3.2: Proto-Hominins
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In determining what fossil features denote a specimen is a hominin, many different characteristics are examined, including those related to bipedalism, about which you previously learned, and non-honing chewing. Apes have a canine-premolar honing complex, which means that there is a diastema between the lower canine lower third premolar where the upper canine fits when the jaws close (Larsen 2014). Other characteristics such brain and body size and what, if any, cultural behaviors are associated with the fossil remains are also scrutinized.
The various features associated with hominins developed at different rates, a situation referred to as mosaic evolution . In determining which species a fossil specimen belongs to, paleoanthropologists utilize comparative anatomy. There is much discussion among researchers as to the exact number of species. Some tend to see broad ranges of variation, which results in fewer species. Researchers with this approach are sometimes referred to as "lumpers" because they lump fossil specimens in relatively few species. Other researchers see more narrow ranges of variation and are referred to as "splitters" because they see more variation of species in the fossil record. For the purposes of this course, we are going to use the approach presented in Jurmain et al. (2013), which is more of a lumper approach.
While the hominins will be presented more or less in chronological order, do not mistake chronological order for linear evolutionary relationships; some hominins that are presented are not in the direct line to modern humans. It is also important to keep in mind that new discoveries are made each year that refine what we know about human evolution. What this means is that what you learn this quarter could change somewhat next year as new data is made available. While this can make studying human evolution frustrating at times, the new discoveries help us gain a better understanding of just how our early ancestors evolved.
It is highly recommended that you begin your exploration of human evolution by watching the documentary, Becoming Human.
Proto-hominins
Sahelanthropus tchadensis
Discovered by the Mission Paléoanthropologique Franco-Tchadienne (MPFT) led by Michel Brunet at Toros-Menalla, Chad, during the 2001-2002 field season, Sahelanthropus tchadensis is the oldest hominin discovered to date. Cosmogenic nuclide dating ( https://en.Wikipedia.org/wiki/Surface_exposure_dating ) places Sahelanthropus between 7.2 to 6.8 mya (million years ago) (Lebatard et al. 2008). The binomial recognizes the area where the fossils were found, Sahel. The type specimen, also referred to as a holotype , includes “…a nearly complete cranium and…parts of two mandibles and some isolated teeth” (Bailey 2006: 2044).
Figure \(\PageIndex{1}\) - Sahelanthropus tchadensis
The skull is a combination of ape-like and human-like features. Ape-like features include brain size, heavy brow ridge. Its human-like features include forward position of the foramen magnum (visit http://www.nature.com/scitable/knowl...hecus-67648286 (scroll down) to view image comparing placement of foramen magnum in chimps, humans, and Sahelanthropus ), reduced prognathism, smaller canine teeth, and intermediate thickness of the premolar and molar enamel. Due to the pronounced brow ridge Brunet’s team suggests that the Sahelanthropus specimen is male.
There is debate among researchers as to whether Sahelanthropus is a hominin or an ape. Some suggest that the specimen belongs to that of a female ape because it is likely to find canines worn at the tips in female apes. Critics claim that without postcranial evidence it is premature to claim that Sahelanthropus is bipedal (Su 2013).
Paleoecological data suggest that this Sahelanthropus specimen died near a lakeshore and the area was extensively forested.
Orrorin tugenensis
Found in 2000 by a team led by Martin Pickford and Brigitte Senut, Orrorin tugenensis is represented by a collection of fossils that include a minimum of five individuals. Fragments of numerous fossilized body parts were found: jaw, femur, humerus, and finger bones. Many teeth were found, including molars and canines. The binomial reflects where the fossils were found, the Tugen Hills region of Kenya. Orrorin means “original man” in the Tugen dialect. Using multiple dating techniques, including paleomagnetism and biochronology, the Tugen Hills fossils are dated to about 6.0 mya.
Figure \(\PageIndex{2}\) - Orrorin tugenensis fossils
Like Sahelanthropus , Orrorin has a mix of ape-like and human-like traits. Its teeth are more ape-like so the determination of bipedality is central to attributing the fossils to that of a hominin. The founding research team claims that features of the femur indicate that Orrorin was a biped and in the direct line to modern humans. More recent studies suggest that Orrorin was in fact a bipedal hominin, but not in the direct line to Homo (Richmond and Jungers 2008).
The paleoecological evidence associated with Orrorin fossils suggests that the area was a woodland populated with lakes and streams.
Ardipithecus
Two different species of Ardipithecus have been identified: Ar. kaddaba and Ar. ramidus . The two species are differentiated primarily on the C/P3 complex (canine-premolar features), specifically, that A r. kaddaba’s canines are more primitive than those of Ar. ramidus .
Ar. kaddaba is the older of the two species. It is dated to 5.8-5.2 mya. Tim White, Gen Suwa, and Yohannes Haile Selassie discovered Ar. kaddaba fossils in the Middle Awash region of Ethiopia. The fossil collection is comprised of fragments of the mandible and teeth, forearm, clavicle, and fourth toe. The shape of the upper canine is more human-like than ape-like in that they are smaller with a more circular crown. Overall, the postcranial fragments are more ape-like; however, the toe bone mentioned previously is similar to the toe bones of Australopithecus afarensis , a species that had all the hallmarks of habitual bipedalism. Other researchers claim that a single fourth toe bone does not provide enough evidence to confirm that Ar. kaddaba was a bipedal hominin.
Figure \(\PageIndex{3}\) - Ardipithecus ramidus: Ardi skeleton
Paleoecological data suggest that Ar. kaddaba lived in a “closed, densely-wooded habitat close to permanent water sources (e.g., lakes and/or rivers) with swampy conditions and floodplain grasslands” (Becoming Human c2008).
Tim White is also credited with the discovery of Ar. ramidus in Aramis, Ethiopia. Dated to about 4.4 mya, Ar. ramidus “represents the oldest species that possesses features unequivocally linked to the hominin lineage. Thus, Ar. ramidus is the best evidence discovered thus far for the root of the hominin family tree” (Becoming Human c2008). Paleoanthropologists know more about Ar. ramidus than the previously mentioned species as 110 specimens have been unearthed at Aramis.
Postcranially, Ar. ramidus is still ape-like; however there are some features that suggest the species could walk bipedally, but it most likely spent time in the trees much like modern chimpanzees. In other words, its mosaic characteristics suggest facultative bipedalism. Features that lead researchers to claim Ar. ramidus could walk bipedally include the position of the foramen magnum and features of the spine and ilium.
Early hominins
Australopithecus anamensis
Australopithecus anamensis , meaning “southern ape of the lake,” was found by Maeve Leakey and Alan Walker in 1994 in Kanapoi, Kenya. Additional A u. anamensis fossils were recovered at Allia Bay, Kenya and several sites in Ethiopia: Asa Issie, Woranso-Mille, and Fejej. Fossil specimens include mandibles, maxilla, teeth, a partial humerus, tibia, manual phalanx, capitate, partial femur, several vertebrae, and a partial temporal bone (Ward et al 2013). Using radioisotopic dating methods on volcanic deposits, Au. anamensis dates to 4.1-3.9 mya. The fossil evidence suggests that Au. anamensis is ancestral to Au. afarensis .
Figure \(\PageIndex{4}\) - Australopithecus anamensis fossils
Au. anamensis exhibits a mosaic of ape-like and Homo -like features. The size and shape of the teeth, especially the lower premolar and upper canine, the u-shaped dental arcade, and the prognathism are some of the ape-like features, while the thickness of the enamel and the breadth of the molars are more like early Homo . The single wrist bone is also like Homo . Lower limb bones suggest Au. anamensis was fully bipedal.
Paleoecological data suggest that Au. anamensis lived in forested areas near streams.
Australopithecus afarensis
Discovered by Donald Johanson in 1974 at Hadar, Ethiopia, Australopithecus afarensis is arguably the most well know fossil hominin species. It is dated from 3.7-3.0 mya (Scarre 2014). Johanson’s discovery in 1974 was, at the time, the most complete hominin fossil. Over 40% of the skeleton was recovered, which allowed the team to fully reconstruct the skeleton. This fossil specimen, named Lucy, coupled with footprints found at Laetoli, Tanzania, in 1978 by Mary Leakey, confirmed that Au. afarensis was fully bipedal, albeit not exactly like modern humans. The footprints at Laetoli indicate that Au. afarensis had a short stride and a strolling gait. Since the 1970s, hundreds of specimens of Au. afarensis have been found (60 individuals at least from Hadar alone!) in Ethiopia, Kenya, and Tanzania, allowing paleoanthropologists to make “definitive [emphasis original] statements about the locomotor pattern and stature of” (Jurmain 2013: 211) this early hominin.
Figure \(\PageIndex{5}\) - Reconstruction of the fossil skeleton of "Lucy" the Australopithecus afarensis
Au. afarensis has several primitive, or ape-like, features, including a relatively small brain in comparison to Homo , a u-shaped dental arcade, a flat nose, a flattened forehead (referred to as platycephaly) and prognathic face. Its canines, while larger than Homo , are smaller than earlier hominins. While its brain was larger than earlier hominins, it is still small in comparison to Homo. There is evidence for sexual dimorphism; Au. afarensis males were no taller than 5 feet and females about 3-4 feet, similar in proportion to modern African apes. Au. afarensis has a suite of derived traits associated with bipedalism; i.e., bowl-shaped pelvis, s-curve of the vertebral column, and knee anatomy. However, the curvature of the fingers and toes and the proportion of the arms to legs suggest to some researchers that Au. afarensis spent some time in the trees.
In 2006, Zeresena Alemsegad announced the discovery of a 3.3 million year old Au. afarensis child not 4km from where Lucy was found in 1974. It is not only the oldest juvenile fossil ever found, it is also the most complete hominin fossil found to date. Selam, as the fossil was nicknamed (or Lucy's baby or Dikika's baby), confirmed earlier suggestions that Au. afarensis was bipedal, yet spent time in the trees. The shoulder structure with its upward pointing shoulder joints and the bony ridge running along the shoulder blades are like that of apes, which would have facilitated arboreal movement even if they were not as fully capable as chimpanzees at moving in trees.
Paleoecological data indicates that Au. afarensis lived in both grassland (savanna) and woodland environments.
Australopithecus africanus
Raymond Dart identified Australopithecus africanus , “African southern ape,” in 1924, the first australopith to be recognized. This specimen was a juvenile australopith, nicknamed the Taung baby. Based on the position of foramen magnum, Dart claimed it was a bipedal hominin, but his contemporaries refuted his claim as they thought the brain was too small. The paleoanthropological community did not recognize the Taung baby as a hominin until the 1950s at which time other fossil specimens attributed to Au. africanus had been found. Au. africanus has only been found in southern Africa at such sites as Makapansgat, Sterkfontein, and Taung.
Figure \(\PageIndex{6}\) - Australopithecus africanus (Mrs. Ples)
Using primarily biochronological methods since South Africa does not have geologic deposits suitable for other types of dating techniques, it has been dated to 3-2 mya (Scarre 2014). In comparison to Au. afarensis , Au. africanus has smaller incisors and larger molars; the canines no longer have the pointed, triangular appearance seen in apes and Au. afarensis ; however, Au. africanus still exhibits some prognathism in the face and has a small brain like that of Au. afarensis . Postcranially, Au. africanus retains some primitive features like those seen in Au. afarensis , e.g., shorter arms than legs and hand/feet shape. Its size is also similar to Au. afarensis . Another derived feature are the nasal pillars. Nasal pillars are a “buttressing of bone on either side of the nasal opening of the skill on the maxilla,” which may be an adaptation for eating hard foods (Becoming Human c.2008). Other derived traits include a longer, flatter occipital bone and a taller frontal bone, two traits seen in the genus Homo . Because of the traits mentioned above, there is general consensus that Au. africanus is a direct descendent of Au. afarensis . Some paleoanthropologists suggest that Au. africanus is the progenitor of Paranthropus robustus (see below). Its relationship to Homo is less clear.
Australopithecus garhi
Found in Bouri, Ethiopia in 1997 by Behane Asfaw and Tim White, Australopithecus garhi is a gracile australopith. “Gracile” refers to the thickness of the bone; in this case it is less robust than its Paranthropus contemporaries. Using radioisotopic and biochronometric dating methods, Au. garhi dates to 2.5 mya. Few fossil specimens have been found and those that have are relatively fragmentary. One cranium and other skull fragments were found and serve as the basis of the species identification. The size and shape of its molar teeth suggest to some researchers that Au. garhi is related to Paranthropus aethiopicus (see below), but its other features, e.g., braincase, face, and other teeth, are more like genus Homo . In light of this, some researchers contend it is ancestral to Homo .
Figure \(\PageIndex{7}\) - Australopithecus garhi
Australopithecus sediba
A relative newcomer to the stage, Australopithecus sediba was found in 2008 at Malapa Cave, South Africa by Matthew Berger, the 9-year-old-son of the project’s lead paleoanthropologist, Lee Berger. Dating to 1.95-1.75 mya using paleomagnetism, uranium-lead dating, and biochronology, Au. sediba has a mosaic of characteristics that suggest it may be transitional from the australopiths to genus Homo , hence its name “wellspring or fountain” in the local Lesotho language. However, this claim is controversial as the earliest dates for Homo predate Au. sediba by about 500,000 years (Becoming Human c2008).
Figure \(\PageIndex{8}\) - Australopithecus sediba
Au. sediba shares some traits with Au. africanus , e.g., cranial capacity, brow ridges, and enlarged tooth cusps (the pointed tops of teeth), causing some to claim the two species are related. Its arm-to-leg proportions are likewise similar to the australopiths. The features that link Au. sediba to Homo include the pelvis shape, more vertical brain case, smaller cheek bones, and molar shape.
Another controversy recently emerged in 2014 when Ella Been and Yoel Rak presented their spinal cord study (Barras 2014). They claim that the spinal cord features and the jawbones of the two specimens identified by Berger are actually two different species: early Homo and an australopith. Additionally, Been and Rak claim the Malapa collection contains the remains of four individuals, not two. Berger disputes this claim that there are two species present. You can read more details about this debate atNew Scientist [optional].
Robust Australopiths
Three robust species of hominins emerged in the Plio-Pleistocene period: Paranthropus aethiopicus , Paranthropus boisei , and Paranthropus robustus . They have morphological features that suggest they were well adapted for eating hard foods that needed grinding, which led to their being identified as “robust.” Their incisors and canines are small, while their premolars and molars are quite large. The zygomatic arch is flared, allowing for larger masticatory muscles that are needed to grind hard foods. This tends to make the face dish-like. A prominent sagittal crest tops the skull, yet another chewing adaptation as it the hard-working temporalis muscle a sturdy bone on which to attach. It has been argued that the robust australopiths were so well adapted that they could not respond quickly enough to changing environmental conditions, which led to their extinction by 1.0 mya. Recently, dental evidence from P. boisei suggests that hard foods were not the primary diet of at least P. boisei , but were fall back foods, or foods that were ate when preferred foods were not available (Becoming Human c2008).
Note
There is debate over whether the differences mentioned above qualify the robust australopiths to be in a separate genus from the australopithecines. In some anthropological works the genus Australopithecus is used. In others, such as this work, Paranthropus is used.
Paranthropus aethiopicus
Paranthropus aethiopicus is dated 2.7-2.3 mya. While it was first identified as a species in 1967 by French researchers who found a toothless mandible at Omo, Ethiopia, it was not accepted until 1985 when Alan Walker and Richard Leakey found the “black skull” at Lake Turkana, Kenya. It is called the black skull because during the fossilization process it was stained black by minerals present in the sediment. Other P. aethiopicus fossils have been found at Laetoli, Kenya since the 1985 discovery; however, no postcranial material has ever been recovered.
Figure \(\PageIndex{9}\) - Paranthropus aethiopicus
P. aethiopicus exhibits a powerful jaw, well-developed sagittal crest, and megadont, or extremely large, molars. Its cranial capacity, the joints between the jaw and cranium, and prognathic face are similar to Au. afarensis . The prominence of the sagittal crest toward the back of the skull is also similar to Au. afarensis . These features are not present in other robust australopiths or Au. africanus . These similarities lead some paleoanthropologists to claim Au. afarensis is ancestral to P. aethiopicus .
P. aethiopicus shares several characteristics with other robust species such as forward positioned zygomatic arches, a dished face (see P. boisei reconstruction below), thick palate bones, and large premolars and molars.
Paranthropus boisei
Paranthropus boisei shares several features with P. aethiopicus , including a dished face, strong sagittal crest, and large premolars and molars (in fact the molars are about four times as large as modern humans (Smithsonian 2015)). Unlike P. aethiopicus , the sagittal crest is positioned towards the front of the skull instead of the back. Other unique features include premolars shaped like molars, the zygomatic arch forms a circular arch, the foramen magnum is short and heart-shaped, and the braincase is large than the other robust australopiths. Little was known about the postcranial structures of P. boisei until a 2010/11 discovery of fragments of postcranial remains at Olduvai Gorge, Tanzania. Fragments of the radius, ulna, femur, and tibia support earlier suggestions that P. boisei was sexually dimorphic. These postcranial remains indicate that P. boisei was “...more ruggedly built—combining terrestrial bipedal locomotion and some arboreal behaviors…it [has] more well-formed forearms muscles that were used for climbing, fine-manipulation and all sorts of behavior” (Sci-News.com 2013).
Figure \(\PageIndex{10}\) - Paranthropus boisei
P. boisei was discovered in 1955 at Olduvai Gorge by Mary Leakey. It was not until 1959 that Leakey identified the fossil as a new species and it Zinjanthropus boisei , nicknamed “Zinj.” Subsequent discoveries of similar fossils and other robust australopiths resulted in a consensus among researchers that Zinj belonged in the genus Paranthropus . P. boisei fossils have been found in several East Africa sites, including Peninj, Tanzania, Konso, Ethiopia, and Koobi Fora and West Turkana, both in Kenya. It lived in grasslands, but also forested areas near water sources, between 2.3-1.2 mya, making it a long-lived species. There is no evidence to suggest that P. boisei is ancestral to any subsequent hominin.
Figure \(\PageIndex{11}\) - Paranthropus boisei ; model of adult male (Smithsonian Museum of Natural History)
Paranthropus robustus
Paranthropus robustus is the only robust australopith found in southern Africa. First discovered in 1938 by Robert Broom in Kromdraii, South Africa, P. robustus fossils were also recovered from Swartkrans and Drimolen, South Africa. Like the other robust species, it has megadont cheek teeth (premolars and molars), large zygomatic arches, dish-shaped face, sagittal crest, and a high degree of sexual dimorphism. Its unique characteristics include a larger brain size than other australopiths and hand morphology suggesting a grip capable of tool use. P. robustus is dated 2.0-1.2 mya.
Figure \(\PageIndex{12}\) - Paranthropus robustus
References
- Alemseged Z, Spoor F, Kimbel WH, Bobe R, Geraads D, Reed D, Wynn JG. 2006. A juvenile early hominin skeleton from Dikika, Ethiopoa. Nature 443 (Sep 21): 296-301. Available from: http://www.nature.com.offcampus.lib....ture05047.html . doi:10.1038/nature05047.
- Bailey SE. 2006. Sahelanthropus tchadensis. In: Encyclopedia of anthropology, Vol. 5. Thousand Oaks (CA): SAGE Reference. p. 2044-2045.
- Barras C. 2014. Human 'missing link' fossils may be a jumble of species. New Sci [Internet] [cited 2015 Aug 13]; 222(2964). Available from: https://www.newscientist.com/article/mg22229643-200-human-missing-link-fossils-may-be-jumble-of-species/
- Becoming Human. c2008. The human lineage through time. Institute of Human Origins [Internet] [cited 2015 Aug 3]. Available from: http://www.becominghuman.org/node/human-lineage-through-time
- Domínguez-Rodrigo M, Pickering TR, Baquedano E, Mabulla A, Mark DF, Musiba C, et al. 2013. First partial skeleton of a 1.34-million-year-old Paranthropus boisei from Bed II, Olduvai Gorge, Tanzania. PLoS ONE 8(12): e80347. Available from: http://journals.plos.org/plosone/art...l.pone.0080347 . doi:10.1371/journal.pone.0080347
- eFossils [Internet] [cited 2015 Aug 10]. Department of Anthropology, The University of Texas at Austin. Available from: http://efossils.org/
- Harmand S, Lewis JE, Feibel CS, Lepre CJ, Prat S, Lenoble A, Boës X, Quinn RL, Brenet M, Arroyo A, Taylor N, Clément S, Daver G, Brugal JP, Leakey L, Mortlock RA, Wright JD, Lokorodi S, Kirwa C, Kent DV, Roche H. 2015. 3.3-million-year-old tools from Lomekwi 3, West Turkana, Kenya. Nature 521 (May 21): 310-315. Available from: http://www.nature.com.offcampus.lib....ture14464.html . doi:10.1038/nature14464.
- Hunt KD. Australopithecines. In: Encyclopedia of anthropology, Vol. 1. Thousand Oaks (CA): SAGE Reference, 2006. p.311-317.
- Jurmain R, Kilgore L. Trevathan W. 2013 Essentials in physical anthropology. Belmont (CA): Wadsworth Cengage Learning.
- Larsen, CS. 2014. Our origins: discovering physical anthropology. New York (NY): W. W. Norton & Company, Inc.
- Lebatard AE, Bouriès DL, Duriner P, Jolivet M, Braucjer R, Carcaillet J, Schuster M, Arnaud N, Monié P, Lihoreau F, Likius A, Macaye HT, Vignaud P, Brunet M. 2008. Cosmogenic nuclide dating of Sahelanthropus tchadensis and Australopithecus bahrelghazali: Mio-Pliecene hominids from Chad. Proc Natl Acad Sci U S A [Internet] [cited 2015 Aug 3]; 105(9): 3226-3231. Available from: http://www.pnas.org/content/105/9/3226.full . doi: 10.1073/pnas.0708015105
- Richmond BG, Jungers WL. 2008. Orrorin tugenensis femoral morphology and the evolution of hominin bipedalism. Science [Internet] [cited 2015 Aug 3]; 319(5870): 1662-1665. Available from: www.jstor.org/stable/20053635
- Scarre C. 2013. The human past. London (UK): Thames & Hudson.
- Sci-News.com [Internet]. 2013 Dec 6. Paranthropus boisei: 1.34-million-year-old hominin found in Tanzania. [cited 2015 Aug 12]. Available from: http://www.sci-news.com/othersciences/anthropology/science-paranthropus-boisei-hominin-tanzania-01603.html
- Smithsonian Institution [Internet]. 2015 Aug 4. What does it mean to be human? [cited 2015 Aug 11]. Available from: http://humanorigins.si.edu/evidence/human-fossils/species
- Su DF. 2013. The earliest hominins: Sahelanthropus, Orrorin, and Ardipithecus. The Nature Education Knowledge Project [Internet] [cited 2015 Aug 3]. Available from: http://www.nature.com/scitable/knowl...hecus-67648286
- Ward CV, Manthi FK, Plavcan JM. 2013. New fossils of Australopithecus anamensis from Kanapoi, West Turkana, Kenya (2003-2008). J Hum Evol 65(5): 501-524. Available from doi:10.1016/j.jhevol.2013.05.006
- Wong K. 2006. Special report: Lucy’s baby: an extraordinary new human fossil comes to light. Sci Am [Internet] [cited 2015 Aug 10]; Sep 20. Available from: http://www.scientificamerican.com/ar...rt-lucys-baby/


4.13.3: Water Erosion
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Erosion is the detachment of earth material from the surface. Once detached, agents like water or wind transport the material to a new location where it is deposited. The most ubiquitous form of erosion is that done by water.
Rain splash erosion is caused by the impact of water striking the surface. Rain splash erosion generally takes place in two steps. As precipitation is absorbed by the surface it fills the pore spaces, loosening soil particles and driving them apart. The impact of subsequent rain drops hitting the surface splash the particle away from the point of impact. The effect is to give the surface a dimpled-like appearance.
Surface runoff forms when the rainfall intensity of a storm exceeds the infiltration capacity of the soil. Sheet erosion is caused by the unconfined flow of water running across the surface. The effects of sheet erosion are often hard to distinguish because such thin layers of soil are being removed. It isn't until several years later that significant degradation is perceived.
Rill erosion is caused by water concentrating into innumerable, closely-spaced small channels. Left unchecked, rills can cut vertically and horizontally and when joined form gullies.
Gullies are steep-sided trenches formed by the coalescence of many rills. Once started they are difficult to stop.


22.7: Reactivity of Enolate Ions
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Objectives
After completing this section, you should be able to
- identify the two possible ways in which a given enolate anion could conceivably react with an electrophile.
- write an equation to illustrate the haloform reaction.
- identify the products formed from the reaction of a given methyl ketone with a halogen and excess base.
- identify the methyl ketone, the reagents, or both, needed to obtain a specified carboxylic acid through a haloform reaction.
Key Terms
Make certain that you can define, and use in context, the key terms below.
- haloform
- haloform reaction
Study Notes
Because the negative charge on an enolate ion is delocalized, there are two reactive sites and therefore two potential products. The α ‑substituted product is much more common.
A “haloform” is any compound of the type CHX 3 , where X = Cl, Br or I. Of these three compounds, chloroform is the most common.
The haloform reaction describedin the reading is usually carried out with iodine. This reaction is called the “iodoform test,” and is one of the reactions carried out in the laboratory as a simple qualitative test for methyl ketones.
How Enolates React
Due to their negative charges, enolates are better and more versatile nucleophiles than enols. The increased reactivity of enolates makes them capable of a wider range of reactions than enols. Also, α-hydrogen containing compounds can be completely converted to an enolate by reaction with a strong base. Whereas enols can only be created in small amounts through manipulating their equilibrium.
Since the negative charge of an enolate anion is delocalized between the α-carbon and an oxygen, electrophiles may bond to either atom. Reactants having two or more reactive sites are called ambident, so this term applies to enolate anions. Either the C of the O reactive site in an enolate may act as a nucleophile depending on the reaction conditions. Reactions with the oxygen would create a new O-E bond and produce an enol derivative. Reactions with the α-carbon creates a new C-E bond and creates an α-substituted carbonyl compound. Although reactions with the nucleophilic oxygen are possible, reactions involving the nucleophilic α-carbon are much more common, partially due to the thermodynamic stability of the C=O bonds in the final products. Also, the enolate counter ion, such as Li + or Na + , is more tightly associated with the negatively charged enolate oxygen which can then block incoming electrophiles, reducing their chance of reaction at the oxygen.
Stereochemical Implication of Enolate Formation
During enolate formation, an α-hydrogen is removed to form a sp 2 -hybridized, trigonal planar C=C bond which removes any chiral information from the original α-carbon. Because the enol alkene is planar, the incoming electrophile can attack from either the top or the bottom. If the α-carbon of the starting material has a defined stereochemistry or if a new stereocenter is formed during the reaction, the product will be a racemic mixture of enantiomers.
Base Promoted α-Halogenation
An enolate reacts rapidly with a halogen to produce α-halogenated carbonyl products. This reaction has the tendency to overreact and create polyhalogenated products. If a monohalogenated product is sought, the acid catalyzed halogenation reaction discussed in section 22.3 is preferred. Because complete formation to the enolate is not necessary, weak bases, such as the hydroxide anion, are sufficient to produce this reaction. Once a small amount of enolate is formed, it quickly reacts with the halogen. This removes the enolate and shifts the equilibrium toward forming more enolate by Le Chatelier's principle.
Overreaction During Base Promoted α-Halogenation
The α-hydrogens of halogenated carbonyl products are usually more acidic than the corresponding non-halogenated compounds. The inductive electron withdrawing effect of the electronegative halogen stabilizes the negative charge of the enolate ion. This promotes further enolate formation and also further halogenation of the α-carbon. Monohalogenated carbonyls form an enolate over 100 times faster than their non-halogenated counterparts making multiple halogenations of the α-carbon frequent. This effect is exploited to cause the haloform reaction.
The Haloform Reaction
Overall, the haloform reaction represents a method for the conversion of methyl ketones to carboxylic acids. Due to the increased reactivity of α-halogenated products, methyl ketones typically undergo base promoted halogenation three times to give a trihalo-ketone. A halomethyl ion leaving group is then substituted with a hydroxide ion during nucleophilic acyl substitution. The resulting carboxylate can then be protonated to form a carboxylic acid.
Example
Mechanism
Note! This reaction is considered to be base promoted and not base catalyzed because an entire equivalent of base is required for each α-halogenation. Deprotonation of an α-hydrogen with hydroxide produces the nucleophilic enolate ion which subsequently reacts with the halogen. The increasing acidity of α-halogenated ketone causes this reaction to occur two more times. Once formed, the -CX 3 group attached to the carbonyl can act as a leaving group. Nucleophilic acyl substitution with a hydroxide anion causes C-C bond cleavage and eventually produces a haloform (CHCl 3 , CHBr 3 , CHI 3 ) and a carboxylate anion. The carboxylate ion is easily protonated with acid to form a carboxylic acid functional group. Often, this reaction is performed using iodine (I 2 ) because the subsequent iodoform (CHI 3 ) side-product is a bright yellow solid which is easily filtered off.
This reaction represents one of the few examples of a carbanion leaving group. The trihalomethyl ion ( - :CX 3 ) is particularly stabilized due to the inductive electron-withdrawing effects of the three halogens. The stability of the carbanion can be seen when considering the pK a corresponding conjugate acid. In particular, bromoform (CHBr 3 ) has a pK a of 13.7 which is more than 10 20 times more acidic than a typical alkane C-H bond.
1) Enolate formation
2) Nucleophilic attack on the halogen
3) Repeat the halogenation two more times
4) Nucleophilic attack on the electrophilic carbonyl carbon
5) Nucleophilic acyl substitution
6) Deprotonation
7) Protonation of the carboxylate
Biological Haloform Reaction
Interest in the haloform reaction has increased since the discovery that certain plants and marine algae can biosynthize chloroform, bromoform, and other small halocarbons through an analogous process. Previously it was assumed that these toxic compounds were present in the environment as a man-made pollutants.
The likely starting material of the biosynthesis are biogenic methyl ketones, a halogen anion, and oxygen. The enzyme, chloroperoxidase, catalyzes the polyhalogenation of the methyl groups. As in the haloform reaction, the final biosynthesis step involves a nucleophilic acyl substitution with a hydroxide anion to create a haloform and a carboxylate anion.
Exercises
1) Please predict the expected products of the following reactions:
a)
b)
Solutions
a)
b)


7.7: Standard States of Pure Substances
It is often useful to refer to a reference pressure, the standard pressure , denoted \(p\st\). The standard pressure has an arbitrary but constant value in any given application. Until 1982, chemists used a standard pressure of \(1\units{atm}\) (\(1.01325\timesten{5}\Pa\)). The IUPAC now recommends the value \(p\st = 1\br\) (exactly \(10^5\Pa\)). This e-book uses the latter value unless stated otherwise. (Note that there is no defined standard temperature .)
A superscript degree symbol (\(\circ\)) denotes a standard quantity or standard-state conditions. An alternative symbol for this purpose, used extensively outside the U.S., is a superscript Plimsoll mark (\(\unicode{x29B5}\)). (The Plimsoll mark is named after the British merchant Samuel Plimsoll, at whose instigation Parliament passed an act in 1875 requiring the symbol to be placed on the hulls of cargo ships to indicate the maximum depth for safe loading.)
A standard state of a pure substance is a particular reference state appropriate for the kind of phase and is described by intensive variables. This e-book follows the recommendations of the IUPAC Green Book (E. Richard Cohen et al, Quantities, Units and Symbols in Physical Chemistry , 3rd edition, RSC Publishing, Cambridge, 2007, p. 61–62) for various standard states.
- Section 9.7 will introduce additional standard states for constituents of mixtures.


4.7: Summary Questions
4.7 Summary Questions
1. A 50 yr-old tree has a 20” dbh. A 50 yr-old tree of the same species has a 36” dbh. What are some possible reasons for the difference in the diameter of these trees even though they are the same age?
2. A Douglas-fir is cored at dbh, resulting in a ring count of 36. What is the tree’s estimated total age?
3. Estimate the age of the core sample illustrated below.
4. A young tree is illustrated below. Count the whorls to estimate its total age.
5. Would core samples from all sides of the tree result in the same ring count? Why or why not? (Consider trees on slopes, wind patterns, coring angles and false whorls.)
Answers to Summary Questions
1. The key to remember here is that tree diameter is a function of crown volume. So any growing condition that would result in a greater crown for one tree, would also result in a larger diameter for it. These conditions might include: a) more physical growing space for the larger tree; b) greater access to light, nutrients, water and other necessary plant resources; c) a genotype (genetic makeup) more suited to the growing conditions present or less palatable to animals, insects or pathogens; or d) activities of neighboring trees over time that resulted in more favorable growing conditions.
2. For Douglas-fir, we generally add 7 years to a core sample to obtain total age in a stand that appears to have naturally regenerated. This number would increase if it appeared the tree was stagnated under shade for much of its early life (10-12 yrs) or decrease if it was planted from nursery stock and grew in full sunlight (4-5 yrs).
3. Assuming the lines on the drawing represent the dark summer wood or late wood on the tree, they indicate the end of the growing year, Therefore, there are 14 rings present; the shaded one being the bark. If the core sample had not hit the pith, we would have had to reconstruct the pith area, drawing circles as described in Field Techniques number 10.
4.The whorls and knots indicate 10 years. Add 3-4 years to that for the time it took the tree to grow to the first knot, and the total estimated age would be about 13 years.
5.Core samples do not vary widely from one side of the tree to the other, but it is possible for differences to be present. These may result from off-center piths or inconsistent coring directions (due to a tree’s position on a slope, subjectivity to strong winds, or tendency to grow toward a light source). Rot or fire scars may destroy evidence of rings. In addition, false rings do not always extend all the way around the tree.


20.3: Blood Flow, Blood Pressure, and Resistance
By the end of this section, you will be able to:
- Distinguish between systolic pressure, diastolic pressure, pulse pressure, and mean arterial pressure
- Describe the clinical measurement of pulse and blood pressure
- Identify and discuss five variables affecting arterial blood flow and blood pressure
- Discuss several factors affecting blood flow in the venous system
Blood flow refers to the movement of blood through a vessel, tissue, or organ, and is usually expressed in terms of volume of blood per unit of time. It is initiated by the contraction of the ventricles of the heart. Ventricular contraction ejects blood into the major arteries, resulting in flow from regions of higher pressure to regions of lower pressure, as blood encounters smaller arteries and arterioles, then capillaries, then the venules and veins of the venous system. This section discusses a number of critical variables that contribute to blood flow throughout the body. It also discusses the factors that impede or slow blood flow, a phenomenon known as resistance .
As noted earlier, hydrostatic pressure is the force exerted by a fluid due to gravitational pull, usually against the wall of the container in which it is located. One form of hydrostatic pressure is blood pressure , the force exerted by blood upon the walls of the blood vessels or the chambers of the heart. Blood pressure may be measured in capillaries and veins, as well as the vessels of the pulmonary circulation; however, the term blood pressure without any specific descriptors typically refers to systemic arterial blood pressure—that is, the pressure of blood flowing in the arteries of the systemic circulation. In clinical practice, this pressure is measured in mm Hg and is usually obtained using the brachial artery of the arm.
Components of Arterial Blood Pressure
Arterial blood pressure in the larger vessels consists of several distinct components (Figure \(\PageIndex{1}\)): systolic and diastolic pressures, pulse pressure, and mean arterial pressure.
Systolic and Diastolic Pressures
When systemic arterial blood pressure is measured, it is recorded as a ratio of two numbers (e.g., 120/80 is a normal adult blood pressure), expressed as systolic pressure over diastolic pressure. The systolic pressure is the higher value (typically around 120 mm Hg) and reflects the arterial pressure resulting from the ejection of blood during ventricular contraction, or systole. The diastolic pressure is the lower value (usually about 80 mm Hg) and represents the arterial pressure of blood during ventricular relaxation, or diastole.
Pulse Pressure
As shown in Figure 20.10, the difference between the systolic pressure and the diastolic pressure is the pulse pressure . For example, an individual with a systolic pressure of 120 mm Hg and a diastolic pressure of 80 mm Hg would have a pulse pressure of 40 mmHg.
Generally, a pulse pressure should be at least 25 percent of the systolic pressure. A pulse pressure below this level is described as low or narrow. This may occur, for example, in patients with a low stroke volume, which may be seen in congestive heart failure, stenosis of the aortic valve, or significant blood loss following trauma. In contrast, a high or wide pulse pressure is common in healthy people following strenuous exercise, when their resting pulse pressure of 30–40 mm Hg may increase temporarily to 100 mm Hg as stroke volume increases. A persistently high pulse pressure at or above 100 mm Hg may indicate excessive resistance in the arteries and can be caused by a variety of disorders. Chronic high resting pulse pressures can degrade the heart, brain, and kidneys, and warrant medical treatment.
Mean Arterial Pressure
Mean arterial pressure (MAP) represents the “average” pressure of blood in the arteries, that is, the average force driving blood into vessels that serve the tissues. Mean is a statistical concept and is calculated by taking the sum of the values divided by the number of values. Although complicated to measure directly and complicated to calculate, MAP can be approximated by adding the diastolic pressure to one-third of the pulse pressure or systolic pressure minus the diastolic pressure:
\[\mathrm{MAP}=\text { diastolic } \mathrm{BP}+\frac{\text { (systolic BP-diastolic BP })}{3}\]
or
\[\mathrm{MAP}=\text { diastolic } \mathrm{BP}+\frac{\text { (pulse pressure) }}{3}\]
In Figure \(\ PageIndex {1}\), this value is approximately 80 + (120 − 80) / 3, or 93.33. Normally, the MAP falls within the range of 70–110 mm Hg. If the value falls below 60 mm Hg for an extended time, blood pressure will not be high enough to ensure circulation to and through the tissues, which results in ischemia, or insufficient blood flow. A condition called hypoxia, inadequate oxygenation of tissues, commonly accompanies ischemia. The term hypoxemia refers to low levels of oxygen in systemic arterial blood. Neurons are especially sensitive to hypoxia and may die or be damaged if blood flow and oxygen supplies are not quickly restored.
Pulse
After blood is ejected from the heart, elastic fibers in the arteries help maintain a high-pressure gradient as they expand to accommodate the blood, then recoil. This expansion and recoiling effect, known as the pulse , can be palpated manually or measured electronically. Although the effect diminishes over distance from the heart, elements of the systolic and diastolic components of the pulse are still evident down to the level of the arterioles.
Because pulse indicates heart rate, it is measured clinically to provide clues to a patient’s state of health. It is recorded as beats per minute. Both the rate and the strength of the pulse are important clinically. A high or irregular pulse rate can be caused by physical activity or other temporary factors, but it may also indicate a heart condition. The pulse strength indicates the strength of ventricular contraction and cardiac output. If the pulse is strong, then systolic pressure is high. If it is weak, systolic pressure has fallen, and medical intervention may be warranted.
Pulse can be palpated manually by placing the tips of the fingers across an artery that runs close to the body surface and pressing lightly. While this procedure is normally performed using the radial artery in the wrist or the common carotid artery in the neck, any superficial artery that can be palpated may be used (Figure \(\PageIndex{2}\)). Common sites to find a pulse include temporal and facial arteries in the head, brachial arteries in the upper arm, femoral arteries in the thigh, popliteal arteries behind the knees, posterior tibial arteries near the medial tarsal regions, and dorsalis pedis arteries in the feet. A variety of commercial electronic devices are also available to measure pulse.
Measurement of Blood Pressure
Blood pressure is one of the critical parameters measured on virtually every patient in every healthcare setting. The technique used today was developed more than 100 years ago by a pioneering Russian physician, Dr. Nikolai Korotkoff. Turbulent blood flow through the vessels can be heard as a soft ticking while measuring blood pressure; these sounds are known as Korotkoff sounds . The technique of measuring blood pressure requires the use of a sphygmomanometer (a blood pressure cuff attached to a measuring device) and a stethoscope. The technique is as follows:
- The clinician wraps an inflatable cuff tightly around the patient’s arm at about the level of the heart.
- The clinician squeezes a rubber pump to inject air into the cuff, raising pressure around the artery and temporarily cutting off blood flow into the patient’s arm.
- The clinician places the stethoscope on the patient’s antecubital region and, while gradually allowing air within the cuff to escape, listens for the Korotkoff sounds.
Although there are five recognized Korotkoff sounds, only two are normally recorded. Initially, no sounds are heard since there is no blood flow through the vessels, but as air pressure drops, the cuff relaxes, and blood flow returns to the arm. As shown in Figure \(\PageIndex{3}\), the first sound heard through the stethoscope—the first Korotkoff sound—indicates systolic pressure. As more air is released from the cuff, blood is able to flow freely through the brachial artery and all sounds disappear. The point at which the last sound is heard is recorded as the patient’s diastolic pressure.
The majority of hospitals and clinics have automated equipment for measuring blood pressure that work on the same principles. An even more recent innovation is a small instrument that wraps around a patient’s wrist. The patient then holds the wrist over the heart while the device measures blood flow and records pressure.
Variables Affecting Blood Flow and Blood Pressure
Five variables influence blood flow and blood pressure:
- Cardiac output
- Compliance
- Volume of the blood
- Viscosity of the blood
- Blood vessel length and diameter
Recall that blood moves from higher pressure to lower pressure. It is pumped from the heart into the arteries at high pressure. If you increase pressure in the arteries (afterload), and cardiac function does not compensate, blood flow will actually decrease. In the venous system, the opposite relationship is true. Increased pressure in the veins does not decrease flow as it does in arteries, but actually increases flow. Since pressure in the veins is normally relatively low, for blood to flow back into the heart, the pressure in the atria during atrial diastole must be even lower. It normally approaches zero, except when the atria contract (see Figure \(\PageIndex{1}\)).
Cardiac Output
Cardiac output is the measurement of blood flow from the heart through the ventricles, and is usually measured in liters per minute. Any factor that causes cardiac output to increase, by elevating heart rate or stroke volume or both, will elevate blood pressure and promote blood flow. These factors include sympathetic stimulation, the catecholamines epinephrine and norepinephrine, thyroid hormones, and increased calcium ion levels. Conversely, any factor that decreases cardiac output, by decreasing heart rate or stroke volume or both, will decrease arterial pressure and blood flow. These factors include parasympathetic stimulation, elevated or decreased potassium ion levels, decreased calcium levels, anoxia, and acidosis.
Compliance
Compliance is the ability of any compartment to expand to accommodate increased content. A metal pipe, for example, is not compliant, whereas a balloon is. The greater the compliance of an artery, the more effectively it is able to expand to accommodate surges in blood flow without increased resistance or blood pressure. Veins are more compliant than arteries and can expand to hold more blood. When vascular disease causes stiffening of arteries, compliance is reduced and resistance to blood flow is increased. The result is more turbulence, higher pressure within the vessel, and reduced blood flow. This increases the work of the heart.
A Mathematical Approach to Factors Affecting Blood Flow
Jean Louis Marie Poiseuille was a French physician and physiologist who devised a mathematical equation describing blood flow and its relationship to known parameters. The same equation also applies to engineering studies of the flow of fluids. Although understanding the math behind the relationships among the factors affecting blood flow is not necessary to understand blood flow, it can help solidify an understanding of their relationships. Please note that even if the equation looks intimidating, breaking it down into its components and following the relationships will make these relationships clearer, even if you are weak in math. Focus on the three critical variables: radius (r), vessel length (λ), and viscosity (η).
Poiseuille’s equation:
\[\text { Blood flow }=\frac{\pi \Delta \mathrm{P} \mathrm{r}^4}{8 \eta \lambda}\]
- π is the Greek letter pi, used to represent the mathematical constant that is the ratio of a circle’s circumference to its diameter. It may commonly be represented as 3.14, although the actual number extends to infinity.
- ΔP represents the difference in pressure.
- r 4 is the radius (one-half of the diameter) of the vessel to the fourth power.
- η is the Greek letter eta and represents the viscosity of the blood.
One of several things this equation allows us to do is calculate the resistance in the vascular system. Normally this value is extremely difficult to measure, but it can be calculated from this known relationship:
\[\text { Blood flow }=\frac{\Delta \mathrm{P}}{\text { Resistance }}\]
If we rearrange this slightly,
\[\text { Resistance }=\frac{\Delta \mathrm{P}}{\text { Blood flow }}\]
Then by substituting Pouseille’s equation for blood flow
\[\text { Resistance }=\frac{8 \eta \lambda}{\pi \mathrm{r}^4}\]
By examining this equation, you can see that there are only three variables: viscosity, vessel length, and radius, since 8 and π are both constants. The important thing to remember is this: Two of these variables, viscosity and vessel length, will change slowly in the body. Only one of these factors, the radius, can be changed rapidly by vasoconstriction and vasodilation, thus dramatically impacting resistance and flow. Further, small changes in the radius will greatly affect flow, since it is raised to the fourth power in the equation.
We have briefly considered how cardiac output and blood volume impact blood flow and pressure; the next step is to see how the other variables (contraction, vessel length, and viscosity) articulate with Pouseille’s equation and what they can teach us about the impact on blood flow.
 Water may merely trickle along a creek bed in a dry season, but rush quickly and under great pressure after a heavy rain. Similarly, as blood volume decreases, pressure and flow decrease. As blood volume increases, pressure and flow increase.
Under normal circumstances, blood volume varies little. Low blood volume, called hypovolemia , may be caused by bleeding, dehydration, vomiting, severe burns, or some medications used to treat hypertension. It is important to recognize that other regulatory mechanisms in the body are so effective at maintaining blood pressure that an individual may be asymptomatic until 10–20 percent of the blood volume has been lost. Treatment typically includes intravenous fluid replacement.
Hypervolemia , excessive fluid volume, may be caused by retention of water and sodium, as seen in patients with heart failure, liver cirrhosis, some forms of kidney disease, hyperaldosteronism, and some glucocorticoid steroid treatments. Restoring homeostasis in these patients depends upon reversing the condition that triggered the hypervolemia.
Blood Viscosity
Viscosity is the thickness of fluids that affects their ability to flow. Clean water, for example, is less viscous than mud. The viscosity of blood is directly proportional to resistance and inversely proportional to flow; therefore, any condition that causes viscosity to increase will also increase resistance and decrease flow. For example, imagine sipping milk, then a milkshake, through the same size straw. You experience more resistance and therefore less flow from the milkshake. Conversely, any condition that causes viscosity to decrease (such as when the milkshake melts) will decrease resistance and increase flow.
Normally the viscosity of blood does not change over short periods of time. The two primary determinants of blood viscosity are the formed elements and plasma proteins. Since the vast majority of formed elements are erythrocytes, any condition affecting erythropoiesis, such as polycythemia or anemia, can alter viscosity. Since most plasma proteins are produced by the liver, any condition affecting liver function can also change the viscosity slightly and therefore alter blood flow. Liver abnormalities such as hepatitis, cirrhosis, alcohol damage, and drug toxicities result in decreased levels of plasma proteins, which decrease blood viscosity. While leukocytes and platelets are normally a small component of the formed elements, there are some rare conditions in which severe overproduction can impact viscosity as well.
Vessel Length and Diameter
The length of a vessel is directly proportional to its resistance: the longer the vessel, the greater the resistance and the lower the flow. As with blood volume, this makes intuitive sense, since the increased surface area of the vessel will impede the flow of blood. Likewise, if the vessel is shortened, the resistance will decrease and flow will increase.
The length of our blood vessels increases throughout childhood as we grow, of course, but is unchanging in adults under normal physiological circumstances. Further, the distribution of vessels is not the same in all tissues. Adipose tissue does not have an extensive vascular supply. One pound of adipose tissue contains approximately 200 miles of vessels, whereas skeletal muscle contains more than twice that. Overall, vessels decrease in length only during loss of mass or amputation. An individual weighing 150 pounds has approximately 60,000 miles of vessels in the body. Gaining about 10 pounds adds from 2000 to 4000 miles of vessels, depending upon the nature of the gained tissue. One of the great benefits of weight reduction is the reduced stress to the heart, which does not have to overcome the resistance of as many miles of vessels.
In contrast to length, the diameter of blood vessels changes throughout the body, according to the type of vessel, as we discussed earlier. The diameter of any given vessel may also change frequently throughout the day in response to neural and chemical signals that trigger vasodilation and vasoconstriction. The vascular tone of the vessel is the contractile state of the smooth muscle and the primary determinant of diameter, and thus of resistance and flow. The effect of vessel diameter on resistance is inverse: Given the same volume of blood, an increased diameter means there is less blood contacting the vessel wall, thus lower friction and lower resistance, subsequently increasing flow. A decreased diameter means more of the blood contacts the vessel wall, and resistance increases, subsequently decreasing flow.
The influence of lumen diameter on resistance is dramatic: A slight increase or decrease in diameter causes a huge decrease or increase in resistance. This is because resistance is inversely proportional to the radius of the blood vessel (one-half of the vessel’s diameter) raised to the fourth power (R = 1/r 4 ). This means, for example, that if an artery or arteriole constricts to one-half of its original radius, the resistance to flow will increase 16 times. And if an artery or arteriole dilates to twice its initial radius, then resistance in the vessel will decrease to 1/16 of its original value and flow will increase 16 times.
The Roles of Vessel Diameter and Total Area in Blood Flow and Blood Pressure
Recall that we classified arterioles as resistance vessels, because given their small lumen, they dramatically slow the flow of blood from arteries. In fact, arterioles are the site of greatest resistance in the entire vascular network. This may seem surprising, given that capillaries have a smaller size. How can this phenomenon be explained?
Figure \(\PageIndex{4}\) compares vessel diameter, total cross-sectional area, average blood pressure, and blood velocity through the systemic vessels. Notice in parts (a) and (b) that the total cross-sectional area of the body’s capillary beds is far greater than any other type of vessel. Although the diameter of an individual capillary is significantly smaller than the diameter of an arteriole, there are vastly more capillaries in the body than there are other types of blood vessels. Part (c) shows that blood pressure drops unevenly as blood travels from arteries to arterioles, capillaries, venules, and veins, and encounters greater resistance. However, the site of the most precipitous drop, and the site of greatest resistance, is the arterioles. This explains why vasodilation and vasoconstriction of arterioles play more significant roles in regulating blood pressure than do the vasodilation and vasoconstriction of other vessels.
Part (d) shows that the velocity (speed) of blood flow decreases dramatically as the blood moves from arteries to arterioles to capillaries. This slow flow rate allows more time for exchange processes to occur. As blood flows through the veins, the rate of velocity increases, as blood is returned to the heart.
Disorders of the...
Cardiovascular System: Arteriosclerosis
Compliance allows an artery to expand when blood is pumped through it from the heart, and then to recoil after the surge has passed. This helps promote blood flow. In arteriosclerosis, compliance is reduced, and pressure and resistance within the vessel increase. This is a leading cause of hypertension and coronary heart disease, as it causes the heart to work harder to generate a pressure great enough to overcome the resistance.
Arteriosclerosis begins with injury to the endothelium of an artery, which may be caused by irritation from high blood glucose, infection, tobacco use, excessive blood lipids, and other factors. Artery walls that are constantly stressed by blood flowing at high pressure are also more likely to be injured—which means that hypertension can promote arteriosclerosis, as well as result from it.
Recall that tissue injury causes inflammation. As inflammation spreads into the artery wall, it weakens and scars it, leaving it stiff (sclerotic). As a result, compliance is reduced. Moreover, circulating triglycerides and cholesterol can seep between the damaged lining cells and become trapped within the artery wall, where they are frequently joined by leukocytes, calcium, and cellular debris. Eventually, this buildup, called plaque, can narrow arteries enough to impair blood flow. The term for this condition, atherosclerosis (athero- = “porridge”) describes the mealy deposits (Figure \(\PageIndex{5}\)).
Sometimes a plaque can rupture, causing microscopic tears in the artery wall that allow blood to leak into the tissue on the other side. When this happens, platelets rush to the site to clot the blood. This clot can further obstruct the artery and—if it occurs in a coronary or cerebral artery—cause a sudden heart attack or stroke. Alternatively, plaque can break off and travel through the bloodstream as an embolus until it blocks a more distant, smaller artery.
Even without total blockage, vessel narrowing leads to ischemia—reduced blood flow—to the tissue region “downstream” of the narrowed vessel. Ischemia in turn leads to hypoxia—decreased supply of oxygen to the tissues. Hypoxia involving cardiac muscle or brain tissue can lead to cell death and severe impairment of brain or heart function.
A major risk factor for both arteriosclerosis and atherosclerosis is advanced age, as the conditions tend to progress over time. Arteriosclerosis is normally defined as the more generalized loss of compliance, “hardening of the arteries,” whereas atherosclerosis is a more specific term for the build-up of plaque in the walls of the vessel and is a specific type of arteriosclerosis. There is also a distinct genetic component, and pre-existing hypertension and/or diabetes also greatly increase the risk. However, obesity, poor nutrition, lack of physical activity, and tobacco use all are major risk factors.
Treatment includes lifestyle changes, such as weight loss, smoking cessation, regular exercise, and adoption of a diet low in sodium and saturated fats. Medications to reduce cholesterol and blood pressure may be prescribed. For blocked coronary arteries, surgery is warranted. In angioplasty, a catheter is inserted into the vessel at the point of narrowing, and a second catheter with a balloon-like tip is inflated to widen the opening. To prevent subsequent collapse of the vessel, a small mesh tube called a stent is often inserted. In an endarterectomy, plaque is surgically removed from the walls of a vessel. This operation is typically performed on the carotid arteries of the neck, which are a prime source of oxygenated blood for the brain. In a coronary bypass procedure, a non-vital superficial vessel from another part of the body (often the great saphenous vein) or a synthetic vessel is inserted to create a path around the blocked area of a coronary artery.
Venous System
The pumping action of the heart propels the blood into the arteries, from an area of higher pressure toward an area of lower pressure. If blood is to flow from the veins back into the heart, the pressure in the veins must be greater than the pressure in the atria of the heart. Two factors help maintain this pressure gradient between the veins and the heart. First, the pressure in the atria during diastole is very low, often approaching zero when the atria are relaxed (atrial diastole). Second, two physiologic “pumps” increase pressure in the venous system. The use of the term “pump” implies a physical device that speeds flow. These physiological pumps are less obvious.
Skeletal Muscle Pump
In many body regions, the pressure within the veins can be increased by the contraction of the surrounding skeletal muscle. This mechanism, known as the skeletal muscle pump (Figure \(\PageIndex{6}\)), helps the lower-pressure veins counteract the force of gravity, increasing pressure to move blood back to the heart. As leg muscles contract, for example during walking or running, they exert pressure on nearby veins with their numerous one-way valves. This increased pressure causes blood to flow upward, opening valves superior to the contracting muscles so blood flows through. Simultaneously, valves inferior to the contracting muscles close; thus, blood should not seep back downward toward the feet. Military recruits are trained to flex their legs slightly while standing at attention for prolonged periods. Failure to do so may allow blood to pool in the lower limbs rather than returning to the heart. Consequently, the brain will not receive enough oxygenated blood, and the individual may lose consciousness.
Respiratory Pump
The respiratory pump aids blood flow through the veins of the thorax and abdomen. During inhalation, the volume of the thorax increases, largely through the contraction of the diaphragm, which moves downward and compresses the abdominal cavity. The elevation of the chest caused by the contraction of the external intercostal muscles also contributes to the increased volume of the thorax. The volume increase causes air pressure within the thorax to decrease, allowing us to inhale. Additionally, as air pressure within the thorax drops, blood pressure in the thoracic veins also decreases, falling below the pressure in the abdominal veins. This causes blood to flow along its pressure gradient from veins outside the thorax, where pressure is higher, into the thoracic region, where pressure is now lower. This in turn promotes the return of blood from the thoracic veins to the atria. During exhalation, when air pressure increases within the thoracic cavity, pressure in the thoracic veins increases, speeding blood flow into the heart while valves in the veins prevent blood from flowing backward from the thoracic and abdominal veins.
Pressure Relationships in the Venous System
Although vessel diameter increases from the smaller venules to the larger veins and eventually to the venae cavae (singular = vena cava), the total cross-sectional area actually decreases (see Figure \(\PageIndex{2}\) a and b ). The individual veins are larger in diameter than the venules, but their total number is much lower, so their total cross-sectional area is also lower.
Also notice that, as blood moves from venules to veins, the average blood pressure drops (see Figure 20.13 c ), but the blood velocity actually increases (see Figure 20.13d). This pressure gradient drives blood back toward the heart. Again, the presence of one-way valves and the skeletal muscle and respiratory pumps contribute to this increased flow. Since approximately 64 percent of the total blood volume resides in systemic veins, any action that increases the flow of blood through the veins will increase venous return to the heart. Maintaining vascular tone within the veins prevents the veins from merely distending, dampening the flow of blood, and as you will see, vasoconstriction actually enhances the flow.
The Role of Venoconstriction in Resistance, Blood Pressure, and Flow
As previously discussed, vasoconstriction of an artery or arteriole decreases the radius, increasing resistance and pressure, but decreasing flow. Venoconstriction, on the other hand, has a very different outcome. The walls of veins are thin but irregular; thus, when the smooth muscle in those walls constricts, the lumen becomes more rounded. The more rounded the lumen, the less surface area the blood encounters, and the less resistance the vessel offers. Vasoconstriction increases pressure within a vein as it does in an artery, but in veins, the increased pressure increases flow. Recall that the pressure in the atria, into which the venous blood will flow, is very low, approaching zero for at least part of the relaxation phase of the cardiac cycle. Thus, venoconstriction increases the return of blood to the heart. Another way of stating this is that venoconstriction increases the preload or stretch of the cardiac muscle and increases contraction.


7.4: Immunization competencies for healthcare providers
Any healthcare professional prescribing vaccines requires specific competencies in order to ensure that vaccines, like other medications, are provided in a safe, effective, and ethical manner. In order to promote safe and competent practice, the Public Health Agency of Canada (PHAC) developed a handbook in 2008 entitled Immunization Competencies for Health Professionals . These foundational competencies include:
- Explaining how vaccines work using basic knowledge of the immune system.
- Understanding the rationale and benefits of immunization.
- Integrating into practice knowledge about the main steps in vaccine development and evaluation.
- Applying knowledge of the components and properties of immunizing agents as needed for safe and effective practice.
- Applying relevant principles of population health for improving immunization coverage rates.
- Communicating effectively about immunization.
- Implementing guidelines for safe storage and handling of vaccines.
- Preparing and administering immunization agents correctly.
- Anticipating, identifying, and managing adverse events following immunization.
- Understanding documentation requirements for immunizations.
- Recognizing and responding to the unique immunization needs of certain population groups.
- Demonstrating an understanding of the immunization system in Canada.
- Addressing immunization issues using an evidence-based approach.
- Acting in accordance with legal and ethical standards in all aspects of immunization practice (PHAC, 2008).
Health professionals need to be able to anticipate, identify, and manage adverse events that may occur following immunizations (PHAC, 2008). As you have learned in earlier chapters of this resource, adverse events following immunizations are rare. Although these events are rare, monitoring vaccine safety through mandatory adverse event reporting is an important aspect of the immunization program in Ontario. Adverse events following immunization can be reported with a form from the PHAC, which can be submitted to the local public health agency where the patient lives.
Optimizing the Role of Ontario RNs in Immunization Through RN Prescribing
Pending government approval of the proposed CNO regulation, RN prescribing will be authorized for certain medications that will allow RNs to manage non-complex patient care needs (CNO, 2019b). In the first phase of RN prescribing in Ontario, these medications will include some vaccines (CNO, 2019b).
While RNs in Ontario have typically participated in immunization as front-line providers in schools and community settings, this change will allow RNs to not only administer vaccines but prescribe them as well. Given the important role RNs play in primary health care and health promotion, a strategic focus on maximizing the involvement of RNs in immunization should help advance the public health goal of immunization for everyone across the life cycle (International Council of Nurses, 2013).
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https://ecampusontario.pressbooks.pub/immunizations/?p=215