ACUTE BIOLOGIC

CRISIS
Nina Hamili G. Piao RN
 HEMODYNAMICS
The heart, large blood vessels, and the microcirculation (capillary circulation)
interact to keep all body tissues perfused with blood. Effective perfusion
requires good cardiac pumping ability, an adequate amount of blood to be
pumped, and ability of blood vessels to constrict and to dilate to maintain
blood pressure.
 Heart rate
Increased by sympathetic and decreased by parasympathetic nervous
system stimulation.
Stroke volume
Volume of blood ejected by the ventricle with each heartbeat.
Normal: 6070 ml.
 HEMODYNAMICS
The hearts ability to pump is measured by cardiac output (CO), the amount of blood
pumped per minute.
CO =HR x SV ; SV depends on three factors: preload, afterload, and contractility
Normal: 46 l/min.
Preload is the amount of blood presented to the ventricle just before systole.
Right ventricular preload is measured by CVP (normal range 24 mmHg).
Left ventricular preload volume pressure is measured as the pulmonary artery wedge
pressure (PAWP) (normal
range 512 mmHg).
Afterload refers to the amount of resistance to the ejection of blood from the ventricle.
Contractility, the force of contraction, is related to the status of the myocardium.
(contractile force of the heart or inotropy)
 HEMODYNAMICS
Central venous pressure (CVP)
Pressure created by blood volume in the right side of the heart.
Normal: 24 mmHg.

Systemic vascular resistance (SVR)

Resistance in the arteries and the arterioles against which the left ventricle must
pump. As SVR increases,CO decreases.
Normal: 9001400 dynes/sec/cm-5.
 HEMODYNAMICS
Pulmonary vascular resistance
Resistance in the pulmonary arteries and the arterioles against which the
right ventricle must pump.
Normal: 30100 dynes/sec/cm-5
 HEMODYNAMICS
Hemodynamic parameters which reflect these functions are
CVP is the pressure of the blood in the right atrium. It reflects right
ventricular heart function and venous blood return. It indicates the hearts
ability to manage fluid load.
Uses: CVP is a hemodynamic measure to manage a clients fluid volume
status; it is used as a guide to the safe administration of intravenous fluid
volume.
 HEMODYNAMICS
pulmonary artery pressure (PAP)
Pulmonary artery catheter is often referred to as SwanGanz catheter.
It has four to five lumens to measure various cardiac pressures.
Uses: PAP measurement is used in hemodynamic monitoring to provide
information about the efficiency of the right and left sides of the heart and
evaluating a clients response to medical treatment.
SwanGanz catheter video presentation
 HEART FAILURE
Heart failure (HF) is also referred to as congestive heart failure (CHF).
Its onset can be chronic or acute heart failure (pulmonary edema or
cardiogenic shock).
It refers to the inability of the heart to pump sufficient blood to meet the
needs of tissues for oxygen and nutrients.
The incidence and prevalence of CHF increase with age.
 HEART FAILURE (Etiology: )
Damage to the heart, regardless of the cause, leads to decreased cardiac
output and decreased tissue perfusion. Fluid overload or inadequate tissue
perfusion results in altered ventricular filling and emptying.
 HEART FAILURE (Types)

Left-sided heart failure

Left ventricle is unable to pump blood effectively into systemic circulation
and thus blood returns back into pulmonary circulation
 HEART FAILURE (Types)

Right-sided heart failure

Right ventricle is unable to effectively pump blood into pulmonary
circulation and blood returns back into systemic circulation.
 Signs & Symptoms:

Left heart failure (pulmonary symptoms remember

Left and Lung)tachypnea, tachycardia, cough,
bibasilar crackles, gallop rhythm, increased
pulmonary artery pressure,hemoptysis, fatigue,
cyanosis, dyspnea, orthopnea, nocturia,and
paroxysmal nocturnal dyspnea (PND)
 Signs & Symptoms:

Right heart failure (systemic symptoms remember Right

and Rest of the body)peripheral edema, hepatomegally,
splenomegaly, ascites, jugular vein distension (
JVD),increased central venous pressure, weakness,
anorexia, nausea, indigestion, weight gain, mental changes,
bounding pulses, oliguria, and cool extremities.
Dx:

Clinical manifestations, chest X-ray,

echocardiogram, increased CVP, increased
pulmonary artery pressure, ABG analysis, and
liver function test
Rx
Reduce oxygen demands of the myocardium by eliminating and managing
contributing factors
Decrease cardiac workload by decreasing afterload and preload
Improve contractility and manage symptoms
Rx
Low-sodium diet

Medications:
-angiotensin-converting enzyme (ACE) inhibitors
-diuretics
-digitalis
Rx
-beta blockers
-nitrates
-antihypertensives
-positive inotropes (dopamine, dobutamine)
-direct vasodilators
-morphine sulfate
Rx
Physical and psychological rest
Oxygen
If medical intervention is unsuccessful then mechanical assist devices (intra-
aortic balloon pump [IABP]
left ventricular assist devices
heart transplant
Nursing Interventions:
Monitor I&O
Check weight daily
Assess for signs of fluid overload
Monitor level of consciousness
Assess VS, heart and lung sounds
Monitor for cardiac dysrhythmias
Maintain bed rest with HOB elevated
Instruct client to avoid valsalva maneuver
Nursing Interventions:
Assess and record abdominal girth
Monitor ABGs
Oxygen as prescribed
Provide emotional rest
Monitor electrolytes
Administer medications as ordered
Provide client teaching
Provide low-sodium diet as ordered
Client teaching for self-care
Client teaching for self-care
Instruct client
to perform activity without adding to fatigue, so he/she should pace and
prioritize daily activities to avoid extremes in temperature that would tax
cardiac function
to stop activity if experiencing lightheadedness or shortness of breath
to plan for periods of rest alternating with periods of activity
Client teaching for self-care
to maintain a low-sodium diet
to take potassium replacement if taking a potassium depleting diuretic and/or
include foods high in potassium in the diet, e.g., orange and tomato juice,
bananas, raisins, figs,prunes, apricots, spinach, cauliflower, and potatoes
to take diuretics at times that allow for uninterrupted sleep
to adhere to medical regime
to weigh self daily and report to physician a greater than 3-lb weight gain
 ACUTE MYOCARDIAL INFARCTION
Myocardial infarction (MI) is also known as Acute Coronary Syndrome.
It refers to the chest pain brought on by acute obstruction of coronary blood
flow.
MI occurs suddenly.
It results in imbalance of myocardial oxygen supply and demand.
It causes the death of myocardial cells.
 ACUTE MYOCARDIAL INFARCTION
Remember the three Is of the progression of pathophysiology
of an MI: Ischemic tissue progresses to
Injured tissue, which in turn progresses to Infarcted or dead tissue.
ACUTE MYOCARDIAL INFARCTION

As the cells are deprived of oxygen, ischemia develops,

cellular injury occurs, and over time, the lack of oxygen
results in infarction, or the death of cells.
MI (Etiology: )

Obstruction of coronary blood flow due to

thrombus, emboli, or vasospasm. May also result if
oxygen supply is diminished such as with acute
hypovolemia or if oxygen demand is increased as
with tachycardia.
Precipitating factors:

Hypertension, hyperlipidemia, obesity, elevated serum

triglyceride level, smoking, genetic predisposition, high-
fat diets, physical inactivity, stress, age, gender, disease
processes such as diabetes mellitus, hormone , status and
use of oral contraceptives, elevated serum iron levels,
toxic substances in the environment.
S/S:

Acute substernal pain described as crushing which may radiate to back or jaw
Levines sign (chest hand-clutching). This is the universal sign of distress
in agina pectoris and MI.
- Cessation of blood supply to myocardium due to thrombotic occlusion
causes accumulation of metabolites (e.g. lactic acid) within ischemic part of
myocardium. Lactic acid irritates nerve endings resulting to pain.
 S/S:
Feeling of impending doom, restlessness
-Severe pain of a heart attack is terrifying
-Pain lasts more than 20 minutes and is not relieved with rest and/or
nitroglycerine.
Shortness of breath
Shock
-Manifested by SBP <80mmHg, lethargic, cold diaphoresis, peripheral
cyanosis, weak pulse.
-Due to severe pain, severe reduction of C. O. and inadequate tissue
perfusion causing tissue hypoxia
S/Sx.
Oliguria
-Urine flow less than 30 ml/hr. indicates renal hypoxia due to inadequate
tissue perfusion.
Gas pains around the heart, nausea and vomiting
=nausea and vomiting may result from the severe pain or from vasovagal
reflexes conducted from an area of damaged myocardium to GI tract.
S/Sx
Fever-occurs within 24 hours and extens to 3-7 days
-due to destruction of myocardial tissue and inflammatory process
Acute Pulmonary Edema- dyspnea, orthopnea
-LV becomes severely weakened in pumping action due to the infarction
Dx:

Based on presenting symptoms, history of risk

factors, ECG (T-wave inversion, ST-segment
elevation, and abnormal Q wave), and serum
cardiac enzyme values (CK-MB, Myoglobin, and
Troponin)
Dx
Eleveated CK-MB (creatine kinase (CK), elevated LDH lactic
Dehydrogenase , elevated AST
-these cardiac enzymes are produced in abnormally large amounts because of
cellular damage and death.
CK-MB is the most cardiac specific enzyme
Elevated troponin levels-most definitive laboratory findings in MI.
Collaborative Management
Medications:
1. Analgesic-priority
-Morphine Sulfate, Lidocaine, Nitroglycerine are administered via IV.
Morphine is Drug of Choice.
2. Thrombolytic therapy
-to disintegrate blood clot by activating the fibrinolytic process.
e.g. Streptokinase, Urokinase, Tissue plasminogen activator (TPA)
Collaborative Management
Medications:
-crucial between 3-6 hours after the initial infarction has occurred
3. Anticoagulant & Antiplatelet meds-given after thrombolytic therapy to
maintain arterial patency.
Collaborative mgt.

Have client stop activity and rest in semi-Fowlers position

Administer oxygen
Reperfuse area of damage with thrombolytic
medicationGoal is to give within 30 minutes of arrival in
ER
Collaborative mgt.
Analgesics, generally morphine sulfate given IV bolus
Drugs that reduce oxygen demand or increase oxygen supply to the
myocardium include nitrates, beta blockers, ACE inhibitors, calcium channel
blockers, antihypertensives, and antiplatelet agents such as low-dose aspirin
Revascularization procedures such as percutaneous transluminal coronary
angioplasty (PTCA)
 PERCUTANEOUS TRANSLUMINAL
CORONARY ANGIOPLASTY (PTCA)
a type of percutaneous coronary intervention in
which a balloon is inflated within a coronary artery
to break an atheroma and open the vessel lumen,
improving coronary artery blood flow
PERCUTANEOUS TRANSLUMINAL
CORONARY ANGIOPLASTY (PTCA)
Video presentation
Take home quiz:
1. Research on Cardiac Rehabilitation (Brunner and Suddharths). Submit it
handwritten. Use long bond paper.
2. Prepare for an oral quiz next meeting.