NUR 305 exam prep Sam Fox Flashcards
Name the four components of psychological patient care
- Anxiety
- Delirium
- Pain
- Sleep
Name six precipitating factors of anxiety
- Concern about current illness/underlying chronic disease
- Current experiences and feelings
- Current care interventions
- Medication side effects
- Environmental considerations
- Concern about ongoing impact of illness on recovery
List four reasons why patients may have anxiety
- Patient is overly dependent on the nurse
- Are occupied with internal dialog
- Have a long term recovery ahead
- Perceive treat to their wellbeing
List four contributing factors of anxiety
- Duration and severity of illness
- Loss of sense of control
- Impact of illness on the family
- Frequency and complexity of invasion interventions
List and briefly discuss two types of anxiety management
- Pharmacological treatment – treat pain & any other reversible psychological causes of anxiety and agitation
- Non-Pharmacological treatment – such as: massage, music therapy & noise reduction
Sleep deprivation in patients who are critically ill is often attributed to:
a) Bed baths during the evening shift
b) Untreated pain & anxiety
c) Family visiting
d) Altered melatonin levels
b) Untreated pain & anxiety
Discuss how nurses can help promote patients sleep
Plan treatments together, daily baths to suit the patients requirements, reduce environmental noise, encourage quiet time, reduce lighting and interventions.
What are the normal ABG values?
pH 7.36 - 7.44
PaC02 35 - 45 mmHg
Pa02 80 - 100 mmHg
HC03 22 - 32 mmEq/L
Base excess + - 3 Eq/L
Sa02 > 94%
Interpret the following:
pH - 7.48
PaC02 - 30 mmHg
Pa02 - 90 mmHg
HC03 - 24 mmEq/L
Sa02 - 98%
pH = >
PaC02 =
Acidosis / alkalosis readings =
acidosis alkalosis
6.8 8
= =
Death Death
pH homeostasis = 7.36 - 7.44
Metabolic readings:
pH and C02 go in equal direction = metabolic
pH, > C02 =
metabolic alkalosis
Respiratory readings:
pH and C02 go in opposite directions = respiratory
C02 =
Respiratory acidosis
> pH,
R.O.M.E stands for?
Respiratory
Opposite
Metabolic
Equal
Recognition of uncompensated blood values:
If pH, PaC02 and HC03 are abnormal
uncompensated
Recognition of compensated blood values:
If pH is normal - but - PaC02 and HC03 are abnormal
=
Compensated
Ventilation (VQ) Perfusion ratio
- Ventilation and perfusion differ depending on the region of the lung. On average, the alveolar ventilation is about 4 L/min.
- Normal pulmonary capillary blood flow is about 5 L/min
- Therefore, ventilation/perfusion ratio is 4:5, or 0.8. (VQ = 0.8)
Metabolic Acidosis S and S:
• resp rate and depth,
Metabolic Alkalosis, S and S:
- > pH > Bicarbonate
- > bicarbonate in the ECF
- Commonly due to vomiting, gastric suction, long term diuretics = fluid loss
- Hypokalaemia produces alkalosis
- S and S:
Respiratory Acidosis, S and S:
- PaCO2
- > Carbonic acid in the ECF
- Due to resp problem with inadequate excretion of CO2 (COPD)
- Body may compensate or may to asymptomatic
- S and S: > HR, > RR, > BP, mental changes, feeling of fullness in head, >? intracranial pressure, alveolar hypoventilation, alveolar hyperventilation, mechanical ventilation, inadequate perfusion
- Treatment: need to improve ventilation
Respiratory Alkalosis, S and S:
• > pH,
What are the two different types of oxygen delivery systems?
- High flow oxygen system – venturi mask
• Guarantees FI02 irrespective of breathing pattern
• High & low concentrations are possible - Low flow oxygen system – all other devices
• Mixes with room air
• Is influenced by breathing pattern
Disassociation curve:
- In the tissues the oxygen – haemoglobin dissociation curve shifts to the right as the pH increases or temperature rises
- In the lungs, the oxygen – haemoglobin dissociation curve shifts to the left as the pH increases or the temperature falls resulting in an increased ability of haemoglobin to pick up oxygen
Disassociation curve:
In the TISSUE the oxygen – haemoglobin dissociation curve shifts to the RIGHT as the pH increases or temperature rises
= lower affinity for oxygen (not good)
• In the LUNGS, the oxygen – haemoglobin dissociation curve shifts to the LEFT as the pH increases or the temperature falls resulting in an increased ability of haemoglobin to pick up oxygen
= the greater the affiniuty for oxygen (good)
CPAP (Continuous Positive Airway Pressure)
- Support for spontaneously breathing patients & ventilated patients
- Non-invasive via a mask
- Addition to mechanical ventilation
- Raised positive pressure assists in reducing the work of breathing on inspiration
- Increases gas exchange and reduces hypoxia
- Commonly used in patients with: pulmonary oedema, COPD & asthma
While CPAP generally delivers a single pressure, BiPAP delivers an inhale pressure and an exhale pressure
BiPAP (Bilevel positive airway pressure)
Involves:
IPAP (Inspiratory positive airway pressure
• A higher pressure is delivered on inspiration
EPAP (Expiratory positive airway pressure)
• Lower pressure but still positive on expiration
BiPAP is sometimes used in patients who have pulmonary lung issues, like COPD. The difference in pressures helps to eliminate extra CO2 carbon dioxide gas from the body.
NIV, CPAP and BiPAP are all commonly used in?
- High dependency patients
- Neurological disorders ( Guillain Barre syndrome)
- Obstructive sleep apnoea
- COPD
- Asthma
- Post intubation weening issues
Clinical conditions for mechanical ventilation include?
- Respiratory failure (type 1, post anaesthetic)
- Acute lung injury
- Asthma
- Pulmonary embolism
- Pneumonia
- Severe acute respiratory syndrome
Mechanical Ventilation Parameters
- Fraction of inspired 02 (Fi02) os 0.6 = 60%
- Inspiratory : expiratory ratio
- Tidal volume / minute volume
- Ventilator breath rate
- Pressure support
Type 1 and type 2 respiratory failure
Type 1: Post anesthetic Lung injury Asthma Pneumothorax (collection of air in the cavity causing the lung to collapse) Pneumonia
Type 2: Asthma COPD Upper airway Obstruction
Clinical markers of shock:
- Lactate & acid base disturbances
- Need to assess – ABG, pH, base excess
- Increased lactate is a warning sign of organ failure
02 delivery
Nasal canula 2 - 4L/min
25 - 45%
Venturi 4 - 8 L/min
24 - 50% (COPD)
Hudson 6 - 10/Lmin
40 - 60%
Non-rebreather 10 - 15 L/min
60 - 100%
Clinical markers of shock:
- Lactate & acid base disturbances
- Need to assess – ABG, pH, base excess
- Increased lactate is a warning sign of organ failure
definition of shock?
Homeostatic imbalance occurs between nutrient supply and demand
Is the inability of the body to meet the metabolic demands of the tissues = hypoperfusion (the amount of 02 reaching the cells)
Adaptive responses can no longer accommodate circulatory changes
Clinical markers of shock:
- Lactate & acid base disturbances
- Need to assess – ABG, pH, base excess
- Increased lactate is a warning sign of organ failure
List the early indicators of shock
- Tachycardia
- Altered GCS
- Cold skin
- Tachypnoea
- Shallow resps
6.
There are five main sites for significant blood loss:
“on the floor and 4 more”
a.) external haemorrhage.
b.) in the chest i.e. haemothorax.
c.) in the abdomen. Spleen and liver are common.
d.) pelvic fractures.
e.) long bone fractures.
Feel: Skin temp., capillary refill. Pulse rate and volume.
(Use a central pulse – femoral or carotid)
You should have already examined the chest. Inspect the abdomen.
Palpate the pelvis. Look for signs of long bone fractures. Useful adjuncts at this stage include a urinary catheter and a nasogastric tube.
There are five main sites for significant blood loss:
“on the floor and 4 more”
a. ) external haemorrhage.
b. ) in the chest i.e. haemothorax.
c. ) in the abdomen. Spleen and liver are common.
d. ) pelvic fractures.
e. ) long bone fractures.
Feel: Skin temp., capillary refill. Pulse rate and volume.
(Use a central pulse – femoral or carotid)
You should have already examined the chest. Inspect the abdomen.
Palpate the pelvis. Look for signs of long bone fractures. Useful adjuncts at this stage include a urinary catheter and a nasogastric tube.
There are five main sites for significant blood loss:
“on the floor and 4 more”
a.) external haemorrhage
If blood is not on the floor it could be….
b. ) in the chest i.e. haemothorax
c. ) in the abdomen. Spleen and liver are common
d. ) pelvic fractures
e. ) long bone fractures
Feel: Skin temp., capillary refill. Pulse rate and volume.
(Use a central pulse – femoral or carotid)
You should have already examined the chest. Inspect the abdomen.
Palpate the pelvis. Look for signs of long bone fractures. Useful adjuncts at this stage include a urinary catheter and a nasogastric tube.
Name the types of shock
- Hypovolemic
- Cardiogenic
- Distributive shock:
• Sepsis
• Anaphylaxis
• Neurogenic
Identifying types of shock:
Primary Survey: A – E assessment
Secondary Survey – top to toe
Identifying types of shock:
Primary Survey: A – E assessment
Secondary Survey – top to toe
Hypovolemic Shock:
- Low volume of blood or fluid – bleeding (internal/external), vomiting, diarrhoea, burns, dehydration
- Most common cause is bleeding
- Easy to diagnose & treat
Treatment of hypovolemic shock:
- Rapid A - E
- Secure airway/breathing
- Fluid resuscitation
- Increase preload - cardiac output
- minimize further fluid loss
- Fluid infused to reflect loss (burns = plasma, hemorrhage = blood/colloid/crystalloid) to maintain agreed MAP and SBP
- NOTE: can cause overload- need to monitor ABGs, Vitals, cap refill
- Keep patient warm
- Bolus dose = Vol/Kg
- Prepare for theatre
Cardiogenic Shock
• Is the inability to maintain adequate perfusion despite adequate circulatory volume
02 is not clinging to the molecules and therefore, not reaching the tissue
Shift to right of dis curve = high affinity
Base excess is out of normal range (+- 3) = compensating
(body has used up all compensatory mechanisms) = deterioration
- Increase lactate = warning sign of organ failure
• Difficult to diagnose
• Usually occurs within 48 hrs after a MI
• Main cause if left ventricular failure
- Mortality 50 - 80%
Cardiogenic shock S and S:
- Low cardiac output
- Sever pulmonary congestion (feel like drowning)
- Hypotension 10 sec
- Anxiety
- Dyspnea (
Cardiogenic treatment:
- Multi system approach
- Frequent assessments
- Increase oxygen supply – CPAP / BiPAP as required
- Decrease physical activity
- Holistic care & support
- ?fluids
- Inotropes
Inotropes:
Inotropes are a group of drugs that alter the contractility of the heart. Positive inotropes increase the force of contraction of the heart, whereas negative inotropes weaken it.
Inotropes are indicated in acute conditions where there is low cardiac output (CO), such as cardiogenic shock following myocardial infarction, acute decompensated heart failure and low CO states after cardiac surgery.
Reduced CO leads to tissue hypo-perfusion and subsequent hypoxia. Metabolism switches from aerobic to anaerobic, resulting in the formation of lactic acid. If left untreated, this can result in multi-organ failure and death
Disruptive shock
• Tissue has impaired oxygen & nutrient delivery • Failure of the vascular system • Leading to widespread vasodilation Septic shock Anaphylaxis Neurogenic
Septic Shock
• Is systematic inflammation –
Caused by – sepsis, burns, pancreatitis, trauma
• restricts blood flow
• oxygen delivery to tissue is compromised
• cardiac output increases
• hypovolemia occurs – the blood dilates & distributes
• the patient will need >fluid to accommodate tissue = which is bad, the blood will continue to expand & the patient will become over loaded
• patient will present – warm, pink & well perfused
• decompensation will lead to cell death & multiple organ failure
Treatment for septic shock
similar to hypovolemia, assess, fluid management, treat underlying infection, administer inotrope vasopressin
Anaphylaxis
• severe allergic reaction
• 1st expose to the allergen – no anaphylaxis (poss reaction)
• 2nd exposure to allergen = anaphylaxis
Patient may present - anxiety, dizzy, faint, stridor (high pitch sound), wheeze, tachypnoea, dyspnoea (SOB), pharyl/laryngeal oedema, bronchospasm, cyanosis, tachycardia, hypotension, arrhythmias, N & V, diarrhoea, rash, itchy, erythema
Anaphylaxis treatment
Rapid A - E
- Adrenaline
- Antihistamine
- Corticosteriods
Neurogenic shock
- spinal shock
• Spinal cord injury above T6
• Commonly caused by trauma
• Loss of vasomotor tone – disruption to neural output
Neurogenic shock S and S:
Hypotension ( HR does NOT occur
Neurogenic treatment
- ABC
- Stabilise neck & torso
- Fluids if needed
- Resp assessment (risk of pneumonia & atelectasis
- Maintain core temp
- Initiate NBM
- Pressure area care
Name four areas of nursing care for shocked patients
- Rapid A – E
- Holistic care – involve family
- Communication – patient, staff, family
- Interventions – fluids, obs, scribe, meds, transfer
Remember VIP - shock
Ventilation - airway, added and ventilation
Infusion - of appropriate volume expanders
Pumping - improve heart pumping with drugs - antiarrythmics, inotropes, diurectics, vasodilators
Patient assessments for shock
- Cardiovascular
- Neurological
- Renal function - insert catheter to measure urine output
Observations for shock include:
Resps, Temp, HR, BP, Sa02, U/o, GCS, ABGs, - bloods to measure lactate = > lactate warning sign of organ failure cardiac output – central line
Vasopressors:
class of drugs that evlevate mean arterial pressure by inducing vasoconstriction
common inotropes
Heart failure:
- Dobutamine
- Dopamine
Septic shock, Cariogenic shock, anaphlatic shock, neurogenic shock and hypotension (following anesthethic):
- Adrenaline - Epinephrine
- Phenlepfine
- Noradrenaline
second line agent for septic and anaphlatic:
- Vasopressin
Treatment pathway for shock
fluid resus medication management theartre rehab transfer - ICU, spinal unit
Cardiac conduction system
- Sinoatrial - SA node (pacemaker) fires
- excitation spreads through atrial myocardium
- Atrioventricular - AV node fires
- Excitation spreads down AV bundle
- Perkinje fibres distribute excitation through ventricular myocardium
Need to find where the blockage is to know the extent of damage
- large arteries = > damage
* artery branches =
Cardiac output
- the amount of blood pumped by the heart each minute
- regulated by homeostatic mechanisms
- regulated in response to stress & disease
- is affected by preload, afterload & contractility
- critically ill patients do not compensate as well as healthy people
- maybe unable to >HR to compensate BP & hypertension
Cardiac output - CO =
HR x Stroke volume
Stroke Volume
• the volume of blood pumped with heart beat (50-100ml/beat)
Preload
Pressure of stretch exerted on the walls of the ventricle by the volume of blood filling the ventricles at the end of diastole; used as an indication of volume status
Factors that can reduce preload:
- volume loss – haemorrhage
- venous dilation – hyperthermia / medication
- tachycardia’s AF / super ventricular tachycardia (SVT)
- raised intrathoracic pressure – need to use NIV, BiPAP, CPAP
- raised intracardiac pressure – tamponade - Cardiac tamponade is pressure on the heart that occurs when blood or fluid builds up in the space between the heart muscle (myocardium) and the outer covering sac of the heart (pericardium).
- Body position can affect preload due to the effect on venous return
Central venous pressure (CVP)
• Preload of the right ventricle measured by the CVP
Contractility
The ability of a muscle to shorten when stimulated; in particular the force of the myocardial contraction
• Is difficult to measure clinically
• Decreased by:
1. Hypoxia Both cause MI’s
2. Ischemia
3. Drugs: thiopentone, calcium channel blockers
• Increasing contractility will increase myocardial oxygen demand
Mean Arterial Pressure (MAP)
• Average pressure within the arterial system throughout the cardiac cycle 70 – 90 mmHg
Assessment of CO & haemodynamic monitoring
- Establish Dx
- Determine therapy & monitor response to it
- Heart rate & rhythm - 4 or 5 lead or 12 lead ECG
- Non- invasive monitoring – obs, check all pulses (don’t just relay on monitors)
- Invasive – catheter – arterial pressure monitoring, central venous pressure, pulmonary artery pressure, pulmonary capillary wedge pressure
ECG - Calculate the rate:
- Count the number of large boxes between R to the next R
* Divide 300 by the number of large squares
Electrical activity with the associated ECG pattern
Atrial Depolarization = P wave Delay at AV node = PR segmant Ventricular Depolarization = QRS complex Ventricular Repolarisation = T wave No electrical activity = Isoelectric line (the flat line at the end before it starts again)
Causes of chest pain - cardiovascular
Myocardial ischaemia Coronary artery spasm (angina) Myocardial infarction Pericarditis Pulmonary embolism Mitral valve proplapse Ca - usually secondary cancer
Causes of chest pain - Non-cardiovascular
Dissecting thoracic aneurysm Herpes zoster Oesophageal reflus and spasm Hiatus hernia Pneumonia Pneumonthorax Pleurisy Peptic unlceration Gallbladder disease Musculoskeletal pain Costochondritis
Costochondritis
- Inflammation of the intercostal muscles
- Musculoskeletal pain 10/10
- Non-specific, non-localised (everywhere)
- Resembles MI but clear ECG
- Non-reactive to morphine
- Need I’m ibroprofen
- Skin is pale & sweaty
Stable angina
• Often relieved by rest alone
Symptoms – chest discomfort
Unstable angina
• May come on at rest
Symptoms – Acute MI (occlusion)
Sudden death
Management of angina
- A – E assessment
- 02 at 6L / min via Hudson mask
- Medication as prescribed
Administer 02 b/c of the active chest pain even if sats are normal, however, studies show with holding 02 > survival rates as the body is forced to use the 02 it has in a much better way
Risk factors for CHD -
Non-modifiable
Age Gender Ethnicity Genetic predisposition Low birth weight Diabetes Hormonal/biochemical factors
Risk factors for CHD -
Modifiable
Blood cholesterol Tobacco smoking High BP Overweight/obesity Diet Alcohol consumption Social class Geographical distribution
Acute coronary syndrome
Includes all cases of unstable angina and acute MIs
Underlying pathology is the abrupt, complete or partial obstruction (occlusion) of a coronary artery
Most often triggered by the rupture of an atheromatous plaque
Nearly all deaths from CHD are the result of MI
Myocardial Infarction -MI
Arises when a region of the myocardium becomes irreversibly necrosed.
It is usually due to thromboembolic occusion of the coronary artery supplying that are of the heart muscle
ST elevated segment
All of the myocardium is being damaged
Chest pain assessment:
PQRST
P – What happened, sitting down? Running?
Q – Where is it, how does it feel, stabbing, crushing?
R – Do they have pain anywhere else? Shoulder, jaw?
S – Rating out of 10
T – When did it start?
MI stats
Each year, around 54,000 Australians suffer a heart attack.
More than 100,000 patients
Symptoms of MI
Pain: Chest Left arm Right arm Both arms Neck Jaw back
Skin: Pale Sweaty Clammy cyanosed
Respiratory:
Tachypnoea
Dyspnoeic
Pulmonary oedema
Physical signs:
Nausea
Vomiting
Psychological:
Anxiety
confusion
MI Dx
Patient History
Symptoms
ECG
Bloods
Obs / monitoring MI
Reassure patient – rest Baseline observations ? Need for cardiac monitoring 12 lead ECG IV access Troponin (T & I) levels and cardiac enzymes (CK – creatine kinase) Contact Dr
MI treatment
Thrombolysis
PCI (Percutaneous coronary intervention) Previously called Angioplasty
Thromobolysis
The development of thrombolysis is the single most important advance in the care of coronary patients since defibrillation
Mortality is approximately 30% less than if patients are left untreated, and the NSF for CHD recommended:
Thrombolysis be given within 60 minutes of a call for help
Within 20 minutes of admission to hospital
However, Thrombolysis is now secondary treatment pathway
Types of thrombolytic agent
Streptokinase. Most widely used, and cheapest. A bacterial protein. Patients develop antibodies, and can only be given once.
Recombinant tissue-type plasminogen activator (tPA). A naturally occurring human protease that is fibrin specific and this works predominantly on the clot, with less risk of systemic bleeding
Retaplase. A new generation, appears to be as effective as streptokinase. However can be given as a bolus and is non-antigenic
PCI (Angioplasty) - Primary treatment pathway
Invasive procedure
Access through femoral artery
Catheter inserted into coronary artery
Balloon inflated in CA to open stenosed area
Stenting carried out at same time if required
Risk of cardiac arrhythmias/cardiac arrest
