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NUR 3002 > Heart failure > Flashcards

Heart failure Flashcards

0
Q

Heart Failure Pathophysiology

A

Interference with Co (such as preload, afterload, myocardial contractility, heart rate or metabolic state) leads to decreased ventricular function and heart failure. When the heart becomes overload the body resorts to compensatory mechanism that are aimed at maintain CO and BP. This occurs through the activation of the SNS which releases adrenaline and noradrenaline to increased HR, contractility and peripheral vascular constriction, initially this improves CO. eventually due to increased workload, the myocardium requires addition oxygen and CO falls as a result. The kidney’s notice this decrease in perfusion and activate the renin-angiotensin-aldosterone system which increases sodium retention in the kidneys(aldosterone) and increased peripheral vascular resistance (angiotensin) leading to an increased BP. In addition the brain notices a reduced CPP and secretes ADH to increase water absorption in the kidneys leading to a further increase in blood volume. Due to the increase in blood volume in the heart chambers the heart initially trys to compensate by stetching the ventricle walls (thinning), this works for a while until the muscle fibers become over streched and can no longer contract effectively leading again to a deduced CO. the compensate for this the walls of the ventricle thicken to give it more power, this increases CO and maintains perfusion but the muscles have a poor coronary artery supply and become prone to life threatening ventricular arrhythmias.

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1
Q

Define Heart Failure

A

A progressive condition of impaired cardiac function due to structure or functional disorder that decreases the ability of the ventricles to fill and eject. The heart cannot pump blood at a volume required to meet blood pressure requirements of the body.

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2
Q

Differentiate between clinical manifestations of L and R sided failure

A

LEFT: left heart failure means that the left ventricle is unable to pump the blood forward into the aorta causing the blood to back flow into the pulmonary system causing symptoms of pulmonary oedema (pink throthy sputum). At risk of pneumonia.
•Dyspnoea; orthopnoea (cant lie flat); dry hacking cough (cant bring up fluid); crackles on auscultation; nocturia; chest pain
RIGHT: right heart failure means that the right ventricle is unable to pump blood forward into the pulmonary vasculature causing blood to back flow into the venous system causing symptoms of peripheral oedema (pitting).
•Weight gain (sodium and water retention), GI bloating à nausea à anorexia, ascites (eventually), distended neck veins; behavioural changes
BOTH: suffer fatigue; tachycardia

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3
Q

Discuss Nursing management of chronic Heart Failure

A

Management is aimed at reducing the workload of the heart and preventing complications such as pleural effusion, arrhythmia, stroke from left ventricular thrombus, hepatomegaly from back flow of blood into the liver and renal failure from decreased perfusion.
•May require revascularisation (CABGS, Stents), pacemaker or heart replacement
Fluid volume excess
•Monitor urine output with strict fluid balance (renal function)
•Fluid restriction 1-1.5L per day
•Daily weight
•Dietary restriction (low sodium, high protein, smaller meals)
•Diuretics: thiazides (Hydrocholrothizide), loop diuretics (frusemide) or potassium sparing (spironolactone) which one will depend of other co-morbities.
Activity intolerance
•Encourage activity with regular rest periods as don’t want to over work the heart
•Cardiac rehab
•Paroxysmal nocturnal dyspnoea (additional pillows, positioning)
•Sleep disturbance: educate on effect of diuretics

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4
Q

Briefly explain indications of CABGs

A

Briefly explain indications
•Unstable angina that is not responding to medication or percutaneous coronary intervention (PCI)
•Left main coronary artery disease (wont do PCI as may occlude à massive AMI)
•Multi vessel disease ( don’t like doing multiple stents)
•Treatment of MI or heart failure
•Complications from PCI (coronary artery dissection post PTCA)
•Failed PCI

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5
Q

Differentiate between artery and vein grafts used

A

The selection of artery or vein from grafting will depend on the quality of the vessel, such as Peripheral Vascular Disease.
•Arteries: better quality and last longer, 90% patency at 10years. Have a risk of vasospasm then handling and take longer to re-stenose. Commonly the internally mammary or radial are used
•Veins: not as good quality, only have 60% patency after 10years but no vasospasm and are quicker to re-stenose. Commonly use saphenous (leg).

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6
Q

Discuss complications of CABGS

A
  • High risk of bleeding (may need to return to theatre depending on cause) ?blood transfusion
  • Cardiac tamponade (inflammation)
  • Arrhythmias (heart doesn’t like be touched)
  • Blood pressure alterations
  • Electrolyte and metabolic disturbances (hypokalaemia due to diuresis due to release of ATN from atria due to hypertension during by-pass)
  • Atelectasis (collapse of alveoli à pneumonia) : don’t want to deep breath due to pain
  • Pleural effusion as lungs exposed
  • Neurological (post anaesthetic delirium from long surgery), at risk of stroke.
  • Renal impairment from hypoperfusion
  • Coagulopathy à haemorrhage
  • Infection of wound, donor site, ICC site and arterial line/CVC.
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7
Q

Discuss Nursing management of CABGS

A

Preoperative care
•Comprehensive assessment to obtain base line vitals, history to identify risk factors, CXR, ECG, Pathology (FBE, U&E, clotting)
•Education re: procedure and post-operative expectations (e.g. rehab, analgesia)
Post-operative care
•Usually ICU for first 24hours where they are intubated for first 6-12hours and have multiple haemodynamic monitoring devices (artline, CVC, intercostal x2, ETT)
•Breathing: chest auscultation, CXR, monitor pleural and mediastinal drains (UWSD)
•Circulation: monitor haemodynamic status
•CVC care
•ECG baseline on RTW then every 12 hours at least
•Monitor fluid balance (IDC for 24 hours usually)
•Atrial and ventricular pacing wire monitoring ? Remove in ICU
•Monitor GCS as at risk of stroke
•BGL – stress response
•Analgesia – lots plus splinting ( ribs fractured in theatre)
•Cardiac diet
•TED to prevent DVT
•Day 1 mobilisation with physio ( will start slow, maybe just sit in chair)
•Monitor wound Dx
•Monitor vitals as per hospital policy or surgeons preferences and as per patients condition (clinical decision)

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8
Q

Define APO

A

Is an abnormal accumulation of fluid in the interstitial tissue and alveoli that impairs gas exchange and lung expansion. This can be caused by fluid overload, left ventricular failure, prolonged airway obstruction, sepsis or aspiration. Characterised by hypoxaemia, crackles on auscultation, decreased oxygen saturation, and precence of infiltrates on chest x-ray. And pink frothy sputum.

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9
Q

Discuss Pathophysiology of APO

A

Discuss Pathophysiology
Increased hydrostatic pressure, decreased interstitial pressure or increased capillary permeability leads to a build of fluid in the interstitial space of the lungs which the lymphatics can normally drain, however if the fluid continuesp the lymphatic system becomes overwhelmed and fails to drain the fluid away, eventually this fluid along with red blood cells floods into the alveoli (alveolar oedema).

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10
Q

Clinical manifestations of APO

A 
Altered LOC from hypoxia
•SOB & Increased WOB
•Hypoxaemia
•Chest crackles on auscultation
•Dullness to the base of lungs
•Pink frothy sputum
•Skin pale and diaphoretic
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11
Q

Discuss collaborative Management of APO

A

Discuss collaborative Management of APO
Aimed at reversal of the cause and interventions to treat the symptoms
•High flow Oxygen (consider intubation especially if pink frothy sputum)
•NIPPV/PEEP – high pressure to move fluid back and recruit alveoli
•Monitor ABG’s
•Chest x-ray
•Chest auscultation
•Frequent ECG and Cardiac monitoring
•Fluid balance chart ?IDC
•Monitor pathology – cardiac enzymes, FBE, U&E, lactate
•Cautious IVT
•Depending on cause morphine, digoxin, inotropes(hypotensive)
•Position in semi fowlers with legs dependent
•Diuretics +/-
•Fluid restriction depending on cause

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12
Q

Define Stroke

A

An acute neurovascular injury secondary to cerebrovascular disease that is either ischaemic of haemorrhagic of cause.

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13
Q

Differentitate and discuss

Ischaemic causes

A

Ischaemic causes
-Thrombus: caused by atherosclerosis, vasculitis, polycythaemia or infection
-Embolic: cardiogenic emboli (AF, AMI, atrial or ventricular septal defects), fat emboli or septic emboli
-Hypoperfusion: cardiac failure
Haemorrhagic such as a burst aneurism
Risk factors

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14
Q

Risk factors for stroke

A

HT, age (doubles every 10 years after 55), male, family Hx, smoking, hyperlipidaemia, diabetes, AF, recent AMI, endocarditis and carotid stenosis.

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15
Q

Clinical Manifestations for stroke

A

Clinical Manifestations
Think FAST
Facial weakness: facial symmetry when smiling
Arm movements: get patient to lift arms up, dose one drift down or drop rapidly, or turn
Speech change: slurred speech or is there difficulty finding correct words or phrases
T is for test

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16
Q

Discuss management of a diagnosed patient for stroke

A

Discuss management of a diagnosed patient
-Stroke management requires quick identification as patient may be eligible for thrombolysis.
History exclusion >3hr, seizure, Bgl 22 mmol/. AMI >7 days < 3mth, stroke or serous head trauma < 3mth, major surgery 14 days, GIT urinary haemorrhage 21 days.
Pregnant, check haemorrhage risk INR, platelet, BP >185/>110,
Airway
-Remain NBM due to risk of aspiration
-Intubate if GCS less than 9 or sign of raised ICP
Breathing
-Supplemental oxygen if SaO2 below 95%
Circulation
-Manual blood pressure (must be accurate),
-ECG (may find T wave inversion -75%)
-Manage hypotension carefully
-Aggressive management of hypertension not recommended
-2 x large IVB
-Pathology: FBE, U&E, LFT, COAG, BGL and troponin (need to identify type of stroke)
-Maintain euvolemia with IVT

Disability
-Monitor neurovascular obs every hour at least (GCS, pupil size and reactivity)
-BGL every 2-4 hours (affect mortality), keep in range
-Elevate head of bed 30 degrees
-Urgent CT/ ?MRI
-Hypothermia can help decrease cellular metabolism and prevent secondary injury will need intubation and induced coma to stop shivering
-Anti-platelet therapy for ischaemic stroke (aspirin)
Example of ob for thrombolysis
•15mins for 2hrs
•30mins for 4 hours
•Hourly for 4 hours
•2 hourly for 12 hours
•4 hourly until r/v

17
Q

Identify the inclusion and exclusion criteria for thrombolysis for a stroke

A

Onset of symptoms less than 3 hours (excludes those who wake up with symptoms)
-BSL must be over 2.7 and under 22mmol/L
-Seizure at onset excludes patient
-CT to determine cause (must illuminate haemorrhagic)
-Cant have had an AMI, stroke or serious head trauma within last 3 months,
-Cant have had major surgery within last 14 days as wounds will rebleed
-Cant have had GIT or urinary haemorrhage in last 21 days
-Not pregnant
-Need to check haemorrhage risk: warfarin INR needs to be below 1.7
-Cant have had IV heparin within last 48 hours or on herbal medicines and platlet/anticoags
-Need platlets above 100000/mm3
-Blood pressure below 185/110
NEED to stay in bed for first 24 hours as falling à haemorrhage
Minimise invasive procedures for 24 hours
No razors
Monitor for pressure areas

18
Q

Differentiate and discuss

ØIntra-cerebral

A
  • bleeding inside the brain
    ØEpidural
    • bleeding between the dura mater (outer meninges) and the skull
      ØSubarachnoid
    • bleeding in the subarachnoid (middle meninges) space that can lead to cerebral vasospasm and hydrocephalus (water on the brain)
    • can be caused by ruptured cerebral aneurysm (treatment is to surgically clip or endovascular coiling)
      ØSubdural
    • bleeding between the arachnoid mater and the dura mater (inner meninges)
19
Q

Differentiate and discuss extradural and subdural haematomas

A

Extradural haematoma is a neurosurgical emergency as the haemorrhage causes the dura to separate from the skull, it rapidly expands causing raised ICP and can lead to herniation.
Signs and symptoms
•LOC à consciousness àLOC
•Severe headache
•Hemiparesis
•Ipsilateral (same side) pupil dilation
A subdural is a collection of blood between the dura mater and the arachnoid mater and can be acute, subacute or chronic
Signs and symptoms
•Acute: LOC, hemiparesis, fixed and dilated pupils
•Subacute/Chronic: nausea and vomiting, altered LOC, headache

20
Q

Define Intracerebral Haemorrhage

A

Intracerebral Haemorrhage
Bleeding within the brain tissue, manifestations depend on size and location (may or may not be operable), can lead to neuronal death, raised ICP and secondary ischaemia.

21
Q

Factors affecting CCP

A 
Decreased perfusion pressure
-Decreased BP
-Raised ICP
Decreased oxygen or glucose delivery
-Hypoxia
-Anaemia
-Hypoglycaemia
-Decreased cardiac output
22
Q

Increased metabolic demand on CCP

A

Increased metabolic demand

  • Hyperthermia
  • Seizures
  • Agitation
23
Q

Increased vascular resistance of CCP

A

Increased vascular resistance

  • Vasospasm (post aneurism clipping)
  • Thrombosis
  • Cerebral oedema
  • Hypocapnia (low CO2)
24
Q

Define shock in general

A

Define

state of inadequate tissue perfusion resulting in impaired cellular metabolism and function

25
Q

Pathophysiology of shock

A

Pathophysiology
The cells of the body require both oxygen and glucose in order to function effectively, these components are carried by the blood to the cells. A shock state leads to a decrease in blood delivery to the cells causing them to not have enough oxygen and glucose to function.
Oxygen: without oxygen cells convert to anaerobic metabolism (oxygen is required for ATP energy production), the by product of anaerobic metabolism is lactic acid which causes further cell dysfunction. In an acid environment the cells become leaky due to the loss of cell membrane causing fluid shifts, and because of the loss of ATP the sodium potassium pump cannot function causing potassium to leak out of the cells. The third spacing occurs due to the normal body reaction of osmosis and causes oedema, hypotension and decreased circulating volume. Lysosomal enzymes also leak out of the cells and ‘eat’ the cells. All of this leads to cell death and organ failure.
Glucose: when the cells are lacking energy they look for another source and therefore begin to breakdown fats, proteins (muscle) and carbs. This further increases acidosis and the by products are ketones and ammonia. The acidic environment causing leaking of proteins (big normally cant leave) which causes a decreased oncotic pressure (proteins normally draw fluid into the intravascular space), this leads to further fluid shifts into the interstitial space and further hypotension. All in all leading to impaired cellular metabolism

26
Q

4 stages of shock

A

4 stages of shock
Initial: hypoperfusion begins (decreased supply of oxygen and glucose) with imbalance between demand and supply; anaerobic metabolism begins and cellular acidosis starts developing.
-No clinical signs as yet. ?maybe a little lethargic
Compensatory: blood flow is diverted to major organs (HR, lungs & brain) still maintained but diverted away from skin (pale, diaphoretic) & GIT (N&V).
-Compensatory mechanisms baroreceptors (decreased pressure) and chemoreceptors (increased CO2) respond with the release of adrenaline (increased HR & contractility) and noradrenaline (peripheral vasoconstriction – cool fingers and toes). Next in order to maintain the perfusion of major organs the renin-angiotensin-aldosterone system is activated and causes the reabsorption of sodium, water and further vasoconstriction (thirst, decreased & concentrated UO, cold, pale fingers and toes.
-May present as a little anxious, tachypnoea as trying to rid acid, tachycardia as adrenaline from stress response.
Progressive: compensatory mechanisms are not enough leading to hypoxia to major organs
-HR: chest pain, arrhythmia (tachy-VT)
-Kidneys: further decreased UO, increased Urea and creat as not riding acids à AKI leading to more hyperkalaemia, oedema
-Lungs: hypoxia (decreased oxygen sats)
-GIT: bleeding
-Brain: altered LOC (not really aware of whats happening) – hallucinations if not unconcious
-Metabolic acidosis, more leaky, DIC (cant clot), cyanosed peripheries, APO, jaundice
-If not corrected will get MODs (3 or more organs failing)
Irreversible/refractory: severe tissue hypoxia with ischemia, necrosis and death of cell, build up of toxins, multi organ failure.
- Blood pooling = Futher decrease in circulating volume, profound hypotension, cerebral Ischaemia, resp failure, anuria, oozing blood, more jaundice and extremely high Urea and creat

27
Q

IDENTIFY 3 Major classifications of shock

A 
IDENTIFY 3 Major classifications
Low blood flow
-Hypovolaemic: absolute or relative
-Cardiogenic: MI or cardiomyopathy
Maldistribution
-Septic
-Neurogenic
-Anaphylactic
28
Q

Differentiate between the 3 types of shock

A

Hypovolaemic: not enough plasma to circulate around intravascular
Cardiogenic: enough blood but the heart is unable to pump it around the body
Distributive: The volume is available but leaks out of the intravascular space into areas it shouldn’t be

29
Q

3 Major aims of treatment of shock

A

3 Major aims of treatment

  • treat underlying cause
  • Increase arterial oxygenation
  • improve tissue perfusion
30
Q

Define Hypovolaemic shock

A

Loss of intravascular volume (>15% of circulating volume). Paeds and elderly 10%

31
Q

DESCRIBE Pathophysiology of hypovolaemic shock

A

Loss of circulating volume either absolute or relative leads to decreased venous return, decreased stroke volume and decreased CO, which leads to hypoperfusion and impaired cellular metabolism.

32
Q

Causes of hypovolaemic shock

A 
Causes
-Absolute
•Haemorrhage
•Vomiting
•Diarrhoea
•Diuresis: diabetes, on diuretics
•GIT suctioning
-Relative (fluid shift – its in the body just not in intravascular)
•Burns
•Sepsis (causes vasodilation)
•Allergic reactions
•Ascites
•Pleural effusion
•Loss of blood into fracture site
33
Q

Define anaphylactic shock

A

Systemic hypersensitivity reaction that if not treated can lead to death within minutes

34
Q

DESCRIBE Pathophysiology of anaphylactic shock

A

DESCRIBE Pathophysiology
Allergen enters body à immune system reacts to destroy à extensive immune & inflammatory response à cellular breakdown à vasodilation à fluid shifts and hypovolaemia

35
Q

Causes of anaphylactic shock

A

Causes
•Bites and stings
•Pollens
•Food – eggs, peanuts, shellfish (iodine in radiographic contrast media)
•Medications – anti’s, aspirin, NSAIDs, hormones, local anaesthetics, muscle relaxants, vitamins
•Natural rubber latex
•Blood products

36
Q

Chronic heart failure Drugs

A,B,C,D

A

ACE inhibitor- Angiotensin converting enzyme reduce BP, preload, afterload, (Angio oedema, Cough, Electrolyte, let out sodium
Beta blocker -sympathetic receptors relax decrease amount blood being pushed into R) ventricle L) ventricle
Calcium channel blocker soften heart better squeeze negative
Diuretic - release fluid decrease workload, less peripheral pressure (kidney) fruesmide

37
Q

BETA BLOCKER REDUCES HEART RATE
Beta blocker for hypertensive pt
Beta 1 reduce rate of contraction in the heart (block SA node from contracting) reduce stimulation
Beta 2 in the lung…

A 
Atenolol
Metoprolol
Watch out for
••Brady-cardia HR <Blood pressure
Bronchioles constriction
Blood sugar
38
Q

Diuretic nursing intervention & patient edu

A
  • D - diet
  • I - In/out put strict FBC (daily weight)
  • U - unbalance F & E monitor
  • R - Ready decreases BP, ^ HR
  • E - Not evening
  • T - Take AM
  • I - Increased toilet
  • C - Cigarets
39
Q 
Calcium channel blocker stop depolarisation, contractility of the vessels &amp; heart (soft heart) 
Electrical stimuli decreased
often after heart attack
Amlodipine - Norvase
Nifedipine - Procardia
Diltiazem - Lardizam
-Meal (with)
-Under (100 systolic 
-Ca
-H
A

-Calcium channel blocker stop depolarisation, contractility of the vessels & heart (soft heart)
-Electrical stimuli decreased
often after heart attack
Amlodipine - Norvase
Nifedipine - Procardia
Diltiazem - Lardizam
-Meal (with meal)
-Under (100 systolic)
-Calcium
-HTN

40
Q

Exclusion criteria for thrombolysis treatment of stroke

A

Stroke management requires quick identification as patient may be eligible for thrombolysis.
History exclusion >3hr, seizure, Bgl 22 mmol/. AMI >7 days < 3mth, stroke or serous head trauma < 3mth, major surgery 14 days, GIT urinary haemorrhage 21 days.
Pregnant, check haemorrhage risk INR, platelet, BP >185/>110,

NUR 3002 (8 decks)

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