CAD and Cardiac Emergencies

Question 1

CORONARY ARTERY DISEASE (CAD)

Answer 1

• coronary arteries deliver 250 ml oxygenated blood to the myocardium, each minute
• this translates to about 360,000 ml / day
• the heart contracts constantly (>100,000 times / day) and hence has a constant and very
  large O2 demand
• the heart has very little oxygen reserve, so additional needs will require an increase in
  coronary artery blood flow
• the term CAD is used to describe the effects of impaired coronary artery blood flow to the
  myocardium
• in most cases, CAD is caused by coronary artery atherosclerotic obstruction

Question 2

what is atherosclerosis?…

Answer 2

• atherosclerosis is the primary disease that affects coronary arteries
• it is a progressive process by which fatty substances accumulate as plaque along
  the inner lining of the vessels, which then narrows the artery passages
• CAD exists when atherosclerosis has reached the stage where the blood flow
  through the arteries is not sufficient enough to meet the O2 demands of the
  myocardium
• the extent of CAD depends on the amount of arterial narrowing, and the reduction in blood
  flow resulting from this narrowing

Question 3

• there are 4 grades of atherosclerosis

Answer 3

-Grade 1 - 25% narrowing and reduction in blood flow. Severity is minimal.
- Grade 2 - 50%. Moderate
- Grade 3 - 75%. Severe
- Grade 4 - 100%. Complete blockage.
- this classification is based on the degree of obstruction
- obstruction of about 75% is needed to produce significant reduction in coronary
artery blood flow, resulting in symptoms

• obstruction can occur in any, and/or all arteries
• LAD obstruction would be the most dangerous as this vessel supplies a much
  larger portion of the total myocardial mass (reviewing arteries in Lesson 1 might
  be useful)
• an occlusion of the LCA would be even worse, but is the least common

Question 4

How CAD leads to Acute Coronary Syndromes

Answer 4

• a piece of plaque ruptures, traveling toward the distal portion of the artery
• during the travel, platelets begin to adhere to it, as well as fibrin and thrombin
• in other words, a blood clot forms on the plaque
• this “enlarged” plaque then partially or totally occludes the distal portion of the artery
• a rough atherosclerotic lesion irritates the arterial wall causing bleeding beneath the plaque
• the hemorrhage then dislodges the plaque, and the lesion begins its travel
• the ‘travelling’ clotted plaque obstructs a distal part of the vessel

Question 5

CAD RISK FACTORS

Answer 5

• some are modifiable (ie: diet), while others are termed non-modifiable (ie: gender)

Question 6

Heredity, Genetics

Answer 6

• heredity ranks very high on the list of non-modifiable risk factors
• it is becoming clear that genetic influences play an important role
• the physical structure of the coronary arteries and the rate of atherosclerosis seems to
  be genetically determined

Question 7

Hypertension

Answer 7

• high BP is associated with a 2-5 time greater incidence of CAD
• it predisposes to CAD by accelerating the rate of atherosclerosis
• cumulative arterial damage occurs with sustained hypertension

Question 8

Smoking

Answer 8

• nicotine causes vasoconstriction, thereby reducing coronary artery blood flow
• cardiac workload increases (↑HR & BP) and can therefore produce an oxygen deficiency
• associated with ↑ CO levels in the blood, interfering with O2 supply to the myocardium
• the risk factor is markedly reduced within 2-3 years of smoking cessation

Question 9

Obesity

Answer 9

• the mechanism is not fully understood
• it is believed that the risk of CAD is increased in the overweight populace because they
  are more prone to hypertension, diabetes, elevated cholesterol levels

Question 10

Gender & Age

Answer 10

• CAD is still a little more prevalent in men than in women
• female estrogen appears to have a protective effect, however, with women’s roles
  changing, and more showing type A personalities, females are closing the gap on males
• after menopause, the incidence of CAD in females equals that of the male counterpart
• in both sexes, the incidence of CAD increases with age (almost doubling every 5 years)
• men are affected by CAD as early as their mid 20s
• women in childbearing years seem almost protected from CAD, unless they have some
  underlying factor (ie. diabetes, smoking, hypertension)

Question 11

Diet

Answer 11

• fats are carried in plasma in 2 forms:

1) free fatty acids
- these are used up almost immediately for energy

2) lipoproteins
- these are mostly stored in muscle

• lipoproteins can absorb into the vessel walls, leading to atherosclerosis
• cholesterol is transported in lipoproteins. The 2 types of lipoproteins are:

1) HDL (high density lipoproteins)
- these are transported away and metabolized by the liver
- sometimes called the ‘good’ cholesterol

2) LDL (low density lipoproteins)
- these are absorbed into the vessels’ walls
- sometimes called the ‘bad’ cholesterol

• some factors affect HDLs (the ‘good’ lipoprotein):
• lower HDL levels are seen in:
• diabetics
• the overweight
• cigarette smokers
• post-menopausal women
• sedentary types, with lack of exercise
• elevated HDL levels can be seen in:
• those who exercise
• pre-menopausal women
• moderate alcohol consumers (ie.1-2 glasses red wine/day)

Question 12

Diabetes Mellitus

Answer 12

• CAD seems to develop more frequently and at an earlier age among diabetics, particularly
  those with Type 2 Diabetes
• diabetics seem more prone to:
  - hypertension
  - obesity
  - disturbances in sero-lipoproteins
  - (all of which are CAD risk factors)

Question 13

Sedentary Life Style

Answer 13

• the risk of CAD among those leading a sedentary lifestyle is almost doubled
• the mechanism is not yet fully understood, but exercise appears to decrease the risk of
  CAD, regardless of the presence of other risk factors, or the patient’s age
• it is believed that a sedentary lifestyle is associated with:
  - low HDL levels
  - higher levels of LDLs
  - increased triglycerides, as fats are not burned up with activity
  - hypertension

Question 14

Personality Type

Answer 14

• the coronary prone person is often referred to as a “type A personality”
• this person is rushed, aggressive and ambitious in nature
• sometimes even impatient, easily-provoked, and over-committed
• these people have as much as twice the risk of CAD than type B personalities (those
  with lower keyed, relaxed and satisfied lifestyles)
• type A behaviour might increase sympathetic nervous system activity

Question 15

Race

Answer 15

• CAD affects all races
• it is lowest among those of African and Chinese origin
• it is not understood if the differing risks result from environmental factors, or genetic factors

Question 16

Stress, Anxiety

Answer 16

• industrialized countries reveal a higher incidence of CAD
• this is probably due to the environmental stress imposed by a fast-paced lifestyle
• while trying to cope with a rapidly changing society and culture, chronic anxiety develops
  and somehow promotes atherosclerosis
• anxiety is often accompanied by elevated cholesterol levels and hypertension
• studies are ongoing to better understand the CAD-stress relation

Question 17

MANIFESTATIONS and CLINICAL SPECTRUM OF CAD

Answer 17

• CAD symptoms are caused by the lower blood supply reaching the myocardium, rather
  than the state of the coronary arteries
• even with grossly narrowed arteries, CAD may not produce symptoms if enough blood
  is reaching the myocardium through adequate collateral circulation

Question 18

STABLE ANGINA (ANGINA PECTORIS)

Answer 18

• this is the distinctive type of chest pain that indicates impaired circulation to the myocardium
• the heart’s oxygen demand exceeds the capacity of the coronary artery supply

Question 19

STABLE ANGINA (ANGINA PECTORIS) - Pain Characteristics

Answer 19

• usually substernal (under the breast bone)
• pain may radiate to either arm, neck, jaw, teeth, shoulders, upper back
• sometimes, pain may be absent substernally, and only experienced at sites of radiation
• it may be described as tightness, squeezing, constriction, pressure, indigestion, burning,
  heaviness
• the pain is not influenced by change in position or breathing pattern

Question 20

STABLE ANGINA (ANGINA PECTORIS) - Occurrence & Duration of Pain

Answer 20

• cardiac O2 demand is related to the amount of work the heart performs, so any condition
  that increases myocardial demand for O2 can produce anginal pain
• physical effort or sudden emotional stress (fear, excitement) increases the HR, the cardiac
  workload and therefore the O2 requirement, leading to pain
• provoking factors can include exercise, eating, emotional stress, exposure to elements
  (ie. heat or cold)
• when provoking factors cease (ie. activity stops), the HR drops and O2 demand decreases
• consequently, the pain subsides
• cessation of pain indicates that myocardial O2 demands have been met
• pain is usually of short duration (1-5 min), and relieved with rest
• the oxygen deficit is transient and not destructive to the myocardium
• the pain is predictable and reproducible. Patients can predetermine that certain activities
  will cause chest pain
• associated symptoms may include pallor, nausea, vomiting

Question 21

STABLE ANGINA (ANGINA PECTORIS) - Treatment

Answer 21

• rest
• nitroglycerine: acts by dilating the coronary vessels thereby increasing blood flow
  and oxygen supply to the myocardium
• beta-blockers, Ca+ channel blockers, ASA
• often diagnosed by a positive stress test

Question 22

UNSTABLE ANGINA

Answer 22

• this is the clinical ‘stage’ between stable angina and MI
• it is a worsening of stable angina
• chest pain develops with increasing frequency and less effort
• nitroglycerine has little or no effect
• it is difficult to rule out the possibility that a small area of the myocardium was destroyed
  during the longer period of time with a lack of oxygen
• so, these patients are closely observed and often admitted to hospital, until a diagnosis
  of MI can be excluded
• signs of ischemia are often noted on the ECG

Question 23

UNSTABLE ANGINA - Pain Characteristics

Answer 23

• pain is described with the same terms as those experienced with stable angina
  (ie. crushing, heaviness, squeezing, etc)
• chest pain can persist for 10-20 minutes or longer, even after using nitroglycerine
• associated phenomena often include changes in skin color, diaphoresis, nausea, vomiting,
  dyspnea, anxiety

Question 24

UNSTABLE ANGINA - Treatment

Answer 24

• the main goal is to prevent an MI from occurring
• oxygen: increasing the oxygen supply will help supply the heart’s O2 demand
• pain control (morphine is commonly used)
• cardiac monitoring, ECGs, cardiac enzymes and proteins (troponins)
• decrease stress and activity levels
• nitrates, ASA, beta-blockers, calcium-channel blockers

Question 25

PRINZMETAL ANGINA (also called Variant Angina)

Answer 25

• the mechanism is not fully understood, but this type of angina results from
  coronary artery spasm
• it is a cyclical type of pain that can occur at rest, often during the night
• it appears to be more prevalent in those with a history of migraines or Raynaud’s disease,
  indicating the possibility of a generalized vasospastic process
• episodes can last several minutes or cease spontaneously
• the spasm limits blood supply through the affected artery, so ECG signs of ischemia
  and/or injury are seen during the attacks
• the chest pain usually responds to nitroglycerine
• long-term prevention usually includes the use of calcium-channel blockers

Question 26

MYOCARDIAL INFARCT

Answer 26

-Last stage of CAD
- cells in a portion of the myocardium are deprived of O2, causing immediate cellular
changes, and leading to necrosis (cell death) to this localized area
- this is due to the profound and sustained ischemia (cell damage)
- the coronary artery narrows gradually over time, but the obstruction/blockage is sudden

• pain and radiation sites are the same as angina
• the quality of pain is more severe, often described as severe crushing (ton of bricks on
  chest), heavy weight (elephant sitting on chest), viselike
• the pain is prolonged, lasting 30 minutes or longer
• the patient’s nitroglycerine is no longer effective
• pain is not relieved with breath-holding, attempting to change body position or trying
  home remedies (ie. ‘alka seltzer’)
• provoking factors can be the same as angina or there may be no aggravating factors at all
  (can develop during sleep)
• associated phenomena usually include nausea, vomiting, pallor, changes in skin color,
  dyspnea, diaphoresis, fear, apprehension, weakness, sense of impending doom
• signs of decreased CO can be noted (ie. hypotension)
• bradycardia or tachycardia may be present, along with any other arrhythmia
• MI patients are not usually febrile for the first 24 hours
• tachypnea is common, due to the dyspnea
• crackles may be heard on auscultation (if the patient is in early heart failure)
• edema may be noted in the periphery (if the patient is also in heart failure)
• if CO is compromised, peripheral pulses may be less palpable

Question 27

Sites of Infarction

Answer 27

• the site of necrosis is determined by the affected artery that is occluded and unable to
  deliver the oxygenated blood to the site
• the circumflex artery supplies the lateral wall of the LV, so its occlusion would cause a
  lateral wall MI (LWMI)
• the LAD artery supplies the anterior wall of the LV, so its occlusion would lead to an
  anterior wall MI (AWMI)
• the RCA supplies the inferior wall of the LV, so its occlusion would lead to an
  inferior wall MI (IWMI)
• the RCA also supplies the posterior wall of the LV, so its occlusion could cause a
  posterior wall MI (PWMI)
• the RCA supplies the RV. RVMI is not as common as LVMI because the RV has less oxygen
  needs, and it receives a greater portion of blood for its muscle mass, than the LV does

Question 28

Extent of MI

Answer 28

• several factors can determine the severity of cell necrosis. Some factors are:

1. the size of the vessel obstructed (small distal or large proximal artery)
2. capacity of collateral circulation to supply blood to the deprived area
   (if the tissue is well oxygenated, less tissue damage may occur)
3. oxygen demands following the attack
4. thickness of the area involved

Q wave MI (transmural MI) is necrosis which extends through the
entire thickness of the myocardium
non Q wave MI (non-transmural or subendocardial MI) is a lesser
degree of damage that does not involve the full thickness of the
myocardium, but rather the endocardial surface

5. the size of the three zones of tissue damage (see diagram below)
   1) zone of necrosis is the innermost section of tissue where cells are
   necrotic and irreversibly damaged due to the lack of O2
   2) zone of injury is the area surrounding the zone of necrosis where myocardial
   cells are in jeopardy but will survive with restored and adequate
   circulation
   3) zone of ischemia is the outermost area of tissue damage where the cells
   have not received adequate O2, but are expected to recover and
   survive, unless the lack of O2 continues and the ischemia worsens

Question 29

DIAGNOSIS of MI - Patient History

Answer 29

• complaints of chest pain & all the associated phenomena lead the diagnostician to
  suspect that the patient has suffered an MI
• however, the patient’s history does not always fit the classic MI picture
• patients may also complain of typical MI signs & symptoms, and not have suffered an MI
  (ie. esophageal spasm can resemble MI pain)
• therefore, other steps are taken to confirm the diagnosis

Question 30

DIAGNOSIS of MI -Chest X-Ray

Answer 30

• the CXR is usually clear
• if early complications occur, the CXR can help with diagnosing these (ie. LVF,
  pulmonary edema, pleural effusion)

Question 31

DIAGNOSIS of MI - Cardiac Enzyme and Protein Studies

Answer 31

• the patient may have a classic history but the early ECG may fail to show signs of MI,
  making the diagnosis of MI a little difficult
• as discussed in Lesson 3…
• several cardiac enzymes and proteins are normally present in myocardial cells
• following myocardial injury, these enzymes are released into the blood stream
• so, following an MI, elevation of these enzymes is expected
• blood work is drawn serially because of the time needed for enzymes to elevate and peak

Question 32

DIAGNOSIS of MI - Electrocardiogram

Answer 32

• diagnosis of a Q wave MI can easily be obtained from the 12 lead ECG
  (detailed 12 lead interpretation is explored in Coronary Care 2)
• the first ECG may not reflect any changes that indicate MI, so serial ECGs are done
  to monitor changes as well as the patient’s progress or deterioration
• ECGs are also performed on a prn basis (ie. should the patient develop chest pain)
• following Q wave MI, there are 3 major ECG changes
• these reflect the 3 zones of tissue damage in Lesson 5, Part 2 (necrosis, injury, ischemia)

Question 33

1) ECG sign of necrosis

Answer 33

• the necrotic tissue is inert/dead so it cannot conduct any electricity
• this is manifested by the development of a pathological Q wave
• the pathological Q wave is deep (at least ¼ the height of the R wave)
• the Q wave may not be noted for the first 24 hours following the MI
• subendocardial MIs do not develop Q waves (hence the term ‘non-Q wave MI’)
• Q waves that are not at least ¼ the size of the R wave are not necessarily pathological
  and may not be a concern

Question 34

2) ECG sign of injury

Answer 34

• myocardial injury is manifested by changes in the ST segment
• normally the ST segment is iso-electric (on the baseline)
• during acute MI, the ST segment can be elevated or depressed
• ST segment elevation >1mm (1 small box) above the baseline is considered abnormal
• ST segment depression > 0.1mm (1 small box) below the baseline is also abnormal
• ST segment changes are often the first ECG sign of MI, as a Q wave may not have developed yet

Question 35

3) ECG sign of ischemia

Answer 35

• cardiac ischemia is manifested by changes in the T wave configuration
• the T waves are abnormal and can be inverted, peaked, widened
• T waves changes are not exclusively used to diagnose MI (they can be seen with other disorders (ie. pericarditis, bundle branch blocks)

Question 36

3 ECG signs …of MI

Answer 36

1) ECG sign of necrosis
2) ECG sign of injury
3) ECG sign of ischemia

Question 37

CLINICAL MANAGEMENT of MI -

Answer 37

Oxygen
Aspirin
Pain relief
IV therapy
Continuous Cardiac Monitoring
Beta-Blocking Agents
Thrombolytic Therapy
Intake and Output
Physical rest
Emotional rest
Diet
Exercise
Elimination

Question 38

CLINICAL MANAGEMENT of MI - Oxygen

Answer 38

• O2 is administered without delay to all MI patients
• increasing the blood’s O2 content allows for improved myocardial oxygenation
• the main need in the acute phase is to oxygenate the cardiac cells, and decrease the risk
  of further tissue injury
• nasal specs used at 5-8L/min only deliver 30-40% oxygen concentration
• ventimasks deliver a predetermined oxygen concentration
• non-rebreather masks used with 10L/m will deliver 100% oxygen concentration

Question 39

CLINICAL MANAGEMENT of MI - Aspirin

Answer 39

• ASA is given to inhibit platelet aggregation

- it is administered to all MI patients without sensitivity to ASA

Question 40

CLINICAL MANAGEMENT of MI - Pain relief

Answer 40

• always instruct patients that they must inform the staff of pain or discomfort
• many patients believe that staff know when they are experiencing pain, because they
  are on a cardiac monitor
• two medications dilate blood vessels and therefore enhance myocardial oxygenation

1) nitroglycerine
- nitroglycerine spray or s/l tablets can be attempted
- most hospitals allow the CCU or ER nurse to titrate
nitroglycerine IV drips (always follow your institution’s policy)
2) morphine
- administered IV in small amounts until pain relief is achieved
(2.5mg-5mg, Q5min prn, as per hospital policy)

• both drugs reduce preload by increasing venous capacitance
• both drugs reduce afterload by decreasing systemic vascular resistance
• due to its vasodilating effect, both drugs can lower BP very quickly
• close monitoring of VS is important (ie. Q5-15min)

Question 41

CLINICAL MANAGEMENT of MI - IV therapy

Answer 41

• an indwelling venous catheter is inserted and remains in place for several days
• it is used for hydration as well as an emergency access route for medications
• an infusion pump or minidrip should be used with a low flow rate to prevent overloading
  the vascular system (ie. 15-50ml/hr, as per hospital policy)

Question 42

CLINICAL MANAGEMENT of MI - Continuous Cardiac Monitoring

Answer 42

• death producing arrhythmias may develop at any time
• set all alarms & ensure that they are turned on, not silenced
• explain the purpose of monitoring and allow the patient to hear the sound of the alarms,
  and explain that not alarms suggest a sinister scenario

Question 43

CLINICAL MANAGEMENT of MI - Beta-Blocking Agents

Answer 43

• beta-blockers are commonly used in early MI
• they help reduce the HR and cardiac workload, thereby reducing myocardial O2
  requirements

Question 44

CLINICAL MANAGEMENT of MI - Thrombolytic Therapy

Answer 44

• thrombolytics should be started within 2-4 hours following onset of MI symptoms
• hospital policy dictates criteria for thrombolytic therapy and procedures for its delivery
• the patient’s hemodynamic status must be monitored closely throughout the infusion

Question 45

CLINICAL MANAGEMENT of MI - Intake and Output

Answer 45

• maintaining an accurate fluid balance is important
• overhydration and underhydration can pose problems (especially with failure or shock)
• measuring urinary output serves 2 purposes
• calculating the fluid balance
• determining the effectiveness of diuretic therapy

Question 46

CLINICAL MANAGEMENT of MI - Physical rest

Answer 46

• length of time spent on complete bedrest is approximately 24 hours
  (depending on hospital policy and patient stability)
• bedrest decreases the workload on the heart
• while in bed, attempt to maintain at least a semi-fowlers position to allow for lowering of
  the diaphragm, to enhance full lung expansion
• complete restriction of all activities is not necessary (ie. eating, dental care, bathing)
• activity levels are slowly increased after the first 24 hours
• if on exertion, the patient develops symptoms, the degree of activity is curtailed

Question 47

CLINICAL MANAGEMENT of MI - Emotional rest

Answer 47

• maintaining a calm and serene atmosphere is important
• control noise levels, reduce the amount of traffic, and limit visitors
• providing efficient yet unhurried care should be part of the care plan
• allow for rest periods (most hospitals set aside a specific rest hour without visitors)
• attempt to perform scheduled tests around these rest periods (ie. blood work, ECG)

Question 48

CLINICAL MANAGEMENT of MI - Diet

Answer 48

• a fluid diet is often ordered for the first 24 hrs to decrease the heart’s workload by
  decreasing digestion needs
• fluids are also easier to manage when patients are nauseated, especially with narcotics use
• caffeinated drinks are often excluded or given in small amounts, to decrease the risk of
  tachycardia which increases the heart’s workload
• commonly, low cholesterol and no added salt (NAS) cardiac diets are given once nausea
  and vomiting have subsided

Question 49

CLINICAL MANAGEMENT of MI - Exercise

Answer 49

• if on bedrest, passive ROM exercises are performed to prevent muscles from weakening
• anti-embolic stockings are sometimes ordered (usually with bedridden patients) to prevent
  venous pooling and the risk of thromboembolism
• patients should not cross their legs as venous channels can become compressed, thereby
  promoting stasis of blood

Question 50

CLINICAL MANAGEMENT of MI - Elimination

Answer 50

• bedpans are required only if the patient is unable to get out of bed
• most patients can use a commode or urinal at the bedside
• the effort used to sit or stand at the bedside is less than expected
• stool softening agents are commonly administered, by mouth
• enemas and suppositories are avoided as rectal stimulation can induce undesirable
  cardiovascular reflexes (ie. PAT or slow bradycardias)

Question 51

POST-MI REHABILITATION

Answer 51

• one of the most useful methods of helping the patient adjust, is explaining his/her illness
  and clarifying when necessary
• most teaching and rehabilitation can be initiated within 24-48 hours
• the following are some basic guidelines:
• the patient’s concept of an MI may not be factual so, many of his fears may be unrealistic
• offer repeated explanations about various aspects of his/her illness
• answer questions honestly and in a forthright manner
• review any written information and visual aids the patient has been provided with
• do not downplay MI risks and dangers, but emphasize recovery and survival
• encourage and inform the patient of his/her physical and emotional progress
• emphasize that normal activities after recovery are beneficial, rather than harmful
• allow the patient opportunity to express his/her concerns and questions
• listen attentively and show interest in the patient, his/her family, and their needs
• a specific program of increasing activity is protocol in most hospitals
• physical activity is increased gradually, in stages
• walking is the most sensible and effective exercise, with the distance walked being
  gradually increased daily
• the patient will suffer less weakness and fatigue once the regimen begins

Question 52

PSYCHOLOGICAL CARE following MI

Answer 52

• an important facet of cardiac nursing is helping patients cope with MI’s emotional stress
• the patient’s emotional adjustment influences his/her rehabilitation and long term success
• the psychological effects of an acute MI are unique in many ways

Question 53

Sources of emotional stress

Answer 53

• suffering an MI is usually a terrifying feeling right from the onset of symptoms for several
  reasons. Some reasons might be:
• unrelenting chest pain
• dependence on others to provide help
• looks of fear on family and friends’ faces
• strange environment, and sounds of foreign equipment and alarms
• staff and personnel possibly rushing about
• initiation of care and procedures (O2, cardiac monitoring, IV, blood work, ECG, CXR)
• other sources of stress can include concern about home, children, commitments, job
• the suddenness of the illness prevents patients from adequately prepare themselves

Question 54

BEHAVIOURAL RESPONSES following MI

Answer 54

Patients may react to MI with various negative behavioural responses including anxiety,
fear, denial, depression, despair, dejection, anger

Question 55

BEHAVIOURAL RESPONSES following MI - Anxiety

Answer 55

• anxiety is synonymous with fear, and is one of the most common emotions following an MI
• the main source of anxiety is often the prospect of possible death
• anxiety is most often experienced during the first few days
• there is not always a factual relationship between anxiety and the seriousness of the illness
• anxiety may be difficult to identify due to the patient’s attempt to hide the emotion
• what may seem as intellectual curiosity may be a sign of anxiety (ie. asking about
  methods of treatment, lab results, monitoring systems)
• look for signs of tension, apprehension, restlessness, inability to relax, fidgeting

Question 56

BEHAVIOURAL RESPONSES following MI - Denial

Answer 56

• denial can be recognized by the patient’s statements in conjunction with
  his/her actions
• there are two basic types of denial:

1. denial of fact
   - the patient will not acknowledge that s/he has suffered an MI
   - s/he passes it off or minimizes the event
   - may make obvious statements (ie. “I’m sure it’s not a heart attack”)
2. denial of meaning
   - conscious or unconscious effort to deny the emotional feelings
   - the patient will not admit his/her fears, anxieties, depression
   - the patient tries to display optimism

Question 57

BEHAVIOURAL RESPONSES following MI - Depression

Answer 57

• the implications surrounding the MI often lead to depression
• the patient’s concerns can lead to despondency (ie. concerns about his/her usual activities,
  need for life-style changes, earning an income)
• depression, as with a

Question 58

BEHAVIOURAL RESPONSES following MI - Anger

Answer 58

• anger can be self-directed (ie. “Why me, Why now”)
• anger can be directed toward others including hospital staff, family, friends
• these patients can be very complaintive and demanding, and it may be difficult
  to please them or satisfy their needs

Question 59

HEART FAILURE

Answer 59

• the most common complication of MI is the development of arrhythmias
• the vast majority of MI patients will develop at least one arrhythmia, either due to a
  conduction disturbance or a disturbance in impulse formation
• a large percentage of MI patients will also develop heart failure
• heart failure is defined as a state in which the CO is not sufficient enough to supply
  the nutrients necessary to meet the metabolic needs of the body
• in other words, the heart is failing to do its ‘job’
• following an MI, failure is secondary to the heart’s decreased pumping action
• the degree of impairment can vary greatly
• heart failure can involve the R heart, the L heart, or both sides of the heart
• let’s begin by exploring left sided failure…

Question 60

LEFT SIDED FAILURE (LVF)

Answer 60

• following MI, LVF is more common than RVF because most MIs affect the LV, so the
  myocardial damage occurs in the LV, and the damaged LV will fail to perform effectively

Question 61

Pathophysiology of LVF

Answer 61

• because of damage to the L ventricular muscle, the necrosed area and the zone of injury
  cannot contract normally or effectively (so the LV doesn’t contract normally)
• the stroke volume (SV) decreases, which leads to a drop in cardiac output (CO)
• since left ventricular emptying is decreased (↓SV) , excess amounts of blood remain
  in the LV after systole/contraction
• the residual volume in the LV gradually increases, because the uninjured RV continues to
  pump into the pulmonary system, and the lungs keep returning blood to the heart’s L side
• as blood remains in the LV after systole, pressure in the LV will increase during diastole
• so the flow of blood from the LA to the LV during diastole is impeded
• pressure increases in the LA, pulmonary veins and pulmonary capillaries
• the increased pulmonary venous pressure forces fluid into the lung tissues
• this interstitial edema leads to alveolar edema

Question 62

Compensatory Mechanism used in LVF

Answer 62

• a reflex mechanism causes stimulation of the sympathetic nervous system
• the SNS stimulation has 2 effects
  1. it increases the HR
  2. it increases the force of contraction
• because the SV is low, the SNS increases the HR, to improve CO (SV x HR = CO)
• for example: if SV is 30ml, increasing the HR to 150 will produce a satisfactory CO
  of 4500ml (normal CO is 3.6-10L)
• but, this mechanism fatigues the weak heart, and can only be effective for a short time

Question 63

Clinical Manifestations of LVF

Answer 63

Dyspnea

• dyspnea is the earliest and most common sign of LVF
• at first, it begins with exertion, then occurs at rest
• congestion in the pulmonary venous network causes a decrease in lung elasticity,
  as well as less available space for gas exchange
• this interference of O2 and CO2 exchange causes the low saturation levels we detect
• rales (crackles) are heard due to the increase in fluid in the alveoli
• these sounds are confined to the bases at first, and gradually extend higher as the failure
  progresses

Orthopnea

• this is a condition that exists when the patient experiences dyspnea when laying down
• at times, it is relieved with sitting upright

Paroxysmal Nocturnal Dyspnea (PND)

• PND is a sudden development (paroxysmal) of SOB (dyspnea) while asleep (nocturnal)
• the patient awakens with increased SOB, gasping respirations, coughing, wheezing
  (PND is sometimes called ‘cardiac asthma’)
• the condition may or may not subside after sitting up for a period of time
• PND usually indicates that LVF has been progressing slowly and unknowingly

Other Signs

• tachycardia
• hypotension
• diaphoresis
• restlessness
• fatigue, weakness
• ventricular gallop (S3) Refer also to study notes from Lesson 2
  Pulmonary Edema
• pulmonary edema is the most advanced stage of LVF
• pulmonary edema is a massive accumulation of fluid in the interstitial and alveolar
  spaces which interferes with oxygenation
• this leads to hypoxia
• if the hypoxia is not corrected, vital organs are deprived of oxygen, and irreversible
  arrhythmias can occur, leading to death
• pulmonary edema is discussed in more detail shortly

Question 64

Clinical Management of LVF

Answer 64

Oxygen therapy

• SaO2 levels are low because of poor gas exchange in the alveolar tissues
• the goal is to increase the oxygen saturation level
• the O2 should be humidified to prevent drying the air passages

Decrease Preload
- the LV still remains partially filled after systole
- the goal is to decrease the venous return to the heart which would decrease
ventricular filling, and therefore decrease pulmonary venous pressure
- the use of fast-acting diuretics decreases the circulating blood volume (ie. lasix)
- vasodilating agents (ie. nitrates) are used to relax the tone and resistance of the peripheral
venous system, so that venous blood is not forced back to the heart with as much pressure

Decrease Afterload

• the LV lacks energy, strength and oxygen, making it difficult to eject its contents
• this can lead to a further decrease in CO
• the goal is to enhance blood flow out of the LV, into the arterial system
• by dilating the arteries, vasodilating agents will help meet this goal (ie. nitrates)
• the effects of IV nitroglycerine are observed within 2-3 minutes

Morphine
- morphine relieves the patient’s anxiety
- it decreases venous tone (it has a vasodilating effect)
- morphine’s vasodilating effect in the periphery decreases the volume of blood returning to
the heart, therefore reducing preload
Strengthen Myocardial Contractility
- this improves ventricular emptying
- as the residual blood volume in the LV is decreased, the SV increases
- therefore, the CO will improve
- beta-blockers are commonly used to meet this goal and digoxin is sometimes administered
- however, the use of digoxin in the early stages of an MI is controversial, as it increases
the heart’s workload and can provoke unwanted arrhythmias

Controlling the heart rate
- this is directed at maintaining an effective HR, with the use of drugs or pacing
- rapid rates result in shorter ventricular filling time, thereby decreasing SV, which leads to
decreased CO (as examined in Lesson 1)
- slow rates result in decreased CO because the SV cannot increase enough to counteract
the slow HR (as examined in Lesson 1)

Controlling Metabolic Needs
- this can be achieved by providing frequent rest periods to decrease cardiac workload

Question 65

RIGHT SIDED FAILURE (RVF)

Answer 65

• after MI affects the LV, if RVF develops, it is a sequel to left sided failure
• isolated RVF following MI is not as common, as most MIs affect the LV, not the RV
• LVF has led to an increase in pressure in the pulmonary veins and capillaries
• blood being pumped from the RV through the pulmonary arteries meets this increase in
  pressure in the pulmonary system
• therefore, pressure in the pulmonary arteries increases
• as the pressure increases in the pulmonary arteries, emptying of the RV is impaired
• this allows residual amounts of blood to ‘remain’ in the RV after it contracts
• this then impedes blood flow from the RA into the RV, during diastole
• blood returning from the venous system and entering the RA via the vena cavas meets the
  resistance
• this creates a backward pressure throughout the peripheral venous system
• congestion of the venous network follows

Question 66

Clinical Manifestations of RVF

Answer 66

All the Signs of LVF
- because the right sided failure is secondary to LVF

Distended Neck Veins (elevated JVP)

• elevated JVP is caused by increased venous pressure in the superior vena cava
• distended neck veins may even be visualized with the patient in semi to high fowler position

Peripheral and Sacral Edema
- the increased pressure in the venous system forces fluid from the capillaries into the
body’s subcutaneous tissues
- this is sometimes called ‘subcutaneous edema’
- the edema occurs in the dependent areas of the body (bedridden patients develop sacral
edema, while ambulatory patients develop edema of the legs and feet)

Hepatomegaly

• the pressure in the inferior vena cava and hepatic veins causes hepatic engorgement
• as a result, the liver enlarges and can become tender (especially on palpation)

Pleural Effusion

• this is the result of edema fluid also accumulating in the pleural cavity
• a large pleural effusion can compress the lung
• this would then produce or intensify the dyspnea
• a pleural effusion can be suspected with diminished or absent breath sounds
• the effusion is confirmed by CXR

Question 67

Management of RVF

Answer 67

There are 2 basic goals in managing RVF

1) Improve the Cardiac Performance
- the interventions used to meet this goal are similar to those used in LVF

a) the use of vasodilators (drugs that dilate veins and arteries are used (ie. nitroglycerine)
- vasodilators reduce preload, by relaxing the tone and resistance within the
peripheral venous system
- vasodilators reduce afterload, by dilating the arterial system thereby
enhancing blood flow out of the heart

b) decreasing the metabolic needs of body
- this decreases and eases the cardiac workload
- providing frequent rest periods helps meet this goal

2) Control of Sodium and Water Retention
- three interventions can assist with meeting this goal

a) a low sodium diet
b) diuretic therapy to promote excretion of sodium and water
c) fluid restriction to control the volume of fluid in the body

• large amounts of fluid in the system can dilute the limited amount of sodium (Na+),
  especially after diuresis and the low sodium diet
• a fluid restriction can therefore prevent the patient from becoming hyponatremic (↓Na+)
• K+ is also excreted with diuresis. Commonly, potassium supplements are administered
  to prevent hypokalemia (↓K+)
• daily weight should be obtained
• serum electrolytes should be monitored daily

Question 68

PULMONARY EDEMA

Answer 68

• as we’ve learned, pulmonary edema is the most advanced stage of LVF
• there is massive accumulation of fluid in the interstitial and pulmonary alveolar spaces
  which severely interferes with oxygenation
• pulmonary tissues become edematous due to diminished airflow to and from the alveoli
• this edema of the tissues causes airway narrowing
• lung compliance decreases, making breathing very difficult
• this quickly leads to hypoxia
• if the hypoxia is not corrected, vital organs are deprived of O2, irreversible arrhythmias
  occur, resulting in death
• as with LVF, the SNS (sympathetic nervous system) is stimulated in an attempt to
  compensate for the low CO

Question 69

Clinical Manifestations of Pulmonary Edema

Answer 69

• severe dyspnea, tachypnea and orthopnea
• audible gurgling sounds
• incessant cough and wheezing
• blood-tinged, frothy sputum, due to small hemorrhages in the pulmonary system
• extreme anxiety
• cyanosis may be present
• S3 heart sound (may be difficult to hear because of wheezing and gurgling)
• tachycardia and profuse diaphoresis (due to SNS stimulation)

Question 70

Management of Pulmonary Edema

Answer 70

Oxygen therapy

• the SaO2 is very low because of limited gas exchange in the alveolar tissue
• the goal is to increase the oxygen saturation level
• 100% O2 is administered (nasal specs deliver significantly less oxygen concentration)
• the O2 should be humidified to prevent drying the air passages
• airway intubation may be necessary to ensure adequate ventilation

Morphine
- morphine relieves the patient’s intense anxiety
- morphine has a vasodilating effect, so it reduces preload by decreasing venous tone
thereby reducing the volume of blood returning to the heart
- morphine lowers the respiratory rate which means the lungs are not ‘working quite as hard’
- this decreases the volume of blood ejected into the LV, from the pulmonary circulation

Diuretics

• diuretics should produce quick and dramatic improvement, abating dyspnea within minutes
• diuresis then follows, which reduces the volume of blood returning to the heart
• fast-acting diuretics are used (ie. lasix, edecrin)

Vasodilators
- vasodilators decrease preload, by relaxing the tone of the vessels and the resistance in the
peripheral vessels
- the effects of IV nitrates (ie. nitroglycerine) are observed within 2-3 minutes

Bronchodilators

• these are given when pulmonary edema is accompanied by spasm of the bronchial tree
• this spasm interferes with ventilation
• ventolin and/or pulmicort inhalations are the most commonly used drugs
• IV aminophylline is rarely used any longer, due its hypotensive effect

Digitalis
- the use of digoxin can be contra-indicated in pulmonary edema, secondary to MI because
of the strain / workload it can put upon the heart, by forcing it to contract with more strength
- it is not as important as the use of nitrates, diuretics and bronchodilators

Phlebotomy

• this procedure is only performed when other methods are ineffective
• since the advent of nitrates and fast-acting diuretics, this procedure is seldom required
• the goal of phlebotomy is to decrease preload
• it uses the simple phlebotomy technique, with a large bore needle
• the amount of circulating blood volume is decreased, by withdrawing 500-750ml of blood
  from the venous system (into a vacuum bottle)

Rotating tourniquets

• this intervention is only performed when all other methods fail
• rotating tourniquets are seldom necessary and very rarely used
• since the advent of nitrates and fast-acting diuretics, this procedure is seldom required
• the procedure reduces preload
• it is a laborious and very time-consuming intervention. This intervention can require several
  hours at the bedside
• the procedure traps blood in the extremities, thereby reducing venous return
• the procedure involves applying tourniquets to all 4 extremities with enough pressure to
  impede venous return, but not enough to interfere with arterial circulation
• distal pulses must always be palpable, thereby ensuring adequate arterial circulation
• a tourniquet is released from one extremity for 15min, then reapplied
• then another tourniquet is removed for 15 minutes, and reaaplied
• removal of one tourniquet at a time is done in a rotating fashion (limb by limb), Q15min
• when the acute episode subsides, tourniquets are removed one at a time, Q30min
• removing all tourniquets at once would cause a sudden increase in the venous return
  back to the heart, and overload the system

Question 71

CARDIOGENIC SHOCK

Answer 71

• shock develops in the presence of inadequate tissue perfusion
• oxygen and other nutrients become unavailable to the body cells
• the vital organs are not being adequately perfused, most significantly, the brain,
  the heart and the kidneys
• this is due to a marked in decreased CO
• patients in cardiogenic shock are very guarded and often have a grave prognosis
  (even with aggressive interventions)

Question 72

Mechanism of Cardiogenic Shock following MI

Answer 72

• due to LV dysfunction, extensive MI is the most common cause of cardiogenic shock
• extensive left ventricular damage leads to a marked decrease in CO
• this marked decrease in CO causes the BP to fall
• to compensate, the SNS is stimulated to cause
• the HR to increase
• the venous system to constrict, to improve cardiac venous return
• the arteries to constrict, to perfuse vital organs more adequately
• however, the effect of the SNS is only temporary because the SNS cannot
  compensate for the low CO
• the following analogy might help to visualize this concept…
• consider an outside tap where water originates (the heart) and a garden hose (the arteries)
  attached to this tap
• constricting the hose by placing your thumb at the end of the hose will cause the water to
  eject with more pressure (just as constricting the arteries increasing the blood pressure)
• but, if the tap is barely turned on, only a little water is coming out through the
  hose (the LV is extremely damaged and producing very little CO)
• so, constricting the hose will not increase the water pressure (because there
  isn’t enough water)
• regardless of the SNS vasoconstricting effect, the volume of blood ejected by the LV is still
  decreased/minimal
• now the systemic BP begins to fall below critical levels, resulting in an insufficient amount
  of blood and O2 being available to the vital organs
• this inadequate arterial perfusion to the vital organs includes the coronary artery supply
  to the myocardium, causing further cardiac injury
• as a result of inadequate coronary artery supply and the additional myocardial damage,
  the CO diminishes even more. This then becomes a vicious circle
• arterial hypotension leads to coronary artery hypoperfusion and underperfusion of the
  myocardium, producing further LV dysfunction
• because the vital organs are not perfused adequately, findings of shock appear
• other conditions that can progress to cardiogenic shock include:
• dysfunction of papillary muscle
• end-stage cardiomyopathy

Question 73

Clinical Manifestations of Cardiogenic Shock

Answer 73

all body systems become involved because there is underperfusion of all organ tissues

Hypotension

• drop in systolic BP to more than 30mmHg below the patient’s normal baseline
• the systolic BP is usually < 80-90 mmHg, and continues to fall

Narrowing of Pulse Pressure

• pulse pressure is the numerical difference between the systolic and diastolic BP
• the systolic pressure falls before the diastolic pressure

Tachycardia

• the increased HR is due to stimulation of the SNS
• as the shock progresses and the SNS retracts, the effect will be lost, leading to bradycardia

Cool, Clammy and Moist Skin
- due to peripheral vasoconstriction (SNS) which reduces blood flow to the skin

Mental Status Changes
- cerebral underperfusion leads to states of agitation, irritability, restlessness,
confusion, disorientation
- coma will follow

Oliguria
- diminished renal blood flow does not allow for adequate kidney perfusion, so the
kidneys begin to fail
- urinary volume decreases to less than 20ml/hr

Other Signs

• cyanosis
• tachypnea, with shallow respirations

Question 74

Management of Cardiogenic Shock

Answer 74

Prepare for probable cardiac arrest, airway intubation, CPR
Continuously assess hemodynamic stability
- VS, color, level of consciousness, all hemodynamic parameters

Oxygen
- most patients are hypoxic because of decreased lung perfusion, and require 100% O2

ABGs

• arterial blood gas analysis usually reveals acidosis because of poor tissue perfusion
• IV sodium bicarbonate might need to be administered

Monitoring of VS

• frequent, continuous vital signs are monitored, at least Q1min to Q5min
• continuous cardiac monitoring will detect new arrhythmias

Positioning

• patients are placed in trendelenberg position in an attempt to improve the BP
• this may or may not be feasible (ie. pulmonary edema and dyspnea may also be present)

Infusion of Fluids

• a minimum of 2 large bore IVs are required
• to counter-attack the marked hypotension
• to maintain intravascular volume
• to improve the urinary output
• fluids must be well monitored and accurate measurement of intake is important

Pain Relief

• ischemic chest pain is often experienced because of the reduced coronary artery blood flow
• morphine is administered in very small amounts (if at all), because of its hypotensive effect

Sympathomimetic Agents

• these drugs are administered
• to increase the BP
• to improve the strength of the myocardial contraction
• to increase renal and cerebral blood flow
• ie. dopamine, levophed

Diuretics
- diuretics are sometimes administered
- to decrease preload
- to improve urinary output (accurate output measurement is important)
- monitor BP very closely
- diuresis can cause hypovolemia, leading to hypotension
Vasodilators
- nitroglycerine is used to counter-attack the compensatory mechanism of vasoconstriction
- vasoconstriction is desirable at first, but it can lead to a further ↓CO and further myocardial
damage when the LV pumps against the strong resistance of constricted arteries
- monitor BP very closely because vasodilators cause hypotension

Arterial Line

• an arterial line will accurately measure afterload, CO, and arterial BP
• also, accurate arterial blood gases can be drawn and monitored from an arterial line

Pulmonary Artery Catheter
- this catheter will accurately monitor preload, pulmonary artery pressure, and pulmonary
artery wedge pressure

Intra-Aortic Balloon Pumping (IABP)

• usually inserted under fluoroscopy, but blind insertion is possible
• CO can increase by as much as 50% with this procedure
• a narrow balloon catheter, inserted through the femoral artery, is advanced retrogradely
  to the descending aorta, and lies just below the aortic arch
• the balloon inflates with helium during diastole
• this occludes the aorta, pushing any blood still in the aorta back toward the closed
  aortic valve
• this forces blood into the coronary arteries, which are between the aortic valve
  and the positioned balloon
• this increases pressure in the coronary arteries, which will improve
  cerebral and cardiac perfusion during systole
• the balloon is then deflated during systole
• the aortic valve opens with systole, ejecting the LV volume as well as the
  volume of blood that was “trapped” by the balloon during diastole
• blood is propelled with minimal cardiac work
• with the IABP inserted in the femoral artery, NEVER position the patient in a sitting position
• continuous assessment of lower limb circulation is important (peripheral pulses)
• patients can become “balloon dependent”, so that shock returns when the device is weaned
• mechanical assistance with the use of an IABP, and the arterial line and pulmonary
  artery catheter are used in controlled settings (ie. ICU)
• they require specialized skill that would be taught and tested for competence, prior to use
• don’t be alarmed if the basics and mechanism of an arterial line, pulmonary catheter
  and the IABP are a little unclear or difficult to understand
• you will not be tested on the details of these invasive monitoring procedures, in this course

Question 75

CARDIAC TAMPONADE

Answer 75

• cardiac tamponade is an increase in pressure in the pericardial sac
• the pressure in the pericardial sac usually results from accumulation of blood or fluid
• this fluid accumulation might be slow and insidious, or it can develop very rapidly
• the fluid exerts pressure against the heart, not allowing it to fill adequately
• the ventricles have difficulty accommodating blood it receives from the atria
  because the ventricles are being compressed by the pressure surrounding them
• so, there is decreased blood flow into the ventricles during diastole
• this results in decreased blood flow ejected during ventricular systole (↓SV)
• the decreased SV leads to decreased CO
• pressures rise in the systemic veins because venous blood returning to the
  R side of the heart meets the ‘lack of space’ in the R side of the heart
• pressures rise in the pulmonary veins because blood returning to the
  L side of the heart meets the ‘lack of space’ in the L side of the heart
• syncope develops quickly if tamponade events occur rapidly
• post MI deaths usually result from arrhythmias, heart failure or cardiogenic shock
• though rare, LV rupture leading to cardiac tamponade is also fatal
• ventricular rupture usually occurs about 2-5 days post MI
• ventricular rupture is associated with Q wave MI, involving extensive transmural damage
• the necrotic cardiac muscle fibers become soft and weak and a sudden perforation occurs
  in the most center area of the necrotic tissue
• following the rupture, blood ejects through the hole in the LV and fills the pericardial sac
• the accumulation of blood outside the ventricle produces pressure against the heart, and
  compresses it
• this scenario is nearly always manifested by sudden death
• the mechanical action of the heart ceases immediately, so the patient has no palpable
  pulses because mechanical action ceased / the heart is not contracting (there is no CO)
• the heart’s electrical activity may continue, so some form of electrical activity may be
  seen on the cardiac monitor during resuscitation efforts
• this rhythm is called be PEA (pulseless electrical activity)
• other causes of cardiac tamponade can include:
• hemorrhage, secondary to cardiac trauma
• pericarditis with pericardial effusion
• Dressler’s syndrome
  (Dressler’s syndrome is the combined occurrence of pericarditis and pleurisy,
  usually 2-12 weeks post MI)

Question 76

Clinical Manifestations of Cardiac Tamponade

Answer 76

• there are 3 classic features in cardiac tamponade, known as ‘Beck’s triad’
  1. elevated JVP
• distended neck veins are due to increased venous pressure
  2. muffled heart sounds
• the extra fluid obscures the heart sounds
  3. pulsus paradoxus
• an abnormal fall in systolic BP during inspiration
• the BP drops more than 10-15 mmHg with inspiration
• other findings can include:
• hypotension
• due to low CO
• tachycardia
• to compensate for the low CO (CO = SV x HR)
• narrowed pulse pressure
• narrowing of the numerical difference between the systolic
  and the diastolic BP (see above cardiogenic shock BP chart)
• orthopnea
• changes in mental status due to cerebral underperfusion
• anxiety, restlessness
• diaphoresis
• cyanosis

Question 77

Management of Cardiac Tamponade

Answer 77

• continuous assessment and monitoring of the patient’s hemodynamic status is
  required
• the need for airway intubation, CPR and full resuscitation must be anticipated
• when treating cardiac tamponade, the goal is aimed at alleviating the intra-
  pericardial pressure
• this would allow the heart to effectively pump mechanically
• the most common intervention is a pericardiocentesis
• this procedure withdraws the accumulated fluid
• cardiac tamponade can be caused by bleeding into the pericardial sac
• anticoagulant-induced cardiac tamponade might also require additional
  treatment:
• warfarin-induced tamponade might require the administration of Vit K
• heparin-induced cardiac tamponade might necessitate the need for
  protamine sulfate