CAD and Cardiac Emergencies Flashcards
1
Q
CORONARY ARTERY DISEASE (CAD)
A
- 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
2
Q
what is atherosclerosis?…
A
- 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
3
Q
- there are 4 grades of atherosclerosis
A
-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
4
Q
How CAD leads to Acute Coronary Syndromes
A
- 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
5
Q
CAD RISK FACTORS
A
- some are modifiable (ie: diet), while others are termed non-modifiable (ie: gender)
6
Q
Heredity, Genetics
A
- 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
7
Q
Hypertension
A
- 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
8
Q
Smoking
A
- 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
9
Q
Obesity
A
- 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
10
Q
Gender & Age
A
- 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)
11
Q
Diet
A
- 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)
12
Q
Diabetes Mellitus
A
- 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)
13
Q
Sedentary Life Style
A
- 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
14
Q
Personality Type
A
- 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
15
Q
Race
A
- 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
16
Q
Stress, Anxiety
A
- 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
17
Q
MANIFESTATIONS and CLINICAL SPECTRUM OF CAD
A
- 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
18
Q
STABLE ANGINA (ANGINA PECTORIS)
A
- 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
19
Q
STABLE ANGINA (ANGINA PECTORIS) - Pain Characteristics
A
- 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
20
Q
STABLE ANGINA (ANGINA PECTORIS) - Occurrence & Duration of Pain
A
- 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
21
Q
STABLE ANGINA (ANGINA PECTORIS) - Treatment
A
- 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
22
Q
UNSTABLE ANGINA
A
- 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
23
Q
UNSTABLE ANGINA - Pain Characteristics
A
- 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
24
Q
UNSTABLE ANGINA - Treatment
A
- 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
25
Q
PRINZMETAL ANGINA (also called Variant Angina)
A
- 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
26
Q
MYOCARDIAL INFARCT
A
-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
27
Q
Sites of Infarction
A
- 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
28
Q
Extent of MI
A
- several factors can determine the severity of cell necrosis. Some factors are:
- the size of the vessel obstructed (small distal or large proximal artery)
- capacity of collateral circulation to supply blood to the deprived area
(if the tissue is well oxygenated, less tissue damage may occur) - oxygen demands following the attack
- 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
- 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
29
Q
DIAGNOSIS of MI - Patient History
A
- 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
30
Q
DIAGNOSIS of MI -Chest X-Ray
A
- the CXR is usually clear
- if early complications occur, the CXR can help with diagnosing these (ie. LVF,
pulmonary edema, pleural effusion)
31
Q
DIAGNOSIS of MI - Cardiac Enzyme and Protein Studies
A
- 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
32
Q
DIAGNOSIS of MI - Electrocardiogram
A
- 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)
33
Q
1) ECG sign of necrosis
A
- 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
34
Q
2) ECG sign of injury
A
- 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
35
Q
3) ECG sign of ischemia
A
- 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)
36
Q
3 ECG signs …of MI
A
1) ECG sign of necrosis
2) ECG sign of injury
3) ECG sign of ischemia
37
Q
CLINICAL MANAGEMENT of MI -
A
Oxygen Aspirin Pain relief IV therapy Continuous Cardiac Monitoring Beta-Blocking Agents Thrombolytic Therapy Intake and Output Physical rest Emotional rest Diet Exercise Elimination
38
Q
CLINICAL MANAGEMENT of MI - Oxygen
A
- 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
39
Q
CLINICAL MANAGEMENT of MI - Aspirin
A
- ASA is given to inhibit platelet aggregation
- it is administered to all MI patients without sensitivity to ASA
40
Q
CLINICAL MANAGEMENT of MI - Pain relief
A
- 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)
41
Q
CLINICAL MANAGEMENT of MI - IV therapy
A
- 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)
42
Q
CLINICAL MANAGEMENT of MI - Continuous Cardiac Monitoring
A
- 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
43
Q
CLINICAL MANAGEMENT of MI - Beta-Blocking Agents
A
- beta-blockers are commonly used in early MI
- they help reduce the HR and cardiac workload, thereby reducing myocardial O2
requirements
44
Q
CLINICAL MANAGEMENT of MI - Thrombolytic Therapy
A
- 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
45
Q
CLINICAL MANAGEMENT of MI - Intake and Output
A
- 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
46
Q
CLINICAL MANAGEMENT of MI - Physical rest
A
- 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
47
Q
CLINICAL MANAGEMENT of MI - Emotional rest
A
- 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)
48
Q
CLINICAL MANAGEMENT of MI - Diet
A
- 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
49
Q
CLINICAL MANAGEMENT of MI - Exercise
A
- 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
50
Q
CLINICAL MANAGEMENT of MI - Elimination
A
- 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)
51
Q
POST-MI REHABILITATION
A
- 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
52
Q
PSYCHOLOGICAL CARE following MI
A
- 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
53
Q
Sources of emotional stress
A
- 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
54
Q
BEHAVIOURAL RESPONSES following MI
A
Patients may react to MI with various negative behavioural responses including anxiety,
fear, denial, depression, despair, dejection, anger
55
Q
BEHAVIOURAL RESPONSES following MI - Anxiety
A
- 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
56
Q
BEHAVIOURAL RESPONSES following MI - Denial
A
- denial can be recognized by the patient’s statements in conjunction with
his/her actions - there are two basic types of denial:
- 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”) - 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
57
Q
BEHAVIOURAL RESPONSES following MI - Depression
A
- 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
58
Q
BEHAVIOURAL RESPONSES following MI - Anger
A
- 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
59
Q
HEART FAILURE
A
- 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…
60
Q
LEFT SIDED FAILURE (LVF)
A
- 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
61
Q
Pathophysiology of LVF
A
- 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
62
Q
Compensatory Mechanism used in LVF
A
- 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
63
Q
Clinical Manifestations of LVF
A
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
64
Q
Clinical Management of LVF
A
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
65
Q
RIGHT SIDED FAILURE (RVF)
A
- 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
66
Q
Clinical Manifestations of RVF
A
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
67
Q
Management of RVF
A
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
68
Q
PULMONARY EDEMA
A
- 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
69
Q
Clinical Manifestations of Pulmonary Edema
A
- 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)
70
Q
Management of Pulmonary Edema
A
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
71
Q
CARDIOGENIC SHOCK
A
- 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)
72
Q
Mechanism of Cardiogenic Shock following MI
A
- 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
73
Q
Clinical Manifestations of Cardiogenic Shock
A
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
74
Q
Management of Cardiogenic Shock
A
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
75
Q
CARDIAC TAMPONADE
A
- 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)
76
Q
Clinical Manifestations of Cardiac Tamponade
A
- 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
77
Q
Management of Cardiac Tamponade
A
- 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
