Week 1 – Coronary Artery Disease and Stroke
Coronary Artery Disease
 A blood vessel disorder that reduces flow of oxygen and nutrients to the myocardium
 Synonyms include arteriosclerotic heart disease (ASHD), cardiovascular heart disease
(CVHD), ischemic heart disease and coronary heart disease
 Second leading cause of death in Canada
 Leading cause of death among Indigenous people
 Immigrants better heart health which declines the longer they are in Canada and adopt
Western behaviours
 Other marginalized groups (minorities, low income)
 Men > women, until women reach menopause
o Women lose their protective factor at this time
Risk Factors for CAD
 Non modifiable risk factors
o Age
o Gender
o Ethnicity (eg. South Asian)
o Family Hx
o Genetic Predisposition
 Major modifiable risk factors
o Cholesterol Abnormalities – High HDL’s – fatty streaks and hardening of arteries
o Hypertension – additional pressure adds shirring effect on the vessels
o Tobacco use – vasoconstriction, increased carbon monoxide in the body
o Physical Inactivity
o Obesity
 Modifiable Contributing Risk Factors
o Diabetes Mellitus
o Metabolic Syndrome
 High BP
 High Cholesterol
 High Glucose levels
 Waist Circumference – weight carried in abd
o Psychology – anxiety, stress, depression
Coronary Atherosclerosis
 Fatty streaks in lumen of the vessel can begin to develop as early as 15 years old, and
continue to develop until 30
 Complicated lesions  plaque can rupture = thrombosis leading to partial or total
occlusion
Angina
 A syndrome characterized by episodes of paroxysmal pain or pressure in the anterior
chest caused by insufficient coronary blood flow
o 20 minutes without oxygen to the muscle cells causes ischemia in cardiac cells
 Physical exertion or emotional stress increases myocardial oxygen demand = deficiency
of oxygen
 Coronary vessels are unable to supply sufficient blood flow to meet the oxygen demand
 Types of angina:
o Stable
o Unstable  Acute Coronary Syndrome, Preinfarction Angina
o Variant
Anginal Pain
 Mild to severe
 May be described as tightness, choking, or a heavy sensation
 It is frequently retrosternal and may radiate to neck, jaw, shoulders, back, or arms
(usually left)
 Anxiety frequently accompanies the pain
 Other symptoms may occur: dyspnea or shortness of breath, dizziness, nausea, and
vomiting, epigastric pain, impending sense of doom
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The pain of typical angina subsides with rest or NTG
Unstable angina is characterized by increased frequency and severity and is not relieved
by rest and nitro
o Requires medical intervention immediately
Assessment and Care
 P-position/location, provocation; Q-quality, quantity; R-radiation, relief; S-severity,
symptoms; T-timing
o Where is it hurting?
o What does it feel like? (dull, sharp, aching, radiating)
o What makes it worse? What makes it better?
o On a scale of 0-10,
o What were you doing when the pain started? Have you had this pain before? Is it
different from the last time and are your usual interventions not working?
 Risk factors, lifestyle, and health promotion activities
 Does the patient have deficient knowledge about underlying disease and ways to avoid
complications?
 Noncompliance
o have they been diagnosed w/ hypertension?
o when was the last time they took their meds?
o Is the problem being managed as it should?
 Ineffective management of therapeutic regimen, not accepting and making changes to
lifestyle
 Family hx., pt education before dx
Treatment
 Decrease myocardial oxygen demand
 Increase oxygen supply
 Medications
 Oxygen administration
 Reduce and control risk factors
 Reperfusion may be done
o Cath lab or TPA
Medications
 Nitroglycerin (sublingual, spray)
o Usually for patient with chronic stable angina – if their nitro suddenly isn’t
working it has turned into an acute situation
 Beta-adrenergic blocking agents (metoprolol, atenolol)
o This is given initially if they are able to tolerate the side effects (Orthostatic
Hypo)
o Blocking the effects of EPI and NE, so decrease contractility and output to
decrease stress on heart
 Calcium-channel blocking agents (amlodipine/Norvasc, diltiazem/Cardiazem)
o Slowing down electrical activity in the heart to slow down HR
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o This is the next medication that is given if BB is not tolerated well
Antiplatelet (ASA)
o Prevention, but recommendations may be changing
Clopidogrel (Plavix) and ticlopidine (Ticlid)
o Clot busting
Heparin
o SUBQ/IV
Glycoprotein IIB/IIIa agents (abciximab/ReoPro) and tirofiban/Aggrastat)
o Typically used when people go to the cath lab
Acute Coronary Syndrome
1. Unstable Angina
2. NSTEMI
3. STEMI
Coronary Circulation
Right Coronary Arteries
 Supplies Right Atrium, Right Ventricle
Left Coronary Arteries
 Supplies circumflex branch, anterior descending branch
 LEFT SIDED BLOCKS OR MI TEND TO BE MORE SEVERE
Review of PQRST on ECG
1. P wave – SA Node fires
2. QRS – Depolarization of AV node (which allows for contraction of heart)
3. T wave – Ventricles repolarize
4. U wave – Delay of the ventricles repolarizing because of electrolyte imbalance
Non ST Elevation Infarction
 Partial Occlusion
 Possible to have transient elevation of the ST wave, which would still be categorized as
NSTEMI
ST Elevation Infarction
 Total occlusion of vessel
 20 minutes to prevent ischemia
Myoglobin
 Released during injury, first marker that is released on the graph.
 Not specific, can happen during skeletal or cardiac damage
Troponin
 Cardiac specific, myocardial muscle protein that is released when the cardiac muscle is
injured.
 Shows when MI is in the process of occuring.
 Takes 3-12 hours to rise from onset of the MI
 Peaks in 24-48 hours
 5-14 days to return to baseline
CK MB
 Heart specific, helps to quantify damage
 Peaks at 3-12 hours
 Goes back to normal at 24-72 hours
ACS Assessment
 Symptoms:
o Chest pain, palpitations,
o onset of murmur,
o BP elevated,
o pulse may indicate atrial
fibrillation,
o shortness of breath,
o dyspnea,
o tachypnea,
o decreased urinary output,
o skin-cool, clammy,
diaphoretic, anxious, restless,
o light-headed, feeling of
impending doom
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Decreased urine output – due to decreased kidney perfusion. Brain is signalling for O2
to be rerouted to brain and heart
Checking MAP to see how well the organs are perfusing
Inferior wall MI
o Occurs in Right Coronary Artery
o nausea/vomiting occurs because of vagus nerve that is innervated (noxious
stimuli)
Right Ventricle MI –
o Presenting as systemic symptoms
o Increased jugular vein distention, peripheral edema  can end up with heart
failure
Left Ventricle MI
o Crackles occurring due to fluid buildup in lungs that isn’t able to be pumped out
by the heart
o Pulmonary edema
Addressing Anxiety in an Acute Situation
 Use a calm manner
 Stress-reduction techniques – slow down breathing
 Addressing patient’s spiritual needs may assist in allaying anxieties – holding hand ??
 Address both patient and family needs
Potential Complications Post ACS
 Heart failure
 Acute pulmonary edema
 Dysrhythmias (AFIB, VTACH, VFIB) and cardiac arrest
 Cardiogenic shock – so much damage to the heart that it cannot pump effectively – HIGH
RATE OF MORTALITY – Cath lab to get rid of clot
Coronary Artery Bypass Graft Surgery (CABG)
 If the patient is not a candidate for the cath lab (because they have too many vessels
involved in the ACS), then they may need coronary artery bypass
 The vein will be grafted to bypass wherever the clot is
Patient Teaching
 Teaching regarding disease process
 Lifestyle changes and reduction of risk factors
 Explore, recognize, and adapt behaviours to avoid to reduce the incidence of episodes of
ischemia
 Medications - reassessment
 Stress reduction – exercise, meditation, mindfulness
 When to seek emergency care – return of pain, nitro isn’t working, pain is “different”
than before
Stroke
 Stroke occurs when ischemia or hemorrhage into the brain results in death of brain cells.
 Functions are lost or impaired:
o Movement, sensation, or emotions that were controlled by the affected area of the
brain
 Severity of the loss of function varies according to the location and extent of the brain
involved.
 Third most common cause of death in Canada and the United States
 Leading cause of serious, long-term disability
 Physical, cognitive, and emotional impact
Ischemic Stroke
 Ischemic strokes result from inadequate blood flow to the brain from partial or complete
occlusion of an artery.
 87% of all strokes are ischemic strokes.
 Ischemic strokes can be
o thrombotic
o embolic
 A TIA is usually a precursor to ischemic stroke
 Symptoms last less than one hour
 No infarct occurs, but it may develop into one
 Direct to EMERG
TIA – Transient Ischemic Attack
 Transient episode of neurological dysfunction caused by focal brain, spinal cord, or
retinal ischemia, without acute infarction of the brain
 Symptoms last <1 hour.
Thrombotic Stroke
 Thrombosis occurs in relation to injury to a blood vessel wall and formation of a blood
clot.
 Result of thrombosis or narrowing of the blood vessel
 Most common cause of stroke
 Lacunar strokes are typically asymptomatic.
 Clot formed in artery inside the brain
 Plaque in brain, can be partial or total occlusion
Embolic Stroke
 Occurs when an embolus lodges in and occludes a cerebral artery – can travel from other
places
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Results in infarction and edema of the area supplied by the involved vessel
Second most common cause of stroke
Client with an embolic stroke commonly has a rapid occurrence of severe clinical
symptoms.
Onset of embolic stroke is usually sudden and may or may not be related to activity.
Client usually remains conscious, although may have a headache.
Previous MI and high cholesterol levels increase risk for embolic stroke
Hemorrhagic Stroke
 Intracerebral hemorrhage
o Bleeding within the brain caused by rupture of a vessel
o Hypertension is the most important cause.
o Hemorrhage commonly occurs during periods of activity.
o Often a sudden onset of symptoms, with progression over minutes to hours
because of ongoing bleeding
 Subarachnoid hemorrhage
o Intracranial bleeding into cerebro-spinal fluid–filled space between the arachnoid
and pia mater
o Commonly caused by rupture of a cerebral aneurysm
o An aneurysm may be saccular or berry.
o Majority of aneurysms are in the circle
of Willis.
o “Worst headache of one’s life”
o Most frequent surgical procedure to prevent rebleeding is clipping of the
aneurysm.
o Coiling is another procedure.
Clinical Manifestations of Stroke
 Affects many body functions
o Motor activity
o Elimination – losing control of bowels and bladder
o Intellectual function
o Spatial–perceptual alterations
o Personality – changes post-stroke
o Affect
o Sensation
o Communications - Aphasia
Homonymous Hemianopsia
 One side is unable to see
Week 2 – AKI, CKD, FLUIDS/ELECTRO
Acute Kidney Injury
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Abrupt/brief decline in kidney function
Causing rise in serum creatinine
Reduced urine output
OR BOTH
Causes of AKI
Prerenal
 External to the kidney’s themselves, resulting in decreased function (renal blood flow)
 Can occur due to heart failure (poor cardiac output), dehydration, blood loss, GI
hemorrhage, and high protein diets
 Also medication related – eg. tetracycline, glucose steroids
 Unmanaged diabetes
Intrinsic/Intrarenal
 Renal tissue/nephron has been damaged (DIRECT INJURY TO KIDNEY)
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Can occur due to allergic reactions to antibiotics (eg. penicillin), NSAIDS, ACE
inhibitors
Can occur due to hemolytic reaction (blood transfusion)
Contrast dye
Prolonged ischemia from prerenal causes
Postrenal
 Acute renal failure
 Obstruction to kidney tissues
 See picture
LAB STUDIES
BLOOD UREA
NITROGEN (BUN)
2.5-8.0 mmol/L
CREATININE
Male 70-120 umol/L
Female 50-90 umol?L
GFR
90mL/min/1.73m^2 >
SODIUM
135-145 mmol/L
POTASSIUM
3.5-5.0 mmol/L
CALCIUM AND
PHOSPHORUS
Released together
- This is a test that is obtained in
the acute stages
- When levels are high, this means
that urea is not being removed
from the body properly
- More specificity than BUN
- Only reason why creatinine
would rise is due to some sort of
issue happening with the kidneys
- Used more in chronic cases
- Volume of blood filtered per
minute per body surface area
-Tells you how much the
nephrons are able to filter
- Used more in chronic cases
- Sodium gets excreted through
the kidneys, so if the kidneys are
not functioning properly, they
cannot conserve this electrolyte
balance properly
- Too low or too high can cause
ECG changes
- CKD causes retention of
potassium because of retained
urine, so you end up with
hyperkalemia (peaked T waves),
leading to widening QRS wave
when untreated
- Responsible for absorbing
vitamin D, so if kidneys are not
working properly then the GI
cannot properly absorb
-Due to this, the bones will release
calcium  leading to
demineralization
-Phosphate also gets released and
held in body
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As creatinine increases, the glomerular filtration rate is dropping because filtration ability
is decreasing
It takes 3 months to assess and decide if someone has chronic renal damage
AKI symptoms and dysfunction greater than 4 weeks leads into end stage renal disease
Management of AKI
 History and physical examination
 Identification of precipitating cause and treat (eg. uncontrolled blood pressure causing
damage to kidneys, hypertension, HF)
 Serum Cr, GFR
 Serum electrolytes
 Urinalysis and output
 Renal Ultrasound
 Renal Scan
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CT scan (without contrast/dye)
Retrograde pyelogram
Collaborative Therapy
 Treat precipitating cause
 Fluid restrictions
o Restrict fluids if they are not urinating
 Nutritional Therapy (adequate protein and restrict K+ , PO4, Na)
o Moderate amount of protein to maintain muscle in tissues without consuming too
high of an amount to tax the kidneys
o CA+ supplements to prevent demineralization
o Phosphate binders will help to get rid of phosphorus
 Lower K+ if elevated – this must be addressed – give kayexalate, restrict K in diet
 Calcium supplements or phosphate binders
 If necessary, parenteral or enteral nutrition
 If necessary RRT
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NOTE* kidneys could shut down after CABG surgery – there is a large fluid loss that
could send into dysrhythmias
o Ideal situation is that body recovers from the shock of surgery and kidneys
begin to wake up – don’t need to stay on dialysis long term
Chronic Kidney Disease
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Progressive, irreversible loss of kidney function
KDOQI defines CKD as kidney damage OR Glomerular Filtration Rate (GFR) less than
60 mL/min/1.73 m2 for 3 months or longer
Though serum Cr is a common biomarker, its not as effective in early and advanced
CKD. GFR is a better overall measure
Nephrons that die STAY dead
Stage 2-3  Mild to mod kidney loss
 Preventing disease process progression and hold onto as much function as you possibly
can
 Can vary depending on what’s causing CKD
 If patient has other medical conditions like diabetes or hypertension, they need to follow
their regime and have good control over both, take meds on time, etc.
 It is possible to remain in 2-3 stage for 10-20 years if the individual is very engaged in
their regime
Stage 3 Symptoms
 Weak, tired, swelling in extremeties – mild symptoms
 Eventually as disease progresses, these symptoms will be more severe
Stage 4-5
 Matter of time before individual ends up on dialysis
 Patient is usually < 10 GFR before they start dialysis (15 on exam)
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Irritates mucosa of GI lining – bad breath, metallic taste in mouth (later stages)
Anorexic because food doesn’t taste as good as it used to
Anemic – erythropoietin production is reduced in kidney, give EPREX or EPRO (same
thing)
Uremia destroys myelin sheaths – leg cramps and muscle spasm, fatigue
Acute situation with increased uremia can result in confusion
Chronic situation (gradual loss) with increased uremia can result in fogginess in thinking
Increased phosphorus leads to pruritis
Causes
 Diabetes mellitus**
 Hypertension
 Chronic glomerulonephritis
 Pyelonephritis or other infections
 Obstruction of urinary tract
 Hereditary lesions
 Vascular disorders
 Medications or toxic agents
Collaborative Goals of Care for Mild to Moderate CKD
 Main focus is delaying progression and prevent need for renal replacement therapy
(RRT)
 For people with DM, achieve blood glucose goals
 Control hypertension
 Adherence to medication regime
 Consult dietician and develop meal plan (moderate protein restrictions, fluid intake, other
considerations)
 Manage weight
 Regular physical activity
 Smoking cessation – vasoconstriction puts strain on capillaries
 Coping with psychological distress (anxiety and depression)
Stage 5 CKD (End Stage)
1. Hemodialysis (in center or home)
2. Peritoneal dialysis  (Automated Peritoneal Dialysis (APD) or Continuous Ambulatory
Peritoneal Dialysis (CAPD) – membrane functions as filter to get fluid and balance
electrolytes, only done at home
3. Conservative Care
*people avg about 2 chronic illnesses by the age of 60-65*
Home Hemo
 Patient performs dialysis independently in their home
 Patient typically require 1 month of training
 Electrical and plumbing modifications to the home may be required
 Seen in clinic q 2 to 3 months
Hemodialysis Access Options
1. Arteriovenous Fistula – artery + vein, pressure from artery makes vessel get bigger, this
is the best option! (lasts longer & low risk for infection after surgery stage)
2. Graft – synthetic tube attached to vessels (doesn’t last as long, possibility for breakdown
since it is foreign to the body)
3. Central Venous Catheter (central line) – do not use it to put meds, longer term, tunneled
in. MORE PRONE TO INFECTION. Can’t shower
**NO BP OR BLOOD WORK ON THE ARM WHERE THE FISTULA IS* - takes 6-12
weeks for the veins to come together, so it needs to be done pre-emptively
Peritoneal Dialysis
Collaborative Care
 Monitor fluid balance
 Nutritional therapy
 Erythropoietin therapy
 Calcium supplementation, phosphate binders
 Fracture risk- r/t hypocalcemia and hyperphosphatemia
 Risk for infection (suppressed immune system)
 PD patients can have more liberal diet compared to HD
 Make sure that fluids don’t buildup so much, so you don’t have to be as strict with fluids
 In center hemo is done 3x per week
 At home it is done every week
 Immunosuppressed +++
Conservative Care
 Focused on physical and psychological interventions
 Correction of extracellular fluid volume overload or deficit
 Nutritional therapy
 Erythropoietin therapy
 Calcium supplementation, phosphate binders, Kayexelate
 Antihypertensive therapy
 Measures to lower potassium – AVOID ECG CHANGES
 Adjustment of drug dosages to degree of renal function
 Usually this occurs when people do not want dialysis, so we need to keep them as
comfortable as possible
 Some urine output = optimize Lasix dose to keep them comfortable
Fluids, Electrolytes, Acid Base
Sodium
 Extracellular – Where sodium goes, water will follow
 Controls nerve impulses, and is an important factor in the acid base balance
 Obtained MOSTLY through food
 Regulated by the kidneys and antidiuretic hormone
 The ADH is stored in the pituitary gland. If released, it will tell the body to hold onto
water, and therefore also hold onto sodium
Hypernatremia
 What can cause this?
o Muscle weakness, fatigue, confusion, thirst
o Untreated/Uncorrected – seizures
Hyponatremia
 What causes this?
o Too much fluid that has been excreted with sodium (eg. given a bolus after a low
bp)
o GI losses
o Loss through the kidneys  decrease filtering function  losing lots of volune
through excretion and losing sodium with it
o Abdominal cramps
o Shallow respirations
o Muscle spasms
Potassium
 Intracellular
Hyperkalemia
 kidney FAILURE
 burns
 muscle weakness
 leg cramps
 tall peaked T waves, VFIB
Hypokalemia
 starvation,,
 low resps
 low hr
 low bp
 flattened T waves  can lead to U wave
Calcium
 In bones, regulated by the hyperparathyroid hormone
Hypercalcemia
 Cancer in breast or lung
 Confusion
 Fatigue
 Muscle weakness
 Kidney stones
Hypocalcemia
 Thyroidectomy where parathyroid got damaged or removed with it – you lose the
regulation of calcium w PTH
 Prolonged muscle contractions – tetany
 Chvostek – nerve twitching on side of face
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Troussau – inflate BP for 3 minutes, hand will posture (flipping inwardly)
Prolonged QT interval
Hypomagnesemia
 Sits inside the cell
 Chronic alcoholism (cirrhosis of liver)
 Hyperactivity of deep tendon reflexes (overreactive)
Hypermagnesemia
 Excessive consumption of magnesium or milk
 Renal failure
 End up with loss of neuromuscular function
 CNS depression
Acid Base Balance
BLOOD PH
paCO2
BICARB
7.35-7.45
35-45mmHg
21-28 mmol/hg
Acidosis – Decreased pH
 Causes: metabolic issues, respiratory issues, or both
 Patients with impaired breathing are at the biggest risk
 Major changes in the bodily function
o Imbalance of electrolytes, ESP potassium
A. RESPIRATORY ACIDOSIS
 Decreased pH (acidic), increased CO2, normal bicarb HCO3
 Causes:
o Infection – obstruction of airways
o Medications-sedatives, narcotics, anesthetics
o Pneumonia, atelectasis, emphysema
o CHF-pulmonary edema or COPD
o Brain-pressure on respiratory center – injury to medulla causes
decreased RR
o Hypoventilation causes paCO2 retention – decreased RR found in
post op patients
 What to do:
o Patent airway
o O2 as prescribed
o Treating underlying cause
o Semi fowlers to fowlers unless contraindicated
B. METABOLIC ACIDOSIS
 Decreased pH, normal CO2, decreased bicarb
 Causes:
o Starvation
o DKA  give insulin
o Severe diarrhea  eg. ostomy is draining a lot
o Drug use
o Renal failure
o Gastrointestinal fistulas
o Shock
Alkalosis – Increased pH
 Acid-base balance of the blood is disturbed by an excess of bases, especially bicarbonate.
 Problems of alkalosis are serious and potentially life threatening.
A. RESPIRATORY ALKALOSIS
 Increased pH, decreased CO2, normal bicarb
 Causes:
o Excessive exhalation of CO2 (hyperventilation caused by hypoxia)
o Anxiety
o Fear
o Exercise
o Fever
o Septicemia
o Mechanical hyperventilation
 What to do?
o Encourage slow deep breathing
B. METABOLIC ALKALOSIS
 Increased pH, normal CO2, increased bicarb
 Causes:
o Excessive vomiting
o Prolonged gastric suctioning
o Diuretic therapy
 What to do?
o Patent airway
o Vital Signs
Arterial Blood Gases
 Look at pH: if ↓ = acidosis; ↑ = alkalosis;
 Determine primary cause of disturbance:
o If pCO2 is ↑ respiratory acidosis
o If pCO2 is ↓ respiratory alkalosis
o If HCO3 is ↑ metabolic alkalosis
o If HCO3 is ↓ metabolic acidosis
 Fully compensated – ph normal, bicarb out of range to pull ph back into normal range
 Partially – pH out of range bicarb AND CO2 will also be out of range because the body
is trying to fix the imbalance
 Uncompensated – pH out of range but either co2 or bicarb will be out of range
Week 3 – Congestive Heart Failure
Review of Terms
Cardiac Output
 Heart Rate x Stroke Volume
Stroke Volume
 Volume of blood ejected from left ventricle after each contraction
Preload
 Stretch that occurs before the left ventricle contracts
Afterload
 Force which heart has to pump against to push blood out
Myocardial Contractility
 Strength of the muscle contraction
Heart Failure
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An abnormal condition involving impaired cardiac pumping/filling
o Can be weakened
Heart is unable to produce an adequate cardiac output (CO) to meet metabolic needs.
o Therefore, there will be problems perfusing other organs, and oxygen cannot get
out
Heart failure (HF) is not a disease but a “syndrome.”
Associated with longstanding hypertension (inc pressure in vessels), coronary artery
disease (CAD), and myocardial infarction (MI)
Risk Factors
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Primary risk factors
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o CAD
o Hypertension
Contributing risk factors
o Diabetes
o Tobacco use
o Obesity
o High serum cholesterol
Dilated Heart Chamber
 Enlarged ventricles means that muscles
becomes thin, so it cannot pump out the blood
effectively
 Typically happens when there is elevated
pressure in the left ventricle
 Over time, it will not be able to compensate,
therefore the cardiac output will drop down
again
 Because it has been working very hard, the
muscle has thickened (hypertrophy)
 This will increase the oxygen demand since
the muscle is bigger
 Impairs coronary circulation when muscle is
enlarged
 Exercise intolerance
 Milder states of HF may not have as much
difficulty – could be initially manageable since
decreased o2 to body
 Decrease to quality of life
Reduced Ejection Fraction
 Percentage of blood pumped out by the ventricles
 Normal EF = > 55%
 Reduced EF = < 40%
 Heart failure with reduced ejection fraction is caused by:
o Impaired contractile function (e.g., MI)
o Increased afterload (e.g., hypertension)
o Cardiomyopathy
o Mechanical abnormalities (e.g., valve disease)
Preserved Ejection Fraction
 Heart failure with preserved ejection fraction (diastolic HF)
o Impaired ability of the ventricles to relax and fill during diastole, resulting in decreased
stroke volume and CO
o Diagnosis based on the presence of heart failure symptoms and normal EF
 Caused by
o Left ventricular hypertrophy from chronic hypertension
o Aortic stenosis (narrowed opening of aortic valve)
o Hypertrophic cardiomyopathy (inherited abnormality)
 Can be seen in older people who are obese
Mixed HF
 Seen in disease states such as dilated cardiomyopathy
o Poor EF (less than 35%) – not contracting well
o High pulmonary pressures
o Biventricular failure: both ventricles may be dilated and have poor filling and emptying
capacity
o Cardiac output reduced
Compensatory mechanisms
 Sympathetic Nervous System (SNS)
o FIRST and least effective mechanism
o Release EPI and NE
 Increased HR
 Increased contractility
 Peripheral vasoconstriction
o Causes more blood to the heart, but the heart is unable to handle volume  worsening
ventricular functioning
o Overtime, these mechanisms are detrimental as they increase workload of failing
myocardium and increase need for O2
 Neurohormonal Responses (RAAS)
o Blood pressure drops, renin in kidneys is released to convert to ACE1
o Angio 1  Angio 2 causing vasoconstriction
o Antidiuretic hormone is released from the posterior pituitary causing retention of water
o Aldosterone is released from adrenal hormones, causing water and sodium to be retained
 Inflammatory response
o Proinflammatory cytokines (e.g., tumour necrosis factor): released by cardiac myocytes
in response to cardiac injury
o Depression of cardiac function by causing cardiac hypertrophy, contractile dysfunction,
and death of myocytes
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Interleukin 1 and necrotic factors are released
Overtime inflammation will cause fatigue, cardiac and skeletal myopathy (myopathy is
with advanced HF)
 Counterregulatory Processes
o Natriuretic peptides: ANP and BNP
 Released in resp to increase in atrial volume and ventricular pressure
 Promote venous and arterial vasodilation, reducing preload and afterload
 Chronic HF leads to a depletion of these factors.
o The peptides are trying to increase glomerular filtration rate to excrete fluids and sodium
(aldosterone is making you retain)
o Helps with vasodilation
o NT pro BNP helps to determine severity of HF
o BNP > 100 = HF
Types of HF
 Left Sided (Most Common)
o Resulting from left ventricular dysfunction  MI,
hypertension, CAD, cardiomyopathy
o Backup of blood into LA and pulmonary veins
 Pulmonary congestion
 Edema
 Blood tinged sputum
 Right Sided
o Can occur from  Cor pulmonale, LS HF, Right
ventricular MI
o Backup of blood into RA and venous systemic
circulation
 Jugular venous distension
 Hepatomegaly, splenomegaly
 Vascular congestion of GI tract
 Peripheral edema
Diagnostic Studies
 Primary goal: Determine and treat underlying
cause
o History and physical examination
o Chest x-ray
o ECG
o Lab studies (e.g., cardiac enzymes,
BNP)
o Hemodynamic assessment
o Echocardiogram
o Stress testing
o Cardiac catheterization
o Ejection fraction
Acute Decompensated HF
 Pulmonary edema, often life-threatening
 Early
o Increase in the respiratory rate (RR >30)
o Decrease in PaO2
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o Increase in PaCO2
o Fatigue
o Orthopenia – can’t lie flat without SOB
Later (without medical attention)
o Metabolic Acidosis
o Hypoxia
o Death if not treated
Nursing Mgmt of ADHF
 High Fowler’s position
 Supplemental oxygen
 Continuous ECG monitoring
 Ultrafiltration: option for clients with volume overload
 Circulatory assist devices are used to treat clients with deteriorating HF.
 Coexisting psychological disorders should be addressed.
 Keep eye on potassium levels
Chronic Heart Failure
 Fatigue
 Dyspnea, orthopnea, paroxysmal nocturnal dyspnea
 Persistent, dry cough, unrelieved with position change or over-the-counter cough suppressants
 Tachycardia
 Dusky pale look to skin bcz CO is not great
 Progressive worsening of ventricular function
 Clinical presentation depends on severity and underlying disease
 Fluid pooling in the interstitial comes back into circulation, makes them cough
 Can end up with nocturia as well
 Gravity helps get fluid back into vasculature
 At risk for thrombosis and stroke
 At risk for VTACH and VFIB
 Volume overload
Management of CHF
 Oxygen administration
 Self-management teaching
 Exercise and activity – pace self, breaking tasks into chunks (ADL’s exercise etc.)
 Devices
o Cardiac resynchronization therapy (CRT) or biventricular pacing
o Implantable cardioverter defibrillator
 Nonpharmacological therapies
o Mechanical circulatory support
o Intra-aortic balloon pump (IABP)
o Extra-corporeal Membrane Oxygenation (ECMO) - blood is pumped outside of your
body to a heart-lung machine that removes carbon dioxide and sends oxygen-filled blood
back to tissues in the body.
o Ventricular assist device (VAD) - device that helps pump blood from the lower chambers
of your heart (ventricles) to the rest of your body. Typically used in patients waiting for a
transplant
 Drug therapy
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Diuretics
o Thiazide
o Loop – Furosemide/lasix
ACE inhibitors
Neprilysin inhibitors – contains angiotensin receptive blocker and a neprilysin inhibitor (helps
reduce mortality and hospitalization)
-Adrenergic blockers o Positive inotropic agents, helps to slow the HR down – digoxin
o Used in acute situation
o Could be on it chronically if they have had an MI and extent of damage
Dobutamine and milrinone are the two most commonly used agents.
Nutritional therapy
o Fluid restriction not generally required
o Daily weights important - Weight gain of 2 kg (4 lb) over 2 days or a 2.5 kg (5-lb) gain
over a week should be reported to health care provider.
o Diet education and weight management: Individualize recommendations and consider
cultural background
o Recommend Dietary Approaches to Stop Hypertension (DASH) diet.
o Sodium is usually restricted to 2 g per day.
o Heart healthy diet
Weight mgmt if obese
Health Promotion
o Treatment or control of underlying heart disease key to preventing HF and episodes of
ADHF (e.g., valve replacement, control of hypertension, coronary revascularization)
o Early detection of worsening HF may prevent future hospitalizations.
o Client/caregiver teaching: medications, diet, and exercise regimens
o Exercise training (e.g., cardiac rehabilitation) improves symptoms but is often
underprescribed.
o Home nursing care may be required for follow-up and to monitor client’s response to
treatment.
Ambulatory and Home Care
o Explain to client and caregiver physiological changes that have occurred.
o Assist client to adapt to both the physiological and psychological changes.
o Integrate client and caregiver(s) or support system into the overall care plan.
Client Education
o Taking pulse rate
o Know when drugs (e.g., digitalis, -adrenergic blockers) should be withheld and reported
to health care provider.
o Home BP monitoring - +/- 20 from baseline BP will need to hold meds
o Signs of hypokalemia and hyperkalemia if taking diuretics that deplete or spare
potassium
o Instruct client in energy-conserving and energy-efficient behaviours.
Week 4 – Long Covid
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Typically people will recover in 2-6 weeks
People that have previously tested positive - Symptoms that go on for 4 weeks or more after they
initially got sick
No other cause to these symptoms that the person is experiencing
Continuing inflammation or overreactive immune system could be at the root of these symptoms ,
no specific treatment for it
Lingering Symptoms after Covid
 While most people with COVID-19 recover and return to normal health, some people can have
symptoms that last for weeks or even months after recovery from acute illness. People are not
infectious to others during this time
 This persistent state of ill health is known as ‘post COVID condition’ but other names are also
used to describe the condition. However, there is no internationally agreed definition of post
COVID condition as of yet.
 Even people who are not hospitalized and who have mild illness can experience persistent or late
symptoms.
 Some patients develop medical complications that may have lasting health effects.
 Rule out other possible complications (MI, stroke, HF)
 Resembles chronic fatigue symptoms
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Top 5: Fatigue, Headache, Attn Disorders, Hair Loss, Dyspnea
Poor quality of life and psychological distress
Some people had comorbidity already
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The reason why some patients experience long-term symptoms after COVID-19 is uncertain. This
could be partially explained by host-controlled factors that influence the outcome of the viral
infection, including genetic susceptibility, age of the host when infected, dose and route of
infection, induction of anti-inflammatory cells and proteins, presence of concurrent infections,
and past exposure to cross-reactive agents.
It has not yet been established if sex, gender, age, ethnicity, underlying health conditions, viral
dose, or progression of COVID-19 significantly affect the risk of developing long-term effects of
COVID-19.
Seeing people with mild and mod cases also be diagnosed
Mortality rate 2.4x higher in men than women
Can be assoc with post traumatic mental stress
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See the rest of the powerpoint for notes!