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ENV 226: Essential Ecology Final Exam Study Guide — om single-species thinking to the dynamics of many interacting ecies. A community is more even when all species have similar abundances. Diversity: A combined measure of richness and evenness. More diverse = more likely to pull multiple different species out of a 'hat'. Shannon Diversity Index (H′): The most common diversity index. Higher H′ = more diverse (high richness AND high evenness). Formula: H′ = –Σ(pᵢ · ln pᵢ), where pᵢ is the proportion of individuals in species i. Worked example If a community has 4 species, each at 25% (p = 0.25), then H′ = –[4 × (0.25 × ln 0.25)] = 1.39. If one species dominates (e.g., 70/10/10/10), evenness drops and H′ falls even though richness is the same. Why diversity matters — ecosystem function & services Ecosystem function: Biological, geochemical, and physical processes that take place within an ecosystem (e.g., productivity, nutrient cycling, decomposition, pollination). Ecosystem services: The benefits humans derive from ecosystems. Four major categories: Provisioning: food, water, timber, fiber Regulating: climate regulation, flood control, water purification Cultural: recreation, spiritual, aesthetic, educational values Supporting: soil formation, nutrient cycling, primary production How diversity affects function — mechanism Complementary resource use (niche complementarity): Different species use slightly different resources (e.g., water at different soil depths, nutrients at different times). A diverse community captures more of the available resources than any single species could, raising total productivity. Diversity–stability theory Compensation: Species respond differently to environmental fluctuations. When one species declines, another can increase and 'compensate,' keeping overall ecosystem function steady. Insurance hypothesis: A diverse community is more likely to contain at least one species with traits that help the ecosystem cope with change. Diversity acts as ecological 'insurance' against disturbance. Rules of community assembly — what determines diversity at a site Three filters act in sequence on the regional species pool to determine which species actually end up in a local community: Term Definition Dispersal Who can physically get there. Controlled by distance from source populations and by dispersal ability. Connects to the 'mass effect' / rescue effect — regional diversity (gamma) can rescue local diversity (alpha). Environmental filtering What species can tolerate the abiotic conditions (climate, soil, water, salinity). Example: Ponderosa pine will not survive in the Sonoran Desert — environmental filtering excludes it. Biotic filtering What species can coexist given interactions with other species (competition, predation, facilitation). Strongest where abiotic conditions are benign, because more species can be there to interact. Intertidal zonation paradigm — how the filters stack In rocky intertidal communities, abiotic stress (desiccation, wave action) sets the UPPER limit of a species' distribution — an environmental filter. Competition and predation set the LOWER limit — biotic filters. Take-home: environmental filtering dominates in stressful zones; biotic filtering dominates in benign zones. What maintains diversity Intermediate Disturbance Hypothesis (IDH): Diversity is highest at intermediate frequencies or intensities of disturbance. Low disturbance lets competitive dominants exclude others; high disturbance eliminates all but the most disturbance-tolerant species. The middle keeps both groups in the community. Positive species interactions (facilitation): When one species makes conditions better for another (e.g., a nurse shrub providing shade and moisture for seedlings underneath). Facilitation tends to INCREASE biodiversity, especially in stressful environments. 1.2 Succession Primary succession: Colonization of a substrate that has NEVER supported life (e.g., bare bedrock, new volcanic rock, glacial retreat). Soil must be built from scratch, typically by pioneers like lichens and mosses. Secondary succession: Recovery after a disturbance that left soil and some biological legacy behind (e.g., a cleared field, most wildfires). Much faster than primary succession because soil and seed bank persist. Pioneer species: The first species to colonize a disturbed or bare area. Typically fast-growing, high-dispersal, stress-tolerant organisms that modify the site so later-successional species can establish. Quiz-style example The Woodbury Fire burned so intensely on the Tonto NF that only bedrock remained. Recolonization of this area is PRIMARY succession — there is no soil or seed bank left to start from. 1.3 Ecological Energetics Energy: The currency of ecosystems. Most ecological energy originates from the sun as electromagnetic radiation and is stored in tissues (biomass). Trophic level: Organisms that share the same function in the food chain and the same nutritional relationship to primary sources of energy. Level 1 = producers; 2 = primary consumers (herbivores); 3 = secondary consumers (carnivores); 4+ = tertiary / apex predators. Autotroph (primary producer): An organism that produces its own food from inorganic sources — typically plants, algae, and some bacteria via photosynthesis. Consumer (heterotroph): An organism that obtains energy by consuming other organisms. Primary consumers eat producers; secondary consumers eat primary consumers; etc. Production: The rate at which new biomass is created by organisms in an ecosystem (units of mass or energy per area per time). Net primary production (NPP): Gross primary production (total photosynthesis) MINUS the energy plants use for their own respiration. NPP is what is actually available to herbivores. Assimilation and production efficiency Energy is lost at every step of the grazing food chain. Two key efficiencies describe where energy goes: Term Definition Assimilation efficiency (Energy assimilated / energy consumed) × 100%. Assimilated = consumed – egested (waste). Herbivores ≈ 20–50% (tough plant material); carnivores ≈ 80% (similar tissue chemistry). Production efficiency (Energy in new biomass / energy assimilated) × 100%. Endotherms (birds, mammals) are LOW (~1–3%) because most energy is burned as heat; ectotherms (insects, reptiles, fish) are HIGH (~10–50%). Worked example (assimilation efficiency) Eats 400 J, excretes 200 J as waste, puts 50 J into growth. Assimilated = 400 – 200 = 200 J. Assimilation efficiency = 200 / 400 = 50%. The 10% rule Roughly 10% of the energy at one trophic level is transferred to the next. The rest is lost to respiration, heat, and waste. This is WHY food chains are short (usually 4–5 links): there simply isn't enough energy left to support another level. 1.4 Food Webs A food web is many, connected food chains — a map of who eats whom across an entire community. In simple diagrams, arrows point from prey to consumer. Complex diagrams use plus/minus signs to show the direction of effect, and dashed lines to show indirect effects. Top-down control: Higher trophic levels (predators) limit the abundance of lower levels. Removing a top predator releases herbivores, which suppress plants. Bottom-up control: Lower trophic levels (nutrients, producers) limit higher levels. Adding nutrients increases plants, which increases herbivores, which increases predators. Trophic cascade: Indirect effects of a predator propagate down the food web. Classic example: wolves reintroduced to Yellowstone → elk browsing decreases → riparian willow and aspen recover → beavers return → stream ecosystems recover. 2. Ecosystems Ecosystem: A community of organisms PLUS their shared environment. Includes biotic components (plants, herbivores, carnivores, detritivores) and abiotic components (climate, soils, nutrients). 2.1 Ecological building blocks Ecological building block: An atom that (1) makes up organisms and (2) is relatively abundant. Key building blocks: C, H, O, N, P (and sometimes S) — collectively CHONP. Not building blocks: Silicon, aluminum, arsenic, tungsten — they may be abundant in the crust or used by some organisms, but are not core structural elements of life. Potassium is important biologically but is NOT a core 'ecological building block' in this course's sense. 2.2 Liebig's Law of the Minimum Growth is dictated not by the total resources available, but by the SCARCEST resource. The 'limiting nutrient' sets the ceiling on production; adding more of a non-limiting nutrient has no effect until the limit is raised. Application — nutrient pollution A coastal system receives 10 g N, 200 g P, 50 g C, and 20 g O per year as pollutants, and you know the system is N-limited. By Liebig's Law, adding MORE nitrogen is what will most change structure and function — even though phosphorus is arriving in larger quantities, it is not the limiting nutrient. 2.3 Eutrophication Eutrophication is the enrichment of an aquatic system with nutrients (especially N and P) from fertilizer runoff, wastewater, or atmospheric deposition. Process: Excess N fuels algal blooms → algae die and sink → microbial decomposition consumes oxygen → a hypoxic 'dead zone' forms → fish and invertebrates die. Once N is drawn down, the system can become P-limited; phosphorus mined for fertilizer keeps the cycle going. The Gulf of Mexico hypoxic zone is the classic example. 2.4 Nutrient cycles (N, C, P) Term Definition Nitrogen cycle N₂ in atmosphere is biologically inert. Nitrogen-fixing bacteria (free-living and in legume root nodules) convert N₂ → ammonium (NH₄⁺). Nitrification converts NH₄⁺ → nitrite → nitrate (NO₃⁻), the form most plants take up. Denitrification returns N₂ to the atmosphere. Humans roughly DOUBLED global N fixation via the Haber-Bosch process → fertilizer → eutrophication. Phosphorus cycle Largely a SEDIMENTARY cycle — no gaseous phase. P weathers from rock → soil → plants → consumers → back to soil → eventually to ocean sediments. Slow turnover at global scales; a critical component of DNA/RNA, phospholipids, bones, and ATP. Carbon cycle See dedicated section below. C moves among atmospheric, terrestrial, oceanic, and fossil pools. Photosynthesis pulls CO₂ out; respiration and combustion return it. 2.5 Ecotones and cross-ecosystem flows Ecotone: A transition zone between two ecosystems, exhibiting gradients in environmental conditions and a related shift in the composition of plant and/or animal communities (e.g., forest–grassland edge, estuary). Two factors determine how a flow of material/energy from one ecosystem affects another: Relative size of the systems — when the amount of something varies across ecosystems, the LARGER system has a bigger impact on the small system (e.g., a stream flowing into a small pond vs. into the ocean). Quality of the resource — rich subsidies (like salmon carcasses bringing ocean nutrients to streams) matter more than dilute ones. 2.6 Ecological state change & resilience Key components of ecosystems: STRUCTURE (what organisms are there and how they interact), FUNCTION (processes of energy and nutrient movement), and REGIME (which of several possible stable states the system is in). Alternative stable states: An ecosystem can exist in two or more contrasting conditions under the same environmental conditions (e.g., clear lake vs. turbid lake; forest vs. shrubland). Ecological state change (regime shift): A large, persistent, often abrupt shift in the structure and function of an ecosystem, triggered by crossing a critical threshold. Threshold / tipping point: The level of a driver (stressor) at which a system flips to a new state. Hysteresis: Once a system flips, simply reversing the driver does NOT restore the original state — the return path is different from the 'forward' path. Slow vs. fast drivers: Slow drivers (e.g., gradual warming, soil nutrient accumulation) build up until a fast driver (e.g., fire, storm) tips the system across the threshold. Perturbation: Any event (abiotic or biotic) that disturbs the ecosystem. Perturbations that cause regime change can be abiotic (fire, flood, drought) or biotic (pest outbreak, invasion). Resilience: The capacity of a system to absorb disturbance, adapt to change, and recover from adversity while maintaining its essential functions, structure, and identity. The ball-and-cup diagram Picture a ball sitting in a valley (cup) on a hilly landscape. The ball is the current state of the ecosystem; the cup is the 'basin of attraction' for that state. A disturbance pushes the ball; stabilizing (negative) feedback loops pull it back. Strong disturbance or a shrinking cup (loss of resilience) can push the ball over a hill into a NEW cup — that's state change. Negative (stabilizing) feedback loop: A change triggers a response that DAMPENS the change, keeping the system near its current state. Deepens the cup. Positive (amplifying) feedback loop: A change triggers a response that AMPLIFIES the change, pushing the system further from its current state. Flattens the cup and makes state change more likely. Applying resilience to conservation & restoration Manage for resistance — remove stressors that push the ball (exclude high-intensity grazing, reduce pollution). Manage for resilience — rebuild the 'cup' by re-establishing key species, nutrient cycling, and stabilizing feedbacks (planting perennial grasses, restoring hydrology). Passive restoration works when the seed bank, soil, and key species are still intact; active restoration is needed when the system has already crossed the threshold. 3. Landscape Ecology and Biogeography 3.1 Landscape ecology Landscape ecology: The study of spatial patterns of ecosystems and their ecological consequences — explicitly considers the arrangement of habitats across space and how organisms and materials move through them. Spatial elements Term Definition Patch A relatively homogeneous area that differs from its surroundings (e.g., a forest stand in a grassland). Generally the highest-quality habitat. Matrix The background land-cover type that surrounds patches (e.g., desert in Saguaro NP, or agricultural land around forest fragments). Corridor A linear feature connecting patches — allows movement of organisms, genes, and energy. Examples: riparian strips, hedgerows, engineered wildlife crossings (Oracle Road, Tucson). Ecotone See above — the transition zone between landscape elements. Spatial heterogeneity Variability in environmental conditions and habitat types across a landscape. Drives diversity at landscape scales. Scale dependence Ecological patterns and processes depend on the spatial/temporal scale at which they are observed (e.g., a species may look stable regionally but be declining locally). Fragmentation Fragmentation breaks a large continuous habitat into smaller, more isolated patches. Effects include: Loss of total habitat area More edge relative to interior — edge effects (different microclimate, invasives, more predators) penetrate into remaining patches Reduced connectivity — animals cannot move between patches Smaller populations in each patch → inbreeding depression, loss of genetic variability, higher extinction risk Saguaro NP example Mid-sized carnivores in Saguaro NP West crashed after a disease outbreak and never recovered. Why? The city of Tucson grew between Saguaro NP East and West, severing connectivity. No recolonization could occur from the eastern population. Solution: re-establish connectivity — the Oracle Road wildlife crossings documented over 4,400 crossings by 16 species in their first two years. Patch dynamics Patch size, shape, and connectivity change over time because of ecological processes — succession, disturbance (fire, flood, windthrow), and fragmentation — not random chance and not just geology. 3.2 Biomes and realms Biome: A large biological community defined by climate and dominant vegetation type (e.g., tropical rainforest, boreal forest, tundra, desert, savanna, temperate grassland). Biogeographic realm: A large area of the Earth's surface with a distinctive assemblage of taxa, reflecting shared evolutionary history (e.g., Nearctic, Neotropical, Palearctic, Afrotropical, Indomalayan, Australasian, Oceanic, Antarctic). Factors shaping where biomes are found: temperature and precipitation (the primary controls), seasonality, latitude, elevation, continental geography, and evolutionary history. Realms reflect plate tectonics — Pangaea split into Laurasia and Gondwana, then into the continents we have today, producing unique evolutionary trajectories in each realm (e.g., Australia's marsupials, Madagascar's lemurs). 3.3 Island Biogeography and the SLOSS debate MacArthur & Wilson's Theory of Island Biogeography: species richness on an island is set by the balance between the colonization rate (immigration) and the extinction rate. Size effect — larger islands have LOWER extinction rates (bigger populations). Distance effect — islands closer to the mainland have HIGHER colonization rates. Equilibrium species number occurs where colonization and extinction curves INTERSECT. SLOSS debate — Single Large Or Several Small? Originally framed: is a single large reserve or several small reserves of equal total area better for biodiversity? Large favors: lower extinction, room for interior species, bigger populations, full food webs. Several small favors: replication (insurance against one disaster), sampling more habitat types, potentially higher total diversity. Modern answer: it depends — on species' dispersal, the matrix, and whether you value diversity vs. viability. Connectivity (corridors) often matters more than the large/small question alone. Source population: Produces more offspring than can be supported locally — exports individuals to other patches. Population growth rate > 0. Sink population: Organisms arrive but do not reproduce enough to sustain the local population; persists only via immigration from sources. Population growth rate < 0. 4. Extinction and Climate 4.1 The 'Big Five' mass extinctions Term Definition Ordovician–Silurian (~439 Mya) ~85% marine species lost. Cause: rapid glaciation and sea-level drop, then warming. Late Devonian (~364 Mya) Prolonged event; major loss of marine invertebrates, especially reef builders. Probable causes include ocean anoxia and climate change. Permian–Triassic (~251 Mya) 'The Great Dying' — ~96% marine species and ~70% terrestrial vertebrates. THE most severe. Cause: Siberian Traps volcanism → CO₂ spike → warming, ocean acidification, and anoxia. Recovery took 5–10 million years. End Triassic (~199–214 Mya) ~50% of species lost; cleared the way for dinosaurs to dominate. Likely cause: CAMP volcanism and climate change. Cretaceous–Tertiary (K-Pg, ~65 Mya) ~76% of species, including non-avian dinosaurs. Cause: Chicxulub asteroid impact (plus Deccan Traps volcanism) → darkened skies, cooling, then warming. Why scientists are concerned now Current extinction rates are 100–1000× background rates — comparable to mass-extinction levels. Rate of change: current climate change is occurring more rapidly than almost any past episode — faster than many species can adapt or track. Humans have built roads, cities, and agricultural landscapes that BLOCK the range shifts species would otherwise use to follow their climate. Human societies are themselves adapted to current climate (agriculture, supply chains, coastlines) — disruption drives conflict. 4.2 Why climate change affects ecological systems Temperature, precipitation, seasonality, and extreme events all drive the distribution and performance of every species. Shifting climate disrupts energy balance, water balance, food availability, and reproduction; changes the timing of seasonal events; and alters disturbance regimes (fire, floods, storms). All of these cascade through communities and ecosystems. 5. Climate Change — Ecology, Climate, and the Carbon Cycle 5.1 The carbon cycle Term Definition Pool (reservoir) A place where carbon is stored and from which it can be released. Measured as a quantity (e.g., gigatons). Flux The amount of carbon exchanged between pools per unit time (gigatons/year). Measures MOVEMENT. Sink A pool that accumulates more carbon than it releases — net REMOVER of carbon from the active cycle. Source A pool that releases more carbon than it accumulates — net ADDER of carbon to the active cycle. Biggest/smallest pools & fluxes Major carbon pools (approximate, gigatons): Deep ocean: ~37,000 GtC — BY FAR the largest pool Fossil pool (oil, gas, coal): ~10,000 GtC — second largest Reactive ocean sediments: ~6,000 GtC Soils: ~2,300 GtC Surface ocean: ~1,000 GtC Atmosphere: ~800 GtC — this is the pool that drives climate Plant biomass: ~550 GtC (the largest LIVING pool) Major fluxes are photosynthesis and respiration (~120 GtC/yr terrestrial; ~90 GtC/yr ocean), which are normally nearly balanced. Fossil-fuel combustion and deforestation are the (smaller but crucial) fluxes currently unbalancing the system. Why atmospheric CO₂ is increasing Humans are burning fossil fuels — moving carbon from a long-term sink (the fossil pool) into the active atmospheric pool faster than natural sinks can remove it. Deforestation and land-use change also shift carbon from plant biomass and soils to the atmosphere. The balanced photosynthesis/respiration fluxes cannot keep up with the ~10 GtC/yr added by human activity. 5.2 Ocean acidification As atmospheric CO₂ rises, more CO₂ dissolves into the ocean. The chemistry: Step 1: The ocean is slightly alkaline; CO₂ is slightly acidic, so CO₂ dissolves into seawater. Step 2: CO₂ + H₂O → H₂CO₃ (carbonic acid). Step 3: H₂CO₃ dissociates → HCO₃⁻ (bicarbonate) + H⁺. Step 4: Some HCO₃⁻ dissociates → CO₃²⁻ (carbonate) + H⁺. Step 5: Bicarbonate and carbonate exist in equilibrium. Net result: more H⁺ ions → lower pH = acidification. Acidification also reduces carbonate availability, making it harder for corals, shellfish, and plankton to build calcium-carbonate skeletons. Warming and the ocean's ability to sequester carbon Warmer water holds LESS dissolved CO₂ (inverse solubility). As oceans warm, their ability to absorb atmospheric CO₂ decreases — a positive feedback loop that further increases atmospheric CO₂ and warming. 5.3 Important climate feedback loops Term Definition Ice-albedo feedback (POSITIVE) Warming melts polar ice → darker ocean/land replaces reflective white ice → lower albedo, more solar energy absorbed → more warming → more melting. Water vapor feedback (POSITIVE) Warming increases evaporation; water vapor is a greenhouse gas → more warming → more evaporation. Permafrost/methane feedback (POSITIVE) Thawing permafrost releases CO₂ and CH₄ long locked in frozen soils → more warming → more thawing. CO₂ fertilization (NEGATIVE, partially) Higher CO₂ can boost plant photosynthesis, pulling more C out of the atmosphere. Partially counteracts warming but is limited by water, nutrients, and heat stress. Ocean solubility feedback (POSITIVE) Warmer oceans hold less CO₂ → more stays in the atmosphere → more warming. Quiz-style example Melting polar ice caps → decreased albedo → further warming = POSITIVE feedback loop (amplifies the original change). 5.4 Factors affecting Earth's surface temperature Three major controls: Energy arriving from the sun (solar radiation) Earth's albedo — how much of that energy is reflected back to space Greenhouse gases in the atmosphere — how much outgoing infrared is trapped Carbon dioxide is the LARGEST driver of current human-caused climate change (sheer volume, long atmospheric lifetime). Methane is more potent per molecule but far less abundant; water vapor amplifies change via feedback but is not itself a primary driver. 6. Climate Change — Ecological and Human Response 6.1 How climate change affects plants and animals Climate change disrupts performance in three main ways: Term Definition Energy balance Plants: respiration rates rise faster than photosynthesis with warming — net carbon gain (and growth) drops. Animals: thermoregulation costs rise; outside the thermal neutral zone, organisms burn more energy just to stay alive. Water balance Warmer temperatures and higher vapor-pressure deficit mean plants LOSE more water per unit of photosynthesis. Animals face greater dehydration risk; aquatic species face altered hydrology. Food acquisition & reproduction Changed phenology, drought, and heat reduce the resources available for growth and reproduction. Fewer seeds, fewer offspring, lower survival. Examples of species already affected Term Definition Pika Small alpine mammal restricted to cold, rocky talus. Warming pushes them to higher elevations — eventually they 'run out of mountain.' Already extirpated from lower-elevation sites in the Great Basin. Tuatara Reptile with temperature-dependent sex determination. Warming skews sex ratios toward males, threatening population persistence. Wolverine Depends on persistent spring snowpack for denning. Declining snowpack reduces suitable reproductive habitat. 6.2 Responses of species: MOVE, ADAPT, or DIE Move: shift range poleward or upslope to track suitable climate (classic response). Range shifts are highly variable across species — depends on dispersal ability, habitat specificity, and whether barriers (cities, roads, water bodies) intervene. Adapt: through plasticity (phenotypic change within a lifetime) or evolutionary change (genetic change across generations). Long-lived species with small populations adapt slowly. Die: local extirpation or global extinction if neither option is available fast enough. 6.3 Phenology Phenology: The timing of recurring biological events — bud burst, flowering, migration, breeding, hibernation. Climate change is advancing many spring phenological events (earlier bloom, earlier migration). Phenological mismatch occurs when interacting species shift their timing differently — e.g., a migratory bird arrives after its caterpillar prey has already peaked. Mismatches cascade through food webs. 6.4 Characteristics of climate-vulnerable species Narrow thermal tolerance (specialists) Poor dispersal ability (can't move to new climate) Long generation time, low reproductive rate (slow to adapt) Small, fragmented populations (low genetic variation, high stochastic risk) Dependence on climate-sensitive habitats (snowpack, sea ice, coral reefs, alpine tundra) Narrow geographic range, especially on islands or mountain tops (nowhere to go) Tightly tied to a specific phenological window or species interaction 6.5 Why current climate change is especially damaging Rate — change is occurring faster than most species can adapt or move Barriers — human land use has fragmented habitat, blocking the range shifts species used during past climate changes Cumulative stressors — climate change interacts with pollution, invasive species, overharvest, and habitat loss Interconnected systems — ecosystems, human agriculture, and global supply chains are all calibrated to current conditions 6.6 Mitigation vs. Adaptation Term Definition Climate MITIGATION Actions that reduce the magnitude of climate change itself — typically by lowering atmospheric greenhouse gases. Examples: switching to renewables, reforestation (sequestering carbon), reducing fossil-fuel use, more efficient buildings and transport. Climate ADAPTATION Actions that help humans and ecosystems COPE with the climate change that is already happening / unavoidable. Examples: creating migration corridors, building climate-resilient ecosystems through forest thinning, adjusting USDA seed zones, changing crop choices, updating hunting/fishing regulations, designing for sea-level rise. Quick quiz check Planting trees to sequester carbon = MITIGATION (reduces atmospheric CO₂). Thinning Southwest forests to make them more fire-resilient = ADAPTATION (copes with changing fire regime). Geoengineering proposals like stratospheric aerosol injection = a controversial form of mitigation (reduces incoming solar energy). Special cases of adaptation Managed (assisted) relocation: Actively moving species to areas outside their current range that are projected to become climatically suitable. Benefits: may be the only option for species that cannot disperse fast enough; can save species from extinction. Risks: recipient communities may experience novel interactions; potential to create invasive species; ethical questions about intervention. Assisted evolution: Human intervention to increase the rate of evolutionary adaptation — e.g., selective breeding for heat tolerance, or hybridization with warm-adapted populations. Benefits: keeps species in place; works for species that cannot move. Risks: may reduce genetic diversity; unintended consequences; can go wrong (outbreeding depression). 6.7 Corridors, climate refugia, and conservation design Climate refugium: A location whose physical or biological features allow species to persist despite regional climate change — e.g., high-elevation cool pockets, deep canyons, shaded slopes, coastal fog zones. Incorporating corridors (to enable range shifts) and refugia (places species can hold on) into reserve design is essential for climate-integrated conservation. A high-elevation forest that remains cool despite regional warming can serve as a seed source for recolonization — that's the textbook example of a refugium supporting resilience. Final thoughts: making an argument about climate-integrated conservation You should be able to give your own opinion on climate-integrated conservation and defend it. A solid answer acknowledges trade-offs: traditional 'protect what is there' approaches may fail under rapid change, but aggressive interventions (managed relocation, assisted evolution) carry real risks. Most conservation scientists argue for a portfolio approach — protect refugia, build corridors, and use active interventions only where the alternative is extinctionl

NURS 348 — EXAM 4 STUDY GUIDE Hypertension Definition & Overview • Persistent elevation of BP ≥130/80 mmHg (systolic at/greater than 130 OR diastolic at/greater than 80) on at least 2 separate visits, 2+ weeks apart. • Primary (Essential): No identifiable cause, most common (90–95% of cases). • Secondary: Caused by another condition or adverse effects of medications. Etiology/Pathophysiology • ↑ Peripheral resistance and/or ↑ cardiac output → ↑ blood pressure → When blood vessels get narrower (increased resistance) or the heart pumps more forcefully (increased output), pressure inside the vessels rises “like squeezing a hose while water is running” → Over time, this high pressure damages the vessel walls and heart muscle, increasing the risk for atherosclerosis, heart attack (myocardial infarction), and stroke. • ↑ Increased peripheral resistance (arteriolar constriction) → ↑ afterload → left ventricular hypertrophy → heart failure → The heart pushes against more resistance (afterload), making the heart muscle thicker (hypertrophy). Over time, it becomes weaker and can lead to heart failure. • Kidneys retain sodium and water → ↑ circulating volume → The kidneys hold onto extra salt and water, adding more fluid to the blood. More fluid means higher pressure—like overfilling a water balloon. • Activation of renin–angiotensin–aldosterone system (RAAS) = vasoconstriction + fluid retention. RAAS is like the “blood pressure booster” → When this system turns on, blood vessels tighten and the kidneys save even more salt and water, both of which raise blood pressure. Risk Factors: • Primary: family history, ↑ sodium intake, Obesity (BMI >25), African-American ethnicity, smoking, hyperlipidemia, diabetes mellitus, and stress. • Secondary: kidney disease, Cushing’s, pregnancy, pheochromocytoma, medic (steroids, OCPs). Clinical Manifestations (S/S) • Often asymptomatic (“silent killer”)!!! • Headache, dizziness, fainting, vision changes • Retinal damage on exam (cotton wool spots, papilledema). • Note: if blood pressure reading is elevated then take in both arms; pt legs uncrossed, and arms above heart; correct cuff Diagnostics (Dx)/Labs • Multiple BP readings (both arms, sitting and standing) • ECG → Left-Ventricular hypertrophy. evaluates cardiac function. • Labs → ↑ BUN/creatinine (kidney disease), lipids, glucose, cortisol (Cushing’s) Nursing Care / Nursing Interventions • Monitor pt BP regularly and accurately, check both arms/correct cuff • Put on DASH diet (Dietary Approach to Stop Hypertension) Medications • ⭐️Diuretics (first-line): excess fluids, they need to remove; increase urine • Thiazides (hydrochlorothiazide) inhibits water & sodium reabsorption and increases potassium excretion • Side effects/SE: hypokalemia; monitor potassium(K⁺) levels • Loop (furosemide) decreases sodium reabsorption & increase potassium excretion– SE: hypokalemia; monitor potassium(K⁺) levels • Potassium-sparing (spironolactone) – SE: hyperkalemia; monitor potassium levels. EKG: peaked T waves • Also watch out for muscle weakness, irregular, pulse, and dehydration. • ⭐️Calcium channel blockers (verapamil, amlodipine, and diltiazem) Calcium channel blockers relax and widen blood vessels by preventing calcium from entering muscle cells, leading to lower blood pressure (vasodilation) • SE: constipation; take fiber for verapamil, and all can ↓HR • Avoid grapefruit juice ➡️ toxicity, hypotensive effects Calcium= contract • ⭐️ACE inhibitors (lisinopril, enalapril): prevents angiotensin II → vasodilation • SE: - hypotension; monitor BP and pulse HR -hyperkalemia; monitor potassium levels -erectile dysfunction -⭐️cough linked to angioedema (swollen tissue under the skin around lips, tongue, and glottis); report swelling & discontinue med • ⭐️ARBs (valsartan, losartan): for ACE-intolerant pts from cough/hyperkalemia. ARBs lower blood pressure by blocking angiotensin II from binding to its receptors, preventing vasoconstriction, and reducing fluid retention. • SE: angioedema, heart failure, hyperkalemia • Change position, slowly, report, angioedema, edema, and avoid foods that are high in potassium (bananas, potatoes, apricots, spinach, beans); monitor potassium levels • Aldosterone-receptor antagonists (eplerenone, spironolactone): blocks aldosterone action. • SE: kidney damage, hypertriglyceridemia, hyponatremia, and hyperkalemia; monitor kidney function, triglycerides, sodium, and potassium levels • Avoid Grapefruit juice and St. John’s wort, salt substitutes, and potassium rich foods • ⭐️Beta blockers (metoprolol, atenolol): blocks beta receptors (adrenaline/epinephrine) ➡️reduces heart rate, cardiac output, and blood pressure ↓HR, ↓CO; use cautiously in diabetics • SE: -⭐️erectile dysfunction, -Fatigue, weakness, depression -hypoglycemia • Monitor heart rate (hold if HR is less than 60) and do not suddenly stop taking med (cause rebound hypertension); and don’t give to pts with asthma, airway disease (cause bronchospasms) • Central Alpha-2 agonists (clonidine): calm the nerves that raise blood pressure, letting blood vessels, relax, and BP go down, ↓SNS tone • SE: sedation, orthostatic, hypotension, and sexual dysfunction/impotence • Monitor BP and pulse • Alpha-adrenergic blockers (prazosin, doxazosin): vasodilator= relaxed BP; give at night to avoid first-dose hypotension. Start with low dose. • SE: postural hypotension; make sure patient rises slowly and caution. • Monitor BP 2 hrs after initiation Complications • Hypertensive Crisis: usually when patients do not follow the medication regimen • BP >180/120 → organ damage (encephalopathy, renal failure) • S/S: severe headache, dizziness, blurred vision, confusion, epistaxis • Treat: IV antihypertensives (nitroprusside, nicardipine, labetalol); the goal is to lower BP gradually by 20-25% in first hour. Not less than 140/90. Monitor BP every 5-15 mins Patient Education • Adhere to medication regimen, don’t abruptly stop even when you feel better • Change positions slowly • Encourage DASH diet (low sodium, high fruits/veggies, low-fat dairy) ex: grilled salmon, brown rice, steamed broccoli, and low-fat milk • Avoid high-sodium foods. Consume less than 2.3 g/day • Monitor BP at home • Report signs or symptoms of electrolyte imbalances • Encourage Weight loss, exercise 3x weekly • Encourage Smoking cessation • Encourage Limit alcohol (≤2/day men, ≤1/day women) • Manage stress • Report persistent cough or swelling (ACE inhibitor red flag) Peripheral Venous Disorders(PVD) Patho: problems with veins where Deoxygenated blood can't get back to the heart Oxygenated blood pools in the extremities. The valves are preventing backflow. • Venous Thromboembolism (VTE): blood clot that starts in a vein. -Two types: deep vein thrombosis (DVT) and pulmonary embolism (PE) • Venous insufficiency: Improper functioning of the veins. Veins aren’t able to push back blood to the heart which results in swelling, venous stasis ulcers, or cellulitis. Blood can go down into the veins just fine but cannot come back up. a. VTE ex: Deep Vein Thrombosis (DVT) Pathophysiology • Thrombus (Blood clot) forms in deep veins (usually in legs) → can embolize (travel and block vessel) its way to lungs (PE). • Caused by Virchow’s triad: venous/blood flow stasis, endothelial injury, hypercoagulability. Risk Factors • Surgery (hip, knee, prostate) • Immobility • Heart failure • Pregnancy • Family hx • Oral contraceptives or hormone therapy • Cancer • COVID-19 (elevated D-dimer) • Central venous catheters Clinical Manifestations • Note that clients can be asymptomatic • Calf/groin pain (dull/achy), tenderness, warmth, edema • Unilateral swelling • Shallow, irregular shaped wounds • Too much blood, brown/yellow discoloration • Sudden SOB and sharp chest pain → suspect PE • Positioning: “Elevate Veins”, position up in “V” shape, above heart. Worsens: if dangling, sitting/dangling for long periods of time. Diagnostics • ⭐️Venous duplex ultrasonography = gold standard; it’s an ultrasound of Leg to see blood clot/blood flow through the vessel. • ⭐️D-dimer ↑ = clot breakdown evidence • Venogram/MRI if ultrasound inconclusive Nursing Interventions • Bed rest until anticoagulation started • Elevate leg slightly above heart (no knee gatch). Positioning: “EleVate Veins”, think V as veins are up, to keep the veins open. • Warm compresses • DO NOT massage leg • Compression stockings (after swelling ↓) • Encourage early ambulation when safe • SCDS Medications/Procedures (Anticoagulants) stops blood from clotting, another nurse must be with you • Unfractionated heparin (given IV): prevents clots and growth of existing clot; monitor platelets, and aPTT (how long it takes blood to clot) (1.5–2× normal). Must be given in facility. MUST MONITOR CLOSELY • Antidote: protamine sulfate • Low-molecular-weight heparin (Lovenox/enoxaparin): given SubQ, weight-based, prevention and treatment of DVT, given twice daily, can be used in home setting. Don’t need labs. Monitor for bleeding, and take bleeding precautions (Electric razor, soft toothbrush, environment safety) • Warfarin (Coumadin): oral, inhibits vitamin K clotting factors overlaps; combined with heparin 3–4 days until INR 2–3 (takes awhile to kick in; therapeutic affect) • Antidote: vitamin K • Avoid high vitamin K foods (green leafy veggies) • Monitor PT (range: 11-13.5 secs), INR (must know range: 2–3) • Factor Xa inhibitors (fondaparinux; SubQ) (rivaroxaban, apixaban; oral): Prevents development of Thromboses; transitional medication; initial labs are PT and PTT; not routinely • Direct thrombin inhibitors (dabigatran): directly prevents growth of thrombus Formation, given sub Q ; initiate initial lab values only for PT and APTT. • Antidote: idarucizumab • Thrombolytics (tPA): for massive DVT/PE, directly infused into clot, start within 24hrs- 5 days of clot formation; monitor for bleeding, neuro status, dizziness, headache. Take bleeding precautions, pt must use electric razor and, brush teeth with a soft toothbrush. • Inferior vena cava filter: prevents embolus from reaching lungs (PE), inserted in femoral vein; catches blood clot. Used when pt is unresponsive to other treatments. Monitor: bleeding, hematoma, infection, PE (dyspnea, chest pain, tachycardia). Nursing actions: assess circulation and encourage leg exercises/ambulation early, have patient not sit for too long Anticoagulant Therapy Nurse’s Role • Verify labs,;Double-check with another RN for IV heparin, Assess for bleeding (bruises, gums, stools) and Monitor vitals, mental status (signs of intracranial bleed) Reversal Agents • Heparin → protamine sulfate • Warfarin → vitamin K • Dabigatran → idarucizumab Patient Education • Avoid contact sports • Soft toothbrush, electric razor • Avoid sudden diet changes (vitamin K) Complications (anticoagulants) • ⭐️Pulmonary embolism: sudden dyspnea, chest pain, SOB, anxiety, tachypnea → emergency; sit, patient in high Fowlers, and administer oxygen and anticoagulants • ⭐️Ulcer formation(venous): often formed over the medial malleolus, chronic, hard to heal, can reoccur. Can lead to amputation/death. Neuropathic patients might not feel this. Nursing care: Dressing is left 3–7 days; wound vacuums, diet: high in zinc, protein, iron, and vitamins A and C, debride necrotic tissue so wound can heel. Patient Education(Anticoagulants) • Bleeding precautions (soft toothbrush, electric razor) • Report bruising or black stools • Avoid prolonged sitting/crossing legs • Wear compression stockings b. Venous insufficiency Pathophysiology • Valves and legs are damaged due to prolong venous HTN Our previous blood clot Risk factors: • Sitting/standing in one position for a long period of time • Obesity • Pregnancy • Thrombophlebitis Clinical manifestations: • Status dermatitis(brown discoloration along ankles) • Edema • Stasis ulcers around ankles Labs/DX • D-dimer ↑ = clot breakdown evidence, detects clot Nursing interventions: Elevate legs to increase venous return (20 mins, 4-5/day), position: legs above heart, “Elevate Veins”, Apply stockings, and monitor for cellulitis Patient education: avoid sitting/standing still for too long, change positions often, avoid crossing legs, tight clothing. Apply stockings before getting out of bed in the morning Peripheral Arterial Disease (PAD) : affects blood vessels that carry blood away from the heart; artery carries blood away from heart but has difficulty going down to extremities. Pathophysiology • Atherosclerosis in lower extremities → decreased blood flow to tissues. Risk Factors • Smoking, DM, hypertension, hyperlipidemia, obesity, age, sedentary lifestyle. Clinical Manifestations • Intermittent claudication: leg pain with exercise, relieved by rest; not enough oxygen makes the tissue suffer = pain; ischemia • Pain(sharp) that is only relieved when resting in dependent position • Cool, pale, cyanotic skin • Loss of hair on legs, thick toenails • Weak/absent pedal pulses; dorsalis pedis; Doppler(verify), +1 • Numbness, burning at night • No blood and no edema due to an adequate blood flow • Note: think “A” in PAD as Antarctica, where it’s cold! For cold, pale skin! Diagnostics • ⭐️ABI < 0.9 = PAD; ankle pressure compared to break your pressure; expected finding is 0.9–1.3; less than is PAD • ⭐️Arteriography for visualization of occlusion/decreased arterial flow with contrast injection on a x-ray. Monitor for bleeding, hemorrhage, marked, pedal pulses • Doppler studies → decreased flow in DM patients • ⭐️Exercise tolerance testing → decreased pressure in lower limbs, read the workload of the heart/circulation, and clarification during exercise. May use treadmill or meds (dipyridamole, adenosine). Finding of a BP/pulse waveform = arterial disease. Monitor vitals before, during, and after. Stop test if chest pain or symptoms are severe. Nursing Interventions • Encourage graded exercise until pain, rest, repeat • Avoid elevating legs above heart (impairs flow) • Avoid cold, caffeine, nicotine, tight clothing • Keep extremities warm (no heating pad), they can’t feel • Foot care: inspect daily, no bare feet, toenails straight Medications • Antiplatelets: (aspirin, clopidogrel) reduces blood viscosity and increases blood flow and extremities. Monitor: bleeding, abdominal pain, black, tarry stools. • Statins: (atorvastatin, simvastatin). Relieved manifestations like intermittent claudication. • Pentoxifylline: improves RBC flexibility (claudication). Monitor for bleeding, abdominal pain, black tarry stools. Procedures • Angioplasty (balloon/stent). Opens and helps, maintain the patency of the vessel, however, laser vaporizes atherosclerosis plaque. Monitor for bleeding, vital signs, pulses, cap Refill. As patients rest limbs are straight for 2-6 hrs before ambulation. Anticoagulant/Antiplatelet therapy given 1-3 months after. • Atherectomy rotation, device removes, arterial plaque. Monitor for bleeding and distal pulses. rest limbs are straight for 2-6 hrs. Anticoagulant/Antiplatelet therapy given 1-3 months after. • Arterial revascularization bypass surgery • Used for clients at risk for losing a limb, severe claudication, or limb pain at rest. It reroutes the circulation around the arterial occlusion. • Post-op: ⭐️ maintain adequate circulation in repaired artery, mark pedal/dorsalis pulses(compare both), monitor color/temp, pain, cap refill, blood pressure (HTN= risk for bleeding; Hypotension=clot risk). • Complications: for these notify provider first -graft occlusion: acute blockage of bypass graft within 24 hr(absent pulse, cold foot, increased pain) -compartment syndrome: tissue pressure restricting blood flow; causing ischemia (numbness, tingling, edema, worsening/passive pain) -infection: infection of site (warm, tenderness, elevated, WBC, purulent drainage, use sterile technique) Patient Education • Walk until pain → rest → walk more • Stop smoking • Avoid crossing legs • Diet low in cholesterol and fat Postoperative Care – Peripheral Bypass/Revascularization Priorities • Assess extremity: color, temperature, cap refill, sensation, pulses q15min ×1hr • Mark pedal pulses before surgery • Maintain adequate BP (avoid hypo or hypertension) • Do not flex hip/knee excessively • Encourage ambulation when ordered • Report sudden pain, loss of pulse, pale/cool extremity = graft occlusion Complications • Graft occlusion, Compartment syndrome, Wound infection Arterial vs. Venous Ulcers Feature Arterial Ulcer Venous Ulcer Location Toes, feet, lateral ankle Medial ankle Appearance Pale, dry, round “punched out”, no drainage Irregular, leaky/moist, brown discoloration Pain Severe, worse with elevation Achy, relieved with elevation Skin Cool, shiny Warm, thickened Treatment Improve arterial flow Compression therapy, elevate legs Valvular Heart Disease OVERVIEW Overview • Stenosis = narrowed opening/thickening and hardening • Regurgitation = backflow of blood • Causes: rheumatic fever, degenerative calcification, endocarditis Diagnostics • Chest X-ray → chamber enlargement • ⭐️ECG → hypertrophy • Echo → valve dysfunction • TEE → direct view of valves ⭐️ Medications overview • Diuretics [furosemide, hydrochlorothiazide, spironolactone]: reduce pulmonary congestion, by removing excessive extracellular fluid. Monitor: hypokalemia, eats foods high in potassium, and administer furosemide IV slowly over 1 – 2 minutes. • Afterload–reducing agents [Beta-blockers (-lol); calcium channel blockers (-dipine); ACE inhibitors (-pril); angiotensin–receptor blockers (-artan); vasodilators (hydralazine]): control heart rate, by lessening resistance to contraction. Monitor: hypotension. • Inotropic agents (digoxin): increases contractility, improves cardiac output. Hold medication if pulse rate (abnormal) is less than 60/min or greater than 100/min. Take medication same time every day, avoid combining with antacids (2hrs). Monitor: toxicity such as weakness, confusion, visual changes, low appetite. • Anticoagulants: reduces risk of thrombus. Monitor: stroke, PT, INR, bleeding/bruising. Procedures • Valvuloplasty (balloon dilation) • Valve replacement • Mechanical = lifelong anticoagulants • Tissue = replace every 7–10 years Patient Education • Prophylactic antibiotics before dental procedures • Good oral hygiene • Daily weights • Sodium restriction • Avoid caffeine/alcohol • Report HF signs (weight gain, edema, SOB) • Avoid alcohol, epinephrine, and ephedrine= can cause dysrhythmias THE 4 VALVULAR DISORDERS Mitral Stenosis Etiology/Pathophysiology: Narrowed mitral valve obstructs blood flow from left atrium (LA) → left ventricle (LV), increasing LA pressure and pulmonary congestion → right-sided heart failure. Often caused by rheumatic fever. Clinical Manifestations: Dyspnea on exertion, orthopnea, pitting edema, fatigue, palpitations, hemoptysis, apical diastolic murmur. Risk Factors: Rheumatic heart disease, aging, congenital malformations. Labs/Diagnostics: Echocardiogram (valve narrowing, pressure gradient), ECG (A-fib), chest X-ray (LA enlargement). Medications/Management: • Diuretics [furosemide, hydrochlorothiazide, spironolactone]: reduce pulmonary congestion, by removing excessive extracellular fluid. Monitor: hypokalemia, eats foods high in potassium, and administer furosemide IV slowly over 1 – 2 minutes. • Afterload–reducing agents [Beta-blockers (-lol); calcium channel blockers (-dipine): control heart rate, by lessening resistance to contraction. Monitor: hypotension. • Anticoagulants: reduces risk of thrombus; prevent emboli from A-fib. Monitor: stroke, PT, INR, bleeding/bruising. • Surgical: Balloon valvuloplasty or valve replacement. NCLEX Tip: Rheumatic fever is the most common cause. Mitral Insufficiency Etiology/Pathophysiology: Incomplete closure of mitral valve causes blood to leak back into LA during systole → LV dilation and hypertrophy. Clinical Manifestations: Fatigue, dyspnea, orthopnea, palpitations, holosystolic murmur at apex, pitting edema, S3 sounds Risk Factors: Mitral valve prolapse, rheumatic disease, MI, endocarditis. Labs/Diagnostics: Echocardiogram (regurgitant volume), ECG (A-fib), BNP (HF indicator). Medications/Management: • Beta-blockers (-lol); ACE inhibitors (-pril); ARBS/angiotensin–receptor blockers (-artan): reduce afterload /control heart rate, by lessening resistance to contraction. Monitor: hypotension. • Diuretics [furosemide, hydrochlorothiazide, spironolactone]: manage fluid overload. Monitor: hypokalemia, eats foods high in potassium, and administer furosemide IV slowly over 1 – 2 minutes. • Anticoagulants if A-fib present; reduces risk of thrombus; prevent emboli from A-fib. Monitor: stroke, PT, INR, bleeding/bruising. • Surgery for severe cases. NCLEX Tip: Afterload reduction decreases regurgitant flow. Aortic Stenosis Etiology/Pathophysiology: Narrowed aortic valve → obstructed LV outflow → ↑ LV pressure → hypertrophy → ↓ cardiac output. Clinical Manifestations: Triad: angina, syncope, dyspnea (heart failure); systolic murmur radiating to carotids. Risk Factors: Aging (calcification), congenital bicuspid valve, rheumatic fever. Labs/Diagnostics: Echocardiogram (valve area), ECG (LV hypertrophy), cardiac cath (pressure gradient). Medications/Management: • Avoid nitrates/vasodilators (can cause hypotension). • Use beta-blockers (-lol) cautiously. reduce afterload /control heart rate, by lessening resistance to contraction. Monitor: hypotension. • Surgical aortic valve replacement (definitive). NCLEX Tip: Do not aggressively lower preload; maintain perfusion. Aortic Insufficiency Etiology/Pathophysiology: Incomplete closure of aortic valve → backflow of blood into LV → volume overload → dilation and LV hypertrophy. Clinical Manifestations: Dyspnea, palpitations, fatigue, bounding (“water hammer”) pulse, wide pulse pressure, diastolic murmur. Risk Factors: Rheumatic fever, endocarditis, Marfan syndrome, trauma. Labs/Diagnostics: Echocardiogram (backflow volume), ECG (LV enlargement), chest X-ray (cardiomegaly). Medications/Management: • Calcium channel blockers (-dipine); ACE inhibitors (-pril); vasodilators (hydralazine]): reduce afterload /control heart rate, by lessening resistance to contraction. Monitor: hypotension. • Diuretics for volume management. • Surgical valve replacement when severe. NCLEX Tip: Bounding pulse and wide pulse pressure are hallmark findings. General Nursing & Exam Focus • Best diagnostic test: Echocardiogram (for all). • Monitor for A-fib in mitral disorders. • Valve replacement (mechanical): Lifelong anticoagulation. • Daily weights & fluid balance: Detect early HF. • Positioning: High-Fowler’s for dyspnea, low-sodium diet. Inflammatory Heart Disorders (Endocarditis, Pericarditis, Myocarditis, Rheumatic Carditis) Risk Factors • IV drug use, valve replacement, streptococcal infection, immunosuppression, lower socioeconomic status Pericarditis: inflammation of the pericardium (sac around heart) -RF: heart attack, lupus, rheumatoid arthriti -Clinical manifestations: Chest pain (relieved when leaning forward), coughing, Pericardial friction rub, fever, dysrhythmias, and SOB -Labs/DX: • High WBCs, EKG showing ST or T spiking, echocardiogram (inflamed heart) -Nursing care/Intervention: address pain/inflammation, and monitor for cardiac tamponade, position, patient upright, leaning forward, and monitor ECG - Medications: NSAIDs, corticosteroids, anti antibiotics for bacterial • Ibuprofen/NSAIDs for inflammation (pericarditis). Avoid if patient has peptic ulcer, monitor for G.I. bleeding, platelets, liver/kidney function. Must be taken with food, avoid alcohol. • Corticosteroids (prednisone) for autoimmune causes (pericarditis/myocarditis). Low-dose first, take with food, and patient must not stop abruptly. Monitor BP, glucose, electrolytes, wounds, infection, sudden weight gain. -Complication: cardiac tamponade → muffled heart sounds, paradoxical pulse, JVD, hypotension (Beck’s triad) Myocarditis: inflammation of the myocardium (heart muscle itself) -RF: viral (covid, Coxsackie), fungal, or bacterial infection; autoimmune disorder -Clinical Manifestations: Tachycardia, chest pain, murmur, friction rub, dysrhythmias, peripheral swelling, cardiomegaly. -Labs/Dx: ECG, echocardiogram, high troponin, CK – MB, ESR in CRP for inflammation/injury -Nursing Care/interventions: monitor for heart failure, and dysrhythmia’s, provide rest and activity restriction -Medication: • Amphotericin B for fungal infection (myocarditis/endocarditis). Monitor liver/kidney function for a G.I. upset. • Corticosteroids (prednisone) for autoimmune causes (pericarditis/myocarditis). Low-dose first, take with food, and patient must not stop abruptly. Monitor BP, glucose, electrolytes, wounds, infection, sudden weight gain. Endocarditis: bacterial infection that leaves inflammation of the endocardium (inner layer of the heart); bacterial or fungal Infection of endocardial tissues that leads to necrosis and embolization of growth -RF: congenital/valvular heart disease, prosthetic valve, IV drug use -Clinical Manifestations: janeway lesions, Fever, murmur, petechiae, splinter hemorrhages (red streaks under nail beds), Osler’s nodes -labs/dx: positive blood culture, echocardiogram -nursing interventions/care: administer IV antibiotics, antipyretics for fever, and anticoagulants, patient should use soft toothbrush, and prophylactic antibiotics before dental/invasive procedures -medication: • Penicillin for infection (rheumatic fever/endocarditis). Monitor for allergic reaction, kidney function/electrolytes. • Amphotericin B for fungal infection (myocarditis/endocarditis). Monitor liver/kidney function for a G.I. upset. Rheumatic Carditis/heart disease: infection of endocardium due to complication of rheumatic fever; GABHS triggers, rheumatic fever leading to inflammatory lesions in the heart -RF: children, Follows untreated strep infection -Clinical Manifestations: tachycardia, Fever, rash(trunk/extremities), joint pain, murmur, chest pain, muscle spasms, friction rub -Labs/Dx: throat culture (strep infection), positive ASO titer, echocardiogram -Nursing care/Interventions: administering antibiotics to stop strep infection, and promote rest, monitor for heart failure, and encourage life on prophylactic antibiotics. -Medications: antibiotics, valve replacement/repair • Penicillin for infection (rheumatic fever/endocarditis). Monitor for allergic reaction, kidney function/electrolytes. Nursing Interventions (Overview for Inflammatory disorders) • Monitor for tamponade & HF • Administer antibiotics (penicillin) • Pain relief (NSAIDs for pericarditis) • Bed rest • Emotional support • Auscultate heart sounds; murmur or friction rub • Collab with cardiologist and physical therapists Procedures (Overview for Inflammatory disorders) • Pericardiocentesis for fluid removal, then sent to laboratory; monitor for recurrence of cardiac tamponade. ( pericarditis.) • Valve surgery if damaged Complications (Overview for Inflammatory disorders) • Cardiac tamponade: medical emergency resulted from fluid accumulation in pericardial sac. S/S: dyspnea, dizziness, tightness in chest, restlessness. Administer IV fluids, notify the provider, obtain chest, x-ray or ECG Cardiac Diagnostics & Vascular Access (Ch. 28) Transesophageal Echocardiography (TEE) Provides clear heart images via probe in the esophagus to detect valve disease, thrombi, or heart failure. NPO 4–6 hr, monitor VS, ECG, and sedation; check gag reflex before eating post-procedure; keep HOB 45°. Stress Testing (Exercise or Pharmacologic) Assesses heart’s response to stress for angina, HF, MI, or dysrhythmia. NPO 2–4 hr, avoid caffeine/tobacco, wear comfortable clothes; stop test for chest pain, SOB, dizziness. Post: monitor ECG & BP until stable. Coronary Angiography (Cardiac Catheterization) Identifies coronary artery blockages using contrast dye via femoral, radial, or brachial artery. NPO 4–6 hr, assess renal function, allergies (iodine/shellfish), and hold metformin 48 hr before/after. Post: monitor VS and site for bleeding, hematoma, or thrombosis, keep limb straight, maintain bedrest. Complications: cardiac tamponade (↓BP, JVD, muffled heart sounds), embolism, hematoma, AKI—notify provider. Teach: report chest pain, bleeding, SOB, avoid lifting >10 lb, and take antiplatelets as prescribed if stent placed. Vascular Access Devices (VADs) Provide reliable central access for fluids, meds, TPN, or blood. Verify tip placement via x-ray before use. PICC: up to 12 mo use, insert in basilic/cephalic vein → SVC; no BP/venipuncture in that arm, keep dressing dry. Tunneled Catheter: long-term use, subcutaneous tunnel prevents infection; no dressing once healed. Implanted Port: long-term chemo access; access with Huber needle, flush with heparin after use. Complications: • Phlebitis: redness, pain, warmth—maintain sterile technique. • Occlusion: flush gently with 10 mL syringe; never force. • Mechanical issues: swelling or pain at port site = dislodgement → notify provider