacid

Hint 32

Front 33

HF & Kidneys

Back 33

due to impaired pumping ability we have less cardiac output as a result the kidneys get less blood flow & falsely think BP is low or blood volume is low

so mistakenly increases the already high blood volume by

1.stimulating SNS to increase the HR &

constrict the blood vessels

2. initiating the RAAS (Renin Angiotensin Aldosterone System) which retains fluids by locking kidneys & constricting the blood vessels

now we have 2 problems:

an already weak pump with increasingly high blood volume

Front 34

Aldosterone in RAAS

Renin Angiotensin Aldosterone System

Back 34

drugs that blocks/cut the communication line to aldosterone

-pril (ACE) Lisinopril

-sartan (ARBs) Losartan

-actone (Diuretic) Spironolactone

all these drugs increase potassium >5

Front 35

HF diagnostics test

Back 35

Hint 35

Front 36

HF nursing care & interventions

Back 36

Hint 36

Front 37

ACE & ARBS

Back 37

ARBs = Angiotensin Receptor Blockers

if the HR is low ACE & ARBs are the best choices because they act to lower BP only (not HR)

Both ACE & ARBs either inhibit or block the RAAS which retains fluid

Aldosterone:

A: Adds sodium & water in

L: Lets potassium out

side effect: retain potassium

in any potassium Imbalance always the first action by the nurse is cardiac monitoring

Hint 37

Front 38

Calcium Chanel Blocker

Back 38

Front 39

DIGOXIN

Back 39

Hint 39

which patient is most at risk for digoxin toxicity?

patients on potassium wasting diuretics -ide or kidney failure with creatinine>1.3

Low potassium increases the risk for toxicity (digoxin can NOT cause hypokalemia, so you do NOT need eat more green leafy veggies or melons like when we taking Thiazide or loop diuretics that waste potassium)

positive Inotropic = deep contraction

negative chronotropic = decrease HR

monitor elderly & Renal failure patients closely because of digoxin toxicity

Front 40

Back 40

Hint 40

commonly given for chest pain

but also works for HF patients to lower BP

lower pre & Afterload which lowers BP

Front 41

diuretic

Back 41

Hint 41

blocks reabsorption of sodium

Spironolactone like -pril & -sartan Spares potassium instead of blocking RAAS blocks aldosterone(salt water hormone) directly

in any potassium Imbalance always the first action by the nurse is cardiac monitoring

Diuretics

•morning NOT at night

•slow position changes (any BP med)

•daily weight (report 2-3 lbs)

•sunburn

•Low sodium diet (sodium swells)

avoid OTC Meds

C -Cough & Flu meds

A -Antiacids like tums

A -Acetaminophen

N -NSAIDs (Naproxen & ibuprofen)

Furosemide is #1 Drug for worsening HF but if given too fast .....

Front 42

cardiomyopathy

Back 42

All problems lead to LESS cardiac output meaning LESS O2-rich blood OUT to the body.

• Low oxygen

• Restlessness, agitation, altered LOC

• syncope, dizzy + fatigue

• Heart failure signs

• Left-sided = Lung fluid

• Right-sided = Rocks the body with fluid (edema, ascites, JVD)

Hint 42

Front 43

Back 43

Dilated Cardiomyopathy:

Think “Distended heart muscles”

,clients present with fibrosis (stiff hard muscles) of the myocardium & endocardium, dilated chambers, making it hard for the heart to pump out oxygen-rich blood.

so the body thinks we have low pressure so attempts to

•increase BP by stimulating SNS to increase HR

•increase BP by stimulating kidneys to initiate RAAS

Dilated cardiomyopathy s/s :

• S3 murmur

• Cardiomegaly (dilated heart)

Hint 43

All problems lead to LESS cardiac output meaning LESS O2-rich blood OUT to the body.

• Low oxygen

• Restlessness, agitation, altered LOC

• syncope, dizzy + fatigue

• Heart failure signs

• Left-sided = Lung fluid

• Right-sided = Rocks the body with fluid (edema, ascites, JVD)

Front 44

Back 44

• Restrictive Cardiomyopathy: Think “Rockhard heart muscles”, so the heart cannot RE-fill with REstric-tive cardiomyopathy, emboli (blood clots) are common.

Restrictive Cardiomyopathy

• (same general low oxygen & HF)

Hint 44

All problems lead to LESS cardiac output meaning LESS O2-rich blood OUT to the body.

• Low oxygen

• Restlessness, agitation, altered LOC

• syncope, dizzy + fatigue

• Heart failure signs

• Left-sided = Lung fluid

• Right-sided = Rocks the body with fluid (edema, ascites, JVD)

Front 45

most important

most deadly

Back 45

• Hypertrophic Cardiomyopathy: Think “Huge Trophy-like heart muscles” in the middle septum which can obstruct the aorta blocking all oxygenated blood out to the body - very deadly!

Obstructive = blocks the Aortic valve

Non-obstructive = does not block

Hypertrophic Cardiomyopathy

• Typically asymptomatic (no s/s) until heavy exercise & then the child DIES!

treatment: surgery

B: Beta Blocker (Block Beats) AtenoLOL

C: Calcium Channel Blocker (Calm Heart)

Nifedipine, Diltiazem

never give 3D's NO! NO! NO!

D-Dilators (Nitro)

D-Digoxin

D-Diuretics

AVOID! Deadly

•Heavy Lifting (bearing down to poop)

•Burst of activity (sprints)

•Sudden Position changes

Hint 45

All problems lead to LESS cardiac output meaning LESS O2-rich blood OUT to the body.

• Low oxygen

• Restlessness, agitation, altered LOC

• syncope, dizzy + fatigue

• Heart failure signs

• Left-sided = Lung fluid

• Right-sided = Rocks the body with fluid (edema, ascites, JVD)

Front 46

Cardiomyopathy diagnostics

Back 46

Hint 46

in restrictive cardiomyopathy the heart is not enlarged (like dilated Cardiomyopathy) & EF is normal & usually treatment is heart transplant

Front 47

Cardiomyopathy pharmacology

Back 47

Hint 47

these drugs calm ❤ & Low BP / HR

goal: increase CO to increase O2

Front 48

Cardiomyopathy treatment

Back 48

Front 49

Cardiomyopathy patient education

Back 49

Front 50

cardiac tamponade

Back 50

Front 51

cardiac tamponade signs & symptoms

Back 51

Hint 51

Front 52

cardiac tamponade causes

Back 52

Hint 52

ACUTE:

TRAUMA: (Stabbing or MVA)

CHRONIC:

Pericarditis

Front 53

cardiac tamponade diagnostic tests

Back 53

Front 54

cardiac tamponade treatment

Back 54

Front 55

cardiac tamponade wrap up

Back 55

Front 56

endocarditis

Back 56

Hint 56

• Infective = bacteria (mold on heart valves)

• Noninfective = No bacteria (only inflammation)

Heart valves can’t close fully

Less cardiac output = Less oxygen OUT

Front 57

endocarditis signs & symptoms

Back 57

splenomegalia since the spleen is the house for WBCs

Hint 57

Front 58

4 classic signs of endocarditis

Back 58

Splinter Hemorrhage little clots of mole that breaks off heart valves & end up under finger nail beds

Roth Spots in the eye known as Retinal Hemorrhages

Olser's Nodes painful red raised Lesions that found on the hands & feet

Janeway Lesions flat circular Lesions that found on the palms & soles of the feet

Front 59

most deadly complication of endocarditis

Back 59

Risk for stroke or embolic CVA

monitor for :

“agitation”

“change in LOC”

first signs of low o2 to the brain:

confusion, agitation, slurred speech,weakness, facial drooping

Front 60

causes of endocarditis

Back 60

Hint 60

Front 61

diagnostic tests for infective endocarditis

Back 61

Front 62

treatment for infective endocarditis

• Antibiotics

• Valve repair or replacement

Back 62

IV antibiotics last for 4-6 weeks & they can destroy small peripheral vessels so they should be given through central line

Hint 62

never withhold antibiotic therapy while waiting for cultural results even though it might be a fungal infection

Front 63

central venous catheter

Back 63

Front 64

endocarditis ABX

Back 64

penicillin is the antibiotic of choice but a lot of patients have allergy or some type of resistance to penicillin family & can cause less effective birth control & cause accidental pregnancy (deactivates the pill,use alternative form of birth control)

vancomycin if it given too fast or first dose, massive flushing of skin red rashes or hives usually around neck & chest, STOP the infusion & then assess the patient airway

Ceftriaxone radiating shoulder pain, NO alcohol

Front 65

Pericarditis

Back 65

Inflammation OUTside the heart

(heart gets compressed & can’t pump)

Less cardiac OUTput = Less oxygen OUT

Hint 65

Front 66

Pericarditis causes

Back 66

50-80% is unknown (idiopathic)

Hint 66

Front 67

pericarditis signs & symptoms

Back 67

monitor for:

•muffled heart sounds

•pulsus paradoxes Drop in Systolic BP by 10 mmHg

precordial chest pain from friction rub that radiates to the left side of the neck, shoulder, back

worsens with deep breathing/lying supine

gets better when sitting up/leaning forward /tripoding

• Elevated WBC (over 10,000) • C-reactive protein

Hint 67

Front 68

pericarditis diagnostics

Back 68

Hint 68

Front 69

pericarditis treatment

Back 69

Hint 69

•surgery: pericardiocentesis

it's important to have NGT placed prior to pericardiocentesis so we could decompress the stomach & prevent puncture

•never stop Prednisone abruptly

taper off

abrupt stop = Adrenal Crisis

Front 70

Pericarditis vs Endocarditis

Back 70

Hint 70

Front 71

PVD: Peripheral Vascular Disease

types & signs & symptoms

Back 71

Peripheral Vascular Disease

scarring & narrowing of the peripheral blood vessels (veins & arteries) like those in the legs & arms. making them small & stiff become very difficult for blood to get through to the extremities.

2 different conditions for PVD

• PVD: Peripheral Venous Disease - narrowed Veins

• PAD: Peripheral Artery Disease - narrowed Arteries

Hint 71

Front 72

PVD vs PAD

Back 72

PAD = problem pushing oxygen rich blood Away from the heart. Oxygen can’t get to legs! WORSE PROBLEM leading to:

- Ischemia (low oxygen)

- Necrosis (tissue death)

PVD = problem Vacuuming deoxygenated blood back to the heart! Blood begins to pool in the legs manifesting as Varicose Veins

Hint 72

Front 73

intermittent Claudication

Back 73

it's intermittent calf pain in PAD

Hint 73

Front 74

6 P's = O2 assessment

Back 74

Hint 74

Front 75

Peripheral Vascular Disease

nursing interventions

Back 75

Front 76

Peripheral Vascular Disease

causes

Back 76

Front 77

Atherosclerosis

Back 77

Hint 77

Front 78

Peripheral Vascular Disease

treatment

Back 78

Hint 78

Front 79

Peripheral Vascular Disease

Patient Education

Back 79

limited standing

compression socks

Front 80

DVT causes

Back 80

Deep Vein Thrombosis

smoking, diabetes (uncontrolled), HTN (over 140/90)

Front 81

causes of DVT

Back 81

Front 82

DVT diagnostics

Back 82

Hint 82

D-Dimer measures that actual clot break down in the body that happens all the time but elevated d-dimer shows elevated clot break down

Front 83

DVT treatment

Back 83

GOAL: preventing the dislodgment of the blood clot (prevent PE)

TED hose : Compression stockings

SCD : Sequential Compression Device

Hint 83

Front 84

DVT Treatment During Blood Clot

Back 84

Front 85

once DVT is resolved

prevent a DVT after surgery like knee/hip replacement surgery

Back 85

Front 86

DVT Nursing Interventions

Back 86

Front 87

4 rules of potassium

Back 87

Front 88

4 stages of shock

5 types of shock

Back 88

Hint 88

Shock: decreased tissue perfusion eventually leading to organ failure and death

Front 89

Initial

Back 89

There is too little oxygen in the blood to feed the organs, resulting in anaerobic metabolism, meaning metabolism without oxygen - BUT s/s are absent in this stage

Front 90

Compensatory

Back 90

The body is trying to compensate for the LOW oxygen, So the heart will pump faster (tachycardia) & RR increases to get more oxygen (tachypnea) body compensates with the sympathetic nervous system to speed up the vital signs & renin-angiotensin activation to maintain BP and oxygenation to keep the organs perfused

Front 91

Progressive

Back 91

Front 92

Irreversible

Back 92

Death is imminent

Hint 92

imminent: قریب الوقوع

Front 93

Septic Shock

Back 93

a septic widespread bloodborne infection that overwhelms the body typically caused by a bacterial infection like Pneumonia or UTI or kidney infection that gets worse. A systemic cytokine release inside the bloodstream causes extreme vasodilation & fluid leakage from capillaries

Front 94

Septic Shock Signs & Symptoms

Back 94

Hint 94

MUST report to HCP immediately

EMERGENCY treatment is necessary

Front 95

Septic Shock treatment

Back 95

Emergency treatment may include supplemental oxygen, intravenous fluids, antibiotics, and other medications.

Front 96

Neurogenic shock

Back 96

The Autonomic nervous system is damaged resulting in the blockage of the sympathetic nervous system which is supposed to speed up the vitals & vasoconstriction.

Only the parasympathetic system is intact - which puts the breaks on the vitals causing widespread vasodilation & hypotension naturally, we see low & slow vital signs like HR & BP. Vasodilation causes decreased blood flow BACK to the heart leads to decreased cardiac OUTput & this leads to poor tissue perfusion from the lack of oxygen & impaired cell metabolism resulting in organ failure & death.

Front 97

Neurogenic shock S/S

Back 97

Hint 97

Front 98

Neurogenic Shock interventions

Back 98

Front 99

Autonomic Dysreflexia

a deadly complication for any spinal cord injury above T6

Back 99

severe hypertension that can kill the client

Front 100

Hypovolemic shock (hemorrhagic)

Back 100

Caused by excessive fluid volume loss through diarrhea, vomiting, or fluid shifts as in burn patients & from bleeding (hemorrhage) from trauma like a gunshot or knife injury, or even surgery & GI bleed.

Hint 100

Front 101

Hypovolemic shock S/S

Back 101

Hint 101

4. low urinary output <30ml/hr due to fluid volume loss

Front 102

Hypovolemic shock interventions

Back 102

Hint 102

Front 103

Cardiogenic shock

Back 103

The heart fails to pump like in heart failure exacerbation or an MI heart attack heart muscles are weak & fail to pump

Front 104

A client having a… myocardial infarction based on elevated troponin levels … the nurse should alert the primary health care provider because the vital sign changes … are most consistent with which complication? Refer to the exhibit.

Back 104

Hint 104

Front 105

Client with heart failure exacerbation… and suspected state of shock. The nurse knows which intervention is the priority for this client?

Back 105

Front 106

Cardiogenic Shock treatment

Back 106

Front 107

Anaphylactic Shock

Back 107

Hint 107

Anaphylactic reaction vs Mild allergic reaction :

any allergy that affects the ABC

Airway, Breathing, Circulation

or even induces hives

this is anaphylaxis

Front 108

Epinephrine

Back 108

Hint 108

Front 109

Epinephrine Normal side effects

Back 109

Front 110

Back 110

Front 111

HTN

Back 111

Hint 111

Front 112

HTN S/S

Back 112

Front 113

HTN causes

Back 113

Front 114

HTN Complications

Back 114

Front 115

Diagnostics Tests

Back 115

Front 116

HTN Labs

Back 116

Hint 116

Left ventricle Hypertrophy

Front 117

HTN treatment

Back 117

Front 118

HTN pharmacology

Back 118

Hint 118

Front 119

Pacemakers

Back 119

symptoms related to Low O2

Hint 119

Front 120

Types of Pacemakers

Back 120

Hint 120

Front 121

Types & Modes of Permanent Pacemakers

Back 121

Hint 121

Front 122

post operative Pacemakers

interventions & patient education

Back 122

Hint 122

Front 123

can Pacemaker patients use TENS

Transcutaneous electrical nerve stimulation (TENS)

Back 123

Front 124

Valve disorder

Back 124

Hint 124

Front 125

Valve disorder

Pharmacology, Surgeries, Patient Education

Back 125

Hint 125

Front 126

Valve disorder

S/S & Causes

Back 126

Hint 126

Front 127

Back 127

Hint 127

allergy to shellfish isn't using to screen for iodine allergy anymore

after:lie flat (supine) & don't cross the legs

REPORT

over 1.3=Kidney damage/contrast nephropathy

urine: 30ml/h or Less

avoid renal failure patients

STOP Metformin 48 hrs (before/after) cath lab to prevent lactic acidosis & nephropathy

Mucomyst (Acetylcysteine) to protect kidneys

Front 128

Discharge teaching

Back 128

avoid NSAIDS like Ibuprofen & naproxen can cause increased risk for thrombotic effects

Hint 128

Front 129

HF causes & risk factors

Back 129

1. Hypertension (high BP) is the #1 risk factor

2. Atrial fibrillation & other dysrhythmias

3. Mitral valve regurgitation

4. Cardiomyopathy

right sided HF : COPD, Smoking, obstructive sleep apnea

Hint 129

fluid fills the lungs causing pressure (pulmonary hypertension) which in result the right side has trouble pumping blood forward

so left sided HF commonly causes right sided HF

Front 130

HF pharmacology

Back 130

Hint 130

all these drugs drop the BP & take work load off the heart & cause orthostatic hypotension except DIGOXIN since it doesn't affect BP

= Change positions slowly

Front 131

Cardiomyopathy signs & symptoms

Back 131

Hint 131

All problems lead to LESS cardiac output meaning LESS O2-rich blood OUT to the body.

• Low oxygen

• Restlessness, agitation, altered LOC

• syncope, dizzy + fatigue

• Heart failure signs

• Left-sided = Lung fluid

• Right-sided = Rocks the body with fluid (edema, ascites, JVD)

Front 132

potassium foods

Back 132

Front 133

Peripheral Vascular Disease

diagnostics

Back 133

Front 134

DVT signs & symptoms

Back 134

Avoid Humans Sign which can dislodge clot