Perfusion, Circulation and Sleep

The Loop

The fourteen stops bent into a circle: start at stop 1, bottom left, up the blue side, across the lungs, down the red side. The heart is two pumps side by side, in one loop, so they move the same volume with every beat; the left is stronger because it pushes against higher pressure, not because it moves more. (Standard physiology; the deck defines stroke volume and cardiac output but does not compare the two sides.) And the colour changes in exactly two places — red in the lungs, blue in the body — never inside the heart, because the septum keeps the sides apart.

Inside the Heart

The lab worksheet, and very likely any test figure, uses an anatomical outline, so find the same stops on a real shape.

The Word Bank

The only word bank the course has shown you is on the heart lab worksheet, where you labelled the heart and traced the flow in red and blue. Its terms, sorted by whether each is a stop:

The documents disagree on ten blanks or eleven (see the endnote); you cannot predict the subset, so learn the whole chain. Part 2 drills every version.

One Name, Several Labels

A blank that wants “mitral” may sit beside a diagram that says “bicuspid”. A change of label is not a change of answer.

The atrioventricular-and-semilunar terminology is standard anatomy rather than something the cardiac deck spells out; it is how the four valves sort into the two heart sounds in Part 3.

The Quiz, Rehearsed

The blood-flow question as the Quiz 3 blueprint described it: venae cavae given, the rest blank, a word bank with Apex left in to reject. Type into each blank, or click a blank and then a word.

Three versions, because the documents disagree on the count. Eleven is right atrium to aorta with all four valves (the peripheral-vascular prep sheet’s count). Thirteen adds the lungs and the body. Nine drops the two semilunar valves, as the worksheet’s bank does. When you can do all three with the bank hidden, you are ready.

Two Kinds of Valve

The four valves come in two pairs, and the pairing is the key to the heart sounds. Each lets blood through one way only — the Think Conceptually handout’s “Normal Function of the Heart Valves (open and closing)”. (Standard physiology: valves have no muscle; they open and shut passively, on pressure.)

(Standard anatomy, not in the deck: the AV valves are held by chordae tendineae on papillary muscles, which stop the flaps blowing back; semilunar cusps simply fill and seal.)

Lub and Dub

The deck: systole is “myocardial contraction”, diastole the “filling phase”; Jeopardy: the phase “related to relaxing of the heart muscle” is diastole. The two sounds are the borders between the phases.

The clips are played two octaves higher than life so a phone or laptop speaker can carry them; with headphones, open “Original pitch” under each player to hear the true sound a stethoscope gives.

Where Each Valve Is Heard — APETM

The largest block on the Exam 4 blueprint: 8 questions with skeletal figures and locating heart sounds. The five listening posts, top to bottom, spell APETM.

The lab manual words the tricuspid row “S1 > or = S2”; use the deck’s five lines (see the endnote).

Lab manual: normally 1–2 cm and brief, often not palpable in adults, displaced laterally and left in late pregnancy. Slide-16 notes say “4th–5th ICS”; answer fifth, though “4th–5th” is not wrong (endnote).

The technique, in the deck’s order

1. Rate and rhythm first, in one area — “usually apex or Erb’s point”. Regular: count 30 seconds and multiply by 2. Irregular: count a full minute.
2. Then each area: S1, S2 and any extra sounds.

• Erb’s point is the alternative apical-pulse site — the deck’s notes: “Often easier than Apex for large breasted women.”
• Pulse deficit = apical − radial (Jeopardy), for an irregular pulse: 96 at the apex, 80 at the wrist → 16 beats too weak to make a pulse. (Standard: two nurses, same full minute.)
• Draping: displace breast tissue laterally; expose only the part of the chest being assessed.

Bell or Diaphragm

Equipment: a stethoscope and a watch with a second hand. Lab manual: “Listen with bell (light pressure) and diaphragm (heavy pressure) of stethoscope at all sites.”

Finding the Spaces by the Ribs

On a drawing, the only thing you can count is ribs, so learn each site as a rib address.

Rib addresses: aortic and pulmonic between ribs 2 and 3, Erb’s 3–4, tricuspid 4–5, mitral 5–6 at the midclavicular line.

Labelled

12345

Now find them yourself

Press Start. The unmarked copy has no dots: count down from the sternal angle and click where each site is. Some questions ask by name, some by rib address, some by which sound is louder.

StartShow meStop

Where the Valve Is, and Where You Listen

Two maps of the same four valves. Anatomy: all four bunched behind the sternum, from the pulmonic (highest) to the tricuspid (lowest), where their sounds overlap (standard anatomy). Auscultation — APETM — listens downstream instead.

Extra Sounds

Anything beyond two syllables is an extra sound; the sound strip under Lub and Dub marks where each falls.

S3 and S4 — the gallops

Both are quiet, low thuds in diastole from blood hitting a ventricle that cannot take it. The deck: S3 is “rarely normal in older adults”; S4 comes “late in diastole” from “abnormal resistance to ventricular filling”.

The deck lists children among those in whom S4 can be normal; standard teaching says it is S3 that is normal in children (see the endnote).

Murmurs

A “blowing or swooshing sound”, “audible when blood volume [is] increased in [the] heart or blood flow is impeded or altered”, from “cardiovascular disease or circulatory problems”. Systolic: just after S1. Diastolic: just after S2. The lab manual: graded 1 to 6; “a diastolic murmur or murmur > grade 3/6 is never innocent”; abnormal aortic murmurs are heard best at Erb’s point.

The rest of slide 21

The Think Conceptually handout’s sound list adds muffled; in standard teaching that suggests fluid around the heart (pericardial effusion).

Pericardial or Pleural Rub?

Both are a scratchy, grating sound of two membranes rubbing; the difference is what moves them.

Standard teaching: ask for only a brief breath-hold; a pericardial rub is often loudest at the lower left sternal border with the client sitting up and leaning forward.

Bruits and Thrills

Murmur, bruit, thrill: one event found three ways — turbulent flow through a narrowed or damaged opening. Where you find it, and whether you hear or feel it, names it. The Exam IV review: a bruit is “a swishing sound… in the carotid artery or any other artery”.

Standard content: feel a thrill with the palm or base of the fingers; it first appears at murmur grade 4. Lab manual: a bruit can be normal in children and high-output states.

The One Rule: Look One Stop Backwards

The Exam 4 blueprint’s version of the heart lab’s “what happens with abnormalities” adds the clue: “Important to understand blood flow and internal structures to answer these types of questions.” You work the symptoms out from the fourteen stops. Blood is a one-way queue: when a chamber or valve fails, blood waits in whatever comes before it, and whatever comes after it goes short — a backward half (congestion) and a forward half (not enough arriving).

Left- and right-sided failure as named syndromes, and the backward/forward framing, are standard nursing content (Taylor Ch 40; ATI Cardiovascular); this note covers every left-versus-right table in this part.

Left Side Fails — the Lungs Fill

When the left ventricle cannot empty — scarred by an MI, or worn by years of high blood pressure — blood waits in the left atrium, pulmonary veins and lungs, and fluid is pushed into the air spaces: every backward sign is wet lungs.

Standard nursing content: the mechanisms in the “why” column; the cough of pulmonary edema can bring up frothy, pink-tinged sputum; some patients wake suddenly at night short of breath (paroxysmal nocturnal dyspnea).

The forward half: the left ventricle is the only pump that feeds the body, so its failure is decreased cardiac output — see Not Enough Forward, below.

Right Side Fails — the Body Fills

When the right ventricle cannot keep up, blood waits in the right atrium, the venae cavae and every vein that empties into them — neck above; liver, gut and legs below. The lungs are downstream, so they can stay clear.

Standard nursing content: abdominal congestion can cause loss of appetite and nausea; the abdominal fluid is ascites. The lab manual gives the normal finding as no neck vein distention, jugular venous pressure under 3 cm with the patient at 45° (more in Part 5).

Standard nursing content: chronic lung disease, raising pulmonary artery pressure, is the other classic cause — one reason the deck’s history slide asks about “Lung disease”.

Why Heart Patients Get Up at Night

The prior-year review: “Nocturia (frequent night urination) and Edema are symptoms of which Heart Condition?” — heart failure. The deck pairs them on its bolded history list and asks “Do you get up during the night to urinate?” right after the pillows question: orthopnea is the lungs’ answer to lying down, nocturia the kidneys’.

The mechanism is standard physiology (Taylor Ch 40). Nocturia has other causes — prostate, diabetes, an evening diuretic, bedtime fluid — so look for it paired with edema.

Not Enough Forward: Decreased Cardiac Output

Cardiac output: Jeopardy’s “how much blood the left ventricle pumps out in a minute”, “a reflection of blood flowing around the body, especially to the brain and other vital organs.”

Standard: resting output is roughly 4–8 litres a minute; the compensating rise in rate costs the heart oxygen.

Standard: on a nitroglycerin drip, like HB, BP is also what the drug can drop.

Left-Sided Versus Right-Sided, Side by Side

Sort a stem’s findings into the columns; whichever fills is the failing side. Both? The left probably went first.

HB’s case gives both “poor capillary refill” and “< 3 seconds”, so build no answer on his refill time. That an anterior-wall MI involves the left ventricle (left anterior descending artery) is standard anatomy, not stated in the case.

Traps

The Cardiac History

The cardiac deck spends four slides on subjective data (slides 10–13) before it reaches for the stethoscope, and that proportion is the lesson: most of what the exam will later confirm, the history has already found. Crackles, JVD and an S3 are what you hear and see; orthopnea, nocturia and “I can’t keep up any more” are what the patient tells you first. Parts 3 and 4 explain the findings. This part is the conversation that leads to them.

History of present concern — the deck’s bolded list

Slide 10 sets every line of this list in bold. Learn it as a list of cues, each pointing at a part of the heart’s job:

Standard nursing content: diaphoresis in an MI is a sympathetic (“fight or flight”) response to pain and falling output; the deck lists it without explaining it.

Demographics, past history and family history — the speaker notes

Slide 10’s notes and slide 11 give the rest of the history. Demographics first: age, gender, baseline pulse and BP, recent blood work — the baselines you will compare everything else against.

Why the family-history follow-up asks when: heart disease in a parent or sibling at a young age is a stronger risk signal than the same disease at 85 (standard nursing content). HB’s father died of an MI at 57.

Medications — including the ones they buy themselves

Slide 11: “Medications for heart disease? Why? Assess compliance” and “OTC meds and nutritional supplements?” Slide 13’s notes add the reason: “OTC meds/supplements (some can interact with prescribed meds)”, and ask for the medication schedule as well as the names. Three separate questions hide in that line: what do you take, why do you take it (the answer often names a diagnosis the patient forgot to mention), and do you actually take it as prescribed.

Standard examples of OTC products that matter to a cardiac patient: decongestants and NSAIDs can raise blood pressure, and some herbal supplements interact with anticoagulants.

Lifestyle and health practices — slide 12

Slide 13’s notes add three more: usual weight, typical diet, and recreational drug use.

Chest Pain: Ask, Assume, Act

Stable versus unstable angina, standard nursing content (Taylor Ch 40 defines stable angina as a temporary imbalance between the oxygen the heart needs and the oxygen delivered): stable angina is predictable — brought on by exertion, eased by rest or nitroglycerin. Unstable angina is new, worsening, or comes at rest, and is treated as an emergency. Pain that lasts longer and is not relieved points toward an MI.

What to ask about chest pain — a checklist

Once the patient has described the pain, the rest of the questions fill in the picture. OPQRST is a common way to remember them. It is a study aid, not course wording — the course’s own rule is only that the description comes first, so start at Q and use the letters to make sure nothing is missed. HB’s answers, from the cardiac case, are in the third column.

OPQRST (onset, provocation/palliation, quality, region/radiation, severity, time) is a standard pain-assessment mnemonic, not from the course documents; Taylor’s respiratory history asks the same things (when did it start, where, 0–10, worse with breathing or activity).

The first minutes, in order

Putting the review sheet, slide 23, Jeopardy and the handout together. Every step is correct; the question an exam asks is which comes first.

The order is a synthesis, not a list any course document prints. In practice steps 2–5 overlap in the first minute, and standing orders or an emergency protocol may start oxygen before you have finished asking. On a paper question, “describe the pain” wins the what do you ask first item, and BP wins the which vital sign item.

Standard nursing content, not spelled out in the deck: women, older adults and people with diabetes more often have “atypical” symptoms — unusual fatigue, shortness of breath, nausea, indigestion, back, neck or jaw pain — and older adults may present with confusion or breathlessness alone.

Risk Reduction and Teaching That Works

The population goals — slide 9

Slide 9 states the public-health goal as “Reduce CHD deaths”, and lists how: smoking cessation; educate adults on early warning signs and symptoms — call 911; increase timely therapy (an AED in the community); increase HTN control; reduce cholesterol; more medical office visits for people with co-morbid conditions such as diabetes and high cholesterol; and more adults doing vigorous physical activity.

Standard teaching that goes with “call 911”: do not drive yourself to hospital with chest pain, and do not wait to see whether it passes.

Who carries more risk — slide 24

Teaching that motivates

This reading of the review-sheet question is an inference from the Jeopardy answer, not a printed course answer. It matches standard nursing teaching principles (readiness to learn; motivational interviewing): fear-based messages alone tend to produce short-lived change.

The Physical Exam: Prepare, Inspect, Palpate

Slide 15 is two questions — “What equipment is needed? How will the nurse prepare the patient?” — with the answers set to “fly in” one at a time. A slide built as a quiz is a good guess at an exam question.

Slide 16 then names the techniques, in the usual order — inspect, palpate, percuss, auscultate:

Standard nursing content: a PMI that is displaced to the left of the midclavicular line, or larger than about a coin, suggests an enlarged left ventricle — the left ventricular hypertrophy HB’s old ECG showed.

What it looks like written down. HB’s focused assessment is a model of the format: “Neck vessels: positive carotid pulsations, +2 symmetrical. Jugular vein distention noted.” and “Precordium: pulsation noted at point of maximum impulse. Heart sounds: tachycardia, irregular rhythm. S1 > S2 at apex, S2 > S1 at base, positive S3 noted.” Every phrase in it is something this part or Part 3 taught you to look for.

From the Lab-Manual Table: Neck Vessels and Percussion

The lab manual’s cardiovascular assessment table adds three things the deck only names: how to tell a carotid pulsation from a jugular one, a pressure test on the neck veins called abdominojugular (hepatojugular) reflux, and what percussion of the heart finds.

Abdominojugular (hepatojugular) reflux. The table’s palpation row: “Palpate jugular veins and check direction of fill. Check for abdominojugular (hepatojugular) reflux.” The expected finding is “Jugulars easily obliterated and fill appropriately. Negative abdominojugular reflux.” Negative is normal.

Standard nursing content (the table names the test but not the method): with the patient at 30–45°, press firmly over the right upper abdomen, over the liver, for about 10 seconds and watch the neck veins. A jugular pressure that rises and stays up while the pressure is held is a positive reflux: the right side of the heart cannot take the extra blood pushed back to it. That points to right-sided heart failure — the same backup that causes JVD in Part 4.

Percussion of the heart. Slide 16 lists “Percussion (Advanced) — Cardiac Borders — not commonly performed”, so you will not be expected to do it. The lab-manual table says how it is done and what is normal: indirect (mediate) percussion, from the anterior axillary line toward the sternum at the fifth ICS; expected finding, dullness at the third, fourth and fifth ICS to the left of the sternum. The heart is solid, so it sounds dull where the air-filled lung around it sounds resonant — the change from one to the other marks the heart’s border.

Standard nursing content: dullness that reaches further left than expected suggests an enlarged heart. In practice a chest X-ray or echocardiogram answers that question, which is why the deck calls percussion advanced and rarely done.

Labs and Diagnostic Tests

Three of the blueprint’s cardiovascular lines are about tests: the lipid profile, both kinds of echocardiogram, and preparing for a stress test. They get a blue box each. Everything else on slide 22 and the handout’s list is in the tables, so you can recognise it in a stem.

A study aid, not course wording: LDL = Lousy (keep it Low); HDL = Healthy (keep it High). Slide 22 also asks “Patient education?” for the lipid profile. Standard teaching: the patient may be asked to fast beforehand (traditionally 9–12 hours; follow the lab’s instruction); a diet low in saturated fat, weight loss and medication lower LDL; regular exercise raises HDL and smoking lowers it.

Blood tests

Approximate timing, standard nursing content: myoglobin rises first (within a few hours) but is not specific to the heart; CK-MB rises within hours and returns to normal in two to three days; troponin rises within hours and stays raised for one to two weeks, so it can confirm an MI in a patient who arrives days later. Serial draws are usual. BNP is released by stretched ventricles — the higher it is, the worse the failure.

Diagnostic tests

Standard nursing content: other rate-slowing drugs that may be held are calcium channel blockers such as diltiazem and verapamil, and digoxin; beta-blocker names usually end in -olol (metoprolol, atenolol). A chemical stress test gives a drug that mimics exercise for a patient who cannot walk a treadmill; caffeine is avoided for 12–24 hours because it blocks some of those drugs. The test is stopped for chest pain, a falling BP, a serious dysrhythmia or severe breathlessness. The review sheet prints no answer to its VS question; “HR and BP” is this guide’s reading.

From Cues to Care

The deck closes on the clinical judgement model, with cardiac examples at each step. The case sheet for HB asks you to walk the same steps, so learn them as a sequence:

How the three problems map onto forward and backward failure is in Part 4, along with the handout’s monitoring interventions (vital signs, ECG, LOC, lung sounds, oxygen, positioning, JVD, edema, I&O, daily weights, bedrest). This section adds the handout’s framework and the interventions Part 4 does not cover.

What a normal heart depends on

The handout opens with a list that works as a diagnostic checklist in reverse: each thing a normal cardiovascular system depends on has a matching way to fail.

The first row, in the deck’s words. Cardiac deck slide 7, “Cardiac Conduction System”: the notes say “Electrical impulses fire from the SA node to generate a heartbeat. Essentially the conduction system tells the mechanical system when to ‘beat’.” So the SA node starts each beat, the electrical system sets the rate and rhythm, and the muscle and valves do the pumping. An ECG is the tracing of that electrical conduction. The notes add that the detail comes in the second year, with arrhythmias; for now, know that the beat starts at the SA node.

Standard anatomy: the SA (sinoatrial) node sits in the wall of the right atrium and is the heart’s natural pacemaker. The impulse spreads across both atria, then through the AV node and down the ventricles, so the atria contract just before the ventricles.

Interventions not covered in Part 4

The handout’s collaborative broad goal is “to prevent dysfunction — preserve or maximize the heart function,” with interventions individualised to the patient. Beyond the monitoring list in Part 4, it adds:

• Assess chest pain (cardiac pain) — treat promptly if present.
• Educate the patient regarding the importance of reporting chest pain — a patient who says nothing because “it’s only indigestion” is HB.
• Assess GI — indigestion: “can be associated with MI — plan will be to rule out cardiac issue followed by GI work up.”
• Educate — lifestyle modification: smoking cessation, diet, stress management, medications, activity.
• Administer medications as ordered — below.

Medications — learn them by class

The handout’s advice is the method: “Best to learn medications by classification in order to understand what the RN should be evaluating before and after administering.” Pharmacology comes later in the programme; for now, know the classes on the list and the one thing to check for each.

The handout’s last page lists exemplars (coronary artery disease, MI, heart failure, cardiogenic shock, valve disorders, endocarditis, myocarditis, pericarditis) and procedures (percutaneous coronary interventions such as angioplasty and stents, valve repair, bypass grafting, pacemakers, implanted defibrillators, ablation) and says they “will be discussed in conjunction with appropriate exemplars in the NUR courses.” They are not on the Exam 4 blueprint.

Worked Case: HB

HB, 72, presents to the ED with chest discomfort that began after dinner and woke him from a nap. Treated for hypertension for four years. Given aspirin and started on a nitroglycerin drip; ECG and cardiac enzymes drawn; admitted to the cardiac care unit with an anterior wall MI. He asks, “Am I going to die?” The case sheet’s reverse side walks the clinical judgement model. Part 4 sorted his findings into left- and right-sided failure; here is the whole case, every cue tied to where this guide explains it.

Step 1 — identify the cues

Two negatives on HB’s sheet. The case also records “negative clubbing” (with the skin) and “negative hepatomegaly” (with the abdomen). A negative is a finding too: it tells you what has not happened yet. Both are signs of a problem that has gone on for a long time, and HB’s problem is sudden.

Standard nursing content: clubbing is a bulbous swelling of the fingertips, with the angle between the nail and the nail fold flattened to 180° or more. It develops over months from chronic hypoxia — long-standing heart or lung disease — so it is not expected in an acute MI. An enlarged liver (hepatomegaly) comes from long-standing right-sided backup, the same congestion that gives a positive hepatojugular reflux.

Steps 2 to 6 — the case sheet’s questions

The case sheet is blank; these are one defensible set of answers built from the course documents, not an answer key.

Two cautions about the case document (the first repeated from Part 4): it records both “poor capillary refill” and “capillary refill < 3 seconds”, so do not build an answer on his refill time; and the BMI figure is this guide’s calculation (275 lb at 6 ft ≈ 37), not the case’s.

What This Part Covers, and the Words It Uses

The heart is the pump; this part is the pipes. The blueprint’s peripheral vascular heading says “Refer to handouts and case summaries”, and its lines ask for the names of the pulse sites, the normal and abnormal findings, the carotid artery and the symptoms of arterial occlusion — all of which are here. The diseases themselves (PAD, DVT, varicose veins and the rest) are Part 7. The source is the peripheral vascular lecture deck and its recorded lecture; where the instructor said something aloud that the slide does not, what she said wins.

The lecture’s own objectives put one skill above the rest: “be proficient in locating pulse points… so that we’ll be able to pick that out on a test or the NCLEX.” The blueprint’s eight figure questions are heart sounds on a skeletal figure (APETM, Part 3); a pulse-site picture is not promised, but “pick that out on a test” makes the body figure below worth drilling.

The deck lists DVT, embolism, thrombus and varicosities without defining them; those lines are standard definitions.

Structure and Function

Four kinds of vessel, one job: oxygenated blood out to the body, deoxygenated blood back to the heart and lungs. The deck takes them in order — arteries, veins, capillaries, lymphatics — and the contrast between the first two is where the questions come from.

Capillary beds are where the work is done: the exchange of nutrients, gases and metabolites between blood and tissues. Oxygen-rich blood arrives from the arterioles; the venules carry the metabolites away into the veins. The lymphatic system — nodes, vessels running parallel to the arteries and veins, spleen, tonsils, thymus — maintains fluid and protein balance (when it is overloaded the result is lymphedema) and fights infection alongside the immune system.

Getting Blood Back Up the Leg: Venous Return

Arteries have the heart behind them. Veins do not — by the time blood reaches the feet the heartbeat’s push is spent, and the blood has to climb a metre back to the heart against gravity, through thin, non-muscular tubes. The deck names three things that make it possible:

The other answers to slide 10’s question — ambulation (the real calf pump: “as a person walks, the contraction of the calf muscles promotes venous flow”), anti-embolism stockings, leg elevation, range-of-motion exercises and the rest — are gathered into one checklist under the blueprint’s “prevent venous emboli” line in Part 7.

Across the Lifespan

Standard obstetric figures put the rise in blood volume nearer 40–50% than a full doubling. The deck says “doubles”; if an option offers it, it is the course answer.

Subjective Data

Slide 13 lists the present health concerns to ask about: colour or texture changes in the skin, pain, numbness or tingling, cramping, decreased functional ability, edema, bulging veins. The notes — read almost word for word in the lecture — tell you what each one points to:

Risk factors

Slide 14 asks about personal and family history of cardiovascular or circulation problems — blood clots, ulcers, numbness, edema — and then the habits and conditions behind them: smoking, diabetes, a sedentary lifestyle, sitting or standing for long periods, hypertension, genetics, oral contraceptives or estrogen, high cholesterol or a high-fat diet, and recent trauma to an extremity. Three lines from the notes carry the numbers:

Slide 15 then asks you to sort these into modifiable and non-modifiable. That sort sits with the two blueprint lines that ask for it, in Part 7 (the cardiac version of the same sort is in Part 5).

Equipment and Preparation

Slide 16 is two questions that “fly in” — what equipment is needed, and how will the nurse prepare the patient? — with the answers in the notes.

Inspection and the Pitting Edema Scale

Slide 18’s list: size and symmetry, colour of the skin, colour of the nail beds, edema, ecchymosis, wounds, lesions, venous patterns and varicosities. (Ecchymosis is a bruise — the lecture: “If you don’t know, look it up.”) The notes add one instruction above all others: “Stress the importance of comparing one extremity to the other.”

Normal, from the lab-manual assessment table: skin colour uniform, with no erythema, red streaks, edema or lesions; leg hair evenly distributed; no varicosities. If edema is present, the same table says to measure the calf circumference — which is what the measuring tape is for.

The pitting edema scale is the lecture’s “this should be a repeat for many of us” — press a thumb or finger into the swollen tissue over a bone, release, and judge how deep a pit it leaves.

Palpation: Temperature, Turgor, Capillary Refill

Slide 20 lists four things to palpate: temperature, turgor and texture, capillary refill, peripheral pulses. Pulses get their own section next. For temperature the notes give a technique: use the dorsal aspect (the backs) of your hands and assess both extremities at the same time, comparing one with the other.

Why the backs of the hands, standard nursing content: the skin there is thinner and more sensitive to temperature than the palms.

Turgor and texture share slide 22 with capillary refill. To test capillary refill, press on a nail bed until it blanches, release, and count the seconds until the colour returns. The slide only asks the question — “Normal Capillary Refill? (? Seconds)”. The instructor answers it.

The press-and-count technique is standard nursing content; the slide shows it in a photo without describing it.

The Pulse Sites, by Name, Place and Purpose

Slide 23 names eight sites: temporal, carotid, brachial, radial, femoral, popliteal, posterior tibial, pedal. The notes add the technique — use the pads of two or three fingertips — and that the carotid and apical are covered with the heart — the apical with the heart sounds (Part 3), the carotid in the cardiac assessment (Part 5). The lecture adds the apical to the list of reasons, so it is here too. Slide 26 is five photos with no labels, and the instructor’s note is “Have students identify names of pulse sites”; the lecture asks over them, “Do you know the landmarks around each of these photos? Do you know the names of those landmarks?” — so the landmark is part of the answer.

From the lab-manual table: use light palpation with the finger pads, and note rate, rhythm, equality, amplitude and elasticity; normal is regular, equal, +2, with soft, pliable arteries and no thrills. It also says to document pulse amplitudes on a stick figure — the same kind of figure the exam uses. The table lists an ulnar pulse too; the course deck does not. Its grading list also skips 2 — “0 = Absent, 1 = Weak, 3 = Full, 4 = Bounding” — while the same table gives normal as “+2”: answer with the deck and the lecture, 2+ is normal, documented 2+/4. “If indicated”, the table adds an Allen test (arterial flow to the hands) and an ankle–brachial index (flow to the legs, Part 7).

The Allen test, standard nursing content (Taylor uses it before a radial arterial blood gas): press on the radial and ulnar arteries while the patient makes a tight fist, have them open the blanched hand, release the ulnar — colour returning within a few seconds means the ulnar artery alone can supply the hand.

Auscultation: Bruits and the Doppler

Slide 27 has two items. Bruit (carotid / aortic / femoral): the lecture — “we utilize the bell of our stethoscope to listen for bruits. And that’s a swishing sound.” And Doppler pulses if not palpable.

The recording of a real carotid bruit is in Part 3 (Bruits and Thrills), next to the murmurs it must not be confused with. In an adult, a normal carotid makes no swish; the lab-manual table notes a bruit “may be normal in children and with high-output states”.

The lab-manual cardiovascular table gives the technique: “Listen for bruits with bell of stethoscope. Have patient hold breath when auscultating for carotid bruits” — so breath sounds do not mask a soft bruit (Part 3 quotes the same line).

Standard nursing content: a bruit over a narrowed carotid is a stroke risk — the HEENT case client with a soft bilateral carotid bruit also had a blood pressure in the 180s.

The same lab-manual table pairs the carotid with the jugular vein: listen with the bell, breath held, for a venous hum. Normal is none, though a venous hum “may be normal” in children. To tell it from a murmur carried up from the heart, press on the jugular vein — a venous hum disappears.

Blood pressure — the lab-manual lines

The deck does not cover blood pressure; the lab-manual peripheral-vascular table lists it under auscultation:

Two lab-manual figures are older than current practice: it calls a 10–15 mm Hg systolic fall orthostatic (current definitions use 20 systolic or 10 diastolic) and gives normal adult BP as under 140/90 (current guidelines call 130–139/80–89 stage 1 hypertension). If an item quotes the table, answer with the table.

The Doppler

When a pulse cannot be felt, it can often still be heard. The slide 27 notes, read aloud: the Doppler “can assess weak peripheral pulses. It magnifies pulsatile sounds from the heart and blood vessels as an arterial signal. The arterial signal is a rhythmic whooshing sound.” The technique, in the deck’s order:

Standard nursing content: the probe is usually held at about 45 degrees, pointing toward the heart, with light pressure (pressing hard can flatten the artery); once found, the spot is often marked with a pen so the next nurse can find it again. A pulse heard only by Doppler is commonly charted as “D” or “Doppler” rather than a number.

Labs: Arterial Risk, Venous Clot

Standard nursing content: C-reactive protein is a marker of inflammation, and homocysteine is an amino acid whose high levels are linked to vessel damage and clotting. D-dimer is a fragment released when a clot breaks down; a normal D-dimer makes a DVT unlikely, but a raised one is not specific, so the ultrasound (venous duplex) is what confirms it.

The Seven P’s of Arterial Occlusion

The lecture: “So the seven P’s of arterial occlusion in limb. So this is a great way to remember.” They are what a limb looks and feels like when its artery is blocked — limb ischemia — and the review sheet points straight at them: “What are signs of Peripheral Arterial Occlusion/Disease? (See 7 P’s PPT from Peripheral Assessment).”

The automatic transcript of the recorded lecture renders the list as “pain, power, pulselessness…”; the slide makes clear the word is pallor.

Standard nursing content: in acute limb ischemia, paresthesia and paralysis are late signs — the nerves and muscle are already being damaged, and the limb is in danger. Pain and pallor usually come first.

Clinical Judgement: Problems, Goals, Interventions

The last slide runs the findings through the clinical judgement model — hypothesis, generate solutions, take action, evaluate. The lecture: “we see that a patient has pale or cold extremities. So they might have altered tissue perfusion, arterial.”

That is the assessment. Part 7 takes the same findings and sorts them into the disorders the blueprint and the tidbits handout name — PAD, Raynaud’s, Buerger’s, venous thrombosis and DVT, venous insufficiency, varicose veins — with the arterial-against-venous comparison and the case of JH.

Arterial or Venous?

Part 6 taught you how to examine a leg. This part is about what the findings mean, and almost every question on it turns on one decision you make first: is the problem on the way in, or on the way out?

Arteries bring blood in. When they narrow, the tissue below the narrowing is starved — it is pale, cold, hairless, painful when it is asked to work, and it heals badly. Veins take blood out. When they or their valves fail, blood pools — the leg is swollen, warm, stained brown, and it aches after standing. Starved against flooded. Nearly every row of the table below follows from that one difference.

The course’s words for the two sides: the tidbits handout puts the arterial disorders under Peripheral Arterial Disease (PAD) and the venous ones under Peripheral Vascular Disease (PVD), and the peripheral-vascular preparation sheet tells you to “review and understand difference between PAD and PVD.” The blueprint’s heading for this whole area is “Refer to handouts and case summaries”, so the handout and case JH are the backbone of this part.

Arterial ulcer

Venous ulcer

Peripheral Arterial Disease

The handout’s definition: a chronic disorder in which partial or total arterial occlusion deprives the lower extremities of oxygen and nutrients, and tissue damage occurs below the level of the occlusion. Atherosclerosis is the most common cause — narrowing from plaque, the same process as coronary artery disease, and the handout says its risk factors are “very much like in CAD.”

The leg-to-arm pressure comparison is what the ankle–brachial index measures (ankle systolic ÷ brachial systolic; about 1.0 or higher is normal, under about 0.9 suggests PAD). The lab-manual table mentions the index; the number is standard nursing content.

Acute Occlusion, Procedures and Embolectomy

The handout draws a line you should hold onto: everything above is chronic PAD, built up over months or years. A patient with an acute occlusion from an embolus — a clot that has travelled and lodged — is an emergency and “may require an emergency procedure: catheter embolectomy, thrombolytic or surgical embolectomy, depending on severity.”

The acute picture is the P’s of arterial occlusion / limb ischemia (Part 6) and the deck’s one red line: pain, numbness and tingling, coolness or colour change — “urgent/ possible total arterial occlusion.” Jeopardy lists the findings that “need immediate intervention”: absent or diminished pulses, delayed capillary refill, pallor, and numbness and tingling.

The handout also says, of every vascular procedure, that the peri-operative basics always apply: control pain, prevent pneumonia, prevent DVT, prevent wound infection.

Raynaud’s and Buerger’s

Both appear on the deck’s common-disorders slide and in the handout, and both affect the small arteries of the fingers and toes. The difference is spasm against inflammation: Raynaud’s vessels clamp down and then let go; Buerger’s vessels are inflamed and occluded.

Standard nursing content, not in the handout: Buerger’s disease is very strongly tied to tobacco use, typically in younger adult smokers, and stopping tobacco completely is the one treatment that halts it — which is why the handout lists smoking cessation first.

Assessing Risk and Preventing Arterial Disease

The blueprint asks for “assessing risk of arterial disease” and “prevention of arterial disease/ risk factors”. The first is a set of questions you ask (deck slide 14); the second is what you can change (deck slide 15). The handout says the risk factors are “very much like in CAD”, and the deck’s notes say the same: “same as risk factors for CAD that can lead to MI.”

The deck’s notes single out smoking, high-fat diet and limited activity as “the most modifiable.” The blood tests that measure arterial risk (slide 28): lipid levels, HbA1c for diabetic patients, and C-reactive protein and homocysteine. And slide 12: the American Heart Association says prevention begins in childhood — atherosclerosis already shows in young people with familial hypercholesterolaemia, so teach the risk factors early.

Venous Thrombosis

A thrombus can come with inflammation, and inflammation can come with a thrombus: the handout says the inflammation thickens the vein wall and leads to embolisation — the clot breaking loose. That is the whole danger of the venous side: a leg clot becomes a lung clot.

The handout lists eight items; grouping them under stasis, clotting and vessel-wall injury is the textbook’s Virchow’s triad (standard nursing content). If a stem asks why a post-operative orthopaedic patient is at risk, all three apply: immobile (stasis), surgical trauma (wall injury), and the body’s clotting response to surgery.

Pairing hook (standard): heParin → PTT (P with P…T…T), warfarin/Coumadin → PT/INR (“War” and “PT” are the shorter pair). The handout’s “Diet” means, in standard teaching, keeping vitamin K foods (leafy greens) consistent rather than cutting them out, because vitamin K counteracts warfarin.

The IVC filter

An inferior vena cava filter is a wire, umbrella-shaped filter placed in the inferior vena cava to trap emboli and stop them reaching the lungs (tidbits). The deck’s vein slide points to the IVC as the place it sits. It catches clots; it does not dissolve them or stop new ones forming in the leg.

The recorded lecture describes the IVC filter as something that “actually prevents clots”. The handout’s wording is the precise one: it prevents clots moving to the lungs. If an option says a filter treats or dissolves the DVT itself, it is wrong.

Preventing Venous Emboli — The Checklist

Three course documents ask the same question three ways: the blueprint line, the review sheet’s “What interventions are useful in prevention of VTE (Venous Thrombus Embolism)?”, and the deck’s capitals, “HOW CAN WE HELP TO ENHANCE VENOUS RETURN IN OUR HOSPITALIZED PATIENTS?” The answer to all three is the same idea: keep the blood moving out of the legs, because blood that sits still clots.

Venous Insufficiency and Varicose Veins

Venous insufficiency comes from prolonged venous hypertension — high pressure in the veins stretches them and damages the valves. With incompetent valves, blood pools: venous stasis and edema, which lead to venous stasis ulcers, swelling and cellulitis. Assessment: dermatitis from venous stasis — brownish discoloration along the ankles, extending up to the calf; edema; ulcers. The treatment focus is to decrease edema and promote venous return, and once an ulcer exists, to heal it and prevent it coming back.

The handout says the home system is “like ICD in the hospital”. In context that is almost certainly a typing slip for SCD — the sequential compression device the lecture discusses.

The Rest of the Deck’s List

The deck’s common-disorders slide names ten conditions, and the lecture tells you plainly to look up any you do not know. Most are covered above. The three the handout does not cover are below, in one line each.

† Standard nursing content; the deck names these without defining them.

Case JH, Worked Through

JH is a 55-year-old married African American man admitted with a history of CAD, hypertension and diabetes. Chief complaint: “My left leg hurts and I have two ulcers on my toe that will not heal.” The case sheet walks you through the clinical judgement model — the same model as the deck’s slide 31 — one heading at a time. Here it is filled in.

Arithmetic you can check: 220 lb is about 100 kg and 5 ft 9 in is about 1.75 m, so his BMI is about 32.5 — obese (30 and over), standard content. A normal fasting glucose is under 100 mg/dL, so 140–150 is well above it.

Note what is not there: the case never mentions smoking. Do not add it. A nurse assesses it — it is the first question on slide 14 — but you do not teach cessation to a man who has not been shown to smoke.

Standard nursing content for the diabetic, poorly perfused foot that the case does not spell out: never walk barefoot, check between the toes, keep the skin moisturised but not between the toes, and have a professional cut the thickened nails.

What the Blueprint Asks

The sleep block is six questions, and all three blueprint lines end in the same two words: “PP slides”. That means the Rest & Sleep lab deck, not the textbook chapter. When the deck and Taylor disagree in this part, the deck wins and Taylor’s version sits underneath in grey.

“Chemicals present”, all in one line. The deck has three: melatonin regulates the sleep–wake cycle (slide 6) and “helps to induce sleep”, and carbohydrates stimulate it (slide 24, red); protein wakens the brain (slide 24, red); and short sleep lowers leptin, which raises appetite (slide 21) — the only one the deck itself calls a “chemical change”, and the reason obesity heads slide 5’s red list. Melatonin is in What Runs Sleep; leptin is in the next section.

Rest, Sleep and What Losing It Costs

The deck separates two words that people use interchangeably. Rest is a decreased state of activity that leaves you feeling refreshed — you can rest wide awake. Sleep is a state of rest with an altered state of consciousness and relative inactivity, whose job is to restore mental and physical function. Sleep is not one flat state: it is a complex rhythmic state, a progression of repeated cycles, each with different phases of body and brain activity. That last phrase is the whole of the NREM–REM section to come.

Taylor adds that REM is believed to play a role in learning, memory and adaptation, and that sleep and wake states carry distinct hormonal patterns that influence metabolism and glucose homeostasis — one way to make sense of diabetes and obesity on the red list. The deck gives each kind of sleep its job in the stage table further down.

What Runs Sleep

Slide 6 names three brain structures and one hormone. Learn them as a short chain: two systems in the brainstem switch sleep on and off in cycles, the hypothalamus is the control centre, and melatonin is the chemical messenger that tells the body it is time to sleep.

The circadian rhythm (slide 7)

A circadian rhythm completes a full cycle every 24 hours. Circadian synchronization is when your sleep–wake pattern follows your inner biological clock. That clock is influenced by light and dark — but the deck is careful to add, “not primary control” — and by occupational demands and social pressures. Desynchronization is what happens when the sleep–wake pattern is frequently altered: rotating shifts, jet lag, a hospital stay.

Standard physiology, beyond the deck and in grey because the blueprint says “PP slides”: Taylor lists the neurotransmitters involved — norepinephrine, acetylcholine, dopamine, serotonin and histamine with excitation, GABA with inhibition — and explains caffeine as blocking adenosine, a compound that builds up while you are awake and causes drowsiness. Taylor also explains the carbohydrate effect through the amino acid L-tryptophan (carbohydrates make it more available to the brain). If a question offers melatonin among these, the deck’s answer is melatonin.

NREM and REM

There are two kinds of sleep. NREM (non-rapid eye movement) is most of the night — 75–80% — and is split into four stages that get deeper as they go. REM (rapid eye movement) is the other 20–25%: the dreaming sleep. The cleanest way to keep them apart is the one the instructor drew on slide 8 — the vital signs go in opposite directions.

The four NREM stages, and REM

Slide 9 lays the four stages out as a two-by-two grid, and the text runs in a confusing order if you read it as a list — Stage 1 top left, Stage 3 top right, Stage 2 bottom left, Stage 4 bottom right. Read by box, this is what each stage says:

Taylor 10e Box 35-1 adds detail the deck leaves out. Stage I can include involuntary muscle jerking that wakes the person; stage II is 50–55%. In REM the eyes dart, small facial muscles twitch, large muscles are immobile, resembling paralysis, respirations are irregular, sometimes with apnea, the pulse is rapid or irregular, gastric secretions increase, and the EEG is active. Taylor describes the arousal threshold as greatest in stage IV.

The Sleep Cycle

Slide 11 is four sentences, and together they describe one cycle of 90–100 minutes:

1. The person passes consecutively through the four stages of NREM: I → II → III → IV.
2. The pattern then reverses: IV → III → II.
3. Instead of re-entering stage I, the person enters REM.
4. The next cycle re-enters NREM at stage II and moves on to III and IV.

Taylor 10e (Ch 35) still teaches four NREM stages, with the same percentages and the same I–II–III–IV–III–II–REM pattern. It adds: most people go through four or five cycles a night; each lasts about 90 to 110 minutes (the deck says 90–100); and a person woken at any point returns to sleep starting at stage I. The three-stage N1–N3 scheme is the current American Academy of Sleep Medicine scoring standard, not something either course source uses. Two citation notes: the deck’s slide 8 cites “Taylor box 33.1” and slide 12 cites “Taylor Box 34-2” — numbers from older editions (the deck’s reference list is the 9th edition). In the 10th edition they are Box 35-1 (characteristics of NREM and REM) and Box 35-2 (developmental patterns of sleep).

What Gets in the Way

Jeopardy asked for “factors that interfere with any stage of the sleep cycle” and answered alcohol, caffeine, exercise, stress, medications, shift work. Every one of those six is on slide 12, which is the fuller list:

Taylor on alcohol: a drink may help someone fall asleep, but larger amounts limit REM and delta sleep, and sleep fragments once the alcohol is cleared. That is why alcohol is on the “limit at bedtime” list even though patients often describe it as a sleep aid.

How much sleep, by age — Taylor 10e (Chapter 35), not the deck, which says only that needs change with development. Newborns average about 16 hours in 24; infants 12–16 (with naps); toddlers 11–14; preschoolers 10–13; school-aged children 9–12; teenagers 8–10; adults 7 or more; older adults 7–8 (up to 9). Older adults need about as much as younger adults but get it in lighter, more broken sleep, with less stage IV and shorter REM. The deck’s rule still decides an exam item: judge a patient’s sleep against their own usual pattern.

Shift Work

Shift work disrupts the circadian rhythm by making the body sleep when its clock says wake. Slide 22 lists the possible adverse effects: anxiety and depression, GI symptoms, chronic fatigue, and a set of long-term health risks the deck marks with an arrow.

When Sleep Goes Wrong

The deck sorts sleep disorders into two classes. A dyssomnia is a problem with the amount, timing or quality of sleep itself — too little, too much, or broken. A parasomnia is a behaviour that happens during sleep — the sleep may be fine, but something is done in it.

Taylor 10e defines adult obstructive sleep apnea as five or more obstructive events per hour with symptoms (daytime sleepiness, loud snoring, observed apnea, gasping), or more than 15 per hour even without symptoms; pauses last 10–20 seconds and can reach 2 minutes. The sleep study is a polysomnogram (EEG, eye movements and muscle tone recorded overnight). Treatment is commonly CPAP. On the exam, use the deck’s wording: more than 5, lasting 10 seconds, in an hour.

Three review-sheet questions

Assessing Sleep

The sleep assessment is mostly subjective — the patient’s own account — with a few things you or a bed partner can observe. The deck gives it in four pieces.

Helping Patients Sleep

Slide 23 frames the nursing problem — sleep disturbance, showing up as difficulty remaining asleep, premature awakening, excessive daytime sleeping or an altered sleep–wake pattern — and lists the usual causes: emotional stress, exhaustion, a changed bedtime ritual or environment, circadian disruption from travel or work, exercise within 2 hours of bed, caffeine and heavy meals, drug dependency and withdrawal, and physical illness.

Treating a dyssomnia (slide 24)

Standard nursing content, in brief: stimulus control means using the bed only for sleep and getting up if not asleep after a while; sleep restriction limits time in bed to the time actually spent asleep, then lengthens it. Taylor names cognitive behavioural therapy as the first-line treatment for chronic insomnia.

Taylor disagrees on protein: it recommends a small protein-and-carbohydrate snack (it even suggests “cheese and crackers” or peanut butter on toast) because protein supplies L-tryptophan. The course sources all say avoid protein and cheese at bedtime, so answer with the course. Taylor also advises avoiding caffeine for 4–5 hours before bed and avoiding large, heavy or spicy meals — which agrees with the course.

The Week’s Terms

Both preparation sheets end with a “Define Terms” list. Here they are together, each in one plain line, using the decks’ own definitions wherever the decks give one.

Thrombus and embolism are listed but not defined in the decks; those two lines are standard definitions, consistent with the tidbits handout’s use of the words.

The marked items, one more time

The night before: the first five rows of the box are the eight figure questions, and the sixth is the chain every backup question rests on — say every site with its space, its rib address and its louder sound, out loud, top to bottom. The last seven rows are the six sleep questions. Everything between is the thirty-two multiple choice.

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