Exam 4 Flashcards
Most common cause of cardiovascular disease
Definitions:
Abnormal accumulation of fatty substances and fibrous tissues in the blood vessel walls
This reduces blood flow to the heart muscle
-Heart works heart to get blood through narrow artery and BP goes up
Fatty lipids deposited in the arterial wall –> inflammatory response –> injury to the endothelium
Atherosclerosis
Non modifiable: -Age --Men >45 years old --Women >55 years old -Gender -Race --African Americans, Mexican Americans, Native -Americans, Asian Americans -Family history: even in healthy so major prevention Modifiable -Diabetes -Hypertension -Smoking -Obesity -Physical inactivity -High blood cholesterol New risk factors: -Peridontal disease, influenza, sleep apnea (OSA: hypoxia --> heart disease; causes HTN --> artherscelorsis), increased BMI (increased abdominal girth increases risk of atherosclerosis) For a diagnosis of metabolic syndrome: need 3 or more -Insulin resistance -Abdominal obesity -Dyslipidemia -Hypertension -Proinflammatory state (HIGH LEVELS OF CRP) -Prothrombotic state (HIGH FIBRINOGEN) So DMT2
risk factors for atherosclerosis
Ischemia-inadequate blood supply that deprives the heart muscle of oxygen
Angina-chest pain due to ischemia
Myocardial infarction-if the decrease in blood supply is enough or for a long enough duration –> death of myocardial cells
Myocardial damage decreased cardiac output!!
Could lead to heart failure and sudden cardiac death due to lethal cardiac rhythm disturbances r/t increase workload on heart –> disturbed electrical pathways
manifestations of atheroscelorsis
Chest pain
Shortness of breath (especially in elderly)
Extreme fatigue
Diaphoresis
Nausea and vomiting
Women are atypical: shoulder/arm pain, jaw/back pain
How do you know the difference between angina and MI? = Angina isn’t consistent pain and goes away with meds and rest; MI is persistent pain
classic signs of myocardial ischemia
Controlling cholesterol
- High cholesterol=CAD
- Four elements of fat metabolism
- -Total cholesterol
- -LDL - bad: want them to go to liver to be excreted
- -HDL - good: makes LDL go to liver
- -Triglycerides
- -*these all affect the development of heart disease
20 yrs and older: fasting lipid panels every 5 years
under 20 with family history: tests frequently
management of CAD
Goal= low LDL and high HDL
LDL
<160 for patients with one or no risk factors
<70 for patients at very high risk for acute coronary event
How do we control these LDL levels? = Exercise
cholesterol
Treatment:
Meds that lower lipids
Monitor closely, can affect liver labs
Lifestyle changes
Dietary
Physical activity
Smoking cessation- reduce 50% in first year and continues to go down
Stress management
Hypertension management
Diabetes management
hyperlipidemia
HMG-CoA Reductase Inhibitors (STATINS) FYI -Lovastatin -Pravastatin -Simvastatin -Fluvastatin -Atorvastatin -Rosvastatin Nicotinic Acid -Niacin Fibric Acids -Fenofibrate
Bile Acid Sequestrants
- Cholestyramine (Questran)
- Colesevelam (WelChol)
- Colestipol HCL (Colestid)
cholesterol medications
Hypertension:
- Risk of CAD increases with HTN
- Increases workload of left ventricle –> stressed left ventricle –> failing
Diabetes: -Dyslipidemia -Increased platelet aggregation -Altered red blood cell function What do all of these lead to? = thrombus/clot which increases risk of CAD
hypertension and DM
Pain or pressure in the anterior chest
Caused by insufficient blood flow (usually a blocked artery)
-Oxygen demand exceeds the supply
Types of angina:
-Stable: occurs with exhortation and relieved with rest - happens with activity
-Unstable: lasts longer, more severe, can occur with rest
-Intractable/refractory: severe, incapacitating
-Variant/Prinzmetal’s: chest pain, pain at rest, ST elevation with EKF so take to cath lab and will have clean vessels/no blockage: this is vasospasm r/t ST elevation
-Silent: ischemia on EKG but no pain
angina pectoris
Mild indigestion to a heavy sensation in upper chest - From discomfort to agonizing pain Feeling of impending doom/death Radiate to neck, jaw, shoulders and arms (especially left side**) Tightness** Diabetics: neuropathy so can't feel Women: atypical S/S Weakness Numbness Shortness of breath Pallor Diaphoresis Anxiety Dizziness Nausea and vomiting
Nitroglycerin and rest make it go away
Angina S/S
12 lead EKG
Blood biomarkers: usually drawn q 8 hrs 3 times and look for peak
-CK/CKMB, Myoglobin, Troponin T* or Troponin I* (shouldn’t have any; if + it’s released in response to ___Tegrity* and leads to ischemia)
Stress test: treadmill or meds to increases HR
Nuclear scan
Cardiac catheterization: visualization (pt has chest pain, do card cath in femoral/radial artery, thread cath and visualize arteries/vessels for blockages; use dye, so worry about kidney function r/t contrast dye)
Angina diagnosis
Goal is to increase oxygen supply and decrease oxygen demand to myocardium
Oxygen 1st
Meds: beta blockers (lower HR/BP), blood thinners (esp. with concern of thrombus), Morphine (lower workload (preload) on heart), Nitro (vasodilators)
Control risk factors
PTCA AKA balloon/angioplasty/angiogram
Medical management of angina
M-morphine
O-oxygen
N-nitro
A-aspirin
PTCA or stent placement
Goal is to restore oxygen to the heart and prevent further damage
Time is muscle: door to balloon time = 60 minutes; most amount of time to restore blood/O2 supply; goal is to restore muscle
percutaneous coronary intervention
Could be emergent
Balloon tipped catheter opens vessel and resolves ischemia
Sheath inserted in either the femoral artery or radial artery through the aorta –> into coronary arteries
Balloon is inflated and deflated to open vessel
percutaneous transluminal coronary angioplasty
To prevent restenosis
Metal mesh that provides support to a vessel
What are these patients at risk for after stent placement? = clots: put them on Plavix/aspirin
pt. comes in for bleed, see hx of CAD on chart, ask if they have hx of stent, aspirin could cause the bleed
coronary artery stent
Bleeding or hematoma -Strict bedrest -Manual pressure for 30 mins -Monitor CBC-may need transfusion - shows bleeding -Hematoma: BUN/creatinine = low, tachycardia, hypotension; cough/vomit can cause this Lost or weak pulse distal to site -Assess CSM, color, compare pulses* priority Pseudoaneurysm -Notify physician -Anticipate ultrasound -Assess CSM Retroperitoneal bleed -S/S: back pain, hypotension, stop infusion and fill tank back up -Notify physician -Stop anticoagulants -Anticipate giving IVF or PRBC Acute renal failure -Hydration* with IV to flush dye out -Monitor urine output -Monitor BUN/Creatinine -Administer Mucomyst (protects kidneys so give with CAD)
complications after PTCA
Allergic reaction -Administer Prednisone, antihistamines, H2 blockers prior to the procedure if known allergy to contract or shellfish Cardiac tamponade -Anticipate pericardiocentesis Chest pain r/t stent disturbances -Notify physician -Monitor VS Chest pain (always treat; it's an emergency) -Notify physician -Monitor VS -Cardiac & pulmonary assessment -Assess EKG -Assess troponin
complications after PTCA 2
Many go home the next day Monitor for bleeding Angio seal: collagen plug to seal artery Direct manual pressure Femostop: belt across waist, inflate ball to provide pressure Bedrest Leg straight Radial site
post PCI care
PCI = PTCA and Stent
Over 65 million adults in the US Undermanaged 30% of people don’t know they have hypertension Primary hypertension -95% -Unidentifiable cause, don't know it Secondary hypertension -5% -Identifiable cause: pregnancy, renal/kidney failure (renal arter stenosis causes HTN), meds (steroids and vasoconstrictors)
hypertension
White-coat hypertension: Hypertension in the clinic - no aggressive treatment; more common
Masked hypertension: Normal BP in clinic but hypertension at home or work
-When this is suspected, what should the nurse do? = tell pt. to self home monitor; stop smoking/drinking/stress
Increased workload of heart –> Over time will lead to heart disease and stroke
hypertension types
Normotension: -Blood pressure <120/80 -Must look at this on a continuum -Assessment is based on the average of at least 2 readings --longer BP and higher it gets on trend --> increased risk of morbidity and mortality Prehypertension -Blood pressure 120-139/80-89 -Lifestyle changes: exercise, no smoke/drink, eat healthy - time to catch and fix it Hypertension stage 1: -Blood pressure 140-159/90-99 -Lifestyle changes and medication Hypertension stage 2: -Blood pressure 160 or higher/100 or higher -Medications are a must - lifestyle changes are a plus
types of hypertension
Multifactoral
Age (44) and Elderly (noncompliant; kidney/liver have decreased function, so start low and increase slow)
More common in younger men than women until menopause
Obesity - Childhood
Often coexists with dyslipidemia, diabetes mellitus, sedentary lifestyle and metabolic syndrome (increase risk of CVD with all)
African Americans-especially males
Oral contraceptive use-when accompanied with smoking & obesity
Increased sympathetic nervous system activity
Increased absorption of sodium, chloride, and water (heart failure and increased extracellular fluid –> overwork heart –> big/boggy heart –> fails
Increased extracellular fluid volume, increased systemic vascular resistance
risk factors of HTN
Heart disease
Stroke
Chronic kidney disease (low BUN/creatinine) (with HTN have nocturia)
Peripheral artery disease
Retinopathy: retina vascular damage caused by HTN
HTN damages inner lining blood vessels –> vascular damage to organs –> S/S
underlying systemic effects of heart failure
Weight reduction
DASH diet-dietary approaches to stop hypertension
-Eating plan: consistent amount of potassium, low sodium, high protein, fruit/veggie, low bad fat
Sodium restriction
Physical activity 30 mins at least 3X/week
Moderate alcohol consumption (1-2/day for men; 1/day for women)
Smoking cessation
Complimentary and alternative therapies (stress reduction: yoga, acupuncture, herbal meds but watch med interactions and do lots of teaching)
Self management: self monitor/manage at home, self diet/exercise, good teaching from nurse
nursing management of HTN
Must support patient in adherence/compliance! do everything you can to do so Most patients need 2 drugs Thiazide diuretics -Hydrochlorothiazide (K wasting), Furosemide (K wasting), spironolactone (K sparing) Beta Blockers -Atenolol, Metoprolol, Propranolol Alpha2-Agonists -Clonidine: longer acting Vasodilators: dilate blood vessels to lower BP - Hydralazine, Nitropursside, Nitroglycerin ACE inhibitors -Captropril, Enalapril, Lisinopril ARB -Losartan, Valsartan CA channel blockers -Diltazem, Amlodipine
Can reduce when BP is <140/90 for at least 1 year, so self monitor at home and bring log to apts.
*Give simplest treatment possible
Don’t stop taking r/t rebound HTN
pharm therapy for HTN
Blood pressure >180/>120
Poorly controlled HTN or stopped taking meds
More common in men, older adults, African Americans
Head injury, pheochromocytoma, food-drug interactions, eclampsia, substance abuse, renal disease
2 categories
Hypertensive urgency
-Blood pressure is severely elevated but there is no evidence of organ damage*
-Elevated blood pressure with severe headaches, epistaxis, anxiety
-*Goal-reduce bp to 160/110 for several hours to several days
Hypertensive emergency
- Blood pressure >180/120 and must be lowered quickly to stop organ damage
- Hypertension of pregnancy
- MI
- Dissecting aortic aneurysm
- Intracranial hemorrhage
- Can’t lower too quickly r/t pass out r/t decreased perfusion
hypertensive crisis
Blood vessel grafted to occluded coronary artery
Indications:
Alleviation of angina that can’t be controlled
Left main coronary artery stenosis, multi vessel CAD
Prevention & treatment of MI, arrhythmias, heart failure (blocks coronary artery and decreases blood and O2 –> tissue death; the increases work load stresses the heart)
Treatment of complications from unsuccessful PCI
coronary artery bypass graft (CABG)
open heart surgery
General anesthesia
Cardiopulmonary bypass machine (some on pump, some off pump)
Blood vessel from somewhere else (saphenous vein, left internal mammary artery-LIMA) is grafted-bypasses the obstruction
Chest tubes - anytime with open heart; drains stuff from surgery; 2-3 tubes
Pacer wires: in heart, externally stick out of skin; if brady/tachy you can hook up to this connection
MIDCAB: minimally invasive CABG with no chest incision
CABG
MI: common intra/post op from CABG; inta can decrease perfusion so it can decrease O2 to area in heart
-Know post op if they had an MI during surgery by doing EKG
Renal failure: decrease perfusion to kidneys - check I/O, output, labs BUN/Creatinine to check for decrease perfusion
Hypovolemia: most common cause of decreased CO after CABG
-Know if they have it if their tachy/hypotensive and give fluids/blood to fill tank back up
Bleeding: can cause platelet dysfunction; have low hematocrit/hemoglobin, low BP, blood in chest tube r/t internal bleed - do good chest tube assessments and monitor pleura bag
Cardiac tamponade: emergency; fluid around pericardiac sac - not a problem if you have a chest tube
Fluid overload
Hypothermia: keep warm postop to prevent vasoconstriction; cold will constrict vessel
Hypertension: with vasoconstriction; worry about pressure on heart and can rupture/bleed - give antihypertensives
Tachyarrhythmias: a fib on 3rd day r/t volume changes in body (fluid imbalances)
Bradycardias: pace monitor
Heart failure: increased work load on heart
CABG complications
Neurological status-LOC, pupils: decreased perfusion during surgery (stroke r/t clots and hyperperfusion)
- hard post op to assess r/t pain meds so know baseline*
Cardiac-heart rate, rhythm, sounds: higher HR the more decreased in CO; a fib is common; hypervolemia will have S3 sound
Pulmonary-Lung sounds, O2 saturations, respiratory rate, rhythm: note work of breathing; ex: pneumonia r/t alveoli collapse - hear crackles and know why it happened and fix the why
Peripheral vascular status-pulses, color, skin temp, edema: take vessel and bypass so check blood flow, pulse and perfusion
Renal-urine output, labs to see decrease perfusion
Fluid & electrolyte-I/O, skin turgor
Pain-assessment: *know baseline and pts. goal - do frequent vitals and control. In pain, they can’t wait/deep breath/incentive spirometer
Assess lines, tubes: chest tube, IV, pacer wires - hard to ambulate because of this - must be done
nursing care assessment for CABG
Restoring cardiac output: hypovolemia is most common cause, so give fluids/blood-give back what they lost
- watch output, labs, VS, check for a fib (r/t blood pooling) and arrhythmias
- watch mental status change to check perfusion to brain
Maintaining adequate tissue perfusion: ambulate early, watch CSM, peripheral vascular, DVT/clots*
Monitor signs/symptoms of infection: take temp, labs, watch incision site
Fluid and electrolyte imbalance: I/O, labs
Hourly blood sugar for 1st 4 hours. If >150-180 start insulin drip to bring glucose down. Glucose control is very important for healing*
Impaired gas exchange: cough/deep breath/IS 10X/hour, give O2, on vent for 1st hour, pain control, assess lungs
Impaired cerebral circulation: monitor neuro status*
Pain: can’t have good gas exchange if they don’t have good pain control
nursing interventions for CABG
Reduced blood flow
Unstable angina-plaque ruptures, artery not completely occluded
Acute coronary syndrome
Vasospasm: with prinsometals/variant angina r/t vasospam; see ST elevation
Decreased oxygen supply from blood loss (r/t decrease perfusion/tissue death) or hypotension (not enough O2 in body)
Increased oxygen demand from tachycardia, drugs (cocaine)
IMBALANCE BETWEEN OXYGEN SUPPLY AND DEMAND!
Myocardial infarction (MI)
Types:
STEMI: 100% occlusion
NSTEMI: partial occlusion
Q wave: can show MI
Chest pain- can be persistent/sudden or sometimes silent!
**EKG-T wave inverted, ST segment elevation, Q wave
Echocardiogram: ultra sound of heart to look at heart function; if MI see abnormal LV wall function
-r/t lack of O2 –> cell death –> abnormal wall movement
Labs: 1. Triponin (draw 3x/8 hours-look for peak and find downhill slide), 2. CKMB, 3. Myoglobin
manifestations of MI
Chest pain Shortness of breath, pulmonary edema Nausea and vomiting Decreased urine output Cool, clammy, diaphoretic skin, pale Anxiety, restlessness *Fear *Denial
clinical manifestations of MI
Get to the hospital! give good education, like don't drive EKG Labs *Oxygen r/t chest pain and no O2 Nitroglycerin to dilate vessels Aspirin in case of clot Beta blocker decrease BP/work of heart Ace/ARB to decrease BP
medical treatment of MI
Evaluate need to PCI: do you need cath lab? determine this off labs/EKG if theres ST elevation Thrombolytics Morphine to decrease work of heart IV Heparin, Enoxaparin - anticoag Clopidigrel - antiplatelet Bedrest to decrease work on heart
medical management of MI
Education about risk reduction
3 phases-starts with diagnosis of atherosclerosis and continues for months!
Look at page 421, box 14-7 for health promotion education-KNOW THIS!!
cardiac rehabilitation
Relieve pain PCI Aspirin, Nitroglycerin, Beta blockers Anticoagulants Morphine Oxygen *Reduce anxiety Close monitoring MONA
Monitor and report changes in the cardiac rhythm and rate closely Heart sounds* Lung sounds * Blood pressure* Pain* Respiratory status*
nursing management of MI
Function of the Kidney
- Filature out waste
- Regulates BP by fluid balance
- RBC production
- Electrolyte imbalances r/t fluid balance
Sudden
Can happen in hours to days
Oliguria = <400 mL/day (20 mL/hr)
anuria = no U.O. 50 mL/day
Increased serum BUN/CR = waste in the blood
Acidosis: S/S: blow off = resp system compensates and have increased RR and uremic smell
Fluid excess- lungs 1st AMB dyspnea/crackles, then in tissues (edema/periorbital/JVD)
Electrolyte imbalance: potassium is biggest concern - will increase w/o kidney
BP irregularities: FVE hypertension and RAS system (kidney and blood have renin and active by vasoconstriction and can’t rid waste and holds onto fluid)
Anemia: RBC regulation in kidney - w/o kidney = low hemoglobin/hematocrit
acute renal failure
Exact patho isn’t always known
Different categories
Prerenal: perfusion problem/blood flow to area; determined by MAP (average pressure blood pumps with each cycle - measures perfusion and needs to be >65)
Intrarenal
Postrenal
acute renal failure patho
Caused by any condition in which there is Decreased blood flow (MAP <65) Decreased cardiac output -MI - heart is compromised -Shock - heart is compromised -Heart failure - heart is compromised Hypovolemia: not enough fluid that can't support pressure -Dehydration -Hemorrhage -GI disturbances: colitis or diarrhea -Sepsis: drops BP
prerenal of ARF
