1
Q
Fibrous pericardium
A
Outer membrane that protects the heart form overstretching
2
Q
Parietal layer
A
-lines the surface of the fluid filled sac
-produces serious fluid (lubricating)
3
Q
Pericardial cavity
A
-middle layer filed with serious fluid
-allow layers to move without friction
4
Q
Visceral layer
A
Known as epicardium
-inner layer of the serous pericardium
-adheres to the surface tissue of the heart itself
5
Q
AV valves
A
-tricuspid & mitral (bicuspid)
6
Q
What are red blood cells?
A
-carry oxygen through hemoglobin
7
Q
WBC
A
-leukocytes
-body defense against infeciton or disease
8
Q
Platelets
A
Thrombocytes
-help initiate HEMOSTASIS by forming a plug and triggering blood clotting
9
Q
what are the primary function of platelets
A
- Clot formaiton
- Plug leaks
- Clotting support
10
Q
Arteries
A
-carry oxygenated blood away from the heart to perfuse organs and tissues in the body
11
Q
Veins
A
Deoxygenated blood back to the heart for oxygen
12
Q
Pulmonary artery
A
-deoxygenated blood
Form heart to lungs
13
Q
Pulmonary vein
A
-oxygenated blood
14
Q
Superior mesenteric artery
A
-supplies small intestine & the first half of the large intestine
15
Q
Section of the aorta
A
-ascending
-aortic arch
-thoracic aorta
-abdominal aorta
16
Q
What does the RCA supply?
A
-RV
-base of the heart & interventricular septum
-SA ANS av node
17
Q
LCA supply
A
Most of the left ventricle including the anterior wall and lateral apex
-splits into LAD and then into circumflex
-does not mainly supply the muscle bc it splits into 2
18
Q
circumflex supply
A
Lateral wall and wall of LV
-part of LA
-sometimes posterior lv
19
Q
Left anterior descending flow
A
-anterior front wall of left ventricle
-apex of the heart
-anterior 2/3 of inter ventricular septum
20
Q
What is the pathway of the electrical pathway of the heart?
A
Memory trick
s-end
A
B-ig
B-ounding
P-pulse
21
Q
Pacemaker cell
A
SA and AV node
Calcium causes depolarizaiton in the SA and AV node
22
Q
Contractile cell
A
Atria and ventricle
-calcium is essential for prolonged effective contractions during the plateau phase
23
Q
Systole
A
-contraction of a chamber of the heart
Systole think squeezing (contraction)
24
Q
Diastole
A
Heart relaxes and the chamber (atria and ventricles) fill with blood
Diastole and decompressing (Relaxaiton )
25
Preload
-amount of blood in the ventricles at end of diastole
Preload think prepare pump
26
Stroke volume
The amount of blood pumped out of left ventricle with each individual contraction
27
Contractility
Intensity with the heart muscle is able to squeeze or contract to pump blood out of the
-force is deterred by preload, afterload , balance of electrolytes within the body
28
Afterload
Resistance the heart must work against to pump blood of the ventricles
-after load think against the pressure
29
How does the body regulates pressure in two ways:
1.short term BP regulation
-SNS & PSNS system work to quickly adjust BP in respone to immediate changes
2. Long term BP regulation
-RAAS work to maintain blood pressure by controlling blood volume
30
Dilated cardiomyopathy
-dilation of the left ventricle causing enlargement of the inner chamber
Causes
- pregnancy
-chronic HTN
-genetics
-CAD
-alcohol or illicit drug use (they are toxic to the are muscle cell, damage the myocardium, muscle becomes week
31
Hypertrophic cardiomyopathy
Occurs when the heart muscle, typically the left ventricle, thickens, enlarger & stiffens
Causes
-aortic stenosis (narrowing of aortic valve)
-genetics
-chronic HTN
32
Restrictive cardiomyopathy
-stiff ventricular muscle
Causes
-amyloidosis (buildup of amyloid proteins in tissues & organs)
-cancer
-endomycoardial fibrosis (thickening & scarring of the endocardium
-post radiation therapy
33
What is the patho of APO?
-LV with pulmonary venous HTN & alveolar flooding
-LV due to cardiac/ hypoxia (unstable for right side of heart to recieve blood and pump blood into systemic circulation)
-LV stiffen b/c of hypoxia (muscle needs ATP due to hypoxia anaerobic metabolism is required to produce ATP)
-LV pressure increases
-hydrostatic pressure exceeds the onotic pressure the serum portion of blood is forced out into the alveoli
-hydrostatic pressure exceeds the onoctic pressure lymphatic system cannot cope
-V/Q mismatch b/c fluid in insteirsl space and alveoli
-alvoeli can dilute alveolar surfactant
-SNS respone
34
Cardiac arrest patho
-blood flow and oxygen supply to the coranry arteries ceases
-o2 supply and waste removal stops
-hypoxia leads to anoxia and dysrhtymias arise due ot heart inherent demand for oxygen for cardiac muscle contraction and relaxation, and electrical conduction
-depletion of oxygen and glucose to the brain casues LOC
-body forced into anaerobic metabolism increasing lactic acid levels
-ATP become depleted esp in rhythms like VF/VF
-efflux potassium and influx sodium and calcium into cell
-cell burst
-excess calcium damage the mitochondria and increase nitric oxide
-unwanted depolarization
35
What occurs in circulatory obstruction causing cardiac arrest?
-decreased coroanry artery perfusion
-increase pressure on vena cava
-decrease venous return
-decrease preload and afterload
36
Somatic pain
-skin and deep tissues are innervated which tend to stimulate more intense pain that is easier to locate
37
Visceral pain
-internal organs and blood vessels innervated by visceral pain fibers tend to be dull/ vague which is harder to localize
38
How is chest pain casued?
-lack of oxygen supply to the heart ; mismatch between oxygen supply and oxygen required (demand)
-switched to anaerobic metabolism increasing lactic acid in the coroanry vessels which stimulates the visceral afferent nerves
39
Atheroscloeris
-narrowing of the lumen of medium larger size arteries
-thick plaque called atheroma develop in blood vessels
-harden and calcify behind the lumen narrowing th artery reducing blood flow
40
Stable angina
-occurs during exertion
-during rest blood flow is sufficient to meet demand however on exertion oxygen demand is increased beyond the supply restricts
41
Unstable angina
-atheroscloeris plaque has ruptured thrombus delveops at the site of rupture
-severe CAD
-transient reduction in coronary blood supply because of vasoconstricton &
Thrombus formaiton at the site of plaque rupture
-critical narrowing
-occur at rest
-not easily relived
42
Vasospastic angina
-coroanry artery spasm restricting myocardial blood flow
-oxygen supply/ demand mismatch leading to anaerobic metoalism and production of lactic acid -> this is what stimulates the nociceptors
43
What causes a MI?
-cardiac muscle b/c of prolonged hypoxia
-atherosclerotic plaque ruptures, relases toxins, and attracts factors that causes platelet coagulation , and promote clot formaiton
-lactic acid forms and c abuses pain
-further ischemia and leads to sodium/ potassium pump failure causes dysrhtymias
-sodium floods into cells water follows and cells swell and burst
44
What casues tachycardia chest pain?
-chest pain potently may be experienced if a patient is in a prolonged tachcyardia or has rapid SVT
-supply/ demand mismatch as heart is pumping took quickly and there is decreased filing time of the coroanry arteries during diastole
-coroanry arteries poorly perfused
-cardiac muscle put in anaerobic metabolism due to reduced blood supply and lactic acid is produced causing pain
45
What casues bradycardia chest pain?
-prolonged state of bradyacardia
-as the heart rate is reduced diastole occurs less frequently therefore the coroanry attires are perfused less frequently
=cardiac muscle put in aneorbic metoablism into lactic acid produced pain
46
SVT
-AV node should ve the only conduction pathway between atria and ventricles
-acessory pathway where conduction can pass through the ventricles
-Requires PAC to happen
-PAC occur down the slow of depolarize AV node by the time the premature depolarization has occurred and already quick repoalized the abnormal conduction comes through the accessory pathway and is tea of meeting up to cancel out they do not
47
PVC
-early beat that strats in the ventricles instead of the SA node
-the ventricles cell become irritable and depolarize early
48
Common causes that cause the ventricular to become irritable in a PVC?
-hypoxia
-ischemia
-elecolyte problem
-stimulant drug
-heart disease
49
What can PVC cause?
-palpaitaotns
-skipped beat feeling
-brief CO
-can trigger dangerous arrhythmias such as VTACh and vFib
50
PAC
-early beat that starts somewhere in the atrium not the SA node
51
What cases PAC?
-stress
-caffeine
Hypoxia
-illness
52
What can PAC caue?
-atrial fibrillation
-SVT
-atrial flutter
53
PJC
-an early beat that starts the AV junction
-the junction fires before the SA node
54
What causes PJC
-increased automaticity in the AV junction
-SA node slowing
-drug effects
55
What can PJC casue?
-palpitations
-irregular rhythm
-lead to junction rhythms
-contribute to loss of atrial kick
56
How can HTN cause blurred vision?
-retinal arterioles damage less blood / oxygen to retina blurred vision
-capillary leak
-papilledmea -> increased ICP -> optic nerve swelling
57
How can HTN casue headache
-cerebral vasodialiton & vessel stretch -> pain sensitive vessels and mengies this activates the pain receptors
-impaired cerebral autoregulaiton -> brain can’t restrict anymore
-increased ICP
58
What happens if blood pressure raises to the brain?
-autoregulation fails
-arterioles are already maximally constricted
-cannot protect the capillary anymore
-pressure overwhelms
-arteries forced open
59
What happens if autoregulation fails to the kidneys
-failure to afferent Arteriole autoregulaiton allows high pressure stretch and damage to glomerular capirlleask leak , leading to protein leakage
Proteinuria
-normally with pressure damag
-albumin leaks in
AKI
-capillary injury
-swelling + injury rescues filatriaton surfac e
-nephrons stop working
60
What is hypertensive crisis?
SBP >180 or DBP >120
-arteriole constrict t
-shear stress ono vessel walls increase
-endothelium gets injured
-capillary leak
-organs become ischemic and enematous
61
What occurs to the brain in HTN crisis ?
-hypertensive encephalopathy
-ishcemic stroke
-intracerebal hemorrhage
62
What occurs to the heart in HTN crisis
-ACS
-acute left ventrical failure
-pulmoanry edema
-increased aferload
-increase myuocaridla oxygen demand
63
What happens tp the lungs in HTN crisis?
-flash pulmoanry edema
-LV cannot push against extreme pressure blood back up into lungs
64
Left sided heart failure
-LV weak -> poor out put to body
-fluid back up into lungs
-pressure in pulmoanry capillares increase
-capillaries leak fluid into alvoeli
-gas exchange decrease
65
RSHF
-RV weak -> poor output to lung
-fluid back into systemic circulation
-increased venous pressure e
-fluid leaks into tissues ->peripheral edema , ascites, JVD
66
How can RAAS make heart failure worse
-kidney sense low perfusion -> think BP low
-release renin -> angitensin II -> vasoconstricton
-aldosterone -> Na & water retention
-heart struggles more which worsens CHF
67
MI causing A cute pulmoanry edema
-sudden blockage in coranry attires
-part of the LV dies -> pump strength drops
-blood ca’nt move forward -> back up into lungs
-pulmoanry capillary pressure increase -> fluid leaks into alveoli
68
What is vasomotor center
-located in the medulla
-send low level of sympathic signals
-creates vasomotor tone
-loss of vasomtor tone can casue vasodilation
69
Where are the baroreceptors found
-carotid sinu s
-aortic arch
70
Chemorecpeor found
-carotid and aortic bodies
71
Central chemoreceptors found
-medulla senses CO2
72
Peirphal chemoreceptors
Carotid & aortic bodies sense low O2
73
How does the intermediate system work for BP
-JUXTAGLOMERULAR cells in the kidneys rlease renin with decrease renal perfusion decrease Na
-liver make angiotensiongen
-renin coverts to angio I
-happen in the lung
74
What is angiotensin II
Vasoconstrictor
raises BP
1.aldosterone (retains sodium)
2. ADH release (angiotensin II stimulates vasopressin)
3. Thirst stimulaiton (hypothalamus activation) Jo
75
What part of fetal circulation
76
In the fetus where does oxygenation occur?
Placenta
77
Which vessel bring oxygenated blood from the placenta to the fetus
Umbilical vein
78
What does the ductus venosus do?
-shunt blood form the umbical vein past the liver directly into the IVC
79
In fetal circulation what causes the blood to go to the RA and LA
Foramen ovale
80
What is the ductus arteriosum
-a vessel connecting the priamry artery to the aorta
81
What are the two shunts that bypass the lung
-foramen ovale and the ductus arteriosus
82
What does the ductus arteriosus form after birth
-ligamentum arteriosum
83
What does the ductus venous form after birth
Ligamentum venous
84
What does the umbical vein form
-found ligament of liver
85
What does the foramen ovale form after birth
-fossa ovalis
86
In transposition of great vessels what occurs
-Aorta to RV
-pulmoanry artery to LV
87
What is patent ductus ariosusus
-extra vessel
=blood shunt form high pressure left side to lower pressure gift sided
-wended pulse pressure
-left to right shunt
88
What are endothelins
Vasoconstrictor
-made by the endothelium
-peptides
-helps contorl blood vessel tone and blood pressure
89
What are naturetic peptides
Are heart released hormone
-tells the body we have too much volume and pressure get rid of salt and water and relax the vessel
two kinds
-ANP=>relased form atria
-BNP=> released from ventricles
90
What triggers your naturetic peptides to release?
-cardiac wall stretch
91
What do the naturetic peptides do
1. Make kidney dump sodium
2. Dilate blood vessels
3.turn down the fluid retaining system (RAAS, aldosterone, ADH)
92
What is the flow rate for <12 hr of age
15ml /hr of any isotonic crystalloid solution
93
What is the flow rate for >or = 12 yr
30-60 ml/hr in isotonic crystalloids solution.
94
What may be put in the IV line for fluid replacement
1. Max flow rate of up to two ml/kg/ hr to max of 200 ml/hr
2. Thiamine, multivitamin preparations
3. Drugs in PCP level
4. Potassium chloride for >or= 18 yr of age to max of 10 men in 250ml bag
95
What must be escorted for pt with IV
-blood products
-KCL <18
-pump, or ventral line
-neonate or peds <2 yr
96
When must a bag be change for IV
150 ml left
97
IF is patient has a ROSc what must we do for that pt
-ventilate, t remains apenic, or resp are inadequate
-SPO2 94-98%
-assess pt every 15 mins up to the first hour and after that every 30 mins
98
If a pt is pregnant what must we do for CPR
-make sure they are 20 weeks or greater and have a second paramedic perform manual left utuerine replacement
99
Life limb threat for pt with chest pain
-ACS/MI
-dissecting thoraic aorta
-pneumo, tensio pneumonia, ore resp disorders
-PE
-pericarditis
100
Secondary assessment for chest pain
-lungs
-look at abdomen
-look at neck for JVD or TD
-look at extremities for leg and ankle edema
101
Contraindication for STEMI bypass
-CTAS 1 and paramedic cannot secure airway or ventilate
-12 lead with a mimic
-PC I is greater or equal to 60 mins
-CPAP
-resp distress
-hemodynamics instability or symptomatic wiht SBP <90
-VSA without ROSC
102
What happens if the pt becomes STEMI Postive to a hospital that is not a PCI
Reevaluate under STEMI BYPAAS
103
Distributive shock
-septic
-neurogenic
-anaphylactic
-Tank is too large
-Circulating volume is normal
-AV shunting and increase venous cap activate lads to hypeprfeuion of tissues and decreased CO
104
Septic shock
-pt with blood borne pathogen in compensatory mechanism and / or treatment have failed in maintain hemodynamics stability
-endotoxin relase -> immune activation -> widespread vasodilation -> hypoperfusion (immune system in overdrive) (directly damage BV + nitric oxide)
-immune cells activated by hypoxic/ damged vascular endothelium -> immune cells read led damaging substance and imflmmatory mediators
-increased capillary pearmailby
-inflammatory and clotting cascade. May further triggered in states hypoperfusion
-blood clotting
-compensatory response poisoned by combination of endotoxins and cytokine
-comopsimsed vasocosntricotn and SV compensatory mechanism (preload, afterload, contractility negatively effected)
105
Neurogenic shock
-usually caused by trauma
-high level spinal cord injury above T4=6
-Drisuption of ANS pathway within spinal cord
-lead To decreased SVR and peirphal blood pooling
-decreased HR/CO
-shunt sympathic outflow
-blood vessel + HR taken out
-cannot compnsate
-the move the cord affected the hypotension
-loss of compensatory mechanism leads to atypical s/s unable to activate ns, pink , warm, flushed,skin level of injury
106
Anaphylactic shock
-immune system mediated in setting of seve systemic allergic reaction
-vasodialtion, smooth muscle contraction, increased vascular permeability
-usually pre expoed + reexport
-basophils + leukotriens
-Leakey blood vessels
107
Cardiogenic shock
-dysfunction heart result sin decreased CO
-pump failure
-many different causes likely encountered will be seconadry to ischemia / infarct
-decreased CO -> decreased BP -> SHOCK
-impaired contractility (decreased SV)
-arrhtymais
-structural disorders
-trauma
108
Acute right ventricular shock
-most often result from proximal occlusion of the RCA which feed the SA node, AV node, RV and LV
-RV not able to contract effectively and result in hypotension and caridogenic shock
109
Hypovolemic shock hemorrhage
-decrease in intravascular blood volume to point of cardiovascular compromise
-result in blood hemorrhage
-decrease venous return -> decrease filling pressure -> decrase SV -> decrease CO -> decrease BP -> shock
110
Non hemorrhagic hypovolemic shock
-decrease in intravascular blood volume
-casue low voluem is not form bleeding (severe dehydraiton)
-
111
Causes of non hemorrhagic shock
-skin (sweating, burn)
-GI losses (vomiting, diarrhea)
-renal (diabetes, adrenal dysfunction, dirueitcs)
-fluid shifts (trauma, crush injury, ishcemic bowel
-peds
-elderly
112
Obstructive shock
-blocked/ impeded cardiopulmonary blood flow
-shock seconadry to mechanical factors which interfere with filing/ emptying of the heart or greate vessels
-decreae preload decrease CO
113
Mechanism used in compensated shock
-baroreceptors reflect
-activation of RAAS
-release of catecholamines Epi and no Epi
-ADH
-angiotensin II
114
Multi organ dysfunction syndrome
-eventual dysfunction of 2 or more organ system
-reperfusion injury may lead to multi system dysfunction
-most frequent organ affected = the lungs. (Increase memabne permablity lead to pulmonary edema, inflmmaiton and oxygen theapry resistance)
-kidney affected by hypo perfusion
-heart -> reduced coranry perfusion
-GI tract -> hemorrhage May develop
-liver-> decreased production of clotting factors
-coagulating cascade -> disssemiated intravascular coagulation
115
What is coronary dominance
-which artery GIVEs the pda (posterior ascending aorta)
-the artery run the back and the bottom of the heart and feeds posterior and inferior and back of septum)
116
Inferior wall
Ii, Iii, avf
117
Why inferior mi can cause heart block ?
RCA feeds av node av node becomes ischemia leads to heart block
-sa node has problem making the beat
-av node has proble passing it
-bradycardia and heart block
