Everything else Flashcards

1
Q

Signs and symptoms if the left ventricle is affected

A

Shortness of breath, tachypnea and respiratory crackles

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2
Q

Signs and symptoms if the right ventricle is affected

A

distended neck veins, liver enlargement , anorexia and nausea

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3
Q

At risk for heart failure sections and classes

A

At Risk for Heart Failure
* Stage A. At high risk for heart failure, but without structural disease or symptoms of heart failure
* Stage B. Structural heart disease, but without signs or symptoms of heart failure
Cardiac Failure
* Stage C. Structural heart disease with prior or current symptoms of heart failure
* Stage D. Treatment-resistant heart failure requiring specialized intervention

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4
Q

Nursing care for CCF

A

 Maintain the patient in high fowler’s position
 Elevate extremities
 Frequently monitor vital signs
 Change position frequently
 Monitor intake and output and daily weight
 Restrict fluids as ordered

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5
Q

Signs and symptoms left-sided HF

A

ONE: Nearly all of these symptoms can be seen in heart failure, particularly left-sided failure (PND, orthopnea, crackles, S3 gallop).

TWO: Pulmonary Edema: Crackles, dyspnea, orthopnea

THREE: Shock/Hypoxia: Cold, clammy skin, cyanosis, fatigue,

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6
Q

Signs and symptoms right-sided HF

A

Peripheral oedema
jugular venous distension
Hepatomegaly
Abdominal pain
Nausea
Anorexia
Bloating

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7
Q

Diagnostic studies for CCF

A
  1. Electrocardiography (ejection fraction)
  2. MRI
  3. Computed tomography imaging
  4. Cardiac catheterization with angiography
  5. A biopsy of heart muscle may be needed
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8
Q

Complication/largest risk for CCF

A

Pulmonary edema

Acute pulmonary edema is defined as the sudden increase in PCWP - Pulmonary capillary wedge pressure (usually more than 25 mm Hg) as a result of acute and fulminant left ventricular failure. It is a medical emergency and has a very dramatic clinical presentation. The patient appears extremely ill, poorly perfused, restless, sweaty, tachypneic.

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9
Q

AKI Pathophysiology/phases/S+S

A

Acute Kidney Injury (AKI) is a sudden and almost complete loss of kidney function over a period of hours to days.

Glomerular injury, vasoconstriction of capillaries or tubular injury due to sepsis, trauma, nephrotoxins etc. can lead to:
Oliguria (less than 400 mL/day of urine) or anuria (less than 50 mL/day of urine.

High serum creatinine and blood urea nitrogen levels (azotemia) and retention of other metabolic waste products normally excreted by the kidneys.

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10
Q

AKI diagnostic studies

A

Kidney Function Tests:

Blood Urea Nitrogen (BUN) & Creatinine: Elevated levels indicate impaired kidney function.
Complete/Full Blood Count (CBC):

Used to detect underlying conditions that could contribute to or result from AKI.
Serologic Tests:

Assess for autoimmune or infectious causes.
Electrolytes:

Look for imbalances, particularly potassium, sodium, and bicarbonate, which are often disrupted in AKI.
Bladder Pressure Measurement:

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11
Q

AKI Nursing management

A

Auscultation (Lung and Heart Sounds):

Monitor for: Fluid overload, which may lead to pulmonary oedema and heart failure.

Signs: Adventitious breath sounds (crackles), extra heart sounds (e.g., S3, S4).
Assess Level of Consciousness:

Monitor for: Changes in mentation or restlessness.
Indicates: Potential fluid shifts, toxin accumulation, acidosis, electrolyte imbalances, or hypoxia.
Interventions:

Fluid Replacement:

Plan with patient: Set fluid intake within prescribed restrictions.
Suggestions: Offer a variety of drinks (hot, cold, frozen) spaced throughout the day.
Goal: Reduce feelings of deprivation and thirst.
Correct Reversible Causes of Acute Renal Failure (ARF):

Examples:
Replace lost blood.
Maximize cardiac output.
Stop nephrotoxic drugs.
Relieve obstructions (surgery).

Outcome: Restoring normal kidney function and preventing lasting damage.
Skin Care:

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12
Q

AKI clinical assessment/findings

A

Skin:
Digital ischemia, butterfly rash, palpable purpura: Suggests systemic vasculitis.
Maculopapular rash: Indicates allergic interstitial nephritis.

Track marks: Points to intravenous drug abuse.

Eyes:
Dry conjunctivae: Seen in autoimmune vasculitis.

Jaundice: Indicates liver diseases.

Band keratopathy: Associated with hypercalcemia.

Retinopathy: A sign of systemic diseases affecting the kidneys.

Pulmonary System:
Rales: Could indicate fluid overload or pulmonary edema.
Hemoptysis: May suggest an underlying pulmonary-renal syndrome or severe infections.

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13
Q

Complications AKI

A

Fluid Volume overload: Acute kidney failure may lead to an excess of fluid in the lungs, which can cause shortness of breath (Pulmonary oedema).

Neurological disorders: Siezures may occur with the increase in nitrogenous waste accumulating.

Hyperkalaemia: Elevated levels of potassium in blood are particularly dangerous. At risk of developing a life threatening arrhythmia.

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14
Q

Aetiology Resp Failure

A

Smoking
Obesity
^Age
Trauma
Near drowning
Sepsis
Lung diseases (COPD)
Asbestos/chemical inhalation

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15
Q

ARDS diagnostic criteria

A

1Acute onset
2Bilateral pulmonary infiltrates on CXR
3No evidence of left ventricular heart failure

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16
Q

resp failure pathophys types one and 2

A

T1 (HYPOXEMIC too little O2)
PO2 less than 60mmHg or 50PCO2 unaffected
T2 (HYPERCAPNIA too much co2)
Too much PCO2, greater than 50mmHg

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17
Q

Main S+S ARDS

A

^HR, ^RR, RESP alkalosis (Blood PH rising because not enough O2), resp crackles.

18
Q

Treatment Resp failure

A

Antibiotics + Corticosteroids
chest exercise + suctioning
Fluid resuscitation
O2 therapy, nebs, humidify.

19
Q

ARDS pathophys primary insult to resp failure chart

A

triggers inflammatory response - becomes too much for blood vessels in alveoli space - decreased vascular permeability - fluid shift alveoli and into lungs - decreased surfacant production and decreased lung compliance - poor gas exchange -

20
Q

Aetiology of cardiac disturbances

A

Genetics, older age, CCF, AKI, pulmonary diseases

21
Q

Cardiac disturbances pathophys

A

Electrical misfiring in the heart, further in the SA node, purjunki fibres and bundle of his. The electrical misbalance effects the contractibility and it cannot fill to pump correctly. Not enough blood gets through systemic circulation. Decreased tissue perfusion = cell ischemia.

22
Q

Complications of a cardiac arrythmia

A

Stroke
Death

23
Q

Signs and symptoms cardiac arrythmia

A

decreased GCS, Increased RR and decreased O2.

24
Q

Treatment for cardiac disturbances

A

Cardioversion, echocardiogram, beta blockers, angiogram (stents).

25
Which heart rhythm is mono / polymorphic ??
VT
26
Sepsis Aetiology
Lung infections, older age, infant, malignancys, wound infections,
27
discuss some physiology behind sepsis signs
1) hypo / low map reduced blood volume in systemic circulation, as blood vessels have become leaky due to an influx of white cell mediators. Blood forced out of vessels resulting in reduced volume pumped by heart 2) reduced BV results in decreased tissue perfusion, as hemoglobin helps to carry O2 to tissues, isnt happening therefore increase CO2 is in the tissues + pt ^ RR as they trying to get more O2 perfusion into tissue 3) hypoxic inadequate blood flow and subsequent O2 - therefore cell ischemia + inability for tissues to function correctly - therefore GCS/confused as hypoxic
28
pathophysiology sepsis
1) primary insult - response to pathogen 2) Increase cytokines produces dysregulated inflammatory response 3) influx of cell mediators, disrupts vascular permiability - blood leaks from vessels into extracellular matrix. 4) results in decreased systemic circulation, blood pooling, decreased tissue perfusion. 5) cell ischemia 6) tissue death 7) multiorgan failure
29
Trauma aetiology
depends on MOI blunt (baseball bat) mechanical thermal (hot/cold) chemical (acid) electrical O2 dep Radiation expos
30
brief pathophys trauma
MOI - causes inflamm response - vasoconstriction/shock therefore increase HR, RR, SBP, decrease o2
30
Nursing interventions trauma
1) FNO (establish if brain, peripheries, muscle and skin receptors are functioning effectively) 2) C.spine Precautions (ensure stability of cervical spine has not been compromised) 3) Falls risk assessment (could result in further injury)
31
Trauma in special populations (paediatric + pregnant)
Pregnant Supine Hypotensive Syndrome Keep pregnant patients in left lateral decubitus position to avoid excessive hypotension Paediatric treatment focus: 1) Fluid resuscitation – 20ml/kg of 0.9% saline and repeat if necessary 2) Treat raised intracranial pressure – 20% mannitol or 3% saline
32
Complications of trauma
1) Tension pneumothorax MIDLINE SHIFT + ATELECTASIS influx of air into pleural space, resulting in ^ pressure therefore causing decreased space for lung expansion. S+S ?: WOB, SOB, incr RR, uneven breath sounds. 2) Haemothorax - penetrating trauma Blood collecting in pleural space S+S: decreased SBP, increase WOB, SOB, increased RR, diminished breath sounds. 3) Flail chest 2 or more broken ribs that move seperately when breathing. 4) Open pneumothorax Opening of chest cavity where air enters pleural space. Increased air pressure and decreased ability for lungs to expand. S+S: Increased RR, decrease O2, impairs O2 ventilation.
33
Cardiac tamponade
- Blood filling in pericardium - Becks triad 1hypotension 2distended jug veins 3muffled heart sounds
34
types of shock in trauma
ALL decrease tissue perfusion, hypoxia, decrease GCS + SBP with increase HR 1haemorrhagic 2obstructive (CT + tension pneu) 3Neurogenic shock *SPI
35
Treatment for Ten Pneu
1needle decompression 2nd intercostal space, midclav 2tube thoracostomy 5th intercostal anterior axillary line
36
difference bet tracheostomy + cricothrotomy
cricothyrotomy is usually done in an emergent situation when you are unable to intubate someone and need to get access to someone's airway in a hurry. It's done through the cricothyroid membrane (through the Adam's apple). A tracheostomy is placed lower down in the trachea, between the tracheal rings. It can be placed in an operating room or at the bedside in an ICU setting. It is usually placed if someone is going to need the support of a ventilator for a long time This allows the patient to talk and not have the extreme discomfort of a tube going down his mouth into his trachea.
37
stroke risk factors
hypertension, age, DVT prev, bad lifestyle choices etc
38
stroke treatment
Anticoagulant + antiplatelet, angiogram (blood clots + vessel issues)
39
purpose of fluid administration
Fluid Administration: Plasma Volume Expanders Goal: To restore intravascular volume by boosting oncotic pressure space. Effect: Increases several hemodynamic factors: Central Venous Pressure (CVP) Cardiac Output Types of Fluid Expanders: 1. Crystalloid Solutions Common Types: Normal Saline Hartmann’s Solution (CSL) Characteristics: Balanced salt solutions that easily cross capillary walls. Half-Life: 30 to 60 minutes (O'Neill, 2011). Usage: Cause rapid but short-lived plasma expansion. Effective for fluid replacement or maintaining fluid balance. Can be combined with colloids to sustain plasma volume expansion Colloid fluids Commonly used colloids include: ● Gelatins (Gelofusin) ● Albumin 4% or 20% (albumex) Colloids are better than crystalloids at expanding the circulatory volume, because their larger molecules are retained more easily in the intravascular space and increase osmotic pressure. Gelatins can cause anaphylactic reactions and there is concern regarding the possible transmission of bovine spongiform encephalopathy (Mad cow disease) Products also used if shock is due to hemorrhage  whole blood  Packed RBC’s