Cardiovascular Disorders

Chapter 18
Pgs 285-308

Overview
Diagnostic Tests for
Cardiovascular Function
General Treatment
Measures for Cardiac
Disorders
Coronary Artery Disease
(CAD)
Arteriosclerosis
Atherosclerosis
Myocardial Infarction (MI)

Cardiac Arrhythmias
Sinus node abnormalities
Atrial conduction
abnormalities
Cardiac arrest

Congestive Heart Failure

(CHF)
Arterial Diseases
Hypertension

Shock

Homework
Due Tuesday Oct 4
Do the following Case Study questions on Pg. 306
You do not have to type them; Put the answers in your own
words!

Case Study A
a, b, e, g, k, l, m

Case Study B
a-f

You may work together

If you work in a group, you can turn in one paper!
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Diagnostic Tests for Cardiovascular

Function
ECG
Monitors arrhythmias, MI, infection, pericarditis
Studies conduction activation and systemic abnormalities

Ausculation
Studies heart sounds using stethoscope

Exercise stress test

Assess general cardiovascular function
Checks for exercise-induced problems

Chest X-ray Film

Shows shape, size of heart
Evidence of pulmonary congestion associated with heart failure
Nuclear imaging

Diagnostic Tests
Cardiac
Catheterization
Visualize inside of
heart, measure
pressure, assess valve
and heart function
Determine blood flow
to and from heart

Diagnostic Tests
Angiography
Visualization of blood
flow in coronary artery
Obstruction assessed
and treated
Basic catheterization
Balloon angioplasty

Diagnostic Tests
Doppler Studies
Assessment of blood flow in peripheral vessels
Microphone records sounds of blood flow
Can detect obstruction

Blood tests
Assess triglyceride and cholesterol levels
Electrolytes
Hb, hematocrit, cbcs

Arterial Blood Gas Determination

Essential for pts with shock, MI
Check current oxygen levels, acid-base balance

General Treatment Measures for

Cardiac Disorders

Dietary modification
Regular exercise program
Quit smoking
Drug therapy

Drug Therapy
Vasodilators (Nitroglycerin)
Provide better balance of oxygen supply and
demand in heart muscle
May cause low bp

Beta-blockers (Metoprolol or Atenolol)

Treats angina, hypertension, arrhythmias
Blocks beta1-adrenergic receptors in heart
Prevent epine from increasing heart activity

Drug Therapy

Calcium ion channel blockers

Block movement of calcium
Decrease heart contraction
Antiarrhytmatic for excessive atrial activity
Antihypertension and vasodilator

Digoxin
Treats heart failure
Increases efficiency of heart
Decreases conduction of impulses and HR
Increases contraction of heart

Pts must be checked for toxicity

Antihypertensive drugs
Decrease bp to normal levels
Include:

Adrenergic blocking agents

Calcium ion blockers
Diuretics
Angiotensin-converting enzyme (ACE) inhibitors

Used to treat hypertension, CHF, after MI

Drug Therapy
Adrenergic Blocking drugs
Act on SNS, block arteriole alpha adrenergic
receptors, or act directly as vasodilator

ACE Inhibitors
Treat hypertension, CHF

Diuretics
Remove excess water, sodium ions
Block resorption in kidneys
Treat high bp, CHF

Drug Therapy
Anticoagulant
Decrease risk of blood clot formation
ASA decreases platelet adhesion
Block coagulation process

Cholesterol or lipid reducing drugs

When diet and exercise fail
Decrease LDL and cholesterol

CADArteriosclerosis:
Pathophysiology
General term for all
types of arterial
changes
Best for degeneration
in small arteries and
arterioles
Loss of elasticity,
walls thick and hard,
lumen narrows

CADAtherosclerosis:
Pathophysiology
Presence of
atheromas
Plaques
Consist of lipids, cells,
fibrin, cell debris

Lipids usually
transported with
lipoproteins

Lipoproteins and Transport

Atherosclerosis--Pathophysiology
Analysis of serum lipids:
Total cholesterol, triglycerides, LDL, HDL

LDL
High cholesterol content
Transports cholesterol liver cells
Dangerous component

HDL
good
Low cholesterol content
Transports cholesterol cells liver

Development of Atheroma

Consequences of Atherosclerosis

AtherosclerosisEtiology

Age
Gender
Genetic factors
Obesity, diet high in cholesterol, animal fats
Cigarette smoking
Sedentary life style
Diabetes mellitus
Poorly controlled hypertension
Combo of BC pills and smoking

AtherosclerosisDiagnostic Tests
Serum lipid levels
Exercise stress test
Radioisotope

AtherosclerosisTreatment

Decrease cholesterol and LDL

Decrease sodium ion intake
Control primary disorders
Quit smoking
Oral anticoagulant
Surgical intervention
Percutaneous transluminal coronary angioplasty
(PTCA)
Cardiac catheterization
Laser beam technology
Coronary artery bypass grafting

CABG

CAD: Myocardial Infarction

Pathophysiology
Coronary artery completely obstructed
Prolonged ischemia and cell death of myocardium

Most common cause is atherosclerosis with

thrombus
3 ways it may develop:
Thrombus obstructs artery
Vasospasm due to partial occlusion
Embolus blocks small branch of coronary artery

Majority involve L ventricle

Size and location of infarction determine severity of
damage

Myocardial Infarction

MIPathophysiology
Function of myocardium contraction and
conduction quickly lost
Oxygen supplies depleted
1st 20 minutes critical

Time Line

1st 20 min critical

48 hrs inflammation begins to subside
7th day necrosis area replaced by fibrous tissue
6-8 weeks scar forms

MISigns and Symptoms

Pain
Sudden, substernal area
Radiates to L arm and neck
Less severe in females

Pallor, sweating, nausea, dizziness

Anxiety and fear
Hypotension, rapid and weak pulse (low
CO)
Low grade fever

MIDiagnostic Tests
ECG
Serum enzyme and
isoenzyme test
High serum levels of
myosin and troponin
Abnormal electrolytes
Leukocytosis
Arterial blood gases
Pulmonary artery
pressure measure
Determines ventricular
function

MIComplications
Arrhythmias
25% pts sudden death after MI
Due to ventricular arrhythmias and fibrillation

Heart block
Premature ventricular contraction (PVCs)

Cardiogenic shock
CHF

MITreatment

Rest, oxygen therapy, morphine

Anticoagulant
Drugs
Cardiac rehabilitation
Prognosis depends on site/size of infarct,
presence of collateral circulation, time elapsed
before treatment
Mortality rate in 1st year
30-40% due to complications, recurrences

Cardiac Arrhythmias
Alteration in HR or rhythm
ECG monitors
Holter monitors

decreases efficiency of hearts pumping cycle

Slight increase in HR increases CO
Very rapid HR prevents adequate filling in diastole
Very slow HR reduces output to tissues

Irregular contraction inefficient

Interferes with normal filling/emptying cycle

CA: Sinus Node Abnormalities

Brachycardia
Regular but slow HR
Less than 60 beats/min

Results from vagus nerve stimulation or PNS

stimulation

Tachycardia
Regular rapid HR
100-160 beats/min

SNS stimulation, exercise, fever, compensation

for low blood volume

CA: Atrial Conduction

Abnormalities
Premature Atrial Contractions (PAC)
Extra contraction or ectopic beats of atria
Irritable atrial muscle cells outside conduction
pathway
Interfere with timing of next beat

Atrial flutter
HR 160-350 beats/min
AV node delays conduction
Slower ventricular rate

Treatment of CA
Cause should be determined and treated
Easiest to treat are those due to meds
SA node problems may require a
pacemaker
Some may require defibrillators

Cardiac Arrest
Cessation of all activity in the heart
No conduction of impulses (flat line)
May occur b/c:
Excessive vagal nerve stimulation (decreases
heart)
Drug toxicity
Insufficient oxygen to maintain heart tissue

Blood flow to heart and brain must be

maintained to resuscitate

CHFPathophysiology
Heart unable to pump sufficient blood to
meet metabolic needs of body
Complication
Acute or chronic
Results from
Problem in heart itself
Increased demands placed on heart
Combo

One side usually fails 1st

CHFPathophysiology
1st compensation mechanism to maintain CO
Often aggravates instead of assists
Decreased flow to systemic circ
Kidneys increase renin, aldosterone secretion
Vasoconstriction (increase afterload) and increased blood vol
(increased preload) = increased work load for heart

SNS increases HF and periph resistance

Dilatation of heart chambers, myocardium,
hypertrophies

CHFPathophysiology
2nd effect when heart cannot maintain
pumping capability
Decrease in CO or SV
forward effect

backup congestion

CHFEtiology
Causes of failure on affected side:
Infarction that impairs pumping ability or
efficiency of conduction system
Valve defects
Congenital heart defects
Coronary artery disease

CHFEtiology
Increased demands on heart cause failure
Depends on ventricle most adversely affected
Ex: Hypertension increases diastolic bp
Requires L ventricle to contract more forcibly to open
aortic valve

Ex: Pulmonary disease

Damages lung caps, increases pulm resistance
Increase work load to R vent

CHFSigns and Symptoms

Forward effects
Similar with failure on either side
Decrease blood supply to tissue and general
hypoxia
Fatigue, weakness, dyspnea
(breathlessness), cold intolerance, dizziness

Compensation mechanism
Indicated by tachycardia, pallor, daytime
oliguira

CHFSigns and Symptoms

Systemic backup effects of R-sided failure
Edema in feet, legs
Hepatomegaly, splenomegaly
Ascites
Acute R-sided failure
Increased pressure on SVC
Flushed face, distended neck veins, headaches, vision
problems

CHFDiagnostic Tests
Radiographs
Catheterization
Arterial blood gases

CHFTreatment

Underlying problem should be treated

Decrease work load on heart
Prophylactic measures
Other methods
Diet
Drugs

Arterial Diseases: Hypertension

Pathophysiology
Increased bp
Insidious onset, mild symptoms and signs
3 major categories
Essential (primary)
Secondary
Malignant

Can be classified as diastolic or systolic

Develops when bp consistently over 140/90
Diastolic more important

HypertensionPathophysiology
Over long time, high bp damages arterial walls
Sclerosis, decreased lumen
Wall may dilate, tear
Aneurysm

Areas most frequently damaged:

Kidneys, brain, retina

End result of poorly controlled hypertension:

Chronic renal failure

Stroke
Loss of vision
CHF

HypertensionEtiology

Increases with age

Males more freq and severe
Genetic factors
High sodium ion intake
Excessive alcohol
Obesity
Prolonged, recurrent stress

HypertensionSigns and
Symptoms
Asymptomatic in early stages
Initial signs vague, nonspecific
Fatigue, malaise, morning headache

HypertensionTreatment
Treated in sequence of steps
Life style changes
Mild diuretics, ACE inhibitors
One or more drugs added

Pt compliance is an issue
Prognosis depends on treating underlying
problems and maintaining constant control
of bp

Shock (Hypotension)
Results from decreased circulating blood
vol
General hypoxia
Low CO

Classification and Mechanisms of

Shock
Type
Hypovolemic
Cardiogenic

Mechanism
loss of blood or plasma
Decreased pumping
capability of heart

Anaphylactic

Systemic vasodilation
due to severe allergic
reaction

Septic

Vasodilation due to
severe infection

Neurogenic

Vasodilation due to loss

of SNS and vaso-motor
tone

ShockPathophysiology
Bp decreases when blood vol, heart contraction,
or periph resistance fails
Low CO, microcirculation
= decreased oxygen, nutrients for cells

Compensation mechanism

SNS, adrenal medulla stimulated

Renin secreted
Increased secretion of ADH
Secretion of glucocorticoids
Acidosis stimulates respiration

ShockPathophysiology
Complications of decompensation of
shock
Acute renal failure
Adult respiratory distress syndrome (ARDS)
Hepatic failures
Hemorrhagic ulcers
Infection of septicemia
Decreased cardiac function

ShockEtiology
Hypovolemic shock
Loss of blood, plasma
Burn pts, dehydration

Cardiogenic shock
Assoc w/ cardiac impairment

Distributive shock
Blood relocated b/c vasodilation
Anaphylactic shock
Neurogenic shock

Septic shock
Severe infection

ShockSigns and Symptoms

1st signs
Shock, thirst, agitation,
restlessness
Often missed

2nd signs
Cool, moist, pale skin;
tachycardia; oliguria
Compensation
Vasoconstriction

Direct effects
Decrease bp and blood
flow
Acidosis

Prolonged
Decreased responsiveness
in body
Compensated metabolic
acidosis progresses to
decompensated
Acute renal failure
Monitoring

ShockTreatment
Primary problem must be treated
Hypovolemic shock
Whole blood, plasma, electrolytes, bicarbonate required

Anaphylactic shock
Antihistamines, corticosteroids

Septic
Antimicrobials, glucocorticoids

Maximize oxygen supply

Epine reinforces heart action and vasoconstriction
Dopamine, dubutamine increase heart function
Good prognosis in early stages
Mortality increases as irreversible shock develops