CHAPTER 18 PREOPERATIVE CARE

Diagnosis: TO DIAGNOSE (lymph node biopsy, bronchoscopy)

Cure: ELIMINATE or REPAIR(removal of a ruptured appendix, benign ovarian cyst)
Palliation: ALLEVIATE SYMPTOMS WITHOUT CURE (cutting a nerve root [rhizotomy]
to remove symptoms of pain, creating a colostomy to bypass an inoperable bowel
obstruction)
Prevention: PREVENT (remove mole before it becomes malignant or removal of the
colon in a patient with familial polyposis to prevent cancer
Exploration: EXAM, DETERMINE EXTENT (laparotomy)
Cosmetic improvement: LOOKS (repairing a burn scar or breast reconstruction
after a mastectomy

Elective SX = Planned
Emergency SX = Unplanned
Same-Day Admission = Inpatient
Prior to SX Admission = Chronic Medical condition
Ambulatory SX = (Same day/outpatient sx) = Most common
ST. JOHNS WORT = Prolongs Anesthetic effect
GOLDENSEAL = Increase BP and swelling
LICORICE = Increase BP, swelling, or electrolyte imbalance
SCREEN FOR LATEX ALLERGY MUST INFORM PHYSICIAN/SURGEON to USE
NON-LATEX!
RESPIRATORY SCREENING: Airway Infection = Cancelled SX due to increased
risk of bronchospasm or decreased O2. Report to SX for corticosteroids if
asthmatic. Smokers should stop 6 weeks prior though unlikely.
ENDOCRINE SCREENING: PTS with DM- NEED TO TAKE SERUM GLUCOSE or
CAPILLARY IN MORNING OF SX TO GET BASELINE!
PRE-OP TEACHING:
SENSORY = patients want to know what they will see, hear, smell, and feel
during SX.
PROCESS = general flow of what is going to happen
PROCEDURAL********** = Details that are more specific (ex. IV line that
will be started while pt, with marked site w/ indelible marker, etc) THEY
CANNOT DRIVE AFTER SURGERY!
GENERAL SX INFO: ALL pt should be taught deep breathing/coughing/early
amb post op. Let them know of tubes, drains, etc. Tell them specificially what
they will have after waking up (ex. Total joint replacement will have an
immobilizer, or neurogsurgery = might wake up in ICU)
LEGAL PREPARATIONS: Informed consent must be signed (only surgeon can
do this +witness [nurse]). If patient is ALOC, family member can do it. In
emergency, next-in-line kin is contacted, if no response, sx is initiated w/o
consent.
PRE-OP MEDS: DO NOT GIVE PREOP MEDS UNTIL PATIENT SIGNS CONSENT!
PATIENT MUST REMAIN IN BED AFTER MEDS ARE GIVEN!
Hb = measurement of gas carrying capacity of RBC.
(Females: 11.7-16.0 g/dL Males: 13.2-17.3)

Hct= measurement of packed cell volume of RBC shown as % of total

blood volume
(Females = 35% -47%
males: 39%-50%)
Total RBC Count = Count of # of circulating RBC (Female = 3.8-5.1
Male = 4.3-5.7 x 10^6/uL)
Red cell Indices FUK THIS
RBC morphology = Examination of the shape and size of RBC No
variation in RBC morphology
WBC Count = Measurement of total # of leukocytes (4000-11,000)
WBC Differential: Determine each kind of WBC (Neut =50-70, Eos =0-4,
Baso = 0-2, Lymp = 20-40, Mono = 4-8)
Platelet Count = Measurement of # of platelets available for clooting
= 150-400,000
---------------------------------------------------------------------------------------------------------------------CHAPTER 19 INTRAOPERATIVE CARE
Department Layout: Surgical Suite = Designed to minimize SPREAD OF
INFECTION
Filters and controlled airflow, positive air pressure, UV light = to minimize
infection
FRIENDS/FAMILY allowed in Holding Area
Scrub Nurse Functions: Follows designated scrub procedure, Gowned and
gloved in sterile attire, remains in sterile field
The RN FIRST ASSISTANT can PERFORM SUTURING AND INITIAL INCISIONS
under supervision
ACP: They have their own scope of practice, but needs a physician on vicinity.
(can be a nurse)
POSITIONING: Correct Skeletal Alignment (ASSES for HX of MS issues) NOT
ABSENT SENSES!
General Anesthesia: Usually induced by IV first, THEN augmented with
inhalation. IV Agents= USED BEGINNING of VIRTIUALLY ALL GENERAL
ANESTHESIA.
General Anesthesia: Loss of Sensation + LOC, hypnosis, analgesia, and
amnesia. Skeletal Muscle relaxation, impaired ventilator and CV function.
Elimination of cough, gagging, vomiting, and SNS response.
Regional Anesthesia: Loss of sensation to a region of body W/O LOC.
Involves blocking a nerve, includes spinal, caudal, epidural anesthesia, and
IV/peripheral nerve blocks (interscalene, axillary,
infraclvicular/supraclavicular, popliteal, femoral, sciatic)
Local Anesthesia: Loss of sensation W/O LOC, induced TOPICALLY or via
INFILTRATION, INTRACUTANEOUSLY, or SUBCUT. Topical applications may be
aerosolized/nebulized.
Monitored Anesthesia Care (MAC)/Conscious Sedation: Similar to
general, sedatives and opioids are used at lower dosage, doesnt involved

inhaled agents, Relieves anxiety, analgesia+amnesia, remains responsive

and breathes independently, used for minor procedures (colonoscopy)
Dissociative Anesthesia: KETAMINE = HALLUCINATIONS!
BENZODIZEPINES: (-lam/pam) =
Uses during anesthesia: Reduce anxiety preop+postop; induce and
maintain anesthesia; induce amnesia; treat emergence delirium; supplement
sedation in local and regional anesthestia, and MAC.
Adverse Effects: Synergistic effect with opoids, increasing resp depression,
hypotension, tachycardia, prolonged sedation/confusion
Intervention: Monitor LOC; assess for resp depression, hypotension,
tachycardia. Reverse severe benzodiazepine-induced resp depression with
Romazicon/Flurnazenil.
NEUROMUSC BLOCKING AGENT: ANECTINE:
Uses during anesthesia: MUSCLE RELAXATION
Adverse Effects: APNEA , PARALYSIS, WEAKNESS of muscles
Intervention: MONITOR RETURN OF MUSCLE STRENGTH, OBSERVE CLOSELY
FOR AIRWAY PATENCY OF RESP. MUSCLE MOVEMENT
_____________________________________________________________________
CHAPTER 33 HTN
BP = CO x SVR
CO = SV X HR
Alpha 1(vascular smooth muscle and heart): Increases force of contraction
and produces vasoconstriction
Alpha 2 (Vascular smooth muscle): vasoconstriction
Beta 1 (heart): Increases inotropic, chronotropic, and dromotropic effects.
Also found in kidneys which stimulates release of renin.
Beta 2 (Smooth muscle in coronary arteries, and respiratory system): vasoand broncho-dilation
Vascular Endothelium:
Nitric oxide causes vasodilation & inhibits platelet aggregation
Endothelin (ET) is a potent vasoconstrictor
Normal: <120/<80
Pre HTN : 120-139/ 80-89
HTN STAGE 1: 140-159/90-99
HTN STAGE 2: 160+/100+
Atrial Natriuretic Peptide
Promotes vasodilation (natriuresis)
Promotes sodium and water retention
SECONDARY HTN: HTN with a CAUSE! 5-10%. Coarctation of Aorta, Renal DX,
Endo DX, etc. Age 50+
MANIFESTATIONS OF HTN: ASYMPTOMATIC UNTIL ORGAN FAILURE
SILENT KILLER

Complications: NEOPHROSCLEROSIS: LAB VALUES: Microabluminuria,

proteinuria, microscopic hematuria, HIGH creatinine (*INDICATES RENAL
FAILURE!)+BUN,. EARLIEST SIGN = NOCTURIA!
WHITE COAT PHENOMENON: MAY PRECIPITATE NEED TO GET SELFMONITORING BP @ HOME OR AMBULATORY BP MONITORING (ABPM).
BP MEASUREMENT STEPS:
Use auscultatory method with a properly calibrated instrument.
Patient should be seated quietly for 5 minutes in a chair, with feet on
the floor and arms supported at heart level.
Use appropriately sized cuff to ensure accurate readings.
Obtain at least two measurements.
DRUG THERAPY: A GOAL LESS THAN 130/80** IS RECOMMENDED FOR PTS
WITH HIGH RISK OF CAD or EXISITING CAD.
TEACH PATIENTS ABOUT REBOUND HYPERTENSION FROM TAKING BETA
BLOCKERS!!!! ASSESS FOR BRONCHOSPASM!!***
DIURETICS = HYPOKALEMIA!! GIVE THEM A FRUIT!!!! (OJ/BANANA)
ACE INHIBITORS: Hypotension, dizziness, loss of taste, cough,
HYPERKALEMIA, acute renal failure, skin rash, and angioedema. ASSESS
ORTHOSTATIC HYPOTENSION
ARBS = HYPERKALEMIA!!!!
DASH EATING PLAN FOR COLLABORATE CARE!
COMPLIANCE!: Lack of motivation, Side-effects, inadequate teaching, $, no
insurance, etc.
MANAGEMENT: NUTRITIONAL THERAPY = Start w/ DOCUMENTING a 3-DAY
DIETARY INTAKE!
HTN CRISIS: Pts with HX of HTN who have failed to comply with meds
or who have been undermedicated get HTN Crisis);
MANIFESTATIONS OF HTN CRISIS: Hypertensive encephalopathy, cerebral
hemorrhage
Management: USE Automated BP Machine
_______________________________________________________________
CHAPTER 34 CAD
MAJOR MODIFIABLE RISK FACTORS: BIG 5
Elevated Serum Lipids, HTN, Tobacco Use, Physical Inactivity, and Obesity
Chronic Stable Angina: Pain usually lasts 3-5 minutes. SEEK MEDICAL
ATTENTION IF >5 MIN!
DRUG THERAPY for CHRONIC STABLE ANGINA:
1) Short-Acting Nitrate (used first): Dilates systemic+coronary ARTERIES
NTG SL (Sublingual): Pain relieved 3 minutes. If unchanged/worse stop
and contact EMS
IF symptoms improve, repeat NTG q 5 minutes for 3 doses max.
Tablets must be away from heat sources as it degrades strength
Sprayed ON/UNDER tongue not INHALED. THERE SHOULD BE A TINGLING
(if no tingling = outdated)

Can be used prophylactically 5-10 minute before anginal attack

2) Long-Acting Nitrate (used next): SIDE EFFECT = HEADACHES (USE
TYLENOL)
COMPLICATION = ORTHOSTATIC HYPOTENSION 8HR NITRATE FREE AT
NIGHT, UNLESS NOCTURNAL ANGINA.
3) OINTMENT = USE IN PLACSE OF NO HAIR (upper arm) 3-6hrs
prophylactically.
4) TRANSDERMAL CONTROLLED = ADVANTAGE: ONE APP A DAY
- MATRIX > RESERVOIR: RESERVOIC = DUMPING if BROKEN SEAL!
5) BETA BLOCKERS = DECREASES Everything. Side Effects: bradycardia,
hypotension, wheezing, GI complaints. Some may c/o weight gain,
depression, and sexual dysfunction.
It can mask Hypoglycemic signs - so be cautious when giving it to diabetics.
6) Calcium Channel Blockers: Given after b-blockers. Good for Prinzmetals.
Nitrates suck for Prinzmetals. Potentiates DIGOXIN so monitor digoxin
toxicity!
MI PAIN: Severe, immobilizing chest pain not relieved by rest, position
change, or nitrate administration Heaviness, pressure, tightness, burning,
constriction, or crushing. Substernal, retrosternal, or epigastric areas,
radiating pain to neck, jaw, and arms or back. When epigastric pain is
present, patient may relate it to indigestion; take antacids w/o relief
= MI pain.
PQRST! Precipitating Events, Quality of Pain, Radiation of Pain,
Severity of Pain, and Timing!
Diabetics = Silent Angina (asymptomatic) due to diabetic neuropathy.
Cardiogenic Shock:
Noturnal Angina: Pain at night but not necessarily in recombinant position.
Angina Decubitus: Pain while lying down and relieved by sitting up or
standing.
HEPARIN: Administer with NSTEMI/UA/ACS to prevent NEW clot formation..
MANIFESTATIONS OF MI: Result of sustained ischemia (>20minutes)
causes IRREVERISBLE cell death (necrosis).
COMPLICATIONS OF MI: DYSRHYTHMIAS = MOST COMMON COMPLCIATION
Cardiogenic Shock: Occurs when inadequate oxygen and nutrients are
supplied to the tissues because of severe LV failure ; Requires aggressive
management
Pericarditis: 3-4days after MI; Aggravated by inspriatioin, coughin, . Sitting in
forward position relieves pain. Friction ub. Treatment includes
aspirin+corticosteroids.
Healing Process: TAKES 6 WEEKS AFTER MI TO REPLACE NECROTIC TISSUE
WITH SCAR TISSUE.
SERUM CARDIAC MARKERS:
CKMB Rise: 6hrs Peak: 18hrs Return to normal : 24-36hrs

Troponin: Rise: 4-6hrs

Peak: 10-24hrs
Normal: 10-14 days
Myglobin: Rise: 2 hrs Peak: 3-15 hrs Normal: 24 hrs
ACS CARE: Emergent PCI = treatment of choice for confirmed MI (Balloon
angioplasty/stent)
Fibronylotic Therapy: Indications / contraindications; Ideally within 1 st hr of
symptoms. No later than 6 hrs (C/I after 6); 12-EcG LEAD findings consistent
with MI
Internal Mammary Artery always better than Saphenous for CABG
NURSING DX:
Acute Pain, Decreased CO, Anxiety, Activity Intolerance, Ineffective SelfHealth Management
SCD: Most SCDs are caused by VENTRICULAR DYSRHYTHIMIAS! VTACH

_____________________________________________________________
CHAPTER 35 HF

HF HALLMARK: DECREASE IN LEFT VENTRICULAR EJECTION FRACTION

(systolic failure)
RIGHT SIDED HF: Back up of blood into venous circulation JVD,
hepatomegaly, splenomegaly, vascular congestion of GI tract, and
peripheral edema. Primary cause of RSHF is LSHF. Therefore, you get Pul.
Congestion from LSHF and Cor pulmone(RV dilation and hypertrophy
caused by pulmonary disease) can also cause RSHF.
ADHF = PULMONARY EDEMA ACIDODIC, WET-WARM (PAWP increases)
DYSPNEA: Common Manifestation; Orthopnea SOB during recombinant
position. PND. Due to increase pulmonary pressures in lung, Pt may
have PERSISTENT DRY COUH, UNRELIEVED WITH POSITION
CHANGE OR Over-the-Counter Cough SUPRESSIONS. A DRY
HACKING COUGH MAY BE FIRST SYMPTOM OF HF.
Counter regulatory processes
Natriuretic peptides: Atrial natriuretic peptide (ANP), b-type natriuretic
peptide (BNP)
Released in response to increase in atrial volume and ventricular pressure
MANIFESTATIONS: Sudden weight gain of >3 lb (1.4 kg) in 2 days
may indicate an exacerbation of HF
COMPLICATIONS OF HF: A-FIBB! Treatment can include rate control,
cardioversion, antidysrhythmics, and/or systemic anticoagulation
(Heparin).
ADHF MANAGEMENT: Decrease intravascular volume
Reduces venous return and preload
Loop diuretics (e.g., fursemide [Lasix]), IMPROVE GAS EXCHANGE
BY GIVING SUPPLEMENTAL O2.
MORPHINE! REDUCES ANXIETY (SEDATIVE)
ACE INHIBITORS: ACE inhibitors are the primary drugs of choice for
blocking the RAAS system in HF patients with systolic dysfunction.

DX: Difficult bc of unspecific s/s. EMB may be used for those who develop
unexplained, new HF,. EF is used to differentiate systolic and diastolic HF.
BNP levels aid in LEFT VENTRICULAR DYSNFUNCTION.
Nursing diagnoses
Activity intolerance
Fluid volume excess
Impaired gas exchange
Anxiety
Deficient knowledge
Planning: Overall goals
Decrease in symptoms (e.g., shortness of breath, fatigue)
Health promotion
Treatment or control of underlying heart disease key to preventing
HF and episodes of ADHF (e.g., valve replacement, control of
hypertension, coronary revasculariztion)