Prehypertension: 120-139/80-89 mmHg

Hypertension stage 1:
systolic 140-159 diastolic 90-99 mmHg

Hypertension stage 2:
systolic > 160 or diastolic >100mmHg

s/s: "silent killer"

none

dizziness, ha, fatigue

flushed, angina, sob

palpitations, nosebleeds

arterial baroreceptors

body fluid volume

renin-angiotensin-aldosterone system

Pathology: increased CO, increased peripheral resistance

Smoking cessation

exercise

weight reduction

relaxation techniques

Sodium restrictions: less than 2.3 g/day

diuretics

beta-blockers

calcium channel blockers

ACE inhibitors

ARB

central alpha-2 agonist

direct vasodilators

alpha-1 blockers

The formation of plaque within the arterial wall.

Pathology: injury to inner wall of artery

platelet aggregation/lipid accumuclation

fibrous plaque develops/calcifies

narrowing/occlusion of artery

affects small and large arteries

fatty streaks in lining of artery is an early indication of injury

hyperlipidemia

obesity

sedentary lifestyle

htn

dm

renal disease

genetics

 smoking

low cholesterol diet

smoking cessation

exercise

weight loss

bile acid-binding resins

hmg-coa reductatse inhibitors (statins)

nicotinic acid

fibric acid derivatives

cholesterol absorption inhibitors

complementary: garlic, omega 3 fatty acides, fiber, soy

pathology: atherosclerosis leads to narrowing/occlusion

tissue ischemia/necrosis

SMOKING!! DIABETES, HYPERLIPIDEMIA

African American and Hispanic

Chronic Kidney disease, sedentary lifestyle, sress, Hyper-homo-cystein-emia (venous disease), Metabolic Syndrome, Elevated C-reactive protein

weight loss

exercise

smoking cessation

positioning of legs: no crossing, dependent or at heart level

promoting vasodilation: provide warmth, avoid caffeine, nicotine, stress, cold

Wear ted hose stockings

antiplatelet aggregators

antihypertensive

lipid lowering agents

What causes DTV?

What is VIRCHOW's triad of RISKS for DVT?

It is MULTIFACTORIAL however, stasis is the main cause.

Stasis, Hypercoagulability, endothelial injury

Pregnancy, cancer, oral contraceptives, hormone replacement therapy, Protien defficiency (C, S, Antithrombin III), polycythemia

pathology: endothelial injury: trauma/pressure

venous stasis

hypercoagulability

inflammatory process

atherosclerosis of coronary arteries

Ischemia

oxygen deprivation

myocardial injury

temporary/reversible

Angina

chest pain/pressure

with exertion or at rest

stable vs unstable

Elevated Serum Levels

HTN (3x for men, 2x women)

Tobacco Use (2-6x)

Physical Inactivity (increases 20%)

Obesity

Diabetes (earlier age)

Metabolic Syndrome

Psychological States (stress, etc)

Homocysteine LEVEL

Biggest risk reducer: hyperlipidemia, HTN

How: drug therapy, exercise, smoking cessation, weight loss, low cholesterol diet

Drug therapy same for hyperlipidemia to reduce risk

Age (55% are 65+)

Gender (Higher in men until women reach menopause)

Ethnicity (higher in African Americans)

Family History

Genetic Predisposition

When ischemia is prolonged and not immediately reversible this is indicated. Includes Unstable Angina, Non- ST segment- elevation MI (NSTEMI) and ST-segment elevation MI (STEMI).

prolonged chest pain (> 15 min)

not relieved by rest or NTG

Reversible myocardial ischemia. AKA chest pain. O2 demand (of heart) > O2 supply. Primary cause is insufficient blood flow d/t narrowing of coronary arteries by artherosclerosis. The artery is usually 75% + stenosed.  Predictable pattern of onset, duration and intensity. Lasts 3-5 minutes. Manifests as ST segment depression on ECG. 

can be precipitated by physical exertion, exposure to cold, eating a heavy meal, emotion-provoking situation

Silent Ischemia:
Up to 80% of patients w/ ischemia are asymptomatic. Associated most often w/ HTN and DM. Confirmed only by ECG changes

Nocturnal Angina
Occurs only at night, but not necessarily during sleep.

Angina Decubitus: Chest pain that occurs only while lying down. Not very common. Relieved by sitting or standing.

Printzmetal's (variant) Angina:
Occurs at rest usually in response to spasm of major coronary artery. Seen in patients with history of migraine headaches and Raynaud's phenomenon. Spasm may occur in the absence of CAD. Chest pain and marked, transient ST segment elevation. May occur during REM and may be relieved by moderate exercise

nitrates

beta-blockers

calcium channel blockers

antiplatelet aggregation

ranexa (ranolazine)

Percutaneous Transluminal Coronary Angioplasty (PTCA)

stent replacement

Role of nurses

Monitor for acute closure of the vessels (s/s of MI)

Bleeding from insertion site or thrombus at insertion site

reaction to contrast solution

Monitor for hypokalemia, hypotension, dysrhthmias

Administer antiplatelet meds

Educate regarding discharge info

Visualizes coronary arteries, heart chambers, wall motion

visualize great vessels

calculate cardiac output

measures pressures

determine ejection fraction

Check for iodine/shellfish allergies

Monitor for postprocedure bleeding and artery occlusion

Visualizes valves, chambers of heart, wall motion

direction of blood flow through the chambers

Role of Nurse

Pre-op teaching

Mechanical ventilation (usually 3-6 hrs)

Chest tubes

Wound care

Epicardial pacemaker

Monitor pulmonary artery pressure and arterial pressure

Monitor and treat for dysrhythmias

Monitor and treat fluid and electrolyte imbalance

Manage hypo/hypertension

Manage hypothermia

Pain management

splint, cough, turn, deep breath

gradual resumption of activity (begins within hours of extubation)

muscle heart tissue death due to lack of oxygen supply

or

MI occurs as a result of sustained ischemia causing irreversible cellular death

Total occlusion of coronary artery. Result of sustained ischemia (>20 min) causing irreversible myocardial cell necrosis. Necrosis of entire thickness of myocardium takes 4-6 hrs. 80-90% caused by thrombus. Most involve the left ventricle. Degree of altered function depend on are involved and size of infarct.

inus node fires <60 bpm. Normal in athletes and during sleep.

S&S- pale, cool skin, hypotension, weakness, angina, dizziness, confusion, SOB

Associated with- hypothermia, increased vagal tone, parasympathomimetic drugs, Hypothyroidism, increased Intracranial pressure, obstructive jaundice & Inferior wall MI

Treatment- Atropine (use caution if MI suspected), Pacemaker, O2 therapy as needed

Discharge rate from sinus node is increased as a result of vagal inhibition and is >100 bpm.

S&S- Dizziness and hypotension d/t decreased CO, Increased myocardial O2 consumption may lead to Angina.

Associations- exercise, pain, hypovolemia, Myocardial Ischemia, HF, fever, blood loss, anemia, caffeine, nicotine and illicit drugs.

Treatment: Determined by underlying cause. Beta blockers to reduce HR and myocardial O2 consumption. Antipyretics for fever. Analgesics for pain.

Manifests as shark teeth waves on ECG. Common in elderly, and 64% of S/P open heart surgery experience this. Originates from a single ectopic focus. High ventricular rates >100 and loss of Atrial kick.

S&S- SOB, palpitations, anxiety, fatigue. Increased risk for stroke and decreased CO can precipitate angina, HF.

Associations- CHF, Rheumatic HD, Pulmonary Embolism, mitral valve disorders, CAD, HTN, chronic lung disease, hyperthyroid, Digoxin, Quindine, epinephrine.

Treatment: Antidysrhythmics, radiofrequency catheter ablation can be curative.

Total disorganization of atrial electrical activity d/t ectopic foci resulting in loss of effective atrial contraction. Most common dysrhythmia. Prevalence increases w/ age. Manifests as saw tooth on ECG.

S&S- Decreased CO d/t ineffective atrial contractions and rapid ventricular response, thrombi may form in atria d/t blood stasis, Embolus may develop and travel to brain causing a stroke.

Associations- underlying HD (rheumatic HD, CAD), Cardiomyopathy, HF, pericarditis, thyrotoxicosis, alcohol intoxication, caffeine, electrolyte disturbance, cardiac surgery.

Treatment: Digoxin, beta blockers, calcium channel blockers, Coumadin, antidysrhythmics, cardioversion after 4 week coumadin treatment, radiofrequency catheter ablation, maze procedure

Onset

Location

Duration

Character

Associated Symptoms

Radiation

Treatment

Severity

Amino acid that's produced by the body as a result of eating red meat

ncreased levels indicate risk factor for CAD. 12-15= moderate risk

15+= high risk

Causes damage to endothelium

Elevation indicates heart failure. Releases when myocardial fibers are over-stretched.

Normal is below 100, positive up to 3000. Useful to distinguish between cardiac and respiratory symptoms.

Total occlusion --> anaerobic metabolism and lactic acid accumulation --> severe, immobilizing chest pain not relieved by rest, position change or nitrates

Described as heaviness, constriction, tightness, burning, pressure, crushing.

Common locations- substernal, retrosternal, epigastric. Pain may radiate or not

"Pale, clammy and cool." Initially increase HR and BP then decreased BP (secondary to decreased CO), crackles, JVD, Abnormal heart sounds. Nausea, vomiting, fever.

Women- SOB, fatigue, weakness

Diabetics- SOB

Elderly- SOB, change in mental status

transmural: entire thickness of myocardial wall involved

subendocardial: dmage has not penetrated entire thickness of wall

ST segment elevation MI: total occlusion of the infarct artery produces ST-segment elevation.  Most will evolve Q waves on the EKG

Non-ST segment elevation MI: thrombus isn't totally occlusive or rich collaterals.  If cardiac serum marker is detected and non Q wave develops, diagnosis of non Q wave MI is made

1) dysrhythmia- most common. 80% s/p MI. Most common cause of death in prehospital period. Life-threatening types seen most often w/ anterior MI, HF or shock

2) HF- pumping power of heart had diminished

3) Cardiogenic Shock- Inadequate O2 and nutrients  are supplied to tissues b/c of severe LV failure. Requires aggressive mgmt.

4) Papillary muscle dysfunction- mv regurg. Aggravates already compromised LV

5) Ventricular Aneurysm- infacted wall thins and bulges during contraction

6) Acute Pericarditis- inflammation of pericardium. See card

Immediate assessment

Measure VS, O2 stats

Obtain IV access

Obtain 12-lead EKG

Perform brief, targeted H & P including fibrinolytic checklist

Focus on elgibility for reperfusion therapy

Evaluate electrolyte and coagulation studies

Portable chest x-ray

Immediate general tx

O2 at 4 L/min

ASA 162-325 mg

Nitroglycerin SL or spray

Morphine IV (if pain not relieved with nitroglycerin)

Beta-blockers

MONAB

How is an ST-elevation MI determined?

Pain assessment

12 lead EKG

Cardiac markers: cpk, isoenzymes, troponin, myoglobin

If ST-elevation MI occurred and is candidate, start thrombolytic therapy

Indications:

chest pain > 30 min and < 6-12 hours, unrelieved with nitro

Indications of transmural ischemia and injury (ST elevation) on EKG

Absolute CI:

active internal bleeding

recent stroke

recent intracranial or intraspinal surgery

Relative warnings:

severe uncontrolled HTN

trauma or surgery in past 10 days

endocarditis or pericarditis

pregnancy

recent GI or GU bleeding

Thrombolytic Therapy

Nursing Responsibilities

Prophylactic pressure dressings

assess for s/s of bleeding but don't stop for minor surface bleeding

Neuro checks to detect s/s of intracranial bleeding

Test all drainage for blood

reassess for reperfusion: pain relief, ST turns to normal, PVCs,

bradycardia rapid rise in CPK, hypotension

ST elevation

Beta blockers IV

Nitro IV

Heparin IV

ACE inhibitors (after six hours or when stable)

*Don't delay reperfusion therapy

NST elevation

tx similar

heparin, asa, ticlopidine, clopidogrel

glycoprotein IIb/IIIa receptor if planned catheterization and troponin is elevated

-interferes with thrombus formation

-abiximab, tirofiban, eptifbatide

Nitro IV

Beta blockers

Pts don't receive reperfusion therapy

bed/chair rest with continuous EKG monitoring

supplement O2 for low O2 sat or resp distress

NTG prn-possible IV NTG

oral beta-blocker within 24 hours unless contraindicated

Calcium channel blocker is beta blocker is contraindicated

ACE inhibitor within 24 hours if pulmonary congestion or low EF (less than 40%)

Avoid NSAIDs other than ASA

May be used to open occluded coronary arteries, establish blood flow, and save tissues

Not all hospitals offer tx.

Initial bed rest

light diet

stool softeners

continuous EKG monitoring

frequent cardiac and resp monitoring

phase 1 cardiac rehab

denial, anxiety, anger, depression

Maximize and enhance social support systems.

Talk with family and pt.

provide info.

open visitation.

promote constructive coping styles.

Phases: phase one: acute illness to discharge from hospital

Phase two: discharge to convalescence at home.

Phage 3: long term conditioning

Low cholesterol, low sodium diet.

smoking cessation

exercise program: start slow, talk with md

sexual activity: none for awhile

med education

Give ASA at arrival and discharge.

ACE inhibitor or ARB for left ventricular systolic dysfunction.

Give smoking cessation advising if smokes.

Give beta blocker at DC.

Give fibrinolytic med within 30 min of arrival

Give PCI within 90 min of arrival.

NYHA Functional Classification of Heart Disease

Class I

NYHA Functional Classification of Heart Disease

 Class II

NYHA Functional Classification of Heart Disease

Class III

NYHA Functional Classification of Heart Disease

Class IV

1) Written d/c instructions including activity level, diet, meds, follow-up appt, daily weights and symptom mgmt

2) Left ventricular function must be documented in record to indicate it has been (or will be) assessed

3) Ace Inhibitor or Angiotensin II receptor blockers for patients w/ known systolic dysfunction (ef <40%) rx at discharge.

4) Current smokers or smokers who quit w/in last 12 mos will be given cessation advice or counseling while in hospital

Increase venous capacity, inprove EF through improved ventricular contraction, slow the process of ventricular dysfunction, decrease heart size, avoid stimulation of the neurohormonal responses initiated by compensatory mechanisms of HF and enhance neurohormonal blockade.

Proven to increase survival in HF. Includes:

Ace Inhibitors- "Gold standard" for HF. Also loosens the valve and decreases preload, reduce afterload

Angiotensin II receptor blockers

Nitrates- dilation, optimize preload

B-Adrenergic (Beta) Blockers- Block SNS response. Decreases BP, HR & contractility, so not ideal. Lopressor and Coreg do not decrease contractility.

Nesiritide, decrease sympathetic stimulation

Digoxin- Improves contractility, increases CO, improve contractility

Nitrates: optimize preload

morphine sulfate: decreases preload and workload, decrease anxiety, promotes venous pooling

Positive inotropic agents for acute heart failure

dobutamine, milrinone, amirnone, dopamine (vasodilators)

nesiritide

anticoagulants

hydralazine

Teach purpose and dosage.

Adjustments: time of day if dizziness is a problem

time of day for nocturia

dosage adjustment for weight gain

Teach side effects

Look for barriers to med adherence

Create med schedule with client

Education: s/s and when to call the MD

Daily weights: first thing in the AM

Low sodium diet

exercise program: start slow and increase gradually. stop immediately if dyspnea, chest pain, and fatigue occur

Enjoy sex when rested.

Don't have sex if irritated.

Wait one to two hours after a meadl.

Don't have sex if drinking.

If sob or chest discomfort, stop.

Fatigue limits ability to practice developmental skills:

introduce age appropriate toys

create restful home envior.

plan for short play periods after rest.

plan for interactions with healthy children.

Promote growth through nutrition:

frequent small feedings.

feedings should be no more than 30 min

Burp after every half ounce.

Monitor vitals, cognitive status, skin color

ECG

High fowlers/ sitting position

Auscultate heart & lungs

O2, sats

I/O

Meds as ordered (usually IV Lasix, morphine to relax vasculature)

Monitor electrolytes

Provide calm, reassuring environment

CXR

Assess BNP level

High fowlers

O2 mask, biPap

BP, HR, RR, UO q1hour

Continuous ECG, pulse ox

Hemodynamic monitoring

Drugs as prescribed

Daily weights

Vent, cardioversion, VAD

Microbes colonize and attach to valves (usually prosthetic heart valves or in those w/ structural cardiac defects). Colonies break off and enter peripheral blood stream. Also occurs in IV drug users and in those w/ debilitating disease, indwelling catheters or prolonged IV therapy. Acute (onset w/in 2 weeks of infection) that is more virulent, or subacute (onset weeks-months) which is more common. Acute generally caused by Staph aureus, Strep viridians, virus or fungi while subacute caused by entercocci.

Treatment involves long term IV therapy via picc line for 6 weeks & prophalxis before different kinds of procedures.

fever (in 90%), chills, weakness, splinter hemorrhages in nail beds, petechiae, osler's nodes on fingers of toes, Janeway's lesions on palms or soles, Roth's spots, new onset murmur (d/t clumps on valves), HF in up to 80% w/ aortic valve type.

Arthralgia, myalgia, back pain, abd discomfort, wt loss, HA and clubbing of fingers (only w/ SA type).

Recent dental, urologic, surgical or gynecological procedures; heart disease; recent cardiac cath; skin, respiratory or urinary tract infection, IV drug use.

Labs- (2) blood cultures (+bacteria in 90%)

WBC w/ differential

Echocardiogram

CXR

Occurs most often in school age children, after undiagnosed strept throat infection. Injury to heart tissue is caused by inflammatory or sensitivity response to streptococci. Myocardial and pericardial tissue is also affected, but endocarditis results in permanent changes to valves. Treatment includes antimicrobials, salicylates, NSAIDS, corticosteroids and prophylactic antibiotics.

all layers of heart may be involved:

Aschoff's bodies: small nodules of collagen fibers

lesions on the valves

cellular infiltrate

The stretching of an atrioventricular valve leaflet into the atrium during systole. Most patients asymptomatic for life. Murmur from insufficiency that gets more intense through systole. Clicks mid to late systole that may be constant or vary beat to beat. Can lead to dysrhythmia, paroxysmal supraventricular tach, v tach w/ palpitations & dizziness, and chest pain that occurs w/ stress that doesn't respond to antianginal drugs

Valve doesn't close properly and blood backflows through the valve. Asymptomatic for years until devt of some degree of LV failure. During acute episode there is thready peripheral pulses and cool, clammy extremities, weakness, fatigue, palpitations, dyspnea, orthopnea and edema. S3 or murmur is most likely.

Based on backflow of blood over filling chamber before the valve

s/s: dilation and hypertrophy of both chambers, murmur, fatigue, weakness, dysnea on exertion, orthopnea, palpitations, neck vein distension

Dx: echocardiogram, x-ray, ekg, cardiac catheterization (only if surgery is required)

Inflammation of the pericardium (sac that encloses the heart)

acute

chronic constrictive: chronic fibrosis thickening, TB, cardiac surgery, radiation

bacterial, viral, or fungal

grating and oppressive chest pain: aggrevated with breathing, coughing, swallowing and supine position

pericardial friction rub

elevated wbc and esr

ST-T wave elevation in all leads (pericardial inflammation over entire surface of the heart; monitor with series of EKG)

fever

chronic constrictive-right sided heart failure

NSAIDs (escept avoid with acute MI pericarditis)

Corticosteroid therapy (if not bacterial or an acute MI pericarditis)

Antibiotics for acute bacterial

pericardiocentesis if cardiac tamponade

S/S of cardiac tamponade

muffled heart sounds

decreased cardiac output

jugular venous distention

paradoxical pulse (SPB 10 mm HG or more higher on expiration than inspiration)

circulatory collapse: falling arterial pressure, rising venous pressure

Impact: ventricular filling impaired

RX: emergency pericardiocentesis and maintain fluid volume

Inflammation of the heart muscle

Casued by viruses, bacteria, rickettsiae, fungi, parasites, radiation, drug hypersensitivity

S/S: fever, fatigue, general malaise, dyspnea, palpitations, arthralgias, enlarged lymp nodes, S3, crackles, JVD

Disease of the heart muscle affecting structural or function ability

Tx pallative not curative

Three types: dilated, hypertrophic, restrictive

Most common type

dilation of ventricles w/out hypertrophic changes (increased size w/out increased # of cells)

inpaired systolic function, atrial enlargement, LV stasis of blood

S/S: fatigue, weakness, palpitations, dyspnea, dry cough

Moderate to marked cardiomegaly

TX: management of heart failure, diuretics (decrease preload), digoxin (tx atrial fib), ace inhibitors (decrease afterload)

implantable cardiac defibrillator as needed

cardiac transplant

asymmetric ventricular hypertrophy wihtout ventricular dilation: massive ventricular hypertrophy, rapid,forceful contraction, impaired relaxation, obstruction to outflow

S/S: exertional dyspnea, fatigue, angina, syncope or dizziness, palpitations

mild cardiomegaly

TX: beta-blockers

Calcium channel blockers

antidysrhythmic

ICD, dual-chamber pacing

Surgical excision of part of the ventricular septum

avoid strenuous activity and dehydration: should report dizziness, fainting, irregular pulse

digoxin CI in obstructive hypertrophic cardiomyopathy.  Used to tx afib not failure

heart muscle impairs diastolic filling and stretch

S/S: dyspnea, fatigue, palpitations, activity intolerance

mild to moderate cardiomegaly

TX: convention therapy for HF and arrhythmias, heart transplant, exercise restriction, avoid dehydration

Consists of pacing, cardioversion, and defibrillation therapies to treat brady and tachy arrhythmias

External programmer is used to monitor and access the device parameters and therapies for each patient

Cardiac transplant

identify elgible candidate

may have ventricular assist device until heart is available

Postop care: balance risk of rejection with risk of infection

Heart is denervated (affects response to position change, stress,exercise, and certain drugs)

Stenosis

(Valvular heart disease)

usually caused by rheumatic fever

also caused by congenital abnormalities

valve thickened, fibrosed, and calcified

opening smaller than normal

S/S: based on chamber before the stenosis working harder

hypertrophy of camber before narrowing

murmur

dyspnea on exertion

fatigue

orthopnea

paroxysmal nocturnal dyspnea

hepatomegaly, neck vein distention, and edema

angina-aortic stenosis

syncope-aortic  stenosis

atrial fibrillation

prophylactic antibiotic therapy before invasive procedures if high risk

Drugs to control HF: diuretics, digoxin, oxygen, calcium channel blockers or ace inhibitors

Tx afib: meds or synchronized countershock

anticoagulation- avoid clot on valve

rest

After LV failure developed but before irreversible dysfunction

reparative procedures:

valvuloplasty: repair of the valve

1. balloon valvuloplasty for stenotic valves: invasive, surgical, balloon inflated to enlarge orifice

Direct (open) commissurotomy: during open heart surgery: visualize valve: separates fused leaflets, thrombi, and calcifications can be removed

Closed commissurotomy: no cardiopulmonary bypass, midsternal incision, small hole cut into heart, commisure opened with dilator or finger

Annuloplasty: repair of junction between leaflets and muscle wall

Narrows valve orifice and treats regurgitation

Replacement procedures: synthetic/prosthetic, biologic/tissue

PT teaching for Valve Surgery

Sternal incision care

watch for infection

return to normal activity after 6 weeks

avoid heavy and physical labor with upper extremities for 3-6 mos

avoid dental procedures for six mos

anticoagulation therapy

antibiotic prophylaxis

wall of aorta weakness and dilates

caused by congenital weakness, trauma, or disease

most aneurysms found in abdomen below level of renal arteries.  May be in thoracic aorta.

Thrombi can form and embolize.

trauma (MVA)

infection

athersclerosis/HTN: biggest cause

after peripheral artery bypass graft surgery at site of anastomosis

often asymptomatic

s/s of rupture: pain in back, flank, abdomen, or groin

shock with rupture

If AAA is > 6 cm in diameter, may rupture within one year.

If AAA is < 6 cm, risk of rupture very low.

Rupture is life threatening.

                  goal- prevent aneurysm from rupturing

                  early detection/treatment imperative

Determine exact size and location: ultrasound, MRI, CT, angiography

Repeat imaging regularly to determine any changes

Control blood pressure (only if small/asymptomatic)

repair aneurysm before it ruptures

Don't palpate the abdomen if an AAA is known to exist

If rupture not prevented, rapid detection of a rupture: rapid onset of severe back pain with radiation to groin, buttocks, or legs

decreased anesthesia and operative time

smaller operative blood loss

decreased morbidity and mortality

more rapid resumption of physical activity

shortened hospital stay

quicker recovery

higher patient satisfaction

reduction in overall costs

aneurysm growth

aneurysm rupture

perigraft leaks

aortic dissection

bleeding

graft dislocation and embolization

graft thrombosis

incisional site hematoma

site infection

Monitor VS.

Assess for diminished or absent peripheral pulses.

Monitor LOC.

Compare extremities appearance.

Monitor urine output, BUN, and creatinine.

Monitor pressures in heart chambers and cardiac output.

Pulsation from artery is carried through the tubing.  The transducer converts the physical pulsation to an electrical signal.  The monitor shows a digital reading

Measure right atrial and indirect left atrial and ventricular pressures

Left ventricular end-diastolic pressure is determined by pulmonary artery wedge pressure.

Low pressures=low volumes

Measure cardiac output, hydrostatic pressure.

PAP systolic: 15-26

PAP diastolic: 5-15

PAWP: 4-12

balloon inflated in the PA

Balloon occludes forward flow of blood

Static column of blood from the occluded portion of PA, through left atrium and during open mitral valve during systole

reflects LVEDP

Cardiac ouput: 4-8 liters

Cardiac index (CO adjusted for body size): 2.2-4

hemorrhagic shock: hypotension, tachycardia, diaphoresis, oliguria, decreased responsiveness, dysrhythmias

Flank ecchymosis (Grey Turner's sign)

Abdominal distention

Arterial line-monitor bp

contiuous cardiac monitoring

hemodynamic monitoring: pulmonary artery catheter

may be on ventilator overnight

hourly pulse and extremity checks

Limited HOB elevation to avoid flexion of graft

hourly urine output

Monitor BUN and creatinine

T,C, and DB

abdominal assess: paralytic ileus

NG tube for 3-4 days

avoid heavy lifting for 6-12 weeks.

Clinical Manifestations of an Aortic Dissection

Most common: ascending aorta and descending thoracic aorta

s/sx depend on location of intimal tear and extent of dissection

pain characterized as:

sudden, severe pain, in anterior part of chest or intrascapular pain radiating down spine to abdomen or legs

described as tearing or ripping or stabbing

may mimic that of MI

decrease or absence in peripheral pulses

aortic regurgitation with murmur

Severe, life threatening complication

occurs when blood escapes from dissection into pericardial sac

Clinical manifestations include:

hypotension

narrowed pulse pressure

distending neck veins

muffled heart sounds

pulsus paradoxus

 bed rest

pain control with opioids

control BP

Control HR and myocardial contractility

1. IV beta blocker-esmolol

2. oral beta blocker-propranolol

3. sodium nitroprusside

4. calcium channel blockers

5. ACE inhibitors

Descending dissections may be treated with a stent

success of therapy evaluated by pain relief

surgery: resection of segment of aorta with initial tear.  Indicated if drug therapy is ineffective or when complications occur.  The location of the dissection also influences the need for surgery.

Therapeutic Regimen (antihypertensive drugs and side effects)

if pain returns or symptoms progress, instruct patient to seek immediate help

Hourly VS

cardiac monitor

monitor chest tube drainage

assess motion and sensation in all extremities (paraplegia from interruption of blood supply to spinal cord)

May be on ventilator overnight

hourly vs

hourly groin checks

peripheral pulse checks every 4 hrs

pain assessment

encourage c and db

dvt prophylaxis