Perfusion Flashcards
Electrical Conduction of the Heart
"action potential"=electrical impulse SA (sinoatrial) node (P wave) Internodal Tract Right and Left Atria (contract) AV (atrioventricular) Node Bundle of HIS Bundle Branches Purkinje Fibers Ventricle (Contract)
Absolute Refractory Period
Cardiac muscle does not respond to any stimuli during ventricular contraction
Relative refractory period
After absolute refractory when cardiac muscle gradually recovers its excitability (by early distole)
ECG Waves
P-1st, firing of SA node, depolarization of the atria
QRS-2nd, depolarization from AV throughout ventricles
T-3rd, repolarization of the ventricles
U-4th repolarization of Purkinje fibers, or hypokalemia
Intervals between each wave reflect the time it takes for the impulse to travel from one area to another.
ECG lead placement
5 Lead
RA-right arm, on cx where arm/torso meet RL-Left arm, on cx where arm/torso meet RL-Right leg, on abd near hip LL-Left leg, on abd near hip C1-(for V1) 4th IC, rt sternal border
P wave normal
0.06-0.12
firing of SA node, depolarization of atria (contract)
longer: conduction problem within atria or SA node
QRS wave normal
0.04-0.12
depolarization of AV through ventricles (contract)
longer-conduction problem in branches
T wave normal
0.16
repolarization of ventricles
longer: MI or ischemia
inverted: old MI injury
MAP formula
MAP = (SBP + 2(DBP)) / 3
depolarization
contraction
repolarization
rest
ST interval
0.12
MI
elevated = STEMI
PR interval
0.12-0.20
conduction problem AV, bundle of his, bundle of branches, atria
QT interval
0.34-0.44
ventricular Repolarization disturbances
Sinus Bradycardia
Sinus Tachycardia
> 100 bpm
Causes: normal response to increased activity, anxiety, pain, stress, fear, fever, anemia, hypoxemia, hyperthyroidism, pulmonary embolism, decrease cardiac ouput/hypotension, hypovolemic shock, MI, heart failure
caffeine, drugs, alcohol, nicotine
Sx: Decreased blood pressure, Decreased Cerebral perfusion=restlessness, anxiety, confusion, Decreased oxygen saturation, Weakness, Fatigue, Shortness of breath, Decreased urine output, Pain, Palpitations, Orthopnea
Tx: fix the cause!
Sinus Arrhythmia
Ps and Rs irregular
breathing and meds: Morphine, digoxin
asymptomatic
Cardiac output formula
HR x stroke volume = CO
Pathophysiology of PVD
leading cause is atherosclerosis, gradual thickening of intima (innermost layer) and media (middle layer) of the arterial wall from deposit of cholesterol and lipids. also: inflammation and endothelial injury.
collateral circulation develops
mostly affects parts of arterial tree and lower extremity arteries
Plaque develops arterial bifurcations
Symptoms develop when the vessel is occluded by 60% or more
PVD risk factors
tobacco, DM, hyperlipidemia, elevated C-reactive protein, uncontrolled HTN
other factors: family hx, age, gender, hypertriglyceridemia, obesity, sedentary lifestyle, stress, men, cholesterol >240
S/Sx of PVD
Intermittent pain/ cramping with activity [claudication] Rest pain – burning sensation in legs Numbness, decreased sensation Diminished or absent peripheral pulses Extremity pallor with elevation Extremity dark red when dependent Thin, shiny and lack of hair on skin Thickened toenails Skin areas of discoloration Skin breakdown
Treatment for PVD
Clinical therapies:
Smoking cessation
Meticulous foot care
Support hose
Exercise [walk 30-60m, 3-5x week; walk until pain, rest, then walk again until pain for 30min]
Rest for pain
BMI2 priority education topics for PVD
Smoking cessation
DM control, foot care
lipid mgt -statins [lipid-lowering agent; lowers LDL & triglycerides]
HTN [thiazides, ACE-inhibitors, lifestyle changes]
two priority nursing diagnoses for PVD
ineffective tissue perfusion
impaired skin integrity
risk for falls
atropine
–
beta blockers
-olol slows HR, reduces workload angina, BP, HF, heart attack drowsy, fainting, swelling, bradycardia blocks negative effects of SNS watch BP
Ca channel blockers
-VND (vera nifed dilti)
decreases demand for O2 by lowering contractility and conductivity of the heart//relaxes blood vessels
bradycardia, constipation, edema
lipid-lowering agents
–
muscle pain, soreness, GI upset
complications with PVD
gangrene, limb amputation, infection, sepsis
Types of PVD
asymptomatic [found at dr]
intermittent claudication [pain upon activity]
critical limb ischemia [rest pain, tissue loss]
anticoagulants
warfarin, heparin
antihypertensives
–
orthostatic hypoTN, don’t stop abruptly!
antiplatelets
aspirin, clopidogrel
segmented BP
used to check peripheral pulses with doppler
thigh, below knee, ankle
drop in segBP >30 suggests PVD
Ankle Brachial Index
ABI
uses doppler
divides the ankle Systolic BP by the higher of the Lt and Rt brachial Systolic BPs
NOTE: elderly and DM pts-falsely elevated ABIs due to calcification of arteries
DON’T do immediately after revascularization or on distall bypass grafts [risk of graft thrombosis]
ACE-inhibitors
-pril
BP, HF, MI
relaxes blood vessels, reduces heart workload
dry COUGH, dizzy, drowsy, sunburn
digoxin
affects strength, contractility of heart
K+ high or low
early toxicity: anorexia, N/V, fatigue, headache, vision changes
late toxicity: dysrhythmias (brady, AV block)
HOLD if HR
PVD post op care
walk!
no knee flex, or prolonged sitting
if edema, lay with feet above heart level
Acute arterial ischemia
sudden interruption to blood supply
6 Ps: pain, pallor, pulselessness, paresthesia, paralysis, poikilothermia
tissue necrosis and gangrene
paralysis = nerve death
start IV heparin, remove thrombus (meds: tPA, urokinase0 through femoral artery to site of clot (24-48hrs)
a-adrengergic receptors
vasoconstriction
b-adrenergic receptors
vasodilation
classifications of HTN
normal 160/>100
cause of secondary HTN
cirrhosis narrowing of aorta drugs: estrogen, NSAIDs, sympathetic stimulants endocrine disorders neuro disorders pregnancy renal disease sleep apnea
Risk factors for primary HTN
Age alcohol (limit to 1oz) smoking DM (higher risk for organ disease (heart, kidneys)) elevated lipids (atherosclerosis) excess sodium intake gender (men) family hx obesity ethnicity sedentary lifestyle socioeconomic status stress
HTN concept correlation
Altered antecedents: Cardiopulmonary System Fluid Volume Blockages Altered Atrributes: Blood Pressure Capillary Refill Pulses MAP Negative Consequences: Ischemic Pain Loss of Fine Tactile Sensation Confusion ↓ Organ Function
HTN S/Sx
fatigue, dizziness, palpitations, angina, dyspnea
HTNsive crisis: nosebleeds, headache, anxiety, dyspnea
HTN Complications
Heart: CAD (atherosclerosis)
Lt Ventricle Hypertrophy: increase cardiac workload
Heart failure: when heart can’t pump enough blood to meet demand (SOB on exertion, paroxysmal nocturnal dyspnea, fatigue
Brain: CV disease (atherosclerosis -> ischemic attacks, stroke, brain damage bc vessels aren’t able to control blood flow in brain causing cerebral edema)
PVD
Nephrosclerosis: chronic kidney disease (early sign is nocturia)
Renal damage: blurred vision, retinal hemorrhage, loss of vision
Collaborative Care HTN
Lifestyle mod: weight loss, DASH plan, Na reduction, moderate alcohol, physical activity, avoid tobacco, Mgt psychosocial risk factors
HTN diagnostic tools
Thorough H & P
Eye exam – assess retinal damage
Check EKG
UA – check protein
Check labs – BUN, creatinine, lipids, K+,
Renal eval. – IVP, renal arteriogram
Assess BP- for each check - √ BP x 2 at least 2 minutes apart
HTN emergency v. urgency
Hypertensive emergency - BP > 200/150
Evidence of organ damage
Most times d/t patients d/c meds abruptly
Hypertensive urgency- BP > 180/120
BP ↑ but no organ damage
Note: both require quick assessment and initiation of treatment
HTN drugs
Diuretics 2nd drug from other antihypertensive drug classifications All work as vasodilators in some way ACE inhibitors angiotensin receptor blockers beta blockers calcium channel blockers
CHF Patho (systolic)
inability to pump blood effectibely
impaired contractile function (MI), increased afterload (HTN), cardiomyopathy, and mechanical abnormalities (valvular disease)
loses ability to get enough pressure because it’s dilated and hypertrophied.
Ejection Fraction (EF)
CHF patho (diastolic)
inability for vetricles to relax and fill during diastole
“HF with normal EF”
decreased stroke volume and CO
veinous engorgement
result of Lt ventricular hypertrophy from HTN, MI, valve disease, cardiomyopathy
CHF patho (mixed)
dilated lt ventricular walls unable to relax
EF
Compensatory Mechanisms (CHF)
- SNS activation-1st (triggered in low CO states); least effective; releases epi and norepi; increases HR, contractility, vasoconstriction
- Neurohormonal-starts renin-angiotensin-aldosterone system (kidneys, hold water/salt, increase BP and vasoconstrict) ADH released holds more water-all of this leads to increased cardiac workload, myocardial dysfunction, and ventricular remodeling
- Dilation-enlargement of chambers of heart; caused by increased pressure in chambers over time; eventually overstretches
- Hypertrophy-increase in muscle mass and cardiac wall thickness in response to overwork and strain; leads to poor contractility, needs more O2, poor coronary artery circulation (ischemic more easily), prone to dysrhythmia
Left Sided HF
most common
causes blood to back up into lt atrium and pulmonary veins
pulmonary congestion and edema
frothy pink sputum
Right Sided HF
Rt ventricle fails to contract effectively
causes: lt sided HF, rt ventricular infarction, pulmonary embolism, “cor pulmonale”=rt ventricular dilation and hypertrophy from pulmonary disease
JVD, hepatomegaly, splenomegaly, vascular congestion of GI tract and peripheral edema
S/Sx Right Side HF
JVD, edema, weight gain, increased HR, ascites, body edema, hepatomegaly
Fatigue, anxiety, dependent edema, RUQ pain, anorexia, GI bloating, nausea
S/Sx Left Side HF
increased HR, alternating pulses, low PaO2, crackles, S3/S4 heart sounds, pleural effusion, change in mental status, restless/confused
Weakness/fatigue, dyspnea, shallow breaths @ 32-40/min, paroxysmal nocturnal dyspnea, orthopnea, dry hacking cough, nocturia, frothy pink sputum
FACES (CHF)
Fatigue limitations of Activity chest Congestion/cough (dry, nonproductive) Edema Shortness of Breath
Clinical Manifestations CHF
Fatigue, dyspnea, tachycardia (compesation), edema, nocturia, skin changes (dusky, shiny, swollen, X hair growth, brown/brawny), behavioral changes, chest pain (low coronary perfusion), weight changes (edema, muscle waisting)
Complications of CHF
Pleural effusion, dysrhythmias (atrial fibrillation, ventricular tachycardia (VT), ventricular fibrillation (VF)), lt ventricular thrombus (formed in LV), Hepatomegaly (liver congested with venous blood: fibrosis, cirrhosis, cell death), Renal failure
CHF Risk Factors
Hypertension Ischemic Heart Disease Age Obesity Diabetes Renal Failure Valvular Heart Disease Cardiomyopathies Myocarditis Congenital Heart Disease Excessive Alcohol Use Genetics
angiotensin blockers
-sartan
CHF Treatments
Drugs, supp O2, high fowler’s, ultrafiltration or aquapheresis, intraaortic balloon pump (increases coronary blood flow to heart), Ventricular Assist devices, diet, exercise with rest periods, lifestyle change, fluid intake (lowered)
Mitral Valve Prolapse Clinical Manifestations
A mid-systolic click & a late systolic murmur Atypical chest pain; tightness Dizziness; syncope Tachycardia Palpitations r/t dysrhythmias Fatigue; weakness Dyspnea; hyperventilation Anxiety; depression; panic attacks chest pain during emotional stress-nitrates don't work
MVP patient teaching
Take meds as prescribed
avoid caffeine (may exacerbate Sx)
Check OTC drugs for stimulants that may exacerbate Sx
Begin/maintain exercise program
Contact HP if palpitations, fatigue, SoB or anxiety develop or worsen
MVP nursing interventions
stay hydrated, exercise regularly, avoid caffeine Associated Risks Arrhythmias Infective Endocarditis Smoking Cessation Control Blood Pressure Diagnostic/Surgical Procedures Medication Therapy
MVP Collaborative Care
Diagnostics:
Echocardiogram; EKG; CXR; Stress Test; Coronary Angiogram and Cardiac Catheterization
Pharmacological Tx:
Beta Blockers; Diuretics; Vasodilators; Digoxin; Antidysrhythmics; Aspirin; Anticoagulants
Surgical Tx:
Valve Repair
Valve Replacement
Gestational HTN
onset of HTN without proteinuria without proteinuria
doesn’t persist longer than 12 weeks postpartum
Preeclampsia defined
HTN and proteinuria after 20weeks
MAP >105
proteinuria >0.3
Eclampsia defined
Onset of seizure activity or coma in a woman with preeclampsia with no Hx of preexisting condition that causes seizures (seizures usually occur within 48hrs after birth) MAP >105 DTRs +3 headache Urinary OP
Chronic HTN defined
HTN present before 20wks pregnancy, and/or lasts 12wks postpartum
HELLP Syndrome
H-hemolysis
EL- elevated liver enzymes
LP- low platelet count
Sx-malaise, flu-like Sx, Rt upper epigastric pain
Patho Gestational HTN
Uterine arteries don’t widen
decreased placental perfusion and hypoxia
placental ischemia causes endothelial cell dysfunction
generalized vasospasm
poor tissue perfusion to all organs, increased peripheral resistance and increased BP
Labs for preeclampsia & HELLP
H&H up down
platelets normal to down 70 and up
Uric Acid >5.9 >10
bilirubin normal or up up >1.2
Mild Gestational HTN and Preeclampsia Treatment
Activity Restrictions
Diet (protein, Ca, Folic Acid, Zinc) with 48-64oz water
Limit excessive salt, eat roughage, avoid alcohol, tobacco, caffeine
Preeclampsia Pt Teaching
Take BP as directed in right arm, sitting (report increase)
Dipstick clean-catch urine (report >+2)
Assess baby’s activity (report
Sever Gest HTN and Preeclampsia
immediate Mag sulfate (4-6g load dose over 15-30min, 1-2g in LR maintenance)
monitor BP, UO, cerebral status, epigastic pain, labor, vaginal bleeding
after 34 wks, risk of continuing are greater than preterm birth (get baby and placenta out!
Hospital Precautions: Quiet, non-stimulating
Seizure precautions (suction, O2, call light)
Emergency Meds: hydralazine, labetalol, nifedipine, Mag sulfate, Ca gluconate or Ca chloride
Emergency birth pack
Mag Sulfate mild toxicity
normal s/sx: flushed, feels hot, sedated, nauseous, burning at IV site
toxicity: lethargy, muscle weakness, decreased/absent DTRs, double vision, slurred speech
Mag sulfate high toxicity
maternal hypotension, bradycardia, bradypnea, cardiac arrest
antidote! d/c immediately, admin calcium gluconate IV
HTN drugs intrapartum
hydralazine-decreases peripheral resistance
headache, flushing, tachycardia, N/V
labetalol-vasodilator
flushing, orthostatic hypoTN, tremulousness
Methyldopa-CNS suppression
sedation, sleeepiness, constipation
Nifedipine-relaxes smooth muscle (Ca blocker)
headache, flushing
DON’T give with Mag Sulfate-paralysis!!
Seizure care
turn head to one side, side rails up, place pillows/blankets around to avoid injury, call for assistance, document time of onset and duration
after: assess airway, suction if needed, admin O2 in non rebreather @ 10L, check cervix
pathophysiology of CAD
atherosclerosis!
CRP increased
1. fatty streak-earliest lesions of atherosclerosis, characterized by lipid filled smooth muscle cells (tx includes lowering LDLs)
2. fibrous plaque-progessive change in artery wall; narrowing of the vessel wall and reduction in flow to distal tissues
3. Complicated lesion-final stage (most dangerous) inflammation causes rupture, leading to thrombus that further narrows (glycoproteins and fibrinogen cause more clotting) or occludes the artery (plaque is now referred to as a complicated lesion)
Risk Factors for CAD
age, gender, ethnicity, family hx, serum lipids, BP >140/90, DM, tobacco, inactivity, obesity
CAD diet
low saturated fat and cholesterol, high complex carbs (whole grains, fruits, veggies)
Fat 30% of diet
reduce red meat, egg yolks, whole milk
eat omega-3s (salmon or tuna 2x/week)
CAD Treatment
stress-lowers SNS response cholesterol-keeps from buildup BP control-kees from injury angina- coronary angiograms-xray with contrast percutaneous transluminal cornoary angioplasty (PTCA) - balloon/stent stints-holds open vein coronary artery bypass grafts (CABG) -grafts new vein around obstruction
chronic stable angina
reproducible, goes away with rest
notify immediately if ups in frequency or length!
higher demand for O2=angina
Unstable Angina
can happen at rest
plaque rupture
