Pathophysiology Flashcards
1
Q
preterm
A
23-<37 weeks gestation
1
Q
pregnancy term
A
37-42 weeks gestation
2
Q
pregnancy show
A
vaginal discharge of mucous and blood
3
Q
spontaneous rupture of membranes
A
gush of normally clear or pink fluid. Can occur prior to the onset of labour until the baby is born
4
Q
meconium-stained amniotic fluid
A
greenish/brain-stained amniotic fluid
5
Q
first stage labour
A
onset of regular painful contractions to full cervical dilation (i.e. contractions every 2-20minutes, 20-60 seconds duration)
Onset of painful regular, strong, rhythmic contractions resulting in dilation of the cervix until it is 10cm dilated cervix. The initial contractions are 15–30 minutes apart and 10–30 seconds in duration and can be felt at the fundus where they begin. Contractions eventually last 30-90 seconds and can come less than two minutes apart.
Crowning occurs
6
Q
second stage labour
A
full cervical dilation to the birth of a baby (typical duration primipara 1-2 hours, multipart 15-45 minutes)
7
Q
Imminent birth presentation
A
Imminent Delivery
- Active pushing/grunting
- Rectal pressure (urge to use bowels or bladder)
- Anal pouting
- Bulging perineum
- Urge to push
- Crowning (presenting baby’s head)
- mother’s statement “I am going to have the baby”
8
Q
Precuoutate birth
A
usually rapid labour (less than 4 hours) with extremely quick birth). The rapid change in pressure from intrauterine life may cause cerebral irritation
9
Q
causes of PPH
4 T’s
A
- tone: uterine atony ( a soft and weak uterus after childbirth)
- trauma: to genital structures
- tissue: retention of placenta or membranes
- Thrombin: coagulation
10
Q
who is more at risk for PPH
A
- multiple pregnancy
- had more than 4 pregnancies
- past history of PPH
- history of APH
- large baby
11
Q
Pathophysiology of pain:
A
A physiological and emotional response to a noxious stimulus with the potential to cause tissue damage. Pain is subjective and has two aspects, physiological and psychological. Pain stems from pain receptors detecting a painful stimulus and sending the message to the brain, allowing the relevant body parts and pathways to react with pain, swelling and other reactions. Each patient experiences pain differently, and different kinds of pain present in different ways, such as acute and chronic.
12
Q
What are the major airway reflexes and what is their role in protecting the airway?
A
- Contraction of oropharyngeal muscles move food along. During swallowing, the epiglottis moves posteriorly against the glottis preventing food entering the trachea
- Protective reflexes in the upper airway help keep foreign bodies out
- A cough reflex stimulated by laryngeal and respiratory tract receptors involves forced exhalation against a closed glottis which then vigorously expels the air in the lungs as the glottis opens
- The gag reflex (also known as the pharyngeal reflex) – the muscles of the pharynx can contract if stimulated by an unwanted object in the throat producing a forceful expulsion to help prevent choking
- In some cases, the vocal cords within the glottis can close temporarily and occlude the airway from anything entering. This occurs early in drowning keeping water from getting past. When muscle tone is lost, the vocal cords relax and open fully allowing uncontrolled entry to occur where consciousness has been lost
13
Q
What are the four different groups of airway obstruction that can be encountered?
A
Anatomical – positional:
- The tongue and epiglottis are designed to fall back and cover the glottis during swallowing. If consciousness is altered, this airway reflex loses its control since the tongue is a relatively large muscle
Anatomical – Infection or inflammation:
- Infection/inflammation within the upper airway can cause obstruction
Foreign body – external:
- This is an introduced foreign object from outside the body
Foreign bodies can become trapped by pushing the epiglottis down on to the glottis, by lodging within the glottis itself or, if small enough, pass beyond the glottis and lodge in the trachea or bronchi
Foreign body – internal:
- Gastric content is held in the stomach by sphincters and when these relax, when consciousness is lost, it allows the possibility of passive regurgitation (rather than active vomiting)
14
Q
How may larger and obese patients be managed differently?
A
May require modified sniffing position to allow laryngoscopy since increased chest diameter impedes neck flexion.
Correct angle is achieved through ‘ramping’ by either stacking padding beneath the shoulders and head or, alternatively, raising the upper back of the bed/trolley to place the patient’s entire back into a semi-upright posture of approximately 25°.
15
Q
Can you describe the clinical benefits of application of CPAP therapy to the patient presenting with acute pulmonary oedema?
A
- It supports inspiration (inspiratory positive airway pressure) and resists expiration (expiratory positive airway pressure)
- By retaining a small volume of air within the alveoli on expiration, they remain inflated. This has two critical advantages:
- They don’t have to be reopened each breath. This decreases the work of breathing dramatically
Also, alveoli that collapse don’t participate in gas exchange. Alveoli kept open do. All these together dramatically improve oxygenation
16
Q
Describe the clinical benefits of application of CPAP therapy to the patient presenting with acute exacerbation of COPD
A
- As the COPD patient exhales, the gas escapes from the bronchi and trachea quite easily - low airway pressure. For gas on the distal side, in the alveoli, gas escapes slowly due to airway narrowing – higher airway pressure. Change in a pressure causes an obstruction point
- This increases airway pressure which keeps the alveoli inflated for longer, allowing expiration to occur
- The net result is more air can escape from the alveoli, more CO2 is removed and increased oxygen supplied with the next inspiration
17
Q
hyperventilation
define COPD
A
Umbrella term categorised by chronic bronchitis, emphysema and chronic asthma. It’s an irreversible disease. Usually associated with cough, emphysema, airway damage, excessive mucus and sputum production. Depending on the specific disorder, emphysema or chronic bronchitis, the pathophysiology alters.
18
Q
Chronic bronchitis:
define
A
When airways are constantly attacked by pollutants, such as those found in cigarette smoke, they become inflamed and filled with thick, sticky mucous.
19
Q
Emphysema:
define
A
The exchange of oxygen and carbon dioxide takes place in the alveoli. When your alveoli are damaged or destroyed, it becomes difficult for the lungs to exchange oxygen and carbon dioxide and less oxygen gets into your body. Your lungs do not fully empty and air is trapped.
20
Q
Patient presenting with COPD
oxygen levels
A
When treating COPD patients, titrate oxygen flow to stay between 88-92%, the normal range for a COPD patient. Consider low flow oxygen (e.g nasal prongs) to stay in this range. Treat as regular severe hypoxaemia if SpO2 <85%.
21
Q
What is the purpose of endotracheal intubation?
A
- Et reaches further than an OPA/NPA
- Directs air directly into the trachea
- NPA/OPA directs air into the trachea to inflate the abdomen
- ET is direct ventilation to the lungs and prevents aspiration and vomit from getting into the airway compared to OPA/NPA/SGA
22
Q
What is the difference between RSI and DSI?
A
Rapid sequence intubation (RSI)
- Medications administered simultaneously,
- Take effect quickly (within 1 minute),
- Intubation occurs immediately after.
- Prepare patient → Medications administered → Intubation
Delayed sequence intubation (DSI)
- Sedative agent administered early to assist patient compliance
- Intubation occurs several minutes after.
- DSI is typically for patients who cannot be adequately pre-oxygenated to allow safe intubation, i.e. a patient who is agitated or under the influence of psychostimulants.
- Sedation → improved compliance → prepare patient → intubation
23
Q
What is the purpose of administering sedation prior to intubation?
A
- Sedation blunts mental awareness, via decreasing central nervous system (CNS) activity. This reduces sympathetic nervous system activity and the chance of the patient responding to the procedure, including discomfort, panic, anxiety along with physical responses of increased heart rate and blood pressure
- Eg. Ketamine, midazolam, fentanyl
24
What is the purpose of administering a muscle relaxant prior to intubation?
- What is the purpose of administering a muscle relaxant prior to intubation?
- Muscle relaxants aim to remove airway reflexes and motor activity
- Muscle relaxants, or paralysing agents, remove all skeletal muscle function. Arms, legs and, in particular, airway reflexes are stopped for the duration of the drug. The patient is unable to cough or gag and the vocal cords relax to allow intubation
- Eg. Rocuronium, suxamethonium
25
What is end tidal capnography (EtCO2)?
End tidal capnography (EtCO2) measures the proportion of carbon dioxide in exhaled air
EtCO2 monitors show two things:
a waveform of the CO2 escaping and
a numerical reading of the maximum amount of CO2 during each breath
26
What are some key functions of end tidal capnography?
EtCO2 monitoring can be used to evaluate effectiveness of ventilation
Ventilation rate and depth are calculated to approximate normal values (or in some cases intentionally abnormal values). This means a normal EtCO2 reading of 35-45 mmHg can be observed and maintained
It is considered the only definitive means to be sure the ET tube is correctly within the trachea
27
Why are the newborn first breaths so critical?
Opens alveoli for gas exchange
Decreasing intrapulmonary pressures
Decreases vascular resistance
Encourages greater blood flow into the pulmonary circulation
Breathing opens alveoli opens for gas exchange dramatically decreasing intrapulmonary pressures. This decreases vascular resistance encouraging greater blood flow into the pulmonary circulation increasing oxygenated blood flow returning from the pulmonary circulation to the left atrium and ventricle. Cardiac output and systemic blood pressure rise. The combination of cessation of blood through the umbilical cord and pulmonary and systemic pressure changes negate need for foetal circulation bypasses, encouraging their closure and transformation to newborn circulation. The absence of first breaths means much of the pressure changes necessary for circulatory evolution does not occur
28
Why is skin colour not helpful for immediate newborn assessment?
Healthy babies can look blue. Gas exchange is only just starting to build within the lungs even with immediate onset of spontaneous breathing. It can take several minutes for normal pulse oximetry values to be achieved in all babies
29
What is the role of APGAR in newborn assessment?
APGAR is NOT used as a guide for resuscitation. The APGAR system is a scoring tool for one and five minute post evaluation. Some of its components are far more indicative of need for resuscitation than others. Further, the time frames of when it is evaluated do not align at all with resuscitation need.
Do NOT wait one and five minutes to begin resuscitation!
30
What are the two key determinants to assess immediately following birth?
Is the newborn infant spontaneously breathing (or crying)?
Does the newborn infant have good muscle tone (is not floppy/flaccid)?
31
What are the principles guiding newborn cord cutting?
Wait several minutes or until cord stops pulsing to allow additional blood to increase newborns circulating volume.
However, cut the cord if there is a need to remove the newborn away from the mother to effect resuscitation.
Clamp at 10 cm distance from newborn. Place second clamp a further 5 cm. Cut in between the two clamps
32
Pathophysiology of asthma
Asthma is categorised by bronchoconstriction, chronic inflammation and increased mucus secretions. Asthma has an either an impaired autonomic control or inflammatory processes. Asthma is generally caused by an allergen which is detected by the body, such as smoke or dust, which then brings about a response. The pathogenesis of the disease is bought about by certain physiological mediators, such as histamine and prostaglandins. Once these inflammatory mediators are released, the body brings about a response which includes bronchoconstriction, chronic inflammation and increased music secretions.
33
APO
define
APO involves the accumulation of extravascular fluid in lung tissues and alveoli leading to ventilation/perfusion mismatch and an increased work of breathing. It is most commonly caused by congestive heart failure, normally left ventricular failure, but may also be attributed to non-cardiac causes. The consequence of this damage to the myocardium is a build-up of fluid within the pulmonary vasculature and a change in pressures within, leading to the movement of fluid from the intravascular space into the pulmonary space.
34
Seizure
define
A sudden, uncontrolled episode of excessive electrical activity within the brain, which can cause abnormal behaviour, altered conscious state, unnatural movement, impaired perception and altered sensations. It can be either focal or generalised in origin. Status Epilepticus: continuous/recurrent seizures with no return of consciousness between episodes. Can occur with any type of seizure and is considered a neurological emergency.
35
Time is important – by about 30 seconds after birth, the non vigorous newborn must have what commenced?
Getting the newborn breathing is the overwhelming intention. In the first instance, apply basic tactile (not rough) stimulation measures as a means of triggering muscle response and breathing
Pat dry the newborn incorporating foot tapping. Gentle but enough to provoke stimulation
Be wary of wet and slippery newborn!
Gently dry and wrap to maintain warmth as soon as practicable. Where resuscitation is being provided, consider methods to keep the newborn warm including warming the surrounding environment or heat lamp provision.
36
What must happen by 60 seconds post birth for the non vigorous newborn?
Place the head in the neutral anatomical position and commence ventilation with IPPV @ 40-60 minute
Do NOT add supplemental oxygen at this point – air resuscitation. The newborn requires ventilation and, at this point, is accustomed to poor arterial oxygenation and pulse oximetry
37
How is the heart rate determined in the non-vigorous newborn?
Auscultation is preferred over the ECG to avoid attaching electrodes to delicate skin – on right wrist due to it being the last place that is perfused
38
What is the role of airway suctioning in the non-vigorous newborn?
Suctioning can delay the necessary ventilation and oxygenation and can induce bradycardia. Only suction if airway obstruction is suspected. This occurs where there is difficulty in providing assisted ventilation but resistance is encountered. It also occurs where the newborn is attempting to breathe but appears to be having difficulty. This may be caused by airway obstruction.
Suction the mouth first, then the nose using a 10 or 12 FG catheter under low pressure ideally. Newborns are nasal breathers and may gasp and inhale any pharyngeal fluid. Use 5 second burst no deeper than the oropharynx
39
Why is body temperature maintenance critical for all newborns?
- Hypothermia increases oxygen consumption and impedes resuscitation
- Maintain newborn body heat and avoid heat loss. Remember the newborn is wet, naked and exposed to ambient air/breeze. Covering the newborn and addressing ambient air temperature is effective.
- Vigorous newborn – pat dry, lie skin to skin on mother. Maternal body heat is ideal. Cover both with blankets. Wrap the newborn as soon as practicable.
- Maintain normothermia – warm room, protect from breeze
- If resuscitation is required, ideally place the newborn on a warm surface and cover as best as possible to reduce heat loss. Place a protective cap on the newborn’s head to reduce heat loss
For the extreme preterm newborn (<28 weeks gestation) heat loss will be particularly easy and compromising. Do not dry the baby first. Place the newborn immediately inside a plastic zip lock bag with its head (pat dried) protruding
40
What amniotic fluid abnormalities can occur and what can they mean?
The cervix will eventually dilate sufficiently for the amnion to rupture and release amniotic fluid.
- Brownish/green stained fluid suggests meconium indicating foetal distress or a mature gut in a term baby.
- Heavily blood stained fluid may indicate antepartum haemorrhage.
- Offensive-smelling fluid suggests infection.
41
How can you tell the placenta is ready to be expelled?
Readiness for placental (third stage) is noted by a firm, round fundus at the umbilicus. A small fresh blood loss may be noted as the contracted uterus expels any blood within it. A lengthening of the umbilical cord might also be noted. This may be up to 30 minutes after birth. The mother will usually provide some feedback she is ready for third stage delivery including the return of the need to push and deliver the placenta. She will become uncomfortable and ask for the placenta to be delivered
42
What is the definition of primary post partum haemorrhage (PPPH)?
A small amount of blood loss post birth is normal. PPPH is more than 500ml of blood within 24 hours after birth, usually within minutes. Blood loss can be deceptive and difficult to estimate. Bleeding that appears fast or is requiring multiple towels to mop up should be considered seriously and quickly
43
How does primary post partum haemorrhage differ from secondary?
Secondary PPH pertains to period 24 hours to six weeks post birth – usually relates to infection or retained tissue post birth – this instruction does not cater for this problem
44
What are the usual causes of primary PPH?
- Tone - Atonic uterus (soft/weak) – most common cause - this is when your uterine muscles don’t contract enough to clamp the placental blood vessels shut. This leads to a steady loss of blood after delivery.)
- Trauma – concealed (uterine, cervical, vaginal) or visible perineal tear
- Bleeding disorder – if take mediation that encourages clotting (hear) - (If you have a coagulation disorder or pregnancy condition like eclampsia, it can interfere with your body’s clotting ability. This can make even a tiny bleed uncontrollable)
- Retained tissue post-birth - retained placental tissue: This is when the entire placenta doesn't separate from your uterine wall. It’s usually caused by conditions of the placenta that affect your uterus’s ability to contract after delivery.
45
Why do we use Tranexamic acid for PPH?
It reduces bleeding by inhibiting the enzymatic breakdown of fibrin
46
Why do we use oxytocin in PPH
Oxytocin stimulates uterine muscles to contract
- Oxytocin is released from the posterior pituitary and increases uterine contractions by stimulating prostaglandin production and increasing intracellular calcium ion levels in myometrial cells (The muscular outer layer of the uterus)
47
define shoulder dystocia
Shoulder dystocia refers to a situation where, after delivery of the head, the anterior shoulder of the fetus becomes impacted on the maternal pubic symphysis, or (less commonly) the posterior shoulder becomes impacted on the sacral promontory.
48
Breech type
Frank
both legs extended, bum first and legs extend up with head
49
Breech type
Complete
both legs flexed, bum first and legs are cross-legged
50
Beech type
Incomplete
one leg flexed, one leg extended
51
Breech type
Footling
one leg flexed, one leg extended on view
52
Antepartum haemorrhage is defined as?
An external PV (per vagina) bleeding >20 weeks gestation and before labour
53
Antepartum Haemorrhages can be classified as:
- Placenta Praevia
- Placental Abruption
54
Describe Placenta Praevia
- Placenta situated lower on uterine wall, near or over the cervix.
- Bleeding may be minimal during the pregnancy
- As cervix dilates, blood loss can increase
The placenta is an organ that develops inside the uterus during pregnancy. It works to provide oxygen and nutrition to the baby and to remove waste. The placenta connects to your baby through the umbilical cord. Typically, the placenta is attached to the top or side of the inner wall of the uterus.
With placenta previa, the placenta attaches lower in the uterus. This results in some portion of the placental tissue covering the cervix. It can result in bleeding during the pregnancy or during or after delivery.
Changes in the uterus and placenta during pregnancy may lead to the problem correcting on its own. If it doesn't, the baby is delivered by cesarean section (C-section).
55
Placenta Praevia
signs and symptoms
- Bright red bleeding from your vagina. The bleeding often starts near the second half of pregnancy. It can also start, stop, then start again a few days later.
- Mild cramping or contractions in your abdomen, belly or back.
56
What are the risk factors for developing placenta previa?
- You smoke cigarettes or use cocaine.
- You’re 35 or older.
- You’ve been pregnant several times before.
- You’re pregnant with twins, triplets or more.
- You’ve had surgery on your uterus, including a C section or a D&C (dilation and curettage).
- You have a history of uterine fibroids.
57
Can a vaginal delivery be possible with placenta revia?
Depending on where the placenta is situated.
If a patient advertises tht they have placenta praevia when you ask about complications, it is important to determine how low the placenta is lying. If the Placentais covering the cervix like the grade 4/Complete placenta praevia, this needs to be delivered via c-section/cesarian. Be sure to discuss with your patient what the obstetricians plan was, c-section or cephalic delivery.
With a cephalic delivery, expect bleeding (more bleeding) than a cephalic delivery.
58
Placental Abruption is described as
The premature separation of the placenta from the uterine wall
Placental abruption (abruptio placentae) is a pregnancy complication that happens when the placenta separates from your uterus before delivery. The placenta is a temporary organ that connects a growing fetus to your uterus during pregnancy. It attaches to the wall of your uterus, usually on the top or side, and acts as a lifeline that gives nutrients and oxygen to the fetus through the umbilical cord. The placenta also removes waste from the fetus’s blood.
In placental abruption, the placenta may completely or partially detach. This can decrease the amount of oxygen and nutrients the fetus gets. It can also cause heavy bleeding in the birthing parent. Your healthcare provider will need to monitor you closely and determine if an early delivery is necessary.
59
Symptoms of placental Abruption
- Abdominal pain.
- Uterine contractions that are longer and more intense than typical labour contractions.
- Uterine tenderness.
- Backache or back pain.
- Feeling the fetus move less
Vaginal bleeding can vary and isn’t an indication of how severe the abruption is. In some instances, there could be no visible bleeding because the blood is trapped between the placenta and the uterine wall. Pain can range from mild cramping to strong contractions that come on suddenly.
60
Placental Abruption can be caused by/risk factors
Placental Abruption can be caused by:
- Traumatic and this is why we transport all pregnant patients to hospitals >20weeks gestation for assessment
Non-traumatic causes:
- Hypertension
- Smoking
- Uterine atony
Risk factors
- Advanced maternal age
- Prior pregnancy
- Hypertension
- Multiple fetuses
- Prior placental abruption
61
Antepartum haemorrhage
How should we transport this patient and why?
- Position the patient in left lateral position or with a left lateral tilt
- Avoid foetal compression of the vena cava and aorta.
62
Antepartum haemorrhage
If this patient’s perfusion status is deteriorating what management should be considered?
IV fluid resuscitation: titrate volumes to maintain adequate maternal perfusion (up to 40ml/kg)
- May require large fluid resuscitation volumes exceeding visible external blood loss to maintain adequate foetal perfusion.
Maternal circulation will sacrifice foetal circulation when in shock.
63
What is Pre-Eclampsia?
A multi-system pregnancy disorder that occurs after 20 weeks gestation
Preeclampsia is a complication of pregnancy. With preeclampsia, you might have high blood pressure, high levels of protein in urine that indicate kidney damage (proteinuria), or other signs of organ damage. Preeclampsia usually begins after 20 weeks of pregnancy in women whose blood pressure had previously been in the standard range.
Left untreated, preeclampsia can lead to serious — even fatal — complications for both the mother and baby.
Early delivery of the baby is often recommended. The timing of delivery depends on how severe the preeclampsia is and how many weeks pregnant you are. Before delivery, preeclampsia treatment includes careful monitoring and medications to lower blood pressure and manage complications.
Preeclampsia may develop after delivery of a baby, a condition known as postpartum preeclampsia.
64
Performing our maternity focused assessment, what history, signs or symptoms should we consider pre-eclampsia?
- Hypertension (Increase of >20mmHg, consider medication)
- Proteinuria (high levels of protein in urine that indicate kidney damage)
- Compromised organ perfusion, fluid shifting and oedema:
- Neurological: Hypertensive encephalopathy (brain dysfunction caused by extremely high blood pressure), headache, agitation, visual disturbances
- Impaired liver function, upper abdominal pain, nausea/vomiting
_ preganat
- High blood pressure
- headaches
- seizures
- history of it
- hyper reflexia
- visual changes
65
What happens when you have preeclampsia?
When you have preeclampsia, your blood pressure is elevated (higher than 140/90 mmHg), and you may have high levels of protein in your urine. Preeclampsia puts stress on your heart and other organs and can cause serious complications. It can also affect the blood supply to your placenta, impair liver and kidney function or cause fluid to build up in your lungs. The protein in your urine is a sign of kidney dysfunction.
66
How should we manage the pre-eclampsia patient?
- Transport
- Position the patient in left lateral position or with a left lateral tilt.
- Avoid foetal compression of the vena cava and aorta.
- Consider consulting with PIPER
67
Conditions that are linked to a higher risk of preeclampsia include
- Preeclampsia in a previous pregnancy
- Being pregnant with more than one baby
- Chronic high blood pressure (hypertension)
- Type 1 or type 2 diabetes before pregnancy
- Kidney disease
- Autoimmune disorders
68
What is Eclampsia?
Eclampsia is a rare but serious complication of preeclampsia. Eclampsia is when a person with preeclampsia develops seizures (convulsions) during pregnancy. Seizures are episodes of shaking, confusion and disorientation caused by abnormal brain activity. Eclampsia typically occurs after the 20th week of pregnancy.
69
What are the risk factors for eclampsia?
You may also be at higher risk for eclampsia if:
- You’re pregnant with multiples.
- You have an autoimmune condition.
- You consume a poor diet or have obesity (a BMI greater than 30).
- You have diabetes, hypertension or kidney disease.
70
What causes eclampsia?
Eclampsia typically develops from preeclampsia. High blood pressure (from preeclampsia) puts pressure on your blood vessels. There can be swelling in your brain, which may lead to seizures.
Genetics and diet can increase your risk for eclampsia.
71
What are the warning signs of eclampsia?
- Severe headaches.
- Difficulty breathing.
- Nausea or vomiting.
- Trouble urinating or not urinating often.
- Abdominal pain (especially on the upper right side).
- Blurred vision, seeing double or loss of vision.
- Swelling of the hands, face or ankles.
72
What is our management of Eclampsia?
- Midazolam 10m IM
- Repeat if no response after 10 minutes
- Position the patient in left lateral position or with a left lateral tilt.
- High Flow Oxygen
- Transport
- Manage symptomatically
73
Pre-term labour is defined as
The onset of labour prior to 37 weeks gestation
- Preterm labor occurs when regular contractions result in the opening of your cervix after week 20 and before week 37 of pregnancy.
- These contractions are generally lower abdominal or back pain that become regular, and uncomfortable and may be associated with a show or ruptured membranes.
74
Pre-term labour
Risk factors
- Previous preterm labor or premature birth, particularly in the most recent pregnancy or in more than one previous pregnancy
- Pregnancy with twins, triplets or other multiples
- Shortened cervix
- Problems with the uterus or placenta
- Smoking cigarettes or using illicit drugs
75
Pre-term labour prior to 34 weeks gestation, what do we need to consider?
- Newborn resuscitation is likely
- Transport to a facility capable of providing neonatal intensive care.
- Consult with PIPER who will support with you and coordinate with your destination hospital.
76
With Pre-term labour, <34 weeks, but birthing is not imminent, we should?
- Apply a transderm (GTN) patch to the patient’s abdomen
- Smooth muscle relaxant
- Apply a 2nd patch after one hour, if contractions persist.
- Transport
- Left lateral position
- Do not use oral GTN as this can cause significant vasodilation, hypotension and therefore compromise foetal perfusion. If the patient is in true pre-term labour, these methods will not halt labour for long, not even for a few days. All management of a woman in pre-term labour must follow consultation with an obstetric facility/PIPER.
77
With Pre-term labour there are risks of other birthing emergencies, what could these be?
- Breech presentation
- Prolapse cord
78
If birth is not imminent, how is the prolapse cord managed by paramedics?
The strategy seeks to remove any compression from the cord until in-hospital birthing can occur
Place the patient on her front, kneeling and with her chest on the bed. In this way it is intended the foetus falls forward and away from the pelvis and any potential compression. It is not intended the foetus will move sufficient to drag the cord back within the uterus. This is a very temporary measure and will have to be maintained until hospital
79
Cord prolapse symptoms
- They can see or feel the umbilical cord after your water breaks.
- The fetal heart rate drops, slows or changes suddenly.
80
Cord prolapse risk factors
- Breech presentation (when the fetus is in any position other than head first).
- You’re pregnant with twins, triplets or more (also known as having a multiple pregnancy).
- Polyhydramnios (you have too much amniotic fluid).
- Premature rupture of membranes (water breaking) before you reach full term.
81
How is a patient with SVT managed? And why we do not follow the ACS guidelines.
How is a patient with SVT managed?
- Analgesia might be considered but the ideal relief will be achieved by rhythm reversion.
Conventional cardiac therapy might normally include nitrates and aspirin. Nitrate therapy has NO role in the management of SVT – it will only work to reduce right ventricular preload, cardiac output and cause/worsen hypotension. Aspirin might appear to be a reasonable option until it is considered that there is no acute thrombus as there is with acute coronary syndrome. The clotting problem that leads to emboli forming during atrial fibrillation is managed with anticoagulants such as heparin/warfarin. Aspirin is not the most appropriate drug for this – nor is this the same problem with SVT being transient, reversible and without fibrillating atria.
Vagal Manoeuvres
Adenosine
Synchronized cardioversion either haemodynamically unstable or other treatments ineffective.
IV Diltiazem or Verapamil or Beta blockers.
82
Why do we not give GTN to a Pt with SVT?
When combined with the effect of NTG on decreasing venous return, administration in tachy-cardia could plausibly cause a severe drop in blood pressure
83
How does Adenosine help with SVT?
Adenosine = slows conduction through the AV node, resulting in termination of re-entry circuit activity within or including the AV nodal pathway
84
Acute coronary syndrome define/patho
The blanket term covers the spectrum of cardiac illnesses ranging from angina to unstable angina to myocardial infarction (MI). Acute coronary syndrome involves hardening and narrowing of the of coronary arteries due to plaque buildup called atherosclerosis. There is an accumulation of lipids and collagen in the cell wall. The narrowing of the arteries causes a more turbulent blood flow (high blood pressure) which can cause the plaque to rupture and initiate the clotting cascade causing a thrombus. The thrombus causes a blockage within the coronary arteries which can cause a decrease level of oxygenated blood to the heart, which can also lead to the patient feeling pain and/or nausea and vomiting and most importantly chest pain.
85
Unstable angina: define
Unstable angina: This involves sudden, unexpected chest pain or pressure, even while resting. It’s a warning sign of a heart attack and occurs when stable angina worsens.
86
Non-ST-elevation myocardial infarction: define
Non-ST-elevation myocardial infarction: An NSTEMI is a heart attack that providers can detect with blood tests but not with an electrocardiogram (EKG). It means your coronary arteries aren’t fully blocked or were blocked for a short amount of time.
87
ST-elevation myocardial infarction: define
A STEMI is a much more severe heart attack that providers can detect with blood tests and EKG. It occurs when blood flow to your heart is fully blocked for a long time, affecting a large part of your heart.
88
What are the most common risk factors for the development of coronary artery disease?
Damage to the endothelial layer in the arteries creates access for low-density lipoproteins with lipids attached to enter. This damage can be caused by:
- hypertension causing mechanical injury
- diabetes/hyperglycaemia causing complex inflammatory responses within the artery wall
- cigarette smoking releasing toxic chemicals that irritate and damage
- Another risk factor is poor diet containing excessive fats and lipids that increase the accumulation created by the other risk factors
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Coronary arteries fill during diastole. True or False?
Why is the significance to know this?
True
- Anything that adversely affects diastolic blood pressure can cause ischemia of the coronary arteries. This includes hypotension and reduced diastolic time such as occurs during tachycardia
90
Coronary arteries begin on the outside of the heart and run inward.
Coronary artery disease can be found in the larger vessels (outside the heart) or in the smaller vessels within.
Why is it important to know this?
When blood flow is reduced because of coronary artery disease, it is the innermost part that of the ventricle that is affected first. That is furthest away. - This opens up the possibility for partial thickness infarctions, the basis of non-STEMI. It also explains why disease of the smaller blood vessels causes smaller but harder to detect infarcts. This includes those with a history of diabetes and post-menopausal women. Both can be easier to miss unless suspicion remains high for vague and non-specific presentations. Look for history of collapse, syncope, fatigue, breathlessness or even just strong uneasiness of something not being right.
91
How does nitrate therapy (GTN) provide benefit when managing a patient presenting with acute coronary syndrome?
Venous dilation – encourages venous pooling (decreases preload)
- Arterial dilation – reduces SVR and therefore decreases left ventricular afterload (the arterial resistance fighting against ejection)
- This reduces myocardial workload
- Decreases SBP, DBP whilst maintaining coronary perfusion pressure
- Mild collateral coronary arterial dilation – improved blood flow
- Reduced o2 demand
GTN exerts its therapeutic action by relaxing vascular smooth muscle, therefore producing both arterial and venous vasodilation
92
Why are tachycardia and bradycardia of concern when considering administering nitrates for acute coronary syndrome?
CO = HR X SV. Tachycardia greater than 150 is an arbitrary line above which there will not be sufficient time between contractions for adequate ventricular filling – hence additional cardiac output reduction. The same reasoning applies to bradycardia. The heart rate isn’t fast enough to move enough blood each minute with the cardiac output down as a result. Further lowering of blood pressure is likely to only worsen this situation.
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STEMI elevation
Does the monitor ECG interpretation indicate STEMI to 12-lead ECH show ST elevation in two or more contiguous leads:
- ≥ 2.5 mmHg ST elevation in leads V2-3 in men aged <40 years OR
- ≥ 2 mm ST elevation in leads V2-3 in men aged ≥40 years OR
- ≥1.5 mm St elevation in V2-3 in women OR
- ≥1 mm in other leads, OR
- new onset left bundle-branch block?u
94
Why do we use aspirin in ACS
to minimise platelet aggregation nd thrombus formation in order to retard the progression of coronary artery thrombosis in ACS
95
Symptoms of ACS
- Aching
- Burning
- Heaviness
- Numbness
- Pressure
- Tightness
OTHERS
May feel nausea, dizziness, lightheadedness, sweating, fatigue
WOMEN
- Nausea or vomiting.
- Pain that spreads to the shoulders, neck, abdomen or jaw.
- Shortness of breath (dyspnea).
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Risk factors for ACS
- age (over 45)
- Having overweight/obesity.
- Cocaine use.
- Lack of physical activity.
- Smoking.
- Unhealthy diet.
- Family history
97
Signs and symptoms of COPD may include:
- Shortness of breath, especially during physical activities
- Wheezing
- Chest tightness
A chronic cough that may produce mucus (sputum) that may be clear, white, yellow or greenish
- Frequent respiratory infections
- Lack of energy
- Unintended weight loss (in later stages)
- Swelling in ankles, feet or legs
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APO symptoms
Sudden (acute) pulmonary edema symptoms
- Difficulty breathing (dyspnea) or extreme shortness of breath that worsens with activity or when lying down
- A feeling of suffocating or drowning that worsens when lying down
- A cough that produces frothy sputum that may have blood in it
- A rapid, irregular heartbeat (palpitations)
- Anxiety, restlessness or a feeling that something bad is about to happen
- Cold, clammy skin
- Wheezing or gasping for breath
Long-term (chronic) pulmonary edema signs and symptoms
- Awakening at night with a cough or breathless feeling that may be relieved by sitting up
- Difficulty breathing with activity or when lying flat
- Fatigue
- More shortness of breath than usual when you're physically active
- New or worsening cough
- Rapid weight gain
- Swelling in the legs and feet
- Wheezing
99
Why give salbutamol for COPD/asthma
Causes bronchodilation so they widen and relax your airway
100
why give ipratropium bromide for COPD/asthma
It is a bronchodilator that inhibits the cholinergic bonchomotor tone which blocks the vagal reflexes which mediate bronchoconstriction
101
Why do we not give salbutamol to APO Pt
because salbutamol opens up the airway by relaxing and widening it which will allow fluid to move down the airway into the lungs easier
102
Why do we give dexamethasone to COPD/asthma pt
They help reduce the inflammation in your lungs caused by flare-ups.
103
why do we give GTN to pt with pulmonary oedema
to reduce preload and afterload and relax vascular smooth muscle
104
What are the critical determinants of cardiac output and blood pressure?
CO = HR x SV
Cardiac output (CO) = heart rate (HR) x stroke volume (SV)
BP = CO x SVR
or BP = (HR x SV) x SVR (Systemic vascular resistance )
Blood pressure (BP) = Cardiac output (CO) x systemic vascular resistance (SVR)
105
Why does bradycardia have an adverse effect on blood pressure?
Cardiac output reduces since heart rate reduces. Stroke volume remains okay given longer time for ventricular filling
Blood pressure reduces since cardiac output reduced.
To compensate systemic vascular resistance (vasoconstriction) may occur.
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What is the prehospital and subsequent in-hospital management of bradycardia?
- Prehospital treatment is simple – increase the heart rate to one that better contributes to cardiac output using pharmacology such as atropine or adrenaline and, if necessary, temporary external pacing
- In hospital management extends to more permanent pacing options if required and definitively repairing the underlying cause of the problem – i.e. coronary artery reperfusion for MI
107
What prehospital therapy would you not consider when treating a patient with bradycardia?
Anything that reduces systemic vascular resistance since that is the only thing working to maintain blood pressure (e.g. nitrate therapy - giving GTN)
108
What is ‘SENSING’ when regarding pacemakers?
The device is mainly composed by a sensing unit and a pulse generator: the former senses the Sensing is the ability of the device to detect underlying cardiac rhythm. If there is no such activity, the pacemaker should fire regularly. More likely though there is intermittent cardiac activity. It is important where this is the case, the device waits for the heart to be normally stimulated by its own conduction system and only fires in any absence. The device must not compete with the heart’s own conduction system and try to pace when the heart is still working normally. Sensing then forces the pacemaker to wait for and recognise myocardial electrical activity
109
What is ‘CAPTURE’ when regarding pacemakers?
Where the pacemaker correctly fires, capture is the ability of the pacemaker to provide sufficient electrical energy to cause depolarisation of the heart. There is a certain threshold for such stimulation - too little electrical activity and nothing happens. Just enough and the ventricles depolarise (QRS)
110
What management concerns might be relevant for paramedics when a patient has an implanted pacemaker?
- Defibrillation should not occur with any electrode placed over the pacemaker
-Where the pacemaker is located close to where a pad should be positioned, the electrode can be located a few centimetres away and not over the top
- Defibrillating directly over a pacemaker can damage the device or reset its settings from those selected for the patient
- Pacemakers can continue to fire even if the patient is in cardiac arrest. Where this occurs, the pacemaker can effectively be ignored if it is making no contribution to any rhythm or pulse. This includes cessation of resuscitation where the pacemaker might continue to create ineffective spikes despite the patient being deceased.
111
Why does excessive tachycardia have an adverse effect on blood pressure?
There is inadequate time for ventricular filling hence stroke volume is reduced.
There is also little or no input from the atrium
Blood pressure reduces since cardiac output reduces.
Systemic vascular resistance (vasoconstriction) rises to compensate
112
What is the prehospital and subsequent in-hospital management of wide complex tachycardia?
- Aim is to stop the tachycardia to allow the underlying intrinsic cardiac pacemaker (hopefully sinus node) to reassert itself
- This is achieved by either pharmacologically suppressing the aberrant ventricular pacemaker with an antiarrhythmic (such as amiodarone) or using cardioversion to shock the rhythm to a halt
- In hospital management extends to more permanent cardioversion options of implanted ICD and long term pharmacology and definitively repairing the underlying cause of the problem – i.e. coronary artery reperfusion for MI
113
Why does a drop in cardiac output have an adverse effect on blood pressure?
Myocardial Injury/Ischaemia reduces effectiveness of ejection (Stroke Volume)
Normal compensation, heart rate increase, unable to sufficiently compensate for decreased stroke volume from reduced contraction.
which results in reduced cardiac output
Reduced cardiac output reduces the blood pressure.
Systemic vascular resistance (vasoconstriction) rises to compensate but not sufficiently to maintain BP
114
What is the correct posture for a patient with pulmonary oedema and why?
- Upright patient posture is important to encourage venous pooling and decreased venous return (right ventricular preload)
- This reduces the supply of blood from the right side into the pulmonary circulation where the congestion is. It also then reduces preload on the left side of the heart which is already overstretched (Starling’s law)
- An upright posture is critical first management, regardless of conscious state and even systemic blood pressure. When the maximum filling stretch on myocardial muscle is exceeded, anything that increases venous return to the left side of the heart where left ventricular failure is evident will not help. An upright posture also encourages pooling of blood in the lower lungs allowing for greater alveolar filling with less hydrostatic pressure opposing them in the upper lungs.
115
If there in inadequate perfusion to the heart with arrhythmia, pain or hypovolemia what is occurring
Cardiogenic shock is a life-threatening condition in which your heart suddenly can't pump enough blood to meet your body's needs. The condition is most often caused by a severe heart attack, but not everyone who has a heart attack has cardiogenic shock.
In most cases, a lack of oxygen to your heart, usually from a heart attack, damages its main pumping chamber (left ventricle). Without oxygen-rich blood flowing to that area of your heart, the heart muscle can weaken and go into cardiogenic shock.
116
Why do we do a left lateral tilt when transporting mum who is pregnant?
Because we want to take pressure off the amniotic sac (keep baby safe and protected)
117
Pre-eclampsia
patho
Abonormal implantation of placents
- abnormal blood flow through the placenta which leads to vascular dysfunction
Vasoconstriction and capillary leaking in the rest of the body
Capillary leakage leads to cerebral oedema
118
Why do we do the Valsalva Manaue
By blowing into the syringe you increase intrathoracic pressure which decreases pre-load and leads to decreased cardiac output which shows through blood pressure dropping
- The body compensates by increasing sympathetic activity through vasoconstriction
When you stop blowing into the syringe it decreases intrathoracic pressure
The lifting of the legs massively increases preload which creates a massive surge in cardio output
- the baroreceptors detect the changes, which then increase blood pressure and vagus tone which decreases the heart rate which will then break the circit
119
Atherscolosis
