Family Centered Care


Interrupts life (interrupts life)
Not your best self
End-of-Life Care






“Allow natural death” instead of DNR
Palliative care – alternative methods until they’ve been cured or until death
Better for patient, family, hospital (money)
DNR – no compressions no intubating but still treatment. Written orders for
what the pt wants (limited code, chem code etc.)
Comfort care – no BG, benzos/opioids for pain
Pain – assessment facial expression, agitation, vital signs
Sx Management
o Dypnea – position oxygen
o N/V – antiemetics (Zofran), scopolamine patch
o Fever/infection – usually antibiotics are d/c, Tylenol
o Edema – diuretics
o Delirium – holoparadol, avoiding restraints
Withdrawal of Mechanical Ventilation
o Preparing family – don’t know how long, alterations in respirations
Organ Donation
o Brain death (GCS 5 can look into), post cardiac death (isn’t brain dead)
Family care
o Family can be present during resuscitation
Stress Response
Stress response resolves short term stimuli. When long term stressful stimuli body
becomes exhausted, exceeds coping ability.
 Reactive, Anticipatory, Conditional (learned stimuli leading to stress)
Physiologic Response
Limbic system – emotions
Cerebral Cortex - memory attention, thoughts/awareness, *past experiences play
a role in how we perceive stress
Hypothalamus – sends hormones that affects the SNS and the pituitary
o SNS:Catecholamines (epinephrine norepinephrine) vasoconstriction
o Posterior pituitary Corticotropin-releasing hormones CRH (ADH)
increases volume
o Anterior pituitary stimulated by CRH ACTH – increases steroid (cortisol),
aldosterone (holds sodium, water)
SNS Catecholamines:
Epinephrine & Norepinephrine
o Constriction –>Increased venous return -> increase volume (PRELOAD)
–> increase stretch –>better snap
o Increase BP
o Pallor, incrase sweat gland, pilorection, skin at risk for skin
breakdown/ulcer
o Increase pupillary dilation
o Decrease GFR
o Nausea, stress ulcer - Prophylactic PPI
Ephinephrine released in greater amount (shorter acting)
o Bronchodilation increases O2 increases strength
o Increase force and rate of contraction. Increase CO and BP
- Inotropic increases contractility(epinephrine) , negative inotropic decrease
contractility (Beta-Blockers)
o CNS stimulation: more alert, increase muscle tone
o Vasodilation to skeletal muscle: increase function
o Increased lipolysis: increased circulating free fatty acids - over time
increases cholesterol
o Glycogenolysis (glycogen breaks into glucose) gluconeogeniss (glucose
being broken down from non carb sources ): increase BG
Cortisol (released from corticotropin-releasing hormone CRH to Anterior
pituitary to ACTH to Adrenal cortex)
o Increase risk of uclers
o Steroids given during allergic reaction
o
Aldosterone (CRH)
o Retain sodium - Retain water - Increase blood volume – increase BP
- As it holds onto sodium, depletes potassium (potassium sparing diuretic is
a aldosterone antagonist)
ADH (posterior pituitary)
o Water reapsorption - increase blood volume – increase BP
- Neuro pt, SIADH & Diabetes insipidus
Review Chart Slide 10
Acute neuroendocrine response to critical illness
 Serum cortisol level – low levels and adrenal insufficiency with long term critical
illness
 Cosyntropin stimulation test – specific timing, monitoring cortisol response to
stimuli (minimal to no rise with adrenal insufficiency)
 Corticosteroid replacement - going to give short term low dose hydrocortisone
for septic shock. Never d/c abruptly
 Liver and pancreas – liver produces glucagon, doesn’t mean they’ll always need
insulin
Insulin Management in Critically Ill
 Frequent blood glucose monitoring – at least every hour



Continuous insulin infusion – what was previous reading, the rate of change
Transition from continuous to intermittent insulin coverage – how are they
receiving their nutrition? Q4H – Q6H
Corrective insulin coverage
Hypoglycemia management
 D/C continuous infusion of insulin
 Blood glucose concentration monitored Q15 until above 70mg/dl. – glucose given
depending on pt status IV or PO. Hypokalemia risk when given IV infusion
Nursing Management
 Monitor hyperglycemic side effects of vasopressor therapy – norepinephrine and
epinephrine
 Administer prescribed corticosteroids
 Monitor blood glucose, insulin effectiveness, avoid hypoglycemia
 Provide nutrition – enteral (EHA) feedings first few days, TPN within 7 days
 Educate patient and/or family
 Collaborative management
Significant effects of stress response:
↑ BP and ↑ HR – norepinephrine/epinephrine
Bronchodilation and ↑ ventilation ↑ blood glucose levels – epinephrine
Arousal of the CNS
↓ inflammatory and immune responses – what causes?
↑ serum cholesterol levels
These significant effects are necessary to …
 Increase oxygen levels
 Increase circulation
 Increase cell metabolism
* Stress plays a significant role in the development of diseases or the exacerbation of
disease
* Diseases include but not limited to:Hypertension, Diabetes, Coronary artery disease
Adverse Heart Effects during stress response
 Myocardial ischemia – SVR increases because of vasoconstriction peripherally,
increses myocardial oxygen demand
 Left ventricular dysfunction – increased SVR
 Ventricular dysrhythmias – altered brain activity can change in the ventricular
repolarization and electrical instability
Disease and stress – prolonged severe stress
 Acute renal failure – decreased GFR, vasoconstriction





Stress ulcers – prophylactic PPI
Infection
Impeded healing process
Cancer
PTSD – flashback nightmares depression
Strategies to reduce the effects of stress:
 Adequate rest, healthy diet, regular moderate exercise, distracting, counseling,
music, antianxiety medications, methodical approach to problem solving,
meditation, prayer, bible study, recreation, human physical contact, pets
Hemodynamic Monitoring
Physiologic goal of the cardiovascular system is to ‘feed’ the cells oxygen. This is
accomplished by:
 Lungs provide the oxygen supply
 Heart pumps the oxygenated blood
 Blood vessels circulate the blood to the cells
If any one of these systems are not functioning optimally, the others will be affected.
MAP = diastolic X2 + systolic /3 (at least 60-65)`
If a patient requires hemodynamic monitoring, usually one of the 3 following nursing
diagnosis will apply:
 Decreased cardiac output
 Fluid volume excess or deficit
 Ineffective tissue perfusion
Preload “filling pressures”
 The volume in the ventricle at the end-diastole
 Right heart – CVP (central venous pressure) 2-5
 Left heart – LVEDP (left ventricular end diastolic pressure “wedge”)
- Increased SVR from hypertension, cardiac tamponade, aortic valve stenosis
can increase LVDEP
- Pressures tell us there is a problem – we have to figure out what the problem
is
Preload is influenced by:
 Volume
 Compliance
 Atrial “kick”
Afterload –amount of resistance ventricle must overcome to eject the blood
 Right heart – resistance (pressure) exerted from pulmonary vascular bed (PVR)
 Left heart – resistance (pressure) exerted from aorta and systemic vascular beds
(SVR)
Contractility – ability of muscle fibers to contract and eject blood into the pulmonary or
systemic vasculature
 Starlings law – increase blood volume = increase stretch of myocardium =
increased force to pump blood out
 SV – 60-70ml per beat
 Ejection fraction – amount of blood pumped out / total amount of blood in
ventricle 50%
HR X SV = CO (how much blood we pump out each minute 4-6L/minute)
Three invasive tools for measuring hemodynamic pressures:



Intrarterial catheter (A – line, arterial line, art line)
Central venous assess (CVP line) – vena cava, monitor preload,
Pulmonary artery line (PA line) – swan-ganz catheter, high risk (endocarditis,
cardiac tamponade etc.)
Four components of hemodynamic monitoring system
 Invasive catheter
 High-pressure tubing with flush solution
 Transducer - “Brains” of the system
o Fluid filled interface between catheter tip and the monitor (blood/fluid
interface)
o Computer chip that converts pressure signals to waveforms and pressure
values.
 Bedside monitor & cables
Bedside hemodynamic monitoring: equipment, basic setup, heparin. (phlebostatic axis
– 4th intercostal space midaxillary line).
 Zero transducer
 Phlebostatic axis
 Leveling the transducer
Intra-arterial blood pressure monitoring
 Indications – frequent blood pressure monitoring and ABG’s, hypertensive crisis
 Catheters
o Insertion and Allen test
Management:
o Infection
o perfusion pressure (MAP)
o pulse pressure (difference between sys. and dias. ) – if high = aortic
stiffness, if low = poor heart function
o cuff blood pressure
Nursing management
 Monitor peripheral perfusion and document assessment of tissue distal to the art
line

Complications – shows dampened wave form, compare to NIBP (or bubble,
kinked wrist)
o Blood loss
o Emboli – difficulty pulling back when drawing blood
Nursing management (continued)
 Removal of Arterial Line
o Assess for presence of sutures
o Remove sutures if present
o Apply direct pressure
• 5 minute if coagulation studies are normal
• 15 minutes if coagulation studies are elevated
o Chart
• Catheter tip was intact
• Amount of time pressure held if over 5 minutes
• Absence or presence of a hemotoma
WARNING!!!!! NEVER ADMINISTER MEDICATIONS THROUGH AN ART LINE
Preventricular contraction – art line waveform shows nonperfused
Pulsus paradoxus – best state is during exhalation. Inhalation has more pressure in
chest -> effects venous return.
Central Venous Pressure Monitoring
 Indications: a lot of meds to be given (tpn, Propofol, iv antibiotics etc.), can draw
blood from central line, altered fluid status – how much fluids to give.
 Insertion: internal jugular, subclavian, femoral. Increase risk of infection, risk of
pneumo
 Complications: air embolus (right caps), thrombus formation (if can’t draw blood
easily) – measure circumference 2 cm, infection (systemic and local),
 Management: CVP – volume assessment (normal 2-5), removal, patient position
– HOB up to 60 to get accurate reading
Pulmonary Artery (PA) Pressure Monitoring
 Indications: measure Cardiac Index (BMI – cardiac output for YOU 2-4), CHF,
shock,
 Cardiac output determinants
 O2 supply and demand
Preload
• Assess cardiac dysfunction – low or high numbers indicate pressure and need
for fluid. (The higher the pressure in the left ventricle the greater risk of
cardiac dysfunction.)
• CVP – 2-5
• LVEDP – PAOP 5-12
Afterload
• SVR 800-1400
• PVR 100-250
Contractility
o SVR, myocardial oxygen, inotropic medications, electrolyte levels affect
contractility
o Dopamine, dobumamine, milrinine?
After insertion
o Suture in place, verify position (X-ray, also no pneumo), apply plastic
sleeve
o Medical management ?
Nursing Management
 Patient position – can be flat or up to 60, let stabilize after pt movement for 5min phlebo
 Respiratory variation
 Positiven end-expiratory pressure (PEEP)- ARDS/intubated pts, help alveoli stay
open, increases intrathoracic pressure (PEEP 10 > can affect PAOP/LVDEP
lower volume)
 Avoiding complications – valvular damage, clot, hemorrhage, infarction of the
lung, cardiac tamponode, endocarditits
 PA Removal – dysrhythmias
Cardiac Ouput Measurement
 Thermodilution CO bolus method – fill up syringe 5-10mL D5 fluid, push fast,
changes temp how long does the cold fluid take to reach the thermaster = CO
 Patient position and cardiac ouput
 Clinical conditions that alter cardiac output
 Continuous invasive cardiac output measurement
 Calculated hemodynamic profiles
Noninvasive and minimally invasive measurement of cardiac output
 Thoracic electrical bioimpedance  Arterial waveform-pulse contour
 Esophageal Doppler cardiac output
 Partial carbon dioxide rebreathing cardiac output
Continuous monitoring of venous O2 satuation
SVO2 – consumed O2, at the end of circulation – what do I have left?? Don’t want to
come back with 0 or 100. Taken from the pulmonary artery
SCVO2 – from vena cava, end of circulation 02 (not much difference)
Why??? - want to see cells using O2, and sending out enough 02
 SVO2 cardiac output
 SVO2 or SCVO2 hgb, and O2 consumption
- Normal svo2 is 80 with normal value, normal consumption is 10 ish
Cardiac Alterations
Cardiovascular disease: Public education, disease processes, cardiac disorders seen in
crtical care
Coronary Artery Disease
 Description and etiology: atherosclerotic changes in coronary arteries
 Risk factors: age, gender, race, family history – 45 yr. or older, men at a younger
age than women
o Hyperlipidemia: total cholesterol <200, HDL >50, LDL<100,
triglycerides <150
o Obesity >30
o C-reactive protein (CRP) – non-specific sign of inflammation
o CAD risk equivalents – diabetes, CKD, atherosclerotic dzs
o Multifactorial risk – more than two
o Secondary prevention – preventing further issues of someone with
an existing diagnosis
Pathophysiology
 Development of artherosclerosis – the 100% occlusion risk
 Atherosclerotic plaque rupture – plaque can be broken and clot leading to an MI
risk
 Plaque regression – educating lifestyle changes can cause regression of plaque!!
ACS
 Angina – sx, women
 Stable – predictable, precipitating factors, 5 min of rest/SL
 Unstable – worse pain, unrelieved
 Variant (Prinzmetal) – spasm of coronary arteries, at rest same time of the day
 Silent – no sx but shown on EKG, diabetic neuropathy
Medical Management – seen right away within 90 min. door to balloon time
Nursing Management
 Recognizing myocardial ischmia
o EKG – elevated ST segment, they have full thickness damage, full
occlusion?? NSTEMI is not full thickness damage.
 EKG also show where the damage is
o Angiography
 Relieving chest pain
o Aspirin 160-320mg antiplatelet
o O2 – meet demand
o Nitrates – vasodilation of coronary arteries
o Morphine – 2-4mg IV, pain/calm
o Prepare for cath lab – dual antiplatlet medication (aspirin/Plavix),
loading dose of clopidogril, within 30 min. fibronilytic therapy,
heparin (anticoagulant)
 Maintaining calm environment - still ready for acute situation, educate on
avoiding valasava maneuver
MI description & etiology – plaque rupture, a new thrombus, or coronary artery spasm
 Zone of ischmia – can be recovered, inverted T wave (no ST segment changes yet)
 Injury – potentially viable tissue, ST elevation & inverted T wave
 Infarction - dead tissue, pronounced Q wave (deeper wider)
St segment elevation or depression BOTH are concerning, Q wave seen for a while
after an MI (until collateral circulation)
 Transmural Q wave MI – all three layers of heart have been effected
 NSTEMI – still aggressive but can change treatment, - wont receive fibronlytic
but will receive the glycoprotein inhibitiors integrilyn ??
- All same meds except for fibrolytics
 Cardiac biomarkers – reperfusion spikes, monitor for at least 24 hours (q6-8hr)
- Not reperfusing – days long increase and long drop, when reperfused gonna
see sharp increase and sharp drop.
- CKMB & Triponin – both cardiac specific
 Complications – DARTH VADER
o Death, Arrythmias, Rupture, Tamponade, Heart failure, Valve disease,
Aneurysm of ventricle, Dressler’s syndrome (pericarditis), Embolism,
Recurrence/mitral Regurgitation
Complete heart block occurs when specific portinos of condduciton system are
destroyed – no communication between atrium and ventricles. Within first 4 hours of
pain you will see the fatal dysrhythmias (VFIB)
o Heart failure – pumping power diminished, subtle or severe
o Cardiogenic shock – severe LV failure, aggressive management
Heart failure
Neurohormonal compensatory mechanisms in HF
 SNS – releases catecholamines – increases vasoconstriction – increases afterload
& contractility & preload initially
 RAAS – increases fluid retention leading to overload
 Ventricular hypertrophy – increased muscle to combat increased SVR
 Ventricular remodeling – lead to ventricular dilation poor contractility
 Sx – BNP > 100 SOB related to HF, EF < 30%
- HF caused by valvular dysfunction, dyrythmias, myocardium muscle
dysfunction
Nursing Management
 Optimizing cardiopulmonary function
 Promoting comfort and emotional support
 Monitoring the effects of pharmacologic therapy
 Nutritional intake – I/O
 Patient education – daily weight, fluid restrictions, medications
- Ekg monitor to look for dysrhythmias, breath sounds, O2, diuretics,
vasodilators (decrease SVR, preload, BP), morphine
- At risk for respiratory failure = be prepared for intubation
- Weighing daily, restrict activity if needed, HOB raised, maintain skin
Complications of MI
 Papillary muscle dysfunction – affected area at papillary muscle which affects
mitral valve
 Causes mitral valve regurgitation
 rapid clinical deterioration – aggravates LV
 Ventricular aneurysm – infarcted myocardial wall
 Myocardial wall becomes thinned and bulges
 Leads to HF, dysrhythmias, and angina – ventricular rupture, harbors
thrombi lead to embolic stroke “turbulent” blood flow, ventricular
disruption won’t go throw dead tissue
Acute pericarditis
 An inflammation of visceral and/or parietal pericardium – puts pressure on
heart, ventricles can’t expand to contract effectively
 May result in cardiac tamponade, ↓ LV filling and emptying, heart failure – shows
signs of MI
 Chest pain – leaning forward, fever, hypertensive, narrow pulse pressue
 Pericardial friction rub
 ECG changes – ST elevation because of limited blood flow from pressure
 Treated with anti-inflammatory agents
- 2-3 days after MI, treat pain and inflammation NSAIDS, aspirin, and
corticosteroids
Medical Management of MI
 Recanalization of the coronary artery
o Fibrinolytics (tPA) – dissolves clots, high risk, or PCI
 Anticoagulation – stops blood from congealing
o Heparin
 Dysrhythmia prevention
o Amiodarone or beta blockers
 Prevention of ventricular remodeling
o ACE or ARBS – RAAS system interrupted to reduce fluid retention
that increases workload. Long term heart protection by preventing
remodeling by vasodilating
Nursing management
 Balance of myocardial oxygen supply and demand
 Prevention of complications
 Depression after MI
Patient education
 Risk factor reduction – diabetes, cholesterol etc.
 Manifestations of angina – jaw/arm pain, indigestion, doom
 When to call a physician or emergency services -
 Medications
 Resumption of physical and sexual activities
Sudden Cardiac Death
 Description – usually an abnormal arrhythmia (vtach to vfib), might not have
gone to a doctor, spontaneously when they’re out and about
 Etiology
 Pre-existing ventricular dysfunction resulting from cardiac disease
 Medical management – post MI, watch for signs of HF, educate
Cardiomyopathy
- Description and Hypertrophic cardiomyopathy: is not due to overwork, it is
genetic
- Restrictive: third world countries
- Dilated: overdilated, big floppy muscle walls doesn’t snap back as it should.
Could be ischemic, idiopathic, genetics, valvular heart dysfunction,
myocarditis/infection
Nursing mgt. - etiology – treated like HF, positive inotropes, reduce fluid to
reduce workload
Hypertensive Emergency
o Description - >180 sys >120 diastolic
o Emergency- already signs of organ damage. Decreased output/high BUN
o Urgency
o Etiology
o No prior history
o Noncompliance or inadequate medication therapy
 Medical Management
- Nitrocide (Nipride), meds with short half life. Avoid relative ischemia. 20% in
first hour and then another 10-15% in another hour.Hemorrhagic
stroke/aortic dissection are reason to drop BP suddenly. Meds based off of
cause of htn (drip: nitro, Lasix, IV push: labetalol, lisinoprol, hydralazine)
Cardiac Treatments
Fibrinolytic Therapy
Eligibility criteria – high risk ex. surgery/hemorrhagic stroke/recent trauma,
aneurysm clips
 Patients with recent onset of unstable chest pain and persistent ST
elevation
 Patients who present with bundle branch blocks (BBBs) that may obscure
ST segment analysis and a history suggesting an acute MI
- Goal: given within 30 min. of arrival, within 12hr. of onset.
Fibrinolytic agents “ase”
 Streptokinase (SK) – systemically not clot specific, longer half life
 Tissue plasminogen activator (tPA) – short half life
 Recombinant plasminogen activator (rPA) – longer half life, given as a
double bolus
 Tenecteplase (TNKase) – more fibrin specific, more plasma specific,
weight based, bolus – most commonly used
 Outcomes of fibrinolytic therapy
Evidence of reperfusion
 Pain should go away and reperfusion dysrhythmias (short term but
monitor pt decline)
 ST segment – goes away within 60 min.
 Cardiac biomarkers – sharp spike & drop, strict time Q4 ??
Nursing management
 Candidate identification
 Patient preparation – pt, inr, aptt etc.
 Assessment – internal/external bleed, any LOC change
 Bleeding – ensure good patent IVs
Patient education – can’t get up on their own
 Fibrinolytic agents
 Bleeding
Catheter Interventions for Coronary Artery Disease
PCI
 Indications: MI *gold standard,
 Surgical backup: CABG
 PTCA (angioplasty) limitations  Atherectomy: Directional coronary arthrectomy (taking little pieces out) &
Rotablator (like a drill)
 Corony stents: left in place, maintain patency, coated in anticoags,
thrombosis is a risk.
Complications
 Acute: cardiac, bleeding, others
 Late: restonosis, late thrombosis
Nursing management
 Angina
 Renal protection
 Hydration - to flush out IV dye
 Sodium bicarbonate – can help protect kidneys
- Angiography
Nursing management (Cont.)
 Vascular site care - Active closure devices
 Patient education – can’t bend lay flat if femoral.
 Medication regimen
 Risk-factor modification
- Pulling sheath, check pulses, two person job, neurovascular checks,
transparent pressure dressing
Percutaneous valve reparir – balloon valvuloplasty, transcatheter aortic valve
replacement (TAVR). (Arteries or through the chest)
Cardiac Surgery
 CABG : mammory artery or saphenous vein most common
 Valvular surgery – bypass too.
 Cardiopulmonary bypass
Post- op management
 Cardiovascular support: HR/preload/afterload/contractility
 Temp regulation – fever give Tylenol
 Control of bleeding – hematoma, petechiae
 Chest tube patency – mediastinal chest tube, connected to suctin to drain blood
(can cause tamponade effect)
 Pulmonary care – O2 demand, spirometry, get to sit up, cough
 Neurologic – changes in LOC
 Infection – WBC temp
 Renal involvement – BUN, creatine, <30 ml per hour, GFR
IABP –inflates at end of systole giving extra push to support CO, when balloon collapses
it decreases SVR completely. Also helps with coronary artery blood suuply during
diastole.
 Indicated: severe HF or recent MI,
 Management: high risk 1:1
 Balloon catheter position: can’t flex leg, flat, (through fem line), bed rest (below
30)
 Timing
 Dysrhythmias (timing), vascular complications (neurovasc checks), balloon
perforation (plaque in arteries), preventing further complications (log rolling),
psychologic needs, weaning, patient education (pain in back, or leg)
VAD
- used for flow assistance, bypasses ventricle to improve CO
- Heart transplant, not transplant but quality of life, with rest there will be
recovery
 Nursing mgt
 Device failure
- Anticoagulation - Blood 2-3x normal (ptt 25-35, pt 11-16, INR 1-1.1?
normal) PTT – hep, PT INR – coumadin
 Infection – strict aseptic technique and dressing changes, temp, cultures,
insertion site
 Continuous – flow hemodynamics
- Pulses/bp are different. Look at neurovasc. Sys. through doppler.
Vascular Surgery
Carotid Endartectomy – Post op mgt, neurologic assess. : laryngeal nerve,
epiglossal nerve (tongue)
 Bleeding, airway occlusion (tracheal deviation or hematoma),
cardiovascular monitong (potential MI), carotid stents
AAA repair
 Surgical repair (5cm or larger, sx, or expanding)
 post op mgt (monitor for ST elevation),
 endovascular stent grafts
–
distal to aneurysm assess neurovasc, risk for acute renal failure
Peripheral Vascular Procedures
 Surgical revascularization ( fem pop bypass)
 PCI (angioplasty, arthectomy, stent) risk for hematoma, aneurysm, artery
puncture, distal emolization, reocclusion
 Mgt – decrease skin breakdown, monitor st segment
 Neurovasc checks
- First line treatment education: stop smoking, exercise daily, htn/lipid control,
medications
Antidysrhythmics – terminate or prevent abnormal cardiac rhythm
 Sodium channel blockers – lidocaine.
 Beta-adrenergic blockers – blocks release catecholamines (SNS) – slows rate and
vasodilation. “lol”

Amiodarone – slows rate of heart, affect repolarization phase of heart, IV push or
IV drip
 Calcium channel blockers – diltiazem (Cardizem) or amlodipine (Norvasc).
Slows heart, effective for afib, rapid ventricular response, slows rate at AV node.
“pine”
 Unclassified – Adenosine - 6mg rapid IV push. have to give it fast with a flush
behind it. upper extremity IV, given for SVT, risk for asystole, blocks AV node
*chart in book good for NCLEX
Inotropic
 Cardiac glycoside – Digoxin
 Sympathomimetic agents – stimulates SNS
 Dopamine: lower dose minor vasodilation to help with renal perfusion.
Increase dose increased contractility (positive inotropic effect),
vasoconstriction, increase CO
 Dobutamine: positive inotropic effect, increase CO, contractility *cardiac
specific. Increases CO w/o significan increasein HR
 Epinephrine (Adrenaline): increase HR, cardiac conduction, contractility
*short acting
 Norepinephrine (Levophed): contractility, vasoconstriction, CO
Vasodilator medications
- reduce preload, decrease venous return, decrease stretch, decrease afterload
 Direct smooth muscle relaxants – nitropusside, hydralazine, nitroglycerine.
Activates nitric oxide.
 Calcium channel blockers – “pine”, diliazem (Cardizem)
 Angiotensin-converting enzyme (ACE) inhibitors – block angiotension 1 to 2.
 B-type natriuretic peptide – natrocor? BNP released when overstretched, fights
against stretch RAAS & ADH – decreases volume
 Alpha-adrenergic blockers – “zosyn”, BPH
 Dopamine receptor agonists Meds for HF
 Alleviate sx
 Slow progression
 Improve survival
- ACE inhibotors or ARBS, BB, Aldosterone Antagonists
Labs
Cardiac biomarkers in acute coronary syndrome
 Creatine kinase -MB – cardiac specific, elevated 4-8 hrs, peak at 15-24 hours,
remain helvated for 2-3 days.
 Troponin T and troponin I – cardiac specific, most sensitive, elvation 3-6hr,
 Cardiac biomarkers and reperfusion – rise in troponin levels and see them peak
early. Take on admission, before therapy, and then 6-8 hr
Natiruretic peptide biomarkers in HF
-
BNP identifies stretch of walls of ventricle. Kidney failure also can show
elevated levels.
Hematologic study
 RBC – 4.5-6 mil, 4-5.5 mil. anemia & polycythemia
 Hgb – 14-18, 12-16
 Hct – 40-54% 38-49% of RBC in whole blood
 WBC - 5-10,000
 Platelet 150,000-400,000
Blood coagulation studies
 Prothrombin time PT (coumadin/warfarin)
 International normalized ratio INR (coumadin/warfarin)
 Activated partial thromboplastin time aPPT (Heparin!!)
 Anti-factor Xa test of heparin activity (Lovenox)
 Activated coagulation time ACT
Serum lipid studies
 Toal cholesterol <200
 LDL <100
 Triglycerides <150
 High-density lipoproteins >50
Hypokalemia <3.5
 Ventricular dysrhythmias (early beats coming from ventricles, interrupts
conduction, prolongs ventricular repolarization)
 Increased dig toxicity
 ST changes
Hyperkalemia > 4.5
 Peaked T waves (decreased in AV node conduction velocity, slow ventiricular
depolarization and excelerate repolarization)
 Ventricular dysrhythmias
Hypercalcemia
 Slow and strong – positive inotropic effect (increase contractility)negative
chronotropic effect (decrease HR)
Hypocalcemia
 Fast and weak – negative inotropic effective (decrease contractility), positive
chronotropic effect (increase HR)
Hypermagnesemia
 Bradycardia
 Cardiopulmonary arrest
 Hypotension
Hypomagnesemia
 Tachycardia
 Prolonged QT
 Torsades de Pointes
- more common, caused by aggressive use of diuretics, htn and vasospasms lead
to heart spasms.
WS 1
Unit 1 Medications- know your medication templates
norepinephrine
Vasopressor ->Treats hypotension
 Used for pt with cardiogenic shock d/t poor perusion
Causes vasoconstriction peripherally
 Pt has poor blood flow to GI tract, fingers, toes
 Shunts blood up away from the extremities and sends it to the critical portions of
the body
Increases BP and perfuses vital organs.Venous circulation goes up and increases preload
Administration:
 Given IV; Vesicants (can damage tissue if IV is messed up)
 Titrated based on pt BP response
 Goal is to get MAP above 65
Side effects: HTN
DOBUTamine
Positive inotrope: cardiac specific
Slows and strengthens heart
 Given to pt with low CO d/t HF; CHF, post MI
Administration: Given IV
EPINEPHrine
Indications: vasopressor for hypotension, anaphylaxis, cardiac arrest
 Increased BP d/t peripheral vasoconstriction
 Central vasodilation and bronchial dilarion
Administration: Given IV; make sure good placement so that tissue isntruined
Side effects: HTN, tachycardia, can lead to arrythmias
cloNIDine (catopres)
*used for hypertensive urgencies – restricts vasocontriction
Alpha-blacker: anti-hypertensive
Admnistration: Pill, IV, patchy
Side Effects: hypotension, drowsiness, rash, bradycardia, Orthostatic hypotension
Carvedilol
Decreases HR and BP
Indications: dysrhythmias, HTN
Contraindications: asthma
Administration: Check apical pulse, hold if it is lower than 60
Protamine sulfate
Antidoate for heparin
Alprazolam (Xanax)
Benzodiazepine -> Anti-anxiety
Indications: GAD, ICU acquired delirium
Side Effects:
 CNS depression
 Can cause a slight decrease in BP
 Can cause total delirium in elderly population
Avoid abrupt discontinuation
Propofol
Sedative (works quickly and wears off quick)
 Might need for a procedure
 Milk of amnesia?
 Can cause severe hypotension
Side Effects: hyperlipidemia, hypotension
Administration:
 Change line daily, high risk for infection, can affect kidneys overtime
 Need special tubing, or open air vent
Other meds we discussed:
Eptifibatide
Intravenous antiplatelet agent used before and after PCI
Clopidogrel (Plavix)
Oral antiplatelet agent
ASA
Anti platelet aggregator
When giving ASA for MI
 Needs to be non enteric coating
 Let it absorb in the buccal mucosa
 Give 4 baby aspirins (81 mg per pill)
Morphine
 Relieves chest pain in an MI
 Helps with anxiety
 Little bit of dilation effect
Nitrates
Dilation of coronary arteries
Amiodarone
Helps with arrhythmias -> Stabilize electrical conduction in heart
Used after an MI
Beta-Blockers
Stabilize electrical conduction in the heart ->Used after an MI to prevent dysrhythmia
ACE Inhibitors
Angiotensien converting enzymes -> Interrupt raas
Adenosine
Stops the heart ->antidysthymic
Hydralazine
diuretic ->can be used in HF
Alteplase (tPA)
Thrombolytic “clot buster” -> ischemic stroke, PE, MI
Dopamine
positive inotrope ->causes systemic vasoconstriction
Positive inotropes
Increased the contractility of the heart
Examples
 Epi/Norepi
 Digoxin
 Dobuamine-cardiac specific
 Dopamine- causes systemic vasoconstriction
Warfarin
Anticoagulant
Unit 1 notes
Advance directive: medical POA can override this but this is a doc that explains your
wishes, before you are in a medical state where you cant make your own decisions

Never turn off alarms, unless in instance of upcoming purposeful death, alert
other staff first
 Family of pt can be in room during a code or resuscitation
 Before post mortem care: have to notify coroner first
Hemodynamics: answer is usually perfusion
Arterial lines, ventral venous lines, pulmonary artery lines (3 we need to know)
Cardiac cycle!
Math questions
o 1oz=30mL
o 8 oz = 1cup
o 240 mL = 1 cup
Components of hemodynamic monitoring
 transducer (brains of the system), invasive catheter, high pressure tubing with
flush solution (NS), bedside monitoring cables, pressure bag
Three Types:
 Arterial line
 Central lines
 Pulmonary
Callibarate Equipment
How to zero transducer:
o Three way stopcock off to the patient and open to air
o make sure it is level with phlebostatic axis
Phlebostatic axis
o Used in hemodynamic monitoring system, the point of where the
transducer should be
o While patient is laying flat, the fourth intercostal space midaxillary line
o 3 way stop cock, 2 on top, one on bottom, top goes on the patient
o Zero point of circulation
o Need to re-zero everytime the patient gets up
Artherosclerosis
- develops by plaque buildup in the arteries
- to treat non-pharmacologically: keep cholesterol down
- normal:
o HDL: 50
o LDL: 100
o Triglycerides: 150
o Total cholesterol: 200
Critical Care Organizations
- Main association for professional accountability: American association of
critical care nurses (AACN)
DNR
- Must be charted, documented, and ordered before ordered
Preload (LVEDP)
Filling pressures in diastole & Volume entering the ventricles
 Right side of the heart: centeral venous pressure
o Right before its getting ready to contract, this is the lowest pressure point
 Left side of the heart: pressure in the ventricle right after dystole( ventricular
relaxation) , right before systole (ventrictular contraction)
Influenced by:
o Blood volume
o Compliance of the ventricles: Ability of the ventricles to expand and
receive blood and then snap back and contract to push blood forward
o Atrial kick (Right at the end of dystole (ventricular relaxation), right
before systole (ventricular contraction). Ventricle fills just a little bit
more and expand a little extra, then kicks blood out
Right side name: centeal venous pressure (normal amount: 2-5mmHg)
Left side name: Left ventricular end diastole (normal amount: 5-12mmHg)
Afterload
Amount of resistance the ventricles must over come to eject the blood
Right sie of the heart: resistance exerted from the pulmonary vascular bed (PVR)
o Increase PVR: Pulmonary edema, any kind of pulmonary disease
Left side of the heart: resistence/pressure exerted from the aorta and systemic
vascular beds (SVR)
o Increase SVR: kidney failure/disease, vasocontriction, high blood pressure
Cardiac Output SVR? SV
Volume of blood ejected by the left ventricle into circulation in one minute
HR x SV = CO
SV: amount of blood pumped out of the heart per heart beat (60 -70ml)
(If ventricles are holding 120 mL’sand the ejection fraction is 55%... 120x.55= 66
mL SV)
Lowest normal cardiac output: 3,600 - highest normal cardiac output: 7,000
MAP meausres CO
 Formula: {(2xDP) + SP} /3
 Normal amount: in the 90’s
 Lowest acceptable amount: 60; organs are not being perfused if less than this #
Heart Failure
Generic term that describes that the pumping power of the heart has been
diminished leading to backwards flow of blood
- Left HF sx: pulmonary congestion, crackles, pink frothy sputum, SOB…. Can
cause right HF
- Right HF sx: ascites, JVD, dependent edema, hepatosplenomegaly
- Subtle or severe
- Cardiogenic shock
o Severe LV failure
o Have to be aggressive in our management because were losing
perfusion to the body
- Neurohormonal compensatory mechanisms
o Sympathetic nervous system
 Releases catacholamines
Cause peripheral vasoconstriction
o Increasing afterload
o Increases preload
 Pushes fluid back into venous circulation
o Renin-angiotensin aldosterone system (RAAS)
 Hormone system between the kidneys and the heart
 Sodium retention as well as water retention
 Holds on to fluid and makes the heart work harder
o Ventricular hypertrophy
 Muscle is workering harder so the muscle is getting thicker
 Muscle no longer stretches and contracts as well
o Ventricular remondeling
-

Ventricles change morphology and function because thye have
to work harder
- ACE and ARBS
o Going to be given to post MI patients to prevent heart failure by
blocking RAAS
- Decreased blood flow going forward and blood backing up either into the
lungs or back into the body
- Symptoms
o Dyspnea
o Orthopnea
 When they lay down, more blood is returning to the heart, heart
will back up again into the lungs
o Crackles/wheezes
o Cough
o Frothy pink sputum
o Decreased BP
 Pumps not working as well
o Ascites
 Fluid in abd cavity
o Depending pitting edema
o Anxiety
o Decreased o2
o Confusion
o JVD
o Infarct
 If perfusion is not happening well enough
o Fatigue
o S3 gallop, tachycardia
o Enlarged spleen and liver
o Decreased urine output
 Not perfusing to the kidneys well enough, not as much urine is
being created
o Weak oulse
- Nursing management
o Increase cardiopulmonary function
o Promoting comfort and emotional support
o Monitoring the effects fo pharmacologic therapy
 Diuretic
 Getting rid of extra fluids
 Positive inotropes
 Increase the strength of the heart
 Ace/arbs
o Nutritional intake
Hemodynamic Monitoring:
PA line (Swan-ganz line, PAOP, Wedge/PAWP LVEDP?
- Given to patients with heart diease or shock and patients who are hemodynamically
compromised

Is a CVP line with a balloon on the end of the cath, when the balloon is inflated it
goes through the right side of the heart through the right ventricle and into the
pulmonary artery and gets stuck
- Puts a pause on blood flow for a few seconds and this meausres the pressure in the
pulmonary artery and the lungs (pulmonary veins) and into the left atrium and
because the mitral valve is open, the pressure is the same as the left ventricle at end
dystole
- Indirectly measures the pressure in the left side of the heart
- Measures CO by thermodilution blous- cold flush of NS (measures warm blood to
cold NS flush back to warm blood)
- Obtains pressure reading through the balloon
CVP (central venous access/central line)
o Goes into the lowest pressure point of circulation (vena cava/right atrium)
o Can measure the pressure in the right atrium, monitor trends as treatment
occurs
 Normal CVP: 2-5mmHg
o Can be put in the
 intrajugular vein
 subclavian vein
 femoral vein
o Should always get an X-ray done and observe pt before using the central line
to check for pneumothorax and correct placement
o Complications
 Air embolus
 Thrombus formation
 Infection
 pneumothorax
o Nursing mananagement
 CVP volume assessment
 Removal
 Hold pressure for a little bit, not as much as you need for an art
line
 Careful patient positioning
cardiac index
- CO compared to Body surface area
- More accurate cardiac output based on body size
- 2.2-4 is normal
Lab values
- Postassium: 3.5-5
- Calcium: 8.6-10.2
- Magnesium: 1.5-2.5
A-line, Arterial line, art line
- Lines going into an artery that measures BP in real time
- Intra-arterial line
- Placed into the radial artery (sometimes femoral)
-
Need to do the Allens test before placing to make sure both radial and ulnar arteries
are patent first to verify circulation
- NEVER give meds through this line
- When removing an art line
o Remove tape and sutures if present
o Apply pressue above the site
o Remove catheter and oberve the tip
o Apply pressure for 5 min for regular patient and 15 min for patient with
abnormal coagulation studies
Ejection Fraction
- Left ventricle fills up with blood and contracts,its squeezing out a little bit more than
half
- Percentage of blood that is in the left ventricle when it is completely full, is ejected
forward during a contraction
- Normal: 55%
Stress response
- General adaptation system
o 1. Alarm: your body realizing something is going on, the triggering of
the stress response
o 2. Resistance or adaptation: reaction depends on coping mechanisms
or health condition
 temporary response
o 3. Exhaustion: No longer have ability to compensate
Reactive response
o Immediate response to a stimulus
o Something has happened and you are reacting to it
Anticipatory response
o Stress in response to something you are anticipating
Conditional response
o Response that your body has been trained to respond to every time
- SNS activated
o Catacholamines released: norepinephrine (used to help stabilize blood
pressure in the icu) and epinephrine (adrenaline)
 Peripheral arterial vasoconstriction occurs
 Increases BP
 Skin becomes pallor (blood flow not a necessary organ at the time), increased
sweat gland action, goosebumps
 Pupillary dilation
 Decreased GFR in kidneys
 Nausea and stress ulcers d/t decreased blood flow to the GI mucosa
o Epinephrines effects on the body
 Bronchodilation: allows for increased available o2
 Increased force and rate of cardiac contraction: increased
cardiac output, HR, and BP
 Positive inotropic effect: increased cardiac contractility
 CNS stimulation: more alert and increased muscle tone
-
Vasodilation to skeletalk muscles: increased function
Increased lipolysis: increased circulation of free fatty acids,
extra energy source
 Increased glycogenolysis (breaking down of glycogen) and
glucineigenesis (stimulating the production of new sugar)
 Increased blood glucose
o Corticotrophin-releasing hormone
o Cortisol: stress hormone, released by the adrenal glands
 Promotes protein metabiolsim and gluconeogenesis
 Increased blood glucose and serum amino acids
 Delayed healing
 Stabilize CV system
 Increased gasrtic secretion
 Puts you at risk for gastric ulcers
 Decreased allergic and inflammatory responses
 Decreased WBC
 Immune response decreased
 Atrophy of lymphoid tissue
 Decreased lymphocytes
 Increased risk for cancers
 Decreased antibody production
 Alsdosterone
 Retain sodium
 Retain water
 Increased blood volume...increased BP
 ADH
 Water reabsorption
 Increased blood volume and BP
 Preventing the elimination of water
Patient rights
PCI terapy
- Put balloon into a blood vessels
- Want to use on STEMI patients
- 90 min after onset of chest pain to get to cath lab
- start fibrinolytics in 30 min (if stemi) or 120 min if transferring to another
hospital
Fibrinolytic therapy
- Class of medication that breaks apart the clots that are preventing blood
flowto the heart
- Indicated for STEMI patients but not all of them
o Have to do a H&Pto prevent clots from stabilizing anything that may
need to be stabalzied such as on someone who just had surgery… this
would put them at risk for bleeding
- Have to be careful as theyre taking these because they are at risk for bleeding,
watch them carefully
o Start good iv’s before starting


Not used often on non-stemi patients
o Still have some blood flow so you can treat this with nitrates and other
vasodilators
ST segment (STEMI/non-STEMI)
- STEMI
o MI with ST elevation in EKG
o Doesn’t return to baseline and goes into the T wave
o Full occlusion of the coronary artery
o No perfusion to the heart
- Non-stemi
o No ST elevation, Q wave not affected
o Telling us hat there may still be enough perfusion, not a complete
obstruction of blood flow
o Partial occlusion
o Do not give fibronolytics: could rupture plaque
o PCI for balloon angioplasty or stent placement
VAD
- People who are in the end stage of heart failure
- Pt is not goin to have pulse or blood pressure
- Need to be on anticoagulants
IABP
- Pt has to stay still and flat
- Cant move extremity (femoral leg)
Angina
- Acute coronary syndrome: symptoms that we see when someone presents
with a coronary event
o Angina: substernal chest pain
 Most common ACS
- Symptoms
o Chest pain
o Sweating
o Left arm, back, neck, jaw pain
o Patient is acting anxious
o Fatigue
o N/V
o Shortness of breath
o Aytpical presentations especially with women
- Stable angina
o Predictable chest pain that is relieved with medication (nitro) or rest
o Usually already know they have this disease
o Happens because of an inbalance between the oxygen supply and
demand
 Increase in the demand of oxygen as physical activity occurs
o Subsides with nitro or rest; usually exercise induces
- Unstable angina
o An occlusion in the coronary arteries such as plaque build up
o No relief with nitro or rest
-
-
-
o Unpredictable
Variant (prinzmetal) angina
o Spasms of the coronary arteries
o Restriction of blood flow
o Typically happens at the same time everyday
Silent ischemia
o Heart muscle is dying but there are no visible sx
 Common in diabetics or heart transplant pt
 Can see evidence of thsis on an EKG
MI
Sx in men: “crushing” chest pain, radiates to arms (usually L arm)
Sx in women: radiated pain to back, jaw, neck; fatigue, nausea, anxiety, SOB,
indigestion, diaphoresis, dizziness
- 3 causes
o plaque rupture
o thrombus
o coronary spasm
- MONA:
o Morphine
o Oxygen
o Nitro
o Aspirin
- Ischemia vs. Injury vs. Infarction
o Ischemia: tissue is viable
 Inverted T wave
o Injury: tissue might be viable
 Inverted T wave and ST elevation
o Infarction: tissue is no long viable
 Inverted T wave and ST elevation and depressed Q wave
SCVO2 and SVO2 testing
- SVO2
o Can see how much oxygen the body is using
o Venous, measured as the blood is returning to the heart
o Going to see these numbers low in patients that are septic
o Can tell us If our patients are metabolically unstable, using more
oxygen than they need to
Venous and arterial insufficiency
Cardiac biomarkers
- When given fibrinolytics: these rise quickly and then fall
o This means that the therapy has worked
o CK
o CKMB
o Troponin
 CKMB and troponin are most specific to the heart
-