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L2 EBP What information do you need

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Overview

This lecture works through how you turn a clinical or public health uncertainty into an answerable question, decide which study design can answer it, and find and judge the evidence. It sets out the evidence hierarchy and the OCEBM 2011 levels of evidence, places evidence alongside the other domains of decision making (clinical expertise and patient values in clinical settings; environment, population characteristics and resources in public health), and then runs three worked scenarios: pertussis vaccination in pregnancy, the ideal blood pressure target, and road traffic speed limits.

Why this matters and what you should be able to do

Stated purpose: it helps with translating EBP, study design and critical appraisal into clinical practice, and with completing tasks in Med 4/5/6 (study design assignments, EBP tasks in Medicine, Surgery, GP).

Learning outcomes:

  1. Translate clinical uncertainty into an answerable question.
  2. Explain which type(s) of study is best suited to answer that question.
  3. Describe relevant study methods, and the issues to consider when critically appraising a study of that type.
  4. Outline a search strategy to find evidence to answer your question.

Where to look for evidence

  • Consider all relevant evidence when trying to answer a question, and look first for reputable clinical guidelines (e.g. NICE in the UK) and properly conducted systematic reviews and meta-analyses (e.g. Cochrane).
  • If there are no guidelines, systematic reviews or meta-analyses, you may need to search for and appraise individual studies yourself.
  • The choice of information source and study type depends on the research or clinical question.
  • Quoted principle (Oxford CEBM 2011 Levels of Evidence introductory document): “no evidence ranking system or decision tool can be used without a healthy dose of judgment and thought”.

Warning

The transcript flags slides 4 and 5 as scrambled interleaves of two overlapping text runs that were not rendered, so the exact wording and ordering on those slides could not be confirmed. Slide 4 may either restate the learning outcomes in longer form or state the “consider all relevant evidence, look for guidelines and systematic reviews” point, or both as overlapping text boxes.

Hierarchy of evidence

Pyramid “Hierarchy of Scientific Evidence”, strongest at the top to weakest at the bottom:

  1. Meta-analyses and systematic reviews
  2. Randomised controlled trials
  3. Cohort studies
  4. Case-control studies
  5. Cross-sectional studies
  6. Animal trials and in vitro studies
  7. Case reports, opinion papers and letters

The slide’s own qualifier, arrowed at both the top and bottom of the pyramid: not always the right ranking, it depends on your research question and how well the studies were conducted.

OCEBM 2011 Levels of Evidence

The Oxford table maps question type to the best design at each of five steps (Level 1 strongest to Level 5 weakest). Key points to know:

How common is the problem? L1 local and current random sample surveys or censuses; L2 systematic review of surveys allowing matching to local circumstances; L3 local non-random sample; L4 case-series; L5 not applicable.

Is this diagnostic or monitoring test accurate? (diagnosis) L1 systematic review of cross-sectional studies with consistently applied reference standard and blinding; L2 individual such cross-sectional studies; L3 non-consecutive studies, or studies without consistently applied reference standards; L4 case-control studies, or poor or non-independent reference standard; L5 mechanism-based reasoning.

What will happen if we do not add a therapy? (prognosis) L1 systematic review of inception cohort studies; L2 inception cohort studies; L3 cohort study or control arm of a randomised trial; L4 case-series, case-control studies, or poor quality prognostic cohort study; L5 not applicable.

Does this intervention help? (treatment benefits) L1 systematic review of randomised trials or n-of-1 trials; L2 randomised trial, or observational study with dramatic effect; L3 non-randomised controlled cohort/follow-up study; L4 case-series, case-control, or historically controlled studies; L5 mechanism-based reasoning.

What are the COMMON harms? L1 systematic review of randomised trials, systematic review of nested case-control studies, an n-of-1 trial in the patient you are asking about, or an observational study with dramatic effect; L2 individual randomised trial or, exceptionally, observational study with dramatic effect; L3 non-randomised controlled cohort/follow-up study (post-marketing surveillance) provided numbers are sufficient to rule out a common harm, and for long-term harms provided follow-up is long enough; L4 case-series, case-control, or historically controlled studies; L5 mechanism-based reasoning.

What are the RARE harms? L1 systematic review of randomised trials or n-of-1 trial; L2 randomised trial or, exceptionally, observational study with dramatic effect. (Steps 3 to 5 are blank for this row.)

Is this (early detection) test worthwhile? (screening) L1 systematic review of randomised trials; L2 randomised trial; L3 non-randomised controlled cohort/follow-up study; L4 case-series, case-control, or historically controlled studies; L5 mechanism-based reasoning.

Footnotes to the table:

  • A level may be graded down for study quality, imprecision, indirectness (the study PICO does not match the question’s PICO), inconsistency between studies, or a very small absolute effect size; and graded up for a large or very large effect size.
  • A systematic review is generally better than an individual study.

Evidence as one domain of decision making

Clinical settings. Evidence-based practice sits at the intersection of three circles: patient values and choices, best available evidence, and clinical expertise. The slide surrounds these with communities and literature/guidelines on one side, and respect, compassion, cultural safety and competence on the other.

Public health and community settings. EBP is essential when considering interventions. Evidence is underpinned by population needs and values, and many public health interventions occur outside the health sector, for example in transport, environment, agriculture, housing, legislation and finance.

Four overlapping domains influence evidence-based decision making (Spring et al., reproduced by Brownson et al.):

  1. Best available research evidence
  2. Environment and organisational context
  3. Population characteristics, needs, values and preferences
  4. Resources, including practitioner expertise

Brownson et al. on evidence-based public health: its key components are making decisions on the basis of the best available scientific evidence, using data and information systems systematically, applying program-planning frameworks, engaging the community in decision making, conducting sound evaluation, and disseminating what is learned.

The lecture shows the public health four-domain model and the clinical three-circle Venn side by side: the same logic, different surrounding domains.

Scenario 1: pertussis vaccination in pregnancy

The disease. Pertussis (whooping cough) is caused by Bordetella pertussis bacteria and is toxin-mediated. It is highly transmissible. It is most severe in infants in the first few months of life and can be fatal. The effects of immunisation wear off over time, so it is endemic in older children and adults who can pass it to infants. Vaccination in pregnancy provides effective protection of infants under 3 months.

Epidemiology (NZ). Pertussis notifications from January 2010 to February 2025 show recurrent multi-year outbreak peaks, the largest around 2012, 2018 and 2024-2025, each reaching 500 to 600 cases per month, with troughs near zero in between including the COVID period around 2020 to 2022. From mid-2024 a sustained increase began, and on 22 November 2024 an outbreak was declared, with 1,749 cases in 2024 (notification rate 33 per 100,000 population). One young infant aged under 8 weeks died. Māori had the highest rates of pertussis hospitalisation overall, at 45 cases per 100,000.

Rates also vary geographically: by district health board for July to September 2015, Southern had the highest rate (around 40 per 100,000), followed by Whanganui, Nelson-Marlborough, Canterbury and Counties Manukau, down to Tairawhiti lowest; the lowest-ranked boards’ rates were based on fewer than five cases.

Immunisation schedule. The older National Immunisation Schedule gives pertussis-containing vaccine at 6 weeks, 3 months and 5 months (INFANRIX hexa: diphtheria, tetanus, pertussis, polio, hepatitis B, Hib), at 4 years (INFANRIX IPV: diphtheria, tetanus, pertussis, polio) and at 11 years (BOOSTRIX: tetanus, diphtheria, pertussis). Rotavirus (RotaTeq) and pneumococcal (PREVENAR13) accompany the infant doses; Hib (Act-HIB), MMR (M-M-R II) and PREVENAR13 are given at 15 months.

The updated NZ schedule (IMAC, July 2026) adds: every pregnancy Tdap (Boostrix) from the second trimester, influenza in any trimester, and COVID-19 (Comirnaty) in any trimester; MenB (Bexsero) at 2, 4 and 12 months or the alternative approved schedule; MMR (Priorix) at 12 and 15 months; varicella (Varilrix) at 15 months; HPV (Gardasil 9, two doses) in school year 8 / 12 years; Boostrix again at 45 and 65 years; and zoster (Shingrix, two doses) at 65 years. An additional Prevenar 13 dose at 3 months is given to children with an eligible medical condition, and children with high pneumococcal-risk conditions may be eligible for 23PPV.

Timing of the antenatal booster. Women between 28 and 38 weeks of pregnancy are eligible for a free Boostrix, and should have the current booster even if they had a childhood whooping cough vaccination or one more than 5 years ago. For best protection of the newborn the booster should be given by the end of the 36th week, ideally between 31 and 33 weeks. This allows time for the woman’s immune system to produce protection, reducing the risk she has the disease at delivery and for the subsequent year when the baby’s risk of complications is highest. Circulating protection can also cross the placenta, possibly giving the baby some short-lived protection. All other household members and close family such as grandparents should be vaccinated, since they could pass it to the baby. The vaccine is not subsidised for adults but is free for children as part of the normal schedule.

Warning

The transcript flags that the final line of the factsheet text is cut off at the bottom edge of slide 14.

A contrasting source. The lecture shows an anti-vaccination website article (“WAVES NZ”) claiming that vaccinating pregnant women is a “new and extremely disturbing trend”, that vaccine data sheets state the vaccines have never been tested on pregnant women and that effects in breast milk are unknown, and framing antenatal vaccination as experimentation on pregnant women that benefits pharmaceutical companies and leaves a consenting mother without compensation for rare side effects. This is presented as material for critical appraisal, not as the lecturer’s own claim.

Turning it into a question. Suppose your patient wants to know more about the safety of pertussis vaccination in pregnancy. Use the PECOT framework to formulate an answerable question, then ask how you will find the information needed to answer it. Which design is best suited: randomised controlled trial, cohort study, case-control study or cross-sectional study? Why? Then outline how such a study should be done. For a cohort study in particular, ask what the key threats to internal validity are.

The evidence found.

  • Donegan K, King B, Bryan P. Safety of pertussis vaccination in pregnant women in UK: observational study. BMJ 2014; 349: g4219. Observational cohort study in the UK Clinical Practice Research Datalink; 20,074 pregnant women (median age 30) who received pertussis vaccine, plus a matched historical unvaccinated control group. Outcomes were adverse events from clinical diagnoses during pregnancy, with data from the linked child record; the primary event of interest was stillbirth (intrauterine death after 24 weeks’ gestation). Results: no evidence of increased stillbirth risk in the 14 days after vaccination (incidence rate ratio 0.69, 95% CI 0.23 to 1.62) or later in pregnancy (0.85, 0.44 to 1.61) versus historical national rates; no evidence that vaccination accelerated time to delivery (hazard ratio 1.00, 0.97 to 1.02); and no evidence of increased risk of stillbirth, maternal or neonatal death, pre-eclampsia or eclampsia, haemorrhage, fetal distress, uterine rupture, placenta or vasa praevia, caesarean delivery, low birth weight, or neonatal renal failure. Conclusion: in third-trimester vaccination there was no evidence of increased risk across an extensive predefined list of pregnancy-related adverse events.
  • Furuta M, Sin J, Ng ESW, Wang K. Efficacy and safety of pertussis vaccination for pregnant women: a systematic review of randomised controlled trials and observational studies. BMC Pregnancy and Childbirth 2017; 17: 390. Searched Cochrane CENTRAL, Medline, Embase and OpenGrey from inception to 16 May 2016; search terms included pertussis, whooping cough, pertussis vaccine, tetanus/diphtheria/pertussis vaccines, pregnancy and perinatal. Included 15 articles representing 12 study populations, 203,835 mother-infant pairs from the US, UK, Belgium, Israel and Vietnam; two were RCTs and the rest observational. Vaccination at 19 to 37 weeks’ gestation was associated with significantly increased antibody levels in both mothers and newborns versus placebo or no vaccination. There was a lack of robust evidence that these antibodies reduce pertussis incidence (one RCT, n=48, no cases in either group), pertussis-related severe complications (one observational study) or mortality (no study). No evidence of increased risk of serious complications such as stillbirth (two RCTs, n=151, RR 0.86, 95% CI 0.14 to 5.21). Conclusion: maternal vaccination in later pregnancy should continue to be supported while further research fills knowledge gaps.

Bottom line. The evidence is strong that whooping cough vaccine during pregnancy does not increase rates of major pregnancy complications, does not increase serious adverse outcomes in infants, and provides important protection to newborns before they are old enough to be vaccinated themselves. The strongest NZ-specific evidence is the 2018 PIPS study of more than 68,000 pregnancies, which found no unexpected safety risks for mothers or infants from maternal Tdap vaccination.

Other lung-related examples of published evidence used the same way: a retrospective cohort in JAMA Network Open on smoking cessation pharmacotherapy use in pregnancy (varenicline, NRT, bupropion; Australia, New Zealand, Norway and Sweden, 2015-2020), and a national nested case-control study of proton pump inhibitor and H2RA use in infants and risk of community-acquired pneumonia or lower respiratory tract infection (New Zealand, 2002-2018).

Scenario 2: the ideal blood pressure target

History. In the early 20th century elevated blood pressure was thought to be a normal part of ageing, although malignant hypertension was recognised. Franklin D. Roosevelt (US president 1933 until his death in 1945) is the illustrating case.

Observational evidence that BP matters. Dawber (1957, American Journal of Public Health) reported four-year incidence of arteriosclerotic heart disease (defined as myocardial infarction, angina or sudden death attributable to coronary heart disease) in males aged 45 to 62, by hypertension status. Rates per 1,000: all persons 58 (52 new cases in 898 at risk); definite hypertensive heart disease 98 (8/82); definite hypertension 81 (10/124); possible hypertensive heart disease 76 (7/92); borderline hypertension without heart disease 62 (15/243); normotension 26 (8/310). The gradient across categories is the point.

Early RCT of treatment. Veterans Administration Cooperative Study Group on Antihypertensive Agents (1967, JAMA): 143 male hypertensive patients with clinic diastolic BP averaging 115 to 129 mmHg randomly assigned to active treatment (hydrochlorothiazide plus reserpine plus hydralazine hydrochloride) or placebo. Twenty-seven severe complicating events developed in the placebo group versus two in the active group; four deaths in the placebo group and none in the active group. Placebo-group complications included grade 3 or 4 hypertensive retinopathy, congestive heart failure, increasing azotemia, cerebrovascular thrombosis, transient ischaemic attacks, cerebral haemorrhage, myocardial infarction and severely elevated BP; the two active-group events were one cerebrovascular thrombosis and one case of multiple drug toxicity. Conclusion: men with diastolic BP averaging 115 mmHg or above are a high-risk group in which antihypertensive therapy has a significant beneficial effect.

The question to develop. What is the ideal blood pressure target for your patient? Does it depend on age, gender, ethnic group, or other risk factors and comorbidities? What should we advise in guidelines? Is there a PICOT question we can develop?

Meta-analysis of observational data. Prospective Studies Collaboration (2002, Lancet 360: 1903-13), “Age-specific relevance of usual blood pressure to vascular mortality: a meta-analysis of individual data for one million adults in 61 prospective studies”. Individual participant data on one million adults with no previous vascular disease at baseline in 61 prospective observational studies; during 12.7 million person-years there were about 56,000 vascular deaths (12,000 stroke, 34,000 ischaemic heart disease, 10,000 other vascular) and 66,000 other deaths at ages 40 to 89. Meta-analyses used time-dependent correction for regression dilution, relating mortality in each decade of age at death to estimated usual BP at the start of that decade. Findings shown graphically: both stroke mortality and IHD mortality rise continuously with systolic BP (roughly 115 to 180 mmHg) and with diastolic BP (roughly 70 to 110 mmHg) on a log-scale floating absolute risk axis, with each older age band sitting at a higher absolute mortality than the younger ones.

SPRINT (Systolic Blood Pressure Intervention Trial), NEJM, 26 November 2015. An RCT, mapped onto PECOT on the slide:

  • Participants: 9,361 US participants with SBP at or above 130 mmHg and increased cardiovascular risk, without diabetes.
  • Exposure/intervention: intensive treatment, aiming for SBP below 120 mmHg.
  • Comparator: standard treatment, aiming for SBP below 140 mmHg.
  • Outcomes: myocardial infarction, acute coronary syndromes, stroke, heart failure or cardiovascular death, with the primary outcome a composite of these.
  • Time: planned for 5 years but stopped early after a median follow-up of 3.26 years.

Results: primary composite outcome hazard ratio with intensive treatment 0.75 (95% CI 0.64 to 0.89); death from any cause hazard ratio 0.73 (95% CI 0.60 to 0.90). Rates of serious adverse events of hypotension, syncope, electrolyte abnormalities, and acute kidney injury or failure, but not of injurious falls, were higher with intensive treatment. Achieved BP over the trial: standard group around 130 to 135 mmHg, intensive group around 119 to 122 mmHg; the intensive group needed more antihypertensives (for example 2.3 versus 1.9 medications at year 0, and 3.0 versus 1.9 by years 4 to 5).

Interpretation (Whelton, Chen and Krousel-Wood, “Lessons learned from SPRINT”):

  • The optimal BP target during treatment of high BP has been controversial.
  • Observational studies identify a direct, continuous relationship between BP and cardiovascular disease risk.
  • SPRINT provides strong support for intensive treatment of high BP, especially in people with a profile similar to those included in the trial.
  • Experience in other BP-lowering trials is consistent with SPRINT, and the benefit of intensive BP lowering probably applies to other high cardiovascular risk categories not studied in SPRINT.
  • Intensive BP management warrants careful monitoring for adverse effects; the slide’s own callout is “consider adverse events”.
  • Increasing evidence suggests intensive BP lowering is a cost-effective way to improve health in many adults with high BP; implementation trials of feasibility and effectiveness in routine practice, including resource-constrained settings, are warranted.

Warning

Slide 34 was marked text only in the transcript, so the accompanying journal-page image and any callout box on that slide could not be visually verified.

Scenario 3: setting road traffic speed limits

This scenario is worked through the four public health decision-making domains.

Best available research evidence.

  • Risk of pedestrian fatality rises steeply and S-shaped with impact speed, from near 0% at low speeds to about 90 to 100% by roughly 50 to 60 mph (logistic regression on Ashton and Mackay data).
  • Death percentages for pedestrians and cyclists hit by cars by impact speed: 30 gives 10% death, 40 gives 32%, 50 gives 80%, 60 gives 95%.
  • Co-benefits of lower speeds: less congestion, less air pollution and CO2 emissions, stronger communities, more walking and cycling, and reduced obesity (British Academy, “If you could do one thing… Nine local actions to reduce health inequalities”, January 2014).
  • Auckland Transport evaluation of limits lowered on 30 June 2020, in the following 18 months: 47% reduction in deaths, more than 25% reduction in all injury crashes, more than 15% reduction in serious injuries, and more than 20% reduction in total deaths and serious injuries. On rural roads where speeds were changed, a 71% reduction in deaths and more than 25% reduction in serious injuries, equating to a more than 30% reduction in death and serious injury on those dangerous rural roads. AT described these as early results.

Population needs, values and preferences. Local communities are not uniform and are actively engaged: a Nelson parent’s relief as NZTA kept a lower speed limit; Auckland Council voting against higher speed limits in opposition to the government’s plan; and the Far North settlement of Taumatamākuku on State Highway 1 between Kawakawa and Moerewa, where a decades-long residents’ campaign succeeded in August 2020 when NZTA dropped the limit past their homes from 100 km/h to 80 km/h, residents citing “running the gauntlet” to reach the shops and tending to the injured after crashes outside their homes. That highway is one of ten in Northland where recent reductions could be reversed by 1 July under new retrospective rules for setting speed limits.

Resources including practitioner expertise. New Zealand’s Road to Zero road safety strategy 2020-2030, and Waka Kotahi key messages on how to talk about road safety (Vision Zero, Road to Zero, Safe System). The communications approach focuses on solutions, takes a systems approach, and uses multiple community voices. Language guidance: say “the number of people killed or seriously injured on our roads” rather than “road toll”; “crash” not “accident”; focus on injuries rather than crashes; “New Zealand’s road safety strategy” rather than “the Government’s road safety strategy”; and put people first rather than mode or DSI, for example “people who motorcycle” not “motorcycles”, “people walking and cycling” not “pedestrians and cyclists”, and “people make mistakes” rather than “drivers make mistakes”.

Environment and organisational context. This is the domain the lecture circles in red for this scenario, because policy changed against the research evidence.

  • 12 December 2023: government amends speed limit rules to stop blanket speed limit reductions, removing mandatory requirements for Road Controlling Authorities to implement speed management plans and removing the 29 March 2024 deadline for submitting them, so that when limits are set, economic impacts including travel times and the views of road users and local communities are taken into account alongside safety; variable limits near schools at pick-up and drop-off replace permanent reductions.
  • 15 March 2024: Road to Zero was scrapped. An international road safety expert warned that the government must keep applying targets to reduce road fatalities and serious injuries, and that reversing speed limit reductions will drive the road toll up.
  • 28 September 2024: new speed limit rule signed, to reverse blanket reductions on local streets, arterial roads and state highways by 1 July 2025; require reduced variable limits outside schools at pick-up and drop-off by 1 July 2026; and enable limits up to 120 km/h on Roads of National Significance where safe.
  • A safe transport advocacy group took legal action over the rollback after the government announced 38 sections of state highway would revert to previous limits with another 49 sections out for public consultation; some community leaders called the changes reckless.
  • The 2024 Road Safety Objectives document built on the Government Policy Statement on Land Transport 2024 to address road safety challenges, framing road safety as a shared responsibility between road users, authorities and the vehicle industry, under the heading “safer roads, safer drivers, safer vehicles and resetting speed limits”. There has been considerable debate and dissent about some new measures, for example targeted speed limit changes and Warrant of Fitness changes.

Outcome data reported in the lecture. Provisional road deaths in New Zealand were 272 in 2025 and 292 in 2024, a third consecutive annual reduction, credited by police in large part to Operation Open Roads and its focus on deaths on open roads. Separately, ANCAP has changed its vehicle rating system to a “Stages of Safety” framework covering safe driving, crash avoidance, crash protection and post-crash, so crash testing becomes one stage rather than the centre, described as a broadly positive step giving more comprehensive assessments.

Key messages

  • What question or questions are you trying to answer?
  • What is the best available evidence to answer them?
  • Are there any problems with that evidence?
  • Hierarchies of evidence for study design types do not remove the need for critical thought.
  • Evidence sits alongside other domains in clinical medicine and public health, as in the two Venn-style diagrams.

Self-test

  1. List the four learning outcomes of this lecture, that is the four things you should be able to do with a clinical uncertainty.
  2. Where should you look first for evidence, and what do you do if none of those sources exist for your question?
  3. List the levels of the hierarchy of scientific evidence pyramid from strongest to weakest.
  4. Explain the qualification the lecture attaches to the evidence pyramid, and state the quoted principle about evidence ranking systems.
  5. In the OCEBM 2011 table, what is the Level 1 design for a question about diagnostic test accuracy, and what specific features must those studies have?
  6. Distinguish the Level 1 evidence for common harms from the Level 1 evidence for rare harms in the OCEBM table.
  7. List the five criteria for grading a level of evidence down, and the one criterion for grading it up.
  8. Name the three circles of the clinical evidence-based practice Venn diagram and the four domains of the public health decision-making diagram.
  9. Describe the features of pertussis that make maternal vaccination the logical protective strategy for young infants.
  10. What is the recommended window for the antenatal Boostrix booster, and what is the physiological reason for that timing?
  11. Describe the design of the Donegan et al. 2014 study, including the comparator group and the primary event of interest.
  12. State the Donegan et al. results for stillbirth in the 14 days after vaccination and for time to delivery, with their measures of effect.
  13. Contrast what the Furuta et al. 2017 systematic review could and could not demonstrate about maternal pertussis vaccination.
  14. A patient shows you the WAVES NZ webpage. Using only the lecture’s evidence, explain what you can tell her about safety outcomes and about the strongest New Zealand evidence.
  15. Describe the Dawber 1957 findings on four-year incidence of arteriosclerotic heart disease by hypertension category, giving the rates per 1,000.
  16. Describe the design and main result of the 1967 Veterans Administration Cooperative Study.
  17. Set out SPRINT as a PECOT question.
  18. State the SPRINT hazard ratios for the primary composite outcome and for all-cause death, with confidence intervals, and describe the harms that were increased by intensive treatment.
  19. Why was SPRINT stopped early, in the sense of when it stopped relative to plan, and what achieved systolic pressures and medication burdens did the two arms have?
  20. Explain the relationship between usual blood pressure and vascular mortality shown by the Prospective Studies Collaboration, and what “time-dependent correction for regression dilution” was applied to.
  21. Predict what happens to pedestrian fatality risk as impact speed rises from 30 to 60, using the death percentages given.
  22. List the co-benefits of lower speed limits given in the lecture.
  23. Summarise the Auckland Transport 18-month evaluation results for roads with lowered speed limits, including the rural road figures.
  24. Using the speed limit scenario, explain how the “environment and organisational context” domain can override the “best available research evidence” domain.
  25. Distinguish the language Waka Kotahi recommends from the language it advises against, with three examples.
  26. Integrative: the pertussis, blood pressure and speed limit scenarios use different study designs as their strongest evidence. For each, name the design and explain why that design suits that question.

Answers

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