1. Cardiovascular Disruptions

2. Objectives
• Describe the normal structure, function and regulatory
mechanisms of the cardiac system
• Define the factors that can influence cardiac output and their
significance
• State the conditions/situations which can lead to the
development of cardiac disruptions.
• Identify the common disruptions to cardiac function and
discuss each condition according to definition,
pathogenesis, clinical manifestations, and medical/nursing
management.

3. Normal Cardiac System
The heart is the pump of the circulatory system, and sits in the
mediastinal space of the intrathoracic cavity, in loose fitting
sack called the pericardium.
• The heart is suspended by the great vessels and is
positioned with the wide side up, and the apex (narrower
side) down and to the left.
• Heart is comprised of 3 layers
o Epicardium
o Myocardium
o Smooth Endocardium

4. Anterior view of heart and great vessels, and their relationship to lungs & skeletal structures of chest cage

5. Layers of the heart

6. Atria and Ventricles
The heart is broken up into 2 sets of 2 different chambers.
• Atria: Function as a collection chamber for blood returning
to the heart, and as a pump to fill the ventricle.
• Ventricle: Main pumping chamber of the heart.
o Right Ventricle: pumps the blood out of the heart and into
the lungs through the pulmonary artery
o Left Ventricle: pumps the blood out of the heart and into
the body via the aorta

7. Heart Valves
The atria and ventricles have 2 sets of valves that separate the
atria and ventricles from each other, and from the systemic
circulation.
The closure of these valves allows for the filling of the
chambers of the heart and to allow the blood to be pumped out
of the heart during systole.
• Atrioventricular valves: control the flow of blood between
the atria & the ventricles supported by the cordae tendonae
o Tricuspid Valve (RT)
o Bicuspid (Mitral) Valve (LT)
• Semilunar valves: control the flow of blood out of the heart
o Pulmonic Valve
o Aortic Valve

8. Valvular structures of the heart.
Atrioventricular valves are in an open position, semilunar valves are closed.
There are no valves to control blood flow at inflow channels (vena cavae & pulmonary veins) to the heart.

9. Coronary Arteries
Provide oxygenated blood to the heart muscle.
They are broken down into Right and Left Coronary Arteries
and branch directly off the aorta.
• Right Coronary Artery: feeds the right side of the heart
• Left Coronary Artery: breaks into 2 segments
o Left anterior descending artery
o Left circumflex artery

10. Coronary arteries & some of the coronary sinus veins.

11. Function/Cardiac Cycle Events
Cardiac cycle is the rhythmic pumping action of the heart,
which is broken into 2 events:
• Systole: period during which the ventricles are contracting
• Diastole: period during which the ventricles are relaxing and
filling with blood.

12. Regulation of Cardiac Function
The conduction of heart is dependent on the depolarization of
the nerve cells in the heart.
The initial stimulus for a heartbeat originates in the Sinoatrial
Node (P-wave on the EKG)
• P-wave  atrial contraction that moves blood  ventricles
• The AV-valves close (first heart tone S1)
• Ventricular pressure rises
 semilunar valves open
 blood is ejected from the hear
• The Semilunar valves close (second heart tone S2)
• Ventricular pressure < atrial pressure
 AV-valves open
 blood moves from the atria to the ventricle

13. Regulation of Cardiac Function:
Cardiac regulation via the Sinoatrial Node (pacemaker of the
heart) has some functions that make it unique in terms of
regulation of function:
• Automaticity
• Rhymthic
• Speed of spread
The initial depolarization in the Sinoatrial Node, is then spread
to the AV node that transmits the electrical impulse to the
Bundle of His that transmits it to Left/Right Bundle Branches
and ends in the Purkinje fibers

15. What can affect the regulation of the
cardiac cycle?
• Autonomic Nervous System:
o Sympathetic Nervous System: increases the HR, speed
of conduction through the AV node, and increases the
force of atrial and ventricular contractions
o Parasympathetic Nervous System: the vegus nerve
innervation of the SA node directly allows for a slowing of
SA node depolarization rate, and decrease in AV node
conduction
• Baroreceptors: sensitive to stretch or pressure, and when
stimulated cause temporary inhibition of the sympathetic
nervous system stimulation in the heart.
• Chemoreceptors: present in the aorta and carotid bodies,
and are stimulated by a drop in oxygen and an increase in
carbon dioxide levels

16. Cardiac Output:
Definition:
Cardiac Output = Heart Rate x Stroke Volume
The cardiac output can vary from person to person based on:
• body size
• metabolic needs
o physical activity
o rest/sleep
• Ranges from 3.5-8 L/min

17. Influencing factors on cardiac output
• Preload
• Afterload
• Cardiac contractility
• Heart Rate

18. Influencing factors on cardiac output
Preload: Afterload:
• This represents the • This represents the
volume workload of the pressure or tension work
heart of the heart to move blood
• Determined by the amount from the left ventricle into
of blood that the heart has the aorta/pulmonary artery.
to pump with each beat.
o largely comprised of the • Largely determined by the
venous return to the systemic arterial blood
heart pressure for the left
o diuretics have an affect ventricle
on the preload • Pulmonary arterial
pressure determines
afterload for the right
ventricle

19. Influencing factors on cardiac output
Cardiac Contractility: Heart Rate:
• This is the ability of the • this determines the
heart to change the frequency with which blood
strength of it's contraction is ejected from the heart.
without changing it's o increased heart rate can
resting length increase CO to a point,
o increased extracellular however, the quicker the
contraction can increase heart needs to eject
contractile strength blood, the shorter time it
o decreased ATP from has to fill with blood to
ischemia can cause eject.
decreased contractility

20. Overview of Alterations in the Cardiac System
1. Lack of Blood Supply
2. Infections of the heart
3. Immune mediated inflammatory conditions
4. Cardiomyopathy

21. Consequences of decreased blood flow
to the myocardium (heart muscle)
Lack of blood supply or perfusion to the myocardium can result
in ischemia, anginal pain, cardiac arrhythmias, myocardial
infarction (heart attack), conduction defects, heart failure and
sudden death.
Conditions that cause this "ischemic heart disease" are as
follows:
1. Atherosclerosis of the coronary arteries
2. Thrombus within the coronary arteries
3. Vasospasm of the coronary arteries
4. Hypovolemia

22. Atheroscelrosis of the Coronary
Arteries
This disease process of the coronary arteries is the direct
cause of many cases of myocardial ischemia and infarction.
The manifestations of atherosclerosis in the coronary arteries
include:
1. Angina pectoris (myocardial ischemia)
2. Myocardial ischemia (heart attack)
3. Sudden cardiac death

23. Stages in development of atherosclerosis
Developing atherosclerosis in the coronary arteries is a slowly
progressing process, that occurs over many years. Symptoms
often don't occur until the vessel is 75% occluded, which is the
point at which collateral circulation or compensatory
vasodilation cannot keep up with myocardial muscle oxygen
needs.
1. Fatty Streak
2. Fibrous Plaque
3. Complicated lesion

26. Angina Pectoris
Angina comes from a Latin word meaning: "to choke"
• Symptomatic paroxysmal chest pain or pressure sensation
associated with transient myocardial ischemia
• precipitated by situations that increase the work demands of
the heart
o physical exertion
o exposure to cold
o emotional stress
• Pain is described at constricting, squeezing, or suffocating
sensation located in the precordial or substernal area of the
chest

27. Areas of pain due to angina.

28. Myocardial Infarct: Heart Attack
An acute myocardial infarct is characterized by ischemic death
of the myocardial tissue associated with atherosclerotic disease
of the coronary artery.
Area of infarction is determined by the coronary artery that is
affected:
• 30-40% Right Coronary Artery
• 40-50% Left Anterior Descending Artery
• 15-20% Left Circumflex Artery

29. Manifestations of an MI
Onset of an MI can be abrupt or it can progress from unstable
angina.
• pain, usually severe and crushing
• pain substernal radiating to the left arm, neck or jaw
• pain prolonged, not relieved by nitroglycerin
• associated with a feeling of impending doom
• Atypical presentations:
o Women have more atypical ischemic like discomfort
o Elderly people often have more shortness of breath
• Tachycardia, anxiety, restlessness
• pale, cool, moist skin

30. Diagnosing an MI
• EKG changes
o T-wave Inversion
o T-wave Elevation
o ST segment changes
 ST depression (injury confined to the subendothelium)
 ST elevation (injury to the heart is transmural)
• Serum Markers
o myoglobin
o Creatinine Kinase MB (CK-MB)
o Troponin 1 and Troponin T
o C-reactive protein
o B-cell natriuretic peptide (BNP)

31. Top:
A.Normal ECG
B.ST elevation with acute ischemia
C.Q wave with acute MI
Bottom: current of injury patterns with acute ischemia
A.With predominant subendocardial ischemia, resultant ST segment is directed toward inner layer of the affected ventricle &
ventricular cavity. Overlying leads therefore record ST-segment depression.
B.With ischemia involving the outer ventricular layer (transmural/epicardial injury), the ST vector is directed outward. Overlying leads
record ST-segment elevation.

33. Acute MI – X-section of ventricles infarct
(death few days after onset of severe angina pectoris)
• LV transmural infarct in posterior & septal regions.
• Necrotic myocardium is soft, yellowish, and sharply
demarcated.
LV transmural
infarct
in posterior &
septal regions

34. Consequences of AMI
• Damage to the muscle wall of the heart
o ventricular aneurysms
• Damage to the conduction system of the heart
o arrhythmias
• Heart failure
o decreased cardiac output

35. Treatment of AMI
• Administration of Oxygen
• Administration of analgesics
• Aspirin
• Beta-adrenergic blockers
• Nitrates
• If ECG evidence of infarction, Immediate Reperfusion
therapy should be initiated:
o Thrombolytic Therapy
o Revascularization Interventions

36. Sudden Cardiac Death
Unexpected death from cardiac causes, usually within 1 hour of
an MI, can occur up to 24 hours post MI.
• coronary artery disease accounts for 80% of cases
o decreased blood flow causes an acute ventricular
dysrhythmia
o less frequently, the SCD can result from primary left
ventricular outflow obstruction issues
 aortic stenosis
 hypertrophic cardiomyopathy
• abrupt disruption in cardiac function, that produces an
abrupt loss of cardiac output and cerebral blood flow
• Biggest risk factors: left ventricular dysfunction (EF<30%)
and ventricular dysrhythmias following MI

37. Conditions that disrupt blood flow in the
heart
Thrombus within the coronary arteries:
• Areas that have complicated lesions of atherosclerosis can
cause the formation of thrombi.
• The smooth muscle and foam cells in the lipid core
contribute to the expression of tissue factor in unstable
plaques, which leads to the activation of the extrinsic
coagulation cascade and formation of thrombin and the
deposition of fibrin = Red thrombi
• If a plaque is disrupted, the endothelium is damaged and
platelets bind there = white platelet containing thrombi

40. Vasospasm of the Coronary Arteries
This is a spasm of the coronary arteries causing an acute
decrease in coronary blood flow, and ischemia
• occurs most often during rest, or with minimal exercise
• most frequently between midnight and 8am
• can precipitate life threatening arrhythmias, and patient is at
high risk for SCD
• Causes (not totally known)
o hyperactive sympathetic nervous system
o defects in the management of Ca influx into vessel
smooth muscle cells
o alteration in nitric oxide production
o imbalances between endothelium derived relaxing and
contracting factors

41. Hypovolemia
Lack of circulating blood flow throughout the whole body can
lead to a generalized ischemia in the heart due to the overall
decrease in oxygen carrying capacity. Hypovolemia is also
associated with electrolyte abnormalities that can cause
cardiac problems
• Hypokalemia: K+ levels below 3.5 mEq/L
• Hyperkalemia: K+ levels >5.5 mEq/L
• Hypocalcemia: Ca++ levels <8.5 mg/L
• Hypercalcemia: Ca++ levels >12 mg/dL

42. Infections of the Heart
Infections in the pericardium, epicardium, myocardium,
endocardium and the valves
• Result in a decrease in the cardiac output
• Can also cause a backward flow of blood into the ventricles
(due to diseased valves) that can cause congestion of blood
flow

43. Infective Endocarditis
This was previously known as bacterial endocarditis, but other
infectious agents can cause endocarditis. Most common cause
is bacterial though:
• Staphylococcus aureus (can be MRSA)
• Streptococcus viridans
Arise from infections somewhere else in the body, that allows
the infectious organism into the blood stream.
• blood flow turbulence in the heart allows the infective agent
to infect previously damaged heart valves or other
endothelial surfaces
• the infectious agents attach the heart surfaces and form
vegetations of infectious agent, platelets, fibrin, and
leukocytes

44. Infective Endocarditis
• The vegetations are very friable, they can break apart easily
and "embolize"
o 22-50% of patients with IE will experience systemic
emboli from the vegetations
 left side heart vegetations cause emboli to the brain,
kidneys, spleen, or the limbs
 right side of heart vegetations cause emboli to the lung
• The infective vegetations can also cause damage to the
valves and supporting structures

45. Infective Endocarditis
Acute Bacterial Subacute Bacterial
Endocarditis: Endocarditis:
• Usually affects those with • Affects those who have
healthy valves preexisting valve disease
• presents as an acute, • Clinical course may extend
rapidly progressing illness over months
Although this classification system was in
historical use, now clinicians classify IE based on
the cause, or the site of involvement

46. What does endocarditis look like?

48. Immune Mediated Inflammatory
Conditions
These conditions primarily infect the valves, which results in
congestion within the ventricles and in the lung and viseral
circulation
• Rheumatic heart disease is a prime example of this
o sequela to group A (beta hemolytic) streptococcal (GAS)
throat infection
o decreased incidence in the US because of antimicrobial
treatment of GAS infection
• Thought that the untreated GAS leads to antibody formation,
which can affect the heart, joints, CNS and skin.
• the myocardium develops Aschoff Bodies that are nodules
with swelling and fragmentation of the collagen fibers that
become more fibrous as we age

49. Rheumatic Heart Disease
Type III hypersensitivity: antibodies against the strep are
formed, and there is a complex of strep and strep antibodies
that are deposited in the heart, activates complement.
• These complexes can also be deposited into the joints, but
the effects on the joints are reversible
• effects on the myocardium are permanent

52. Cardiomyopathy
A group of disorders that affect the heart muscle, which can
develop as primary or secondary disorders. Often lead to
cardiomegaly and heart failure (dilitation of the heart muscle,
hypertrophy of the the heart, or stiffening of the ventricles).
Primary: Result of disease in the heart muscle itself, but
usually an unknown cause
Secondary: from a secondary disease, like a myocardial
infarction

53. Types of Cardiomyopathy
1. Dilated
2. Hypertrophic
3. Restrictive
Each of these types of cardiomyopathy have their own etiology,
presentation, pathophysiology and treatments.
General Causes of Cardiomyopathy: Toxins such as alcohol,
cocaine, chemotherapy agents, excess thyroid hormone,
uremic disorders, metabolic abnormalities and familial
tendencies

54. Dilated Cardiomyopathy
Characterized by progressive cardiac hypertrophy and dilation
and impaired pumping ability by one or both ventricles. Atria
are also enlarged.
• because of wall thinning that occurs, the hypertrophied
ventricles are thinner than one would expect.
• mural thrombi are common and may be source of
microemboli
• Stasis of blood in the left ventricle
• Causes:
o Alcoholism
o familial condition
o toxic agents (chemotherapy)
Most common form of cardiomyopathy.

55. Hypertrophic Cardiomyopathy
Abnormality that causes excessive ventricular growth or
hypertrophy. Involvement of the interventricular septum tends
to be disproportionate, which produces intermittent left
ventricular outflow obstruction and impaired relaxation of the
heart.
• Genetic disorder identified in many of the cases
o mutation in one of the 10 genes coding for the cardiac
sarcomeres
o found to have myofibril disarray on microscopic
evaluation of the heart
• most common cause of SCD in the young
• need to screen 1st degree relatives once discovered in an
individual

57. Restrictive Cardiomyopathy
Ventricular filling is restricted because of excessive rigidity of
the ventricular walls, although the contractile properties of the
heart remain relatively normal.
• Endemic in parts of Africa, India, South and Central
America, and Asia
• In the U.S., the number 1 cause is amyloidosis, or amyloid
infiltrations of the heart
• Symptoms include: dyspnea, PND, orthopnea, peripheral
edema, ascites, fatigue and weakness.
Least common cardiomyopathy in the U.S.