MEDICAL SURGICAL NURSING OUTLINE Because the blood is deoxygenated it needs to be

I. Oxygenation oxygenated again in the lungs, so it will need to enter

- Processes the heart.
- Organs involved
Starting from the VEINS → HEART, it will enter thru the
- Organ Damage / Failure SVC & IVC, and be received by the (R) ATRIUM (receiving
II. HEART chamber of the heart) it will be pumped downwards thru the
- Chambers of the heart TRICUSPID VALVE (maintains unidirectional flow) and to the
- Valves of the heart (R) VENTRICLE (pumping chamber of the heart) and then it
- Cardiac Activity will be pumped thru the PULMONARY VALVE and to the
- Electrical Conduction System PULMONARY ARTERY, and it will go to the PULMONARY
III. INFECTIOUS DISORDERS CAPILLARIES (smallest vessels in the lungs)
GABHS (Group A Beta Hemolytic Streptococcus)
- Endocarditis, Myocarditis, Pericarditis In the LUNGS lies the ALVEOLI (grape-like sac, site of gas
➢ Diagnostics Test exchange, responsible for ventilation → inspiration O2 IN &
expiration CO2 H20 OUT) The H2CO3 will move from the
- ASO titer, Echocardiogram, ECG/EKG,
pulmonary capillary to the alveoli and the O2 will move
Cardiac Enzymes, CXR
from the alveoli to the capillary using GAS EXCHANGE
➢ Management
thru the process called DIFFUSION.
- Antibiotics/Antibacterials, NSAIDS, Anti-
platelets, Anticonvulsant or P2Y12 inhibitor The OXYGENATED BLOOD will now return to the heart
IV. OBSTRUCTIVE DISORDERS thru PULMONARY VEINS and then received by the (L)
Coronary Artery Disease ATRIUM and be pumped downwards thru
➢ Risk Factors BICUSPID/MITRAL VALVE to the (L) VENTRICLE
➢ Trigger of Symptoms (discharging chamber of the heart) and then discharge the
“Chest Pain” blood thru AORTIC VALVE and to the largest artery AORTA
and it will branch to smaller arteries to the CAPILLARIES
▪ Stable Angina and to the CELLS
▪ Acute Coronary Syndrome
- Unstable Angina
- Non ST Elevated Myocardial Infarction
- ST Elevated Myocardial Infarction
V. COMPLICATION
Heart Failure
- Right Ventricular Heart Failure
- Left Ventricular Heart Failure
➢ Diagnostic Test
➢ Management

OXYGENATION NOTES!
In order for cells to function it needs → ENERGY thru ▪ Passive – kusang loob, matic, no need for effort/energy
▪ Capillary – manipis so kayang maglapas pasok ng mga
the process of gas exchange
glucose → capillary permeability. What blood vessel is the
From the CAPILLARY (blood vessel) the O2 (oxygen) site of gas exchange (diffusion) → CAPILLARY
goes to the CELL using the process called DIFFUSION ▪ Pulmonary – pag may oulmonary na yung vessel ibig
sabihin nasa loob na ng lungs
(from high to low, passive transport)
▪ Ventilation – movement of air in and out of the lungs
The O2 in the cells is combined with GLUCOSE (from
carbohydrates and fats, simple sugar of the blood) which PROCESSES
is from the blood stream thru the process called 1) Respiration → gas exchange
ACTIVE TRANSPORT (from low to high) so it needs ▪ in order for Respiration to happen the requirement is
something to move to higher concentration with the DIFFUSION
▪ Gas exchange between CELLS & BLOOD
help of hormone which is INSULIN (helps the glucose
enter the cell) (capillaries)
Internal respiration, blood becomes
Both will be converted to the energy of the cell → ATP DEOXYGENATED
(Adenosine Triphosphate), if the cell has energy, it will ▪ Gas exchange between LUNGS & BLOOD
function however if may pinasok na nutrients sa cell (pulmonary capillaries)
mayroon ding ilalabas which is the byproduct/waste External respiration, blood becomes
→ H2CO3 (Carbonate Acid, acidic) thru DIFFUSION
OXYGENATED
(move from higher to lower concentration) it will go to the
2) Ventilation → movement of air in and out of the
capillaries in the form of DEOXYGENATED BLOOD
lungs (O2 in, CO2 out)
carrying H2CO3.
@saelounn
 ORGANS INVOLVED VALVES OF THE HEART
- in order for oxygenation to happen - for unidirectional blood flow, and to prevent backflow
1) Lungs → ventilate GOAL: 1) Atrioventricular Valves – found in the atria & ventricles
2) Heart → pump oxygenate the cells (sabay nag open & close, tumutunog pag nag-close)
3) Blood → RBC FAILURE: ▪ Tricuspid valve
Hypoxia (decrease oxygen ▪ Bicuspid / Mitral valve
(carry o2, gases, glucose) in cells/tissues) which can
4) Vessels → pathway result to organ damage 2) Semilunar Valves
(once nag close → second heart sound)
ORGAN DAMAGE / FAILURE ▪ Pulmonary valve
▪ Aortic valve
1) BRAIN damage
▪ EARLY SIGN → ALOC (Restlessness, Confusion,
Disorientation) which can lead to
decrease LOC (Lethargy → stupor → COMA)
2) HEART failure
▪ If the heart fails to pump it will present signs and
symptoms of Heart Failure ABNORMAL HEART SOUND
▪ Primary symptom / EARLY SIGN → congestion ▪ Ventricular Gallop → heard right after S2
▪ LATE SIGN → Cardiac Arrest (valve damage, heart failure) 3 SYLLABLES
3) LUNGS failure ▪ Atrial Gallop → heard right before S1
▪ Respiratory failure → Respiratory Distress (hypertension, hypertrophy) 4 SYLLABLES
Syndrome (tachypnea, alveolar collapse)
4) LIVER & GASTROINTESTINAL failure
CARDIAC ACTIVITY
1) Atrial Depolarization (AV open)
▪ Liver failure → jaundice, malabsorption
2) Ventricular Depolarization (AV close) (S1 lub)
▪ GI lost blood supply → necrosis → ulcers
Atrial Repolarization (SL open)
5) KIDNEYS SYSTEMIC PERFUSION (systole)
▪ renal failure 3) Ventricular Repolarization (SL close) (S2 dub)
CORONARY ARTERY PERFUSION (diastole
HEART
NOTES!
▪ Contract → depolarization
▪ Relax → repolarization
▪ Left Main Coronary Artery — perfuses ANTERIOR
▪ Right Main Coronary Artery — perfuses the
POSTERIOR portion of the heart

CHAMBERS OF THE HEART

RECEIVING CHAMBERS
✓ Right Atrium (DEOXYGENATED BLOOD)
✓ Left Atrium (OXYGENATED BLOOD)
DISCHARGING / PUMPING CHAMBERS
✓ Right Ventricle (DEOXYGENATED BLOOD)
✓ Left Ventricle (OXYGENATED BLOOD)

@saelounn
 ELECTRICAL CONDUCTION SYSTEM (ECS)
- imaginary wires of the heart, controlled by the brain III. PERICARDITIS
▪ Pericardium → pericardial sac: filled with fluid which
will result to decrease friction or cushion
▪ associated to chest pain (sharp) and friction rub →
DANGER → Pericardial Effusion (increase h20 in
seconds) which can result to:
1) decrease myocardial stretch → ↓ perfusion / cariac
output → decrease blood pressure
2) aortic compression (same as #1)
3) vena cava compression → decrease venous return
→ systemic congestion
▪ Pericardial effusion will result to the compression of the
NOTES! heart → CARDIAC TAMPONADE
▪ Cardiac center → Medulla Oblongata
▪ Heart → is a smooth muscle, so it’s attached to autonomic DIAGNOSTIC TEST
ganglia or nerves (ANS → involuntary) 1) ASO Titer (Anti-streptolysin O)
SNS (FOF) — beta 1 receptors → increase HR - (+) blood → (+) Rheumatic Heart Disease
PNS (RAD) — vagal nerve stimulation (CN X) vavagal HR or Culture & Sensitivity (blood and throat)

INFECTIOUS DISORDERS
- Invasion of the microorganisms (bacteria, protozoa,
fungi, parasites, virus → smallest) JONES CRITERIA
- (+) causative agent → culture & sensitivity, PCR MAJOR
Joint inflammation → arthritis (polyarthritis – multiple,
- activates WBC/leukocytes → lysis, killing & destroying
migratory – palipat-lipat)
and activation of chemical mediators which results to
Heart → carditis
inflammation → “itis” Nodes → red & painful nodes
Erythema marginatum → trunk, red rash with fading
GABHS (Group A Beta Hemolytic Streptococcus) margins
- bacteria that causes pharyngitis (strep/sore throat) Seizures / convulsions / sydenham’s chorea / st. vitus dance
→ seizure that only involves NECK & ARMS
▪ Fevers accompanied by sore throat
✓ Rheumatic Fever – high grade fever, joint & muscle pain MINOR (increase)
✓ Scarlet Fever – high grade fever, red rashes Temperature → fever
WBC → Leukocytosis > 11,000 cells/mm3
COMPLICATION OF GABHS CRP → c-reactive protein
- CARDITIS (inflammation of the heart)
ESR → erythrocyte sedimentation rate
I. ENDOCARDITIS (innermost lining) Arthralgia + Myalgia
▪ valve damage → S3 (ventricular gallop) Bradycardia → prolonged PR interval
⤷ Stenosis & Prolapse 2) Echocardiogram
✓ Stenosis (narrowing) — increase cardiac workload → - to visualize one structure of the heart
hypertrophy of the heart → weakness of pump →
3) ECG / EKG
Heart Failure
- monitor the electrical activity & assess cardiac damage
✓ Prolapse (displacement) — incomplete closure →
regurgitation → increase cardiac workload → ✓ T wave inversion → presence of myocardial injury
hypertrophy → weakness of pump → RVHF & LVHF ✓ ST depression → ischemia / angina pectoris
✓ ST elevation → EMERGENCY → MI or STEMI (severe
II. MYOCARDITIS obstruction)
1) decrease pumping action secondary to decrease ✓ Pathologic Q wave → EMERGENCY → developing MI
stretch → DECREASE PERFUSION or NSTEMI (partial obstruction) or UNSTABLE ANGINA
✓ decrease systemic perfusion → multiple organ (pre-infarct)
damage → SHOCK (cardiogenic)
✓ decrease coronary artery perfusion → myocardial
ischemia (↓ O2) → injury & necrosis → 1)
prostaglandin activation 2) increase lactic acid
(because of shifting from aerobic to anaerobic
respiration) → CHEST PAIN → Angina Pectoris
▪ Frank-Starling Doctrine Law — the degree of cardiac
stretch is proportional to the force of contraction.

2) Activation of Platelet Aggregating Factors → small

clots / thrombi formation → obstruction of the coronary
arteries → Myocardial Infarction → Cardiac Arrest (one
shot) or Heart Failure (post cardiac arrest or MI)

@saelounn
 4) Cardiac Enzymes Smoking → strongest risk factor
- increase cardiac enzymes → Myocardial Infarction Sedentary lifestyle
DM 2 → lifestyle related
✓ Myoglobin — the earliest
Diet rich in trans → saturated fats
✓ CK-MB — cardio specific
OCP → oral contraceptive pills
✓ Troponin I — most accurate
Alcoholism
5) Chest X-ray
- to rule out Trigger of Symptoms
✓ Extreme exertion
MANAGEMENT OF GABHS ✓ Extreme emotion
✓ Extreme temperature
1) Antibiotics / Antibacterials ✓ Excessive eating
▪ Penicillin → IV: Pen G (5 – 7 days)
Oral: Amoxicillin, Methicillin, Oxacillin
(4 – 6 weeks)
▪ S/E → tinnitus, diarrhea, increase HCI acid
production
▪ A/E → ototoxicity→ SHL (sensorineural hearing loss)
hepatoxicity → liver failure
peptic ulcer disease → prevention: h2
blockers (famotidine, cimetidine, ranitidine)
2) NSAIDS
- Increases HCI acid and decreases mucosal barrier
- 2nd cause of PUD STABLE ANGINA
▪ or corticosteroids “-sone” - RELIEVED BY REST, O2, Nitroglycerin (3 tabs, 15-30
3) Anti-platelets or P2Y12 inhibitors mins before activity, sublingual → burning sensation)
S/E: headaches, flushing of face, orthotastic hypotension
4) Anticonvulsants WOF: Hypotension → SHOCK
▪ SURGERY
1) Repair: stenosis → valvulotomy (balloon tip catheter) SEVERE ANGINA (Acute Coronary Syndrome)
prolapse → chordoplasty or valvuloplasty - “clots” (thrombi → nonmoving clots) (emboli → moving clot)
2) Replace: transplant ✓ ACS → Unstable Angina, NSTEMI, STEMI
✓ Allogenic → tao ▪ ISCHEMIC – low O2, crushing, tight, squeezing, “vise-like
✓ Xenogenic → hayop: porcine pain” belt around chest (elephant stomping on chest)
✓ Syngeneric → twins ✓ Give Rest O2 Nitroglycerin
- if UNRELIEVED: stable angina
▪ give anti-rejection → immunosuppressants
- if RELIEVED: ACS (UA, NSTEMI, STEMI)
FOR LIFE
✓ Location: substernal
- Corticosteroids, cyclosporine
✓ Radiating: LEFT jaw, shoulder/scapula, arm
✓ Other Sx: Anxiety → ↑ HR, ALOC → ↓ LOC, DOB &
OBSTRUCTIVE DISORDERS SOB, Diaphoresis & cool skin
▪ Coronary Arteries ✓ Early Signs of MI: numbness of L arm, frequent
(L) main → ANTERIOR portion yawning, hypersomnolence, agitation, chest discomfort
(R) main → POSTERIOR portion (2 to 3 weeks)
✓ Atypical Sx: no chest pain
CORONARY ARTERY DISEASE Female, elderly, DM → INDIGESTION
▪ Arteriosclerosis – general term ▪ DIAGNOSTIC TESTS – Chest Xray, Cardiac Enzymes
▪ Atherosclerosis – specific deposition for FATS (Trop I), Cardiac monitor (ECG)
F
Trop I (-) → U.A. Blood test (+) → M.I.
✓ Increase brittleness and rigidity and loss of elasticity
ST elevation → NSTEMI No ST elevation → STEMI
because of deposition SCLEROSIS (deposits of dead
tissues, calcium, fats) which can lead to:
1) High risk for Injury → clot formation
STEMI MANAGEMENT
- FULL OBSTRUCTION
2) Protrusion or Rupture → aneurysm
➢ Priority: PCI within 2 hours
If not possible → give fibrinolytic and perform PCI within
RISK FACTORS
24 hrs; concern is bleeding
NON-MODIFIABLE ➢ POST ACS:
Age & sex: male → 45 years old Maintenance meds → ASA/clopidogrel (1 yr),
Familial tendency → genes, ↑ homocysteine levels Antihypertensives (dilators), Anti-lipids (1-2 mos)
DM 1 → heredity related DM Exercise → light exercise, every other day or 3-4 times a
Anatomy of the coronary artery → small, narrow & week, 30 minutes to 1 hour
numerous twist and turns Diet → LSLF, high fiber
MODIFIABLE Smoking cessation

@saelounn
 Alcohol in moderation ✓ Ascites → GI Sx (anorexia, GI pain) Massive
spirits: male (2 ounce or 60 ml) female (1 ounce or 30 ml) (diaphragmatic, compression = DOB)
beer: male (1-2 glasses) female (1/2 – 1 glass) ✓ Hepatomegaly → ↑ SGPT (ALT), ↑ SGOT (AST)
✓ Splenomegaly → danger is rupture (bleeding)
NSTEMI MANAGEMENT graveyard of RBC
➢ ONAMSBD → fibrinolytic therapy or thrombolytic therapy ✓ JVD, headache
which are CLOT BUSTERS (ateplase, streptokinase)
➢ Procedures → PCI or CABG (within 72 hrs or 3 days) LEFT VENTRICULAR HEART FAILURE
1) Decrease cardiac output
UNSTABLE ANGINA MANAGEMENT - ↓ BP (pressure in the arteries)
1) Oxygen – high flow (non-rebreather) for conscious pt & 2) Pulmonary congestion
intubation + mechanical ventilation for unconscious pt - > 20 mmHg
2) Nitroglycerine (patch) – which is place in a non-hairy
Signs & Symptoms
area, with the nurse wearing gloves and 12 hrs patch time ✓ Decrease cardiac output → weakness, light
3) Aspirin (ASA) – anti-platelet or p2y12 inhibitors, ASA headedness, syncope, low BP
(prevent further myocardial dmg) clopidogrel, ticagrelor ✓ Pulmonary congestion → EARLIEST Sx (orthopnea)
4) Morphine SO4 (opiod) ✓ DOB, SOB, PND (paroxysmal nocturnal dyspnea)
Analgesic → pain ✓ Cough → productive
Dilator → (mild dilating effect) decreases workload of ✓ Adventitious breath sounds → rales (crackles) –
heart because of decrease preload inspiration: popping & rhonchi – expiration: rumbling
Sedative → decrease HR (will not go ↓ normal) & RR ✓ Pink frothy sputum → pulmonary edema
WOF: Respiratory depression; antidote is Naloxone ✓ S3 heart sound
5) Statins (atorvastatin, sinorvastatin, rosuvastatin)
Anti lipids → take at HS (9 pm)
DIAGNOSTIC TEST
S/E: dry cough, rhinitis, irritability, photosensitivity
1) BNP (Brain B-type Notrimetric Peptide → gold
Longterm use of atorvastatin: associated w/ dementia
standard test of HF (↑ BNP = overstretched ventricles)
6) Beta blockers (-olol) – blocks the beta receptors of SNS
2) PAPM (Pulmonary Artery Pressure Monitor)
Beta I → (heart) increase HR contractility, so if blocked it
→ right sided cardiac catheterization insertion
will lead to decrease HR contractility WOF: Myocarditis
(subclavian vein, jugular vein)
Beta II → (lungs) bronchodilation , so if blocked →
(n) 12 – 20 mmHg → <12 – RVHF; >20 – LVHF
bronchoconstriction WOF: asthma, COPD, cystic fibrosis
3) Echocardiogram
7) Dilators – to ↓ peripheral vascular resistance (afterload)
4) ECG/EKG
Ace inhibitor (pril); not suitable for pt w/ renal problems,
5) Cardiac
nepritis syndrome, ESRD
Angiotensin II Receptors Blockers (-sartan)
8) Anti-coagulants – low molecular weight heparin
MANAGEMENT
▪ Diuretics → fluid excretion & electrolytes (do not give
(LMWH) → Enoxaparin
beyond 4 pm) WOF: hypotension
✓ K+ sparring — spironolactone (aldactone)
COMPLICATION
triamterene
HEART FAILURE Effects: na+ → h2o excretion, k+ retention
- weak pumping action of the heart WOF: hyponatremia, hypovolemia, hyperkalemia
- pumping failure → RVHF & LVHFd ✓ K+ wasting — loop diuretics, furosemide (lasix)
Effects: hyponatremia, hypovolemia, hypokalemia
▪ Ejection fraction: < 60% — percentage of blood
▪ Digoxin → cardiac glycosides; (+) inotrophy – ↑ HR
normal → more than 60% (↓ EF — ↓ SV — ↓ CO)
(-) chronotrophy – ↓HR, (-) dromotrophy – ↓O2 demand
▪ Stroke volume – amount of blood in 1 contraction
✓ Before giving digoxin → check apical pulse, renal
▪ Cardiac output – amount in 1 minute contraction
function (BUN → 10-20 mg/dl, Crea → 0.5-1.5 mg/dl),
▪ Preload – amount of blood in the ventricle before a
Serum k+ levels ( 3.5-5.5 mEq/L) hyponatremia
contraction (bala)
✓ During giving digoxin → every week monitor digoxin
▪ Afterload – resistance against the ventricles, Blood
levels (therapeutic level – 0.5-5.5 mEq/L)
viscosity and blood vessel constriction
✓ Monitor sings and symptoms of toxicity
RIGHT VENTRICULAR HEART FAILURE EARLIEST → anorexia & bradycardia (prolonged PR)
1) Decrease blood coming into the lungs Nausea & vomiting, abdominal discomfort,
- ↓ pulmonary pressure: <12 mmHg lightheadedness, syncope, green halos around lights
2) Systemic congestion (photosensitivity), snowy vision (blurring of vision),
- ↑ venous pressure: > 20 mmHg headache, cephalgia
ANTIDOTE: Digibind / Digoxin Immune Fab
Signs & Symptoms ▪ Dilators → Ace inhibitors, ARBS
✓ Hypoxemia → hypoxia ▪ Dopamine → dobutamine
✓ Systemic congestion → EARLIEST Sx (bilateral, ▪ Diet → low salt diet, prudent diet (<800 mg sodium /day)
pitting, dependent) ▪ Daily weight → early morning 6 AM (same time of day,
✓ Sparse hair growth on lower extremities amount of clothes, weighing scale)
✓ Leg fatigue, leg cramps ▪ Decubitus ulcer prevention → CBR (turn pt to side),
✓ Hydrocele egg mattress, avoid dragging force
@saelounn