Disease Process Causes S&S Treatment Nursing Priorities/

Safety
Anemia: too low  Deficiencies  Fatigue Depends on cause-
RBC, Hg or both  Hemolysis  weakness  Replenish
 blood loss dyspnea deficiencies
NOTE: cell  renal failure  pallor address
appearance can  bone marrow depression reason for
help identify the hemolysis
type of anemia  find and
treat
source of
blood loss
 blood
transfusion
Thrombocytopenia:  Immune thrombocytopenia Find the cause and  Avoid ASA
platelet count less purpura (ITP, KNOW THIS) treat the issue & OTCs
than  Heparin-induced accordingly  Monitor
150,000/mm^3 thrombocytopenia (HIT) labs
 Drugs  Avoid IM
 Infections injections
 Can be genetic  Use
electric
razors
 Use soft
brushes
 Use paper
tape
 Use stool
softeners
 Fall
prevention
Neutropenia: WBC  Chemo/immunosuppressant  Neupogen  Watch for
less than 1000 agents  Neulasta low grade
cells/microliter  Leukemias (has longer fevers
 viral infections (HIV) effect)  Isolation
 hemodialysis room
 sepsis  Prevent
infections

Blood Transfusions:
-be certain of blood type and who can receive what kind of blood.
-assess vitals frequently (BP, Pulse, HR, skin reactions) if you notice a reaction- stop infusion immediately but do
not flush. Only run normal saline since it is isotonic.
 Circulatory Function:

Coronary Artery Disease:

- Vascular disorder that narrows or occludes the
coronary arteries leading to MI.
- Atherosclerosis is most common cause. This is build
up of plaque on the artery.
- MI is myocardial cell/tissue death due to long term
oxygen starvation.
- PQRST assessment: Precipitating events, quality of
pain, region/location, severity of pain, timing.
- S&s of CAD:
o increased HR & BP, then drop in BP.
o Crackles
o Jvd
o Abnormal heart sounds= S3 & S4
o Nausea/vomiting due to vasovagal reflex & pain
o Fever in first 2 days
o SIRS
- Diagnostics:
o Detailed health history, physical exam
o Chest xray
o 12 lead Ekg
o Lab studies: biomarkers, lipid panel, CBC, C-
reactive protein, BMP
o Echocardiogram
 o Exercise stress test
o Ct scan
o Coronary angiography

Ischemic Heart Disease

Stable Angina (chest pain) Variant Angina Silent Myocardial Management
“Prinzmetals” Ischemia
 Due to atherosclerosis  Due to coronary  Nitrates:
 Artery unable to constrict artery spasms  Blood still  Beta blockers
or dilate  Restricting blood flowing to  Calcium channel
 Blood flow is decreased flow tissues blockers
but still moves through  dysrhythmias can  Pts don’t suffer
 Increased oxygen demand occur from angina at
decreased oxygen  Pain at rest& all
supply pain nighttime  Symptoms
 Pain with activity  Relief with present in other
 Relief with rest, medications ways such as
medications/nitroglycerin SOB, etc.
 Nursing Interventions:
medications, cardiac
catheterization, coronary
angiography, percutaneous
coronary intervention
(balloon angiography &
stent-placed thru arm or
groin), 12 lead ekg, keep
o2 sat>93%, vital sign
monitoring, treat
dysrhythmias

Nitroglycerin: vasodilator used to treat stable, unstable, and variant angina as well as MI.
o Stable angina: Dilates veins -> decreases pre-load -> decreased o2 demand/
cardiac work
o Variant angina: prevents vasospasms of arteries
o Side Effects: headaches VERY common, othostatic hypotension, reflex
tachycardia after dec. BP.
o Nursing Considerations:
 Assess HR & BP Before
 
Sublingual route. Don’t swallow. Take 1 tab every 5 min. up to 3x. if chest
pain persists 911.
o Drug-Drug Interactions:
 NO ALCOHOL or FENTANYL can cause severe hypotension.
 Heparin= decreased anticoagulation
 Lithium toxicity
 DO NOT use in pts with increased ICP

Beta Blockers (propranolol): antihypertensive treats angina post MI

 Reduces PUMONARY AFTERLOAD
 Negative inotrope= decreased force of contraction
 negative chronotrope= decreased HR
 Negative dromotrope= decreased rate of electrical conduction
 Reduces oxygen demand
 Side Effects:
o Heart failure, AV block, sinus arrest, bradycardia
o Hypotension
o In asthma pt can cause broncospasm
 Nursing considerations:
o Assess apical BP&HR before. NOTIFY PROVIDER IF <60BPM
o Prolongs PR, bradycardia
o DON’T USE IN PT WITH INCREASED ICP. CAN LEAD TO
HEMORRHAGE
o DON’T USE IN PT WITH ANEMIA
 DRUG-DRUG:
o propranolol is contraindicated for patients with asthma, sinus
bradycardia, high-degree heart block, and heart failure.

Calcium channel blockers: antihypertensive& vasodilator treats stable and variant angina.
 Delays conduction thru AV node
 Dilates arterioles
 Reduces myocardial contractility=reduction in myocardial oxygen demand
 Reduces BP-> Reduces ventricular afterload->Reduces oxygen demand
 Side Effects:
o Heart failure, AV block, bradycardia
o PV: hypotension & peripheral edema
o Gi: constipation
o Reflex tachycardia
 Nursing Consid:
o Assess HR & BP BEFORE
o Prolongs PR
o Increased risk of digoxin toxicity
Angiotensin-converting enzyme inhibitors (ACEI) & angiotensin receptor blockers (ARBs):
o block Angiotensin 2, which lowers BP, decreasing the workload of heart.
 Unstable Angina

 Angina (often in the AM)

 More severe, prolonged
or frequent that
previous angina
symptoms
 Artery unable to
constrict or dilate
 PLAQUE RUPTURE only,
no occlusion so no cell
death / no MI
 Pain at rest> 20 min
 No relief with rest or
meds
 Nursing Interventions:
dual heparin and aspirin
use. Cardiac
catheterization with PCI
(balloon angiograph
+stent)

NSTEMI MI STEMI MI

 Small thrombus  Thrombus completely occludes vessel

 Partially occluded vessel 
 Causes less extensive
cardiac damage
 There is myocardial cell
death (yes MI but
insufficient)
 No ST segment elevation
MI
Causes extensive cardiac damage
 ST segment elevation MI
 Tx is aimed at limiting the amount of
myocardium that dies.
 Nursing intervention: EMERGENCY PCI
WITHIN 90 MIN.

Nursing intervention for NSTEMI & STEMI : thrombolytic therapy for sites that don’t have
cardiac catheterization tools. given within 30 min of arrival. Draw blood and start 2 iv SITES,
monitor for signs of bleeding, iv heparin to prevent re-occlusion, assess for signs of reperfusion.

Nursing diagnoses for acute coronary syndromes:

o Decreased cardiac output
 o Acute pain
o Anxiety
o Activity intolerance
o Ineffective health management
o Planning includes: relief of pain, preservation of heart muscle, immediate
and appropriate treatment, effective coping with illness, rehab plan, reduce
risk factors.

Look at 3 biomarkers together to determine if an MI happened. Troponin stays elevated up to 3

days after.

Pathologic changes in an MI:

-Subendocardial infarct: involves inner 1/3 to ½ ventricular wall
-Transmural infarct: full thickness of ventricular wall
-Necrotic myocardial cells are replaced with scar tissue
-Scar tissue cannot contract or conduct action potentials. So you have tissue that is just sitting
there and could become a problem.

3 zones of damage of MI:

-iSCHEMIA: cease to function within minutes
-injury: irreversible damage/death to myocardial cells occurs within 20-40 min
-infarction: early reperfusion after onset of ischemia can prevent further ischemia and necrosis.

Medication anti-platelets, and anti-coagulants

Heart Failure
 Inability of the heart to fulfil its normal role: pumping blood through the pulmonary and
systemic loops.
 Normal pumping ability adjusts to body needs for o2.
 Cardiac reserve: ability to increase CO during increased need!!
 Risk factors for HF: HTN, CAD.
 Comorbidities that contribute to HF: DM, Metabolic syndrome, advanced age, tobacco
use, vascular disease
 Heart failure process:
o Decreased contractility
o Decrease in stroke volume (amount of blood that leaves the heart with each
beat)
o Decrease in output
o Decreased o2 to organs
o Trigger compensatory mechanisms
o Increase blood volume vascular resistance
o Increase cardiac work
o HEART FAILURE OCCURS
 Ppl with heart failure and elderly have poor cardiac reserve.
 Compensatory mechanisms include:
o Frank starling mech: increased stretch
o Increased SNS activity: increased HR & pre-load
o Renin angiotensin aldosterone system (RAAS): increase in pre-load, aldosterone
and ADH
o Myocardial hypertrophy: increased contractile performance
 HF classified into two types: dysfunction failure and side failure
 Dysfunction failure:
o Systolic dysfunction
 Impaired ejection of blood from heart during systole
 Impaired ejection (EF <40%)
  cardiac contractility =  CO
 Causes
 Ischemic Heart Disease
  Preload
 Afterload
o Diastolic dysfunction
 Impaired filling of ventricles during diastole
  LV Filling =  CO
 Causes
 MV Stenosis
 Left Ventricular Hypertrophy
 Aging
 Right side vs Left Side failure:
o RIGHT SIDE:
  fluid accumulation in systemic venous system venous congestion 
lead to peripheral edema
 S&S: enlargement of spleen due to inc. blood + fluid, ascites, congestion,
fatigue, JVD, GI distention, swelling, hard/stiff fingers, EDEMA
o LEFT SIDE:
  Cardiac Output = Left Atrium & pulmonary pressure  eventually
pulmonary edema
 S&S: confusion, altered LOC, blood tinged sputum, cough, crackles,
restlessness, left ventricular hypertrophy= lower PMI,
tachycardia(compensatory), fatigue, cyanosis
 Diagnostics: SAME AS CAD
o Detailed Health History & Physical Exam
o Chest x-ray
o 12-lead ECG/Compare to previous ECG/LOOK 4 Changes in QRS complex, ST
segment, and T wave
o Laboratory studies/ Elevated BNP: natural diuretic
o Echocardiogram: check ejection fraction must be at least at 40%
o Exercise stress test
o Coronary angiography

Nursing Interventions:
Medications:
o vasodilators(nitroglycerin)
o b-blockers
o diuretics (furosemide)
 do not administer if K is < 3.5 mEq/L.
 contraindicated with digoxin= can lead to hypokalemia.
o positive inotrope agent (digoxin): vagotonic effect=
decreased o2 demand. This can lead to A. Fib due to
decreased conduction of AV node.
 SE: bradycardia, fatigue, hypokalemia
 NI: Assess K levels, has to be within normal range 3.5-
5.
 Therapeutic level= .5-1.1
 Assess apical HR for 1 min. notify PCP if <60 bpm
o raas inhibitors:
 ACEI: decreases afterload and pre-load.
 SE: Dry cough common & hyperkalemia.
 NI: Assess BP before/after. Assess K level before
admin. Hold if K is >5.5
 ARB: blocks action of AT @ RECEPTOR SITE.
 Assess bp before/after admin.
 Aldosterone Antagonists: reduces cardiac remodeling,
decreases SNS activation.
 SE: Can cause hyperkalemia
 NI: Assess K level before admin. Hold if > 5.5
Valve Disorders
 Regurgitation= incomplete/ improper closure
o Permits backflow
o Produces distention &  work demands on ejecting chamber
 Mitral Regurgitation( MRS3): Incomplete closure of the mitral valve
o During systole, part of left ventricle stroke volume goes forward into aorta &
regurgitated blood flows back into left atrium
o Results in  CO &/or pulmonary congestion
o Left ventricle enlarges due to  in ventricular pressure
o Left atrium dilates due to extra volume
o Acute
 Occur with MI
 Generally poorly tolerated. New systolic murmur with pulmonary edema
and cardiogenic shock develop rapidly.
o Chronic
 Weakness, fatigue, exertional dyspnea, palpitations, S3 gallop, systolic
murmur
 Aortic Regurg (ARD1)
o Incompetent aortic valve
o  backflow of blood to the left ventricle during diastole
o   left ventricle volume due to blood leaking back thru valve into left atrium
o Turbulent blood flow can cause murmurs. Drop in cardiac output.
o Acute: Abrupt onset of profound dyspnea, chest pain, left ventricular failure and
cardiogenic shock
o Chronic: Fatigue, exertional dyspnea, orthopnea, PND. Diminished or absent S1.
Soft high-pitched diastolic murmur.

 Stenosis= narrowing of valve that doesn’t allow valve to open properly.

o  resistance to blood flow through the valve
o  volume & work of the chamber that empties thru narrowed valve
o Produces distention in one chamber & impaired filling in another

 Mitral Stenosis:
o Incomplete opening of mitral valve during diastole
  Left atrium distention & impaired left ventricle filling
o Resistance  mitral valve
  Left atrium dilates   left atrium pressure
  pulmonary vasculature
  pulmonary congestion & pulmonary HTN
o Symptoms: Dyspnea on exertion, hemoptysis, fatigue. Atrial fibrillation.
Palpitations. Loud, accentuated S1. Low-pitched, diastolic murmur
 Aortic Stenosis:
o  resistance to ejection of blood from the left ventricle into the aorta
 o  resistance =  work of the left ventricle &  volume of blood ejected into
systemic circulation
o S&S: Angina, syncope, dyspnea on exertion, heart failure, normal or soft S 1,
diminished or absent S2, systolic murmur, prominent S4

 Mitral Valve prolapse

o Most asymptomatic
o Usually unknown cause
o Palpitations (awareness of the heartbeat) and dysrhythmias are common
o Dysrhythmias may produce light-headedness or fainting
o Mitral regurgitation may necessitate valve repair or replacement