Midterm Flashcards
Pericardium
-fibrous sac around heart
-Serous layers: Parietal (outer), visceral (on heart and contains fluid within space)
-Innervated by Phrenic Nerve (sensory)
Diastole
-Relaxation
-Filling
Systole
-contraction
-ejection
Afterload
pressure needed to expel blood from the heart
-synonymous with BP
Myocardium
Cardiac muscle fiber
-actin-myosin complex
-Automaticity: contract w/o external stimuli
-Rhythmicity: contract with rhythm
-Conductivity: nerve impulses from one cell to the other due to intercalated discs
-Intercalated disc junctions: Desmosomes (adhesion) and Connexins (conductivity)
Endocardium
-Smooth muscle, innermost layer
Pulmonary Artery
-only artery to carry deoxygenated blood
Pulmonary vein
-only vein to cary oxygenated blood
Right Coronary Artery
-Supplies right ventricle, AV node and SA node
-Right posterior descending
-Right marginal
Left Coronary Artery (supplies)
-supplies left ventricle, L atrium, septum, SA node
SA Node
-sets heart at pace of >100 without other input
-Susceptible to disease due to pericarditis, occulsion
Sympathetic NS
-increase
-norepinephrine
Inotropic
-strength of contraction
Chronotropic
-speed of contraction
Parasympathetic NS
-decrease
-vagus nerve
-acetylcholine
-60-90 bpm
AV Node
-receive from SA
-to Bundle of His to bundle branches to perkinjie fibers
-40-60 bpm without exernal stimuli
-0.04s to contract Vs
Susceptible to disease due to RCA occlusion
P Wave
atrial depolarization
PR interval
-travel of impulse to Vs
QRS Complex
ventricular depolarization
T Wave
ventricular repolarization
QT Internal
Ventricular systole
Low K
Harder to depolarize, slower heart rate
High K
Easier to depolarize as myocardium is excitable, higher heart rate
Cardiac Output
-CO= HR x SV
-5-6L at rest, can increased 4-7x with exercise
-Effects systolic BP
Blood Pressure
BP=HR x SV x Total peripheral Resistance
TPR affects diastolic BP
Mean Arterial Blood Pressure
-average pressure in the systemic system, perfusion of organs and peripheral tissues
MAP= DBP + 1/3 (SBP-DBP)
-Normal: 70- 93 mmHg
-cautions <60mmHg
Determined By:
-BV, CO, Peripheral resistance, distribution of blood in veins
Pulse Pressure
SBP-DBP, difference
-how hard heart is working
>60 working too hard; HTN
<40 failing heart; cardiomyopathy;shock
Effect of Posture on BP
Standing: lower BP, blood pools in legs
Laying: blood evenly in veins, higher BP
BP Normal
<120/<80
BP Elevated
120-129/<80
High BP Stage 1
130-139/80-89
High BP Stage 2
> 140/>90
Hypertensive Crisis
> 180/>120
HR
-Beats per minute
->120bpm @ rest, not enough time to refill, decreases CO
-<45bpm @ rest not enough CO, low bp
Affected by: Baroreceptors, ANS, endocrine, integrity of the system, temperature, emotions
SV
-amount of blood pumped out each beat
-Afterload-Preload, heart contractility
-increases 40-60% during exercise
Cardiac Preload (& determinants)
-End diastolic volume: amount of left ventricular blood volume prior to contraction
Dependent on:
-venous return, BV, LA contraction, Starling law
Cardiac Afterload
-Amount of resistance encountered by left ventricle
Myocardial Contractility
-neural and hormonal influences
Ejection Fraction
Ejection Fraction= SV/EDV
-55-70%
-Low EF indicates systolic heart failure: <40
-EF can be preserved with overall decrease in BV, weak heart increases backflow that increases SV
Hypoxia
O2 concentration of tissues
Hypoxemia
O2 concentration of blood
ESV
End Systolic volume: volume of blood in a ventricle at the end of a contraction
Right Shift in O2 Concentration
-reduced affinity for for O2, higher po2 will result in lower hemoglobin concentrations
-high temp, high acidity
Left Shift in O2 concentration
-increased affinity for O2, lower po2 will result in higher hemoglobin concentrations
-low temp, basic environment
Fick equation
-VO2= HR x SV x (a-vO2 diff)
a-vO2 Diff
-difference in O2 between arteriole and venule
CO Distribution
Muscles: 10-15% (80-85% with exercise)
Trunk: 20-30%
Brain and heart: 5%
Oxygen Extraction
-tissues utilize the same relative amount of o2 in relation to blood o2
Pulmonary O2 Exchange Factors
-Area of capillary membrane
-Diffusion capacity of alveoli
-Pulmonary Capillary volume
-Ventilation to perfusion ratio
Area of Capillary Membrane
invaginations increase the surface area
Diffusion capacity of alveoli
-changes in surface area
-changes in membrane
-gas uptake issues
Pulmonary capillary volume
-increases with exercise
Ventilation to Perfusion Ratio (V/Q)
-blood flow to alveoli must match ventilation or =hypoxemia
-changes with posture
-Norm: 0.8
Reduced: decreased ventilation to perfusion, blood shunted to other parts of the lung, vasoconstriction at arterioles to reduce BV, corrected with O2
Increased: increased ventilation to perfusion, vasodilation to increase BV, dead space
Arteriole Vasoconstriction Mechanism of Action
-alpha receptors
Shunt blood to muscles, from skin and mesenteric
Arteriole Vasodilation Mechanism of Action
-induced by increased vessel stretch
-induced by low O2 or high H+, CO2, metabolites
Beta Receptors
-increased blood flow to Skeletal muscle
-increase ventilation and alveolar perfusion
Cardiac Muscle Dysfunction
-most common cause of Congestive Heart Failure
Symptoms:
-dyspnea
-fluid buildup
-fatigue at rest
Most common cause of pulmonary congestion
-heart failure
-mostly right side affected
Causes of Cardiac Muscle Disease: Hypertension
Increased BP
-increased workload w/o increased blood supply
-decreased BV
-hypertrophy of myocardium that cannot relax well
-BV damage
Causes of Cardiac Muscle Disease: Coronary Artery Disease
-2nd most common cause of CMD
-supply and demand issue
-lipid deposits: atherosclerosis
-scar formation: decreases contractility
Causes of Cardiac Muscle Disease: Myocardial Infarction
-irreversible myocardial necrosis
-most commonly affects left ventricle
PT
-Increased Troponin, CK-MB that needs to come down
-ST elevation on ECG “Stimmy”
Causes of Cardiac Muscle Disease: Cardiac Arrhythmias
-abnormal rate of contractions
-can cause sudden cardiac arrest from SA node
-can lead to decreased CO
-Sick Sinus node syndrome
-Suprasventricular tachycardia
-V fib
Lab Values: Sodium
Increased
-dehydration
Decreased
-overhydration
Lab Values: Potassium
Increased
-Renal retention, decreased insulin
Decreased
-Excess renal secretion, aldosterone, burns
Lab Values: Calcium
Increased:
-hyperparathyroidism, hyperthyroidism
Decreased: hypoparathyroidism, renal failure
Causes of Cardiac Muscle Disease: Renal Insufficiency
-contributes to CMD due to increased fluid triggered by low BP or low BV
-RAAS
-maintains Na and K balance
Causes of Cardiac Muscle Disease: Cardiomyopathy
-disease of heart muscle leading to heart failure
-impaired contractility
-HTN, MI, metabolic disorders, heart valve issues
Causes of Cardiac Muscle Disease: Dilated Cardiomyopathy
Heart failure with reduced ejection fraction (<40)
-systolic dysfunction: less effective pump, decrease CO, fluid back up
-increased LV EDV
-lead to electrical issues
Causes of Cardiac Muscle Disease: Hypertrophic Cardiomyopathy
-enlarged heart that cannot relax
-Heart failure with preserved EF
-diastolic dysfunction: less compliant
-increases left EDP
-rapid ventricular emptying
-muscle cells disorganized
-common cause for sudden cardiac arrest in young athletes
Causes of Cardiac Muscle Disease: Restrictive Cardiomyopathy
-cannot relax
-EF preserved
-diastolic dysfunction; decreased filling
-scar tissue in myocardium (sarcoidosis/radiation) OR defect in myocardial relaxation
-hypertrophy
Heart Valve Abnormalities Consequences
-contracts more forcefully
-induces myocardial hypertrophy
-deceases ventricular distensibility
-decreases CO and BP
Pericardial Effusion
-buildup of fluid compress the heart
Cardiac Tamponade
-pressure on heart leads to decreased heart function
-worse when lying down
-relieved when standing
Pulmonary Embolism
-lung infarction due to decreased BV
-increased pulmonary hypertension
-increases load to right side of heart
-presence of ascities, bilateral LE edema and jugular vein distension
-increases V/Q ratio
Pulmonary Hypertension
-risk for cardiac disease
->20mmHg
-increased R ventricle work (Swangan’s Catheter)
Heart Disease Vitals
-pO2: hypoxia (92-96%)
-RR: tachypnea
-HR: tachycardia
-BP: orthostatic hypotension
Congestive Heart Failure
-decreased CO
-LV failure
-increased BNP (stretch protein in heart)
-attempts compensatory strategies (sympathetic, RAAS, heart receptors, EPO)
Skeletal Muscle Function and CHF
-decreased type 1 fibers
-less contraction strength
Pancreas and CHF
-impairs blood flow
-impairs insulin release
Hematologic function and CHF
-polycythemia (thick blood)
-thrombocytopenia (low platelets)
Anemia
-can cause CHF
-can harm or help
-shifts curve to right; more o2 needed
Neurohumoral Function and CHF
-SNS overstimulation and downreg of B1 receptors
B1: myocardial inotrophy and chronotrophy
B2: arteriole vasodilation and bronchodilation
a1: vasoconstriction
a2: arterial vasodilation (constriction of coronary)
Renal Function and CHF
-RAAS
-a receptor activity
-decreased renal activity
Rate Pressure Product
-SBP*HR
-exercise threshold
-myocardial o2 demand
->10,000 @ rest, increase risk of angina
Stethoscope Diaphragm
-high frequency sounds
Stethoscope Bell
-low frequency sounds
S1
-first heart sound (higher frequency)
-closure of M1 and T1
-best heard in Mitral Area
S2
-second heart sound (lower frequency)
-closure of semilunar valves valves
-best heard in Aortic Area
Aortic Area
-right sternal border
-2nd intercostal space
-S2 best heard
Pulmonic Area
-left sternal border
-2nd intercostal space
Tricuspid Area
-left sternal border
-4th intercostal space
Mitral Area
-left side under nipple
-apex of heart
-5th intercostal space
-S1, S3, S4 best heard
Apical Pulse
Listen to apex of heart for 1 min
S3
-dilated/large ventricle causes rapid flling causes loud sound
-systolic issue
-could be abnormal (heart failure, dilated cardiomyopathy, late diastole) or normal (pregnancy/children, athletes)
-extra heart sound after S2
-“kenTUCKy”
-listen with bell @ apex
S4
-rigid ventricle decreases filling, atria contract late to push past force
-diastole issue
-always abnormal (HTN, MI, atrial kick of blood into stiff ventricle diastolic bad)
-right before S1
-gallop
Respiratory Cycle
Inspiration: 1/3, faster and louder
Expiration: 2/3, slower and softer
Vesicular Breath Sounds
-most of lung area
-inspiratory longer than expiatory
-soft
Brocho-Vesicular Breath Sounds
-near midline around upper spine and sternum
-inspiratory equal expiatory
Bronchial Breath Sounds
-above manubrium
-loud
-inspiratory shorter than expiatory
RV Failure S/S
-venous insufficiency, edema, weightt gain, liver issues
LV Failure S/S
-pulmonary issues, effusion, S3, crackles, decreased O2, paleness, increased HR, increased Breathing
Ischemic heart Disease (Medications)
-restablish balance of o2 supply and demand
-decreasing HR or BP to reduce O2 demand
-increase artery size, remove thrombus,
Heart Failure (Medications)
-maintain CO, adress underlying issue, regulate fluids, decrease preload and afterload, increase conttractility, reduce workload, decrease SNS
Arrhythmias (Medications)
-inhibit abnormal impulses by affectting membrane permeabiliy to specific ions (Cl, K, Ca, Na)
-SA & AV node
-prelong refractory period
Hypertension (Medications)
-reduce fluid, limit SNS, decrease RAAS
Beta Blockers
-olol
-reduced beta receptor binding
-selective of nonselective
B1: increases HR and contractility
B2: bronchoconstriction and vasodilation
CI
-HTN, ischemic HD, heart failure, arrhythmias
SE
-sedation, may mask hypoglycemia, reduced thermoregulatry response, spasms, orthostatic hypotension
Max HR: 164 - (.7 x age)
Orthostatic Hypotension
decreased of BP 20 and HR increase of 30 when standing from sitting
Calcium Channel Blockers
-pine
-decrease HR & BP, conrtactility, O2 demand
-cause vasodilaiton of coronary artieries
CI
-reduce re-infarctions (dead tissue releases Ca), ischemic HD, heart failure, arrhythmias
SE
-negative inotropic effects, blunted HR responses to exercise
Nitrates
-nitr
-slows HR, reduce preload and afterload, decrease contrtactility, lower BP, vasodilation
CI
-HTN, ischemic HD, heart failure, angina
SE
-hypotension, dizziness, reflex tachycardia, skin flushing
Angina (Medications)
-chest pain due to ischemia
-lack of O2 stimulates pain receptors
-treated by nitrates, BB, CC blockers
S/s
-tightness and chest pain
-simular to MI
-ECG ST downward shift
Stable Angina
-pain free at rest
-relieved by nitrates
-predictable
Unstable Angina
-unpredictable
-at rest
->15mins
-progression of disease
Prinzmetal’s Variant Angina
-only at rest; morning
-ST elevation
-cardiac vasospasm (CC blockers)
Thrombolyic Agents
-break clots up quickly
-goal to keep ischemic time <120min
SE
-arrhythmias due to rapid reperfusion (high K, reflex tachycardia), bleeding, hemorrhage CVA
Anti-Platelet Agents
-prevent platelet aggregation and thrombus formation
-decrease platele adverance to site of injury
Anticoagulants
-prevention of blood clots, inhibit thrombin
Common: heparin, pradaxa, xarelto, eliquis
Diuretics
-ide
-decrease blood volume by peeing
-improve cardiac contractility
-reduce cardiac demand
-act of kidneys (loop of henle most potent)
CI
-HTN, heart failure
SE
-hypotension, arrhyhmias (K+)
Carbonic Anyhyrase Inhibitor Diuretics
-mild diuretics
-proximal tubules of kidney
K+ Sparring Diuretics
-mild
-collecting tubules and ducts
Thiazides Diuretics
-moderate
-can cause low K+ and glucose intolerance
Sodium-Glucose Transporter Inhibitors
-ozin
-lower blood sugar, reduce CV deaths and kidney disease, reduce BP, weight loss
SE
-hypoglycemia, Hypotension, UTIs, diabetic ketoacidosis
ACE Inhibitor
-pril
-prevents conversion of ang 1 to 2
SE
-hypotension, dizziness, angioedema (life thrreatening tongue swelling), hyperkalemia
Angiotension II
-vasoconstriction
-water and Na retention
-aldosterone and ADH stimulation
Angiotensin Receptor Blockers (ARBs)
-sartan
-limits effects of ang 2
SE
-hypotension, dizziness, angioedema (life thrreatening tongue swelling), hyperkalemia
Neprolysin Inhibitor
-reduces abnorrmal remodeling
-diuresis
-vasodilation
Aldosterone Antagonists
-suppresses aldosterone
-decreased fluid retention (diuretic)
ex: spironolactone
SE
-hyperkalemia, Orthostatic hypotension
Positive Inotropes
-increase contractions and HR
-opposite of BB
CI
-heart failure
Cardiac Glycosides
-positive inotropes
-increase Ca+
-decrease HR
-increase delay from SA to AV
-increase PR interval
-anti arrhythmics
ex: digoxin
CI
-dilated cardiomyopathy
-a fib
NOT FOR 2nd or 3rd Heart Blocks
SE
-lots of symptoms of digitalis toxicity
Sympathomimetics
-positive inotropes
-mimic SNS, treat shock, heart failure
-short term use only to prevent downrreg
CI
-parenteral use for hheart failure
Phosphodiesterase Inhibitors
-positive inotropes
CI
-severe CHF, strengthen contractions
Vasodilators
-decrease bv, vascular resistance
-Arterial: reduce afterload
-Venous: reduce preload
CI
-HTN, HF, ischemic heart disease
SE
-compensatory SNS actitvation
Alpha Adrenergic Antagonists
-vasodilator
-manage HTN
SE
-reflex tachycardia
-increase in BV
Morphine
-vasodilator
-decrease preload via venodilation
-reduce anxiety and effort during heart failure
Anti-Hypertensive
-regulate BP, decrease HR and CO
-BB, Ca blockers, ACE inhib, vasodilators, diuretics
Anti-Arrhythmics
Membrane stabilizers
-v tach and a fib
-reduces Na+ in cell
SE
-arrhythmias, bradycardia, photosensitivity, hepatotoxicity, hypothyroidism
Risk factors of Critical Illness Weakness
-bed rest
-immobility
-ventilatory suport
-sepsis
-organ failure
Bedrest
-harmful
-no motion against gravity
-skeletal muscle declines 1-1.5% per day
Immobility
-immobility due to meds
-skeletal muscle declines 5-6% per day
3 Causes of Motor Weakness in ICU
-pre-existting neuromuscular disorder
-new neuromuscular disorder
-CIP or CIM
Critical Illness Polyneuropathy
-sensory and motor nerves involved
-main contributor to persistent disability
-sepsis and organ failure
-chronic denervation
Critical Illness Myopathy
-diffuse flaccid weakness in all limbs
-can have complete recovery
-chronic denervation
-can be caused by steroid use
Causes of CIP and CIM
-critical illness and cytokine production lead to cascade of issues
Phase I of ICU Mobility and Walking
-restricted to bed
-unable to bear weight
Phase II of ICU Mobility and Walking
-able to stand
-cannot ambulate
Phase III of ICU Mobility and Walking
-able to ambulate
-improve endurance
Phase IV of ICU Mobility and Walking
-can walk at a high level
-ready to discharge
How much O2 in atmosphere?
21% O2
Nasal Cannula
-24-44% o2
-1-6L
Reservoir Cannula
-conserve o2, stored in reservoir
-100% o2 in each breath
-retains exhhaled air
High Flow Cannula
-1-15L w/ humidification
-24-75% o2
-not harsh on nose
Simple O2 Mask
-6-10L
-30-70%
-6L minimum to brevent rebreathing
Face Tent
-for mouth breathers or facial trauma
-8-15L
-21-40%
Aerosol Mask
-liquid medicatitons into mist
-must be able to see mist
-8-15L
-21-60%
Venturi Mask
-rroom air mixed with specific concentration
-color coded
Nonrebreathing Mask
-highest 02
-75-100%
-8-15L
-bag must be 1/3-1/2 full
-might be close to intubation
Tracheostomy Mask
-straight into tracheostomy tube
-35-60%
-10-15L
High Flow humidification Systems
-up to 60L
-up to 100% o2
-humidified and warmed air
Mechanical Ventilation
-meet physiological needs of pulmonary system
- Rrespiratory failure
- Protection of airway and lung
- Relief of upper airway obstruction
- Improvement of ulmonary toilet (unable to clear airways)
Paradoxical Breathing
-diaphragm fatigued from working hard
-must be inubated
Ventilator Settings to Know
-mode of ventilation
-FiO2: o2 concentration being administered (>60 concern)
-PEEP
Ventilator Patient Data to Know
-Minute ventilation
-respiratory rate
PEEP
-Positive End Expiratory Pressure
-resisdual pressure in alveoli after exhalation
-pressure required to inflate alveoli and prevent collapse
Low PEEP 3-5: normal
Moderate PEEP 5-15: treat refractory hypoxemia
High PEEP >15: severe lung injury
-put pressure on IVC and decreased CO
Mode of Ventilation
-how breath is delivered
- Assist-Control
- SIMV and Pressure Support
- Pressure Support
Assist-Control
-non weaning: breathing for patient
-rate and tidal volume pre-set
-patient can trigger breaths with pre-set tidal volume
SIMV
-synchronized intermittent Mandatory Ventilation
-Weaning mode: starting to take them off
-rate and tidal volume pre-set
-patient can trigger breaths with pressure support instead of pre-set tidal volume
Pressure Support Ventilation
-weaning mode: 0-30cmH20 (10 normal)
-applies to spontaneous breaths
-tidal volume not pre-set
-NOT air, only pressure
CPAP
-constant positive pressure applied in airways
-noninvasive ventilation
BIPAP
-Bi-level pulmonary airway pressure
-noninvasive ventilation
SaO2
-actual o2 content in blood
SpO2
-estimated o2 content in blood
-<88 is concerning, drop in hemoglobin curve
SE
-syncope, dizziness, paleness, quick breathing (>30bpm at rest)
4 Steps to check EKG
- Speed
- QRS Wide or narrow
- P wave
- Regular or Irregular
Rule of 300
5 Boxes: 60bpm
4 Boxes: 75bpm
3 Boxes: 100 bpm
2 Boxes: 150bpm
1 Box: 300bpm
Length of EKG Components
P Wave: 2-3 boxes
PR interval: 3-5 boxes
QRS: 1.5-3 boxes
Lead I
-limb lead
Right arm to Left arm
-normal wave form
-Circumflex A.
-lat wall of LV
Lead II
-limb lead
Right arm to lower limb
-normal wave form
-Right Coronary A.
-Inferior portion of heart/apex
Lead III
-limb lead
-leftt arm to lower limb
-normal wave form (may have inverted P and t wave)
-Right Coronary Artery
-Inferior portion of heart/apex
aVF Lead
-augmented lead
Middle of body to lower limb
-Right coronary Artery
-Inferior portion of heart/apex
-normal wave form
aVL Lead
-augmented lead
From middle to Left arm
-Circumflex A.
-lat wall of LV
-normal wave form
aVR Lead
-augmented lead
From middle of body to right arm
-Top of RV
-inverted wave form
V1
On Right 4th intercostal space
-septal, precordial lead
-L Ant. Descending A.
-inverted P-wave, deep S
-RV
V2
On Left 4th intercostal space
-septal, precordial lead
-L Ant. Descending A.
-inverted P-wave, deep s
-RV, septum
V3
On left between 2 and 4
-Anterior Heart, precordial lead
-Right coronary A.
-RV, septum, ant. heart
V4
On left 5th intercostal space mid clavicular line
-Anterior Heart, precordial lead
-Larger R, small s
-Right coronary A., ant heart
V5
On left 5th intercostal space anterior axillary line
-Lateral heart, precordial lead
-Larger R, small s
-Circumflex A., lat wall of heart
V6
On left 5th intercostal space mid axillary line
-Lateral heart, precordial lead
-Larger R, small s
-Circumflex A., lat wall of heart
Premature Ventricular Contraction
-random cell in ventricles fire out of sync of the rest, prematurely
-wide QRS
Ventricular Bigeminy
-PVCs occur every 2 beats
Ventricular Trigeminy
-PVCs occur every 3 beats
Ventricular Couplet
-PVCs occur in 2s
Ventricular Triplet
-PVCs occurr in 3s
-non sustained ventricular tachycardia
-STOP and check vitals
Ventricular Tachycardia
-fast/large/wide QRS with no p wave, regular
-emergency
Supraventricular Tachycardia
-fast/narrow QRS
-comes from atria not SA node
Junctional Rhythm
-slow (40bpm) /no p wave/inverted T wave
-originates away from atria but depolarizes ventricles
ST Elevation
-Acute MI
-Stimi
ST Depression
-Angina/ischemia/infarction
P Wave Inversion
-Heart block with junctional rhythm
T Wave Inversion
-MI or ischemia
-BBB
-hypertrophy
-pulmonary embolism
Ventricular Fibrilation
-dangerous, call code
-irregular/fast/small
Atrial Fibrilation
-chaos/irregular
-QRS present, no p wave
-multiple cells firing
-valve issues, ischemia, stroke, arrhythmia
Atrial Flutter
-saw tooth/bread knife
-1 cell going crazy
-QRS present and irregular
Torsades De Pointes
-V tach with prolonged QT, irregular
-Looks crazy…how are you alive
Right Bundle Branch Block
-delayed depolarization of RV
-right lead (V1): “M” in QR, deep S
-Left lead (V6): “W” in S wave
R-Wave to find HR
-add up r waves in one strip x 6= HR
Left Bundle Branch Block
-delayed depolarization of LV
-right lead (V1): “W” in R wave
-Left lead (V6): “M” in R wave
-anomally always at tip of QRS
1st Degree AV Block
-husband is late but comes home, long PR interval
-from SA node
-slow HR
2nd Degree AV Block : Type 1
-husband is later and later and then doesn’t come home
-longer PR interval then dropped QRS
-AV node
2nd Degree AV Block : Type 2
-husband randomly doesn’t come home
-normal PR intervals
-randomly dropped QRS
-Bundle of his
-DONT WORK WITHOUT PACEMAKER
3rd Degree AV Block
-normal p wave unrelated to QRS, no correlation of QRS
-random p waves
-DONT WORK WITHOUT PACEMAKER
Percutaneous Revascularization Procedures
-revascularize myocardium
- Angioplasty
- Arthrectomy
- Stenting
Angioplasty
-balloon inflated to push plaque against lumen
-stent then put in
-prone to bleeding
-5-7days no exercise
Arthrectomy
-larger plaque buildup, cut out the plaque
Coronary Artery Bypass Graft
-CABG
-open heart surgery
-place another vessel from one spot to bypass blockage (radial arteries, saphenous veins, mammary arteries)
Cardiac Complications
-infection
-sternal precautions
-scar tissue
-Myocardial Stunning: low cardiac output
-Arryhmias
-Bleeding: migh need blood transfusions
-Neurologic Complications
CABG Complications
-Renal failure: 5-10%
-Pleural Effusions: 90%
-Pericardial Effusion
Sternal Precautions
-limit movement for 6-8 weeks
-gentle coughing
-move “in the tube”: keep arms to the side
-infection control
Intraortic Balloon Pump
-severe heart failure; shock
-restore CO
-inserted in femoral (bedrest) and axillary (might be allowed to exercise) to ascending aorta
-balloon inflates and deflates to increase CO by 40%
Valve Replacements
-aortic most common (pulmonary valve to replace aortic, aortic cannot be repaired)
-Metal: requires life long blood thinners
-Bovine: reduce stroke risk
Arrhythmia Procedures
-Ablation: burn off cells causing arrhythmias
-Pacemaker Implant: need to know rate, what makes it come off
-Defibrillator: prevent arrhyhmias
Peripheral Vascular Interventions
-Endarectomy: plaque removed
-Aneurysm repair
