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204 Cards in this Set
- Front
- Back
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how hospitalizations a year are due to ACS
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Hospitalization due to atherosclerotic disease, particularly acute coronary syndromes, accounts for well over one million admissions to U.S. hospitals each year.
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Epidemiology of ACS in the United States
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Single largest cause of death
515,204 US deaths in 2000 1 in every 5 US deaths Incidence 1,100,000 Americans will have a new or recurrent coronary attack each year and about 45% will die* 550,000 new cases of angina per year Prevalence 12,900,000 with a history of MI, angina, or both need to focus on primary prevention |
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Unstable plaque
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lots of inflammatory cells
thin fibrous cap more oxidized LDL thin smooth muscle lots of activated macrophages to absord the LDL eroded endothelium |
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stable plauque
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thick fibrous cap
thick layer of smooth muscle no inflammatory cells intact endothelium |
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how dow statins affect plaques
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stablilize plaques by decreasing inflammation and enhances the thick fibrous cap
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Coronary thrombosis results from
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rupture of an unstable plaque with resultant thrombus formation
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Unstable plaques are characterized
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a large lipid-rich core and only a thin fibrous cap, vulnerable to rupture or erosion.
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Inflammatory cells and activated macrophages are believed
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are believed to be involved in destabilizing the plaque and the fibrous cap
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ACS Pathophysiology Plaque Rupture, Thrombosis, and Microembolization
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process
Plaque formation (markers: cholesterol and LDL) Inflammation: Multiple factors Infection: (markers: hsCRP, adhesion molecules, interleukin 6, TNF alpha, sCD-40 ligand) Plaque Rupture ? Macrophages Metalloproteinases: markers: MDA modified LDL Thrombosis Platelet Activation Thrombin: markers D-dimer, compliment, fibrinogen, troponin, CRP, CD40L |
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Systemic and Focal Plaque Rupture by IVUS (intrvascular ultrasound) in ACS Patients Undergoing PCI
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fewest plaques rupture at site of culprit lesion
most plaque ruptures are elsewhere than site of culprit lesion second largest number of plaque ruptures occur in a different artery than the culprit lesion there is usually not just one plaque there are diffuse multiple plaqeus |
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______% of patients with more than 2 plaques
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80
that is why primary prevention is essential |
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Progression of coronary plaque over time Clinical Findings
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at 20 years old atherogenic risk factors such as smoking, obesity, age, genetics, male, DM, HTN, and hyperlipidemia
the above can cause endothelium dysfunction and NO is not porduced |
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risk factos for plaque formation
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smoking, obesity, age, genetics, male, DM, HTN, and hyperlipidemia
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what is the start of plaque formation and at what age
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oxidized LDL
20 |
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UA
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occlusion is minimal, no necrosis of myocardial tissue
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NQMI
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non-necrotic, nonst segment elevation but damaged heart
moderate occulsion can progress to STEMI |
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Diagnosis: EKG changes STEMI
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STE ACS: ST segment elevation in two or more
contiguous AND either > 0.2 mV (mm) in leads V1, V2, V3 OR > 0.1 mV in other leads |
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septial views on the EKG
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V1
V2 |
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Summary of unstable angina, NSTEMI, STEMI
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unstable angina: symptoms are present, there are not EKG changes, no biomarkers present
NSTEMI: symptoms are present, EKG changes: ST segement depression, T wave inversion, or no changes STEMI: symptoms are present, EKG changes: ST segement elevation, Increased levels of troponin and CK MB can eliminate unstable angina by looking at biomarkers |
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inferior infarct is in the
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right ventricle
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anterior infarct is in the
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left ventricle
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Short term risk of death or non-fatal MI
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LBBB
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left bundle branch block
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TIMI blood flow
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grade of blood flow is based on how rapidly the blood is flowig through the artries
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Killip II-IV
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I= no clinical s/s of HF
II= (+) for rales and crackles, S3 gallop and JVD III= acute pulmonary edema IV= cardiogenic shock excessive hypotension |
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cardiac catherization
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have to go through roin and get to asending aorta
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stent development
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subacute thrombus
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< 30 days
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late thrombus
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> 30 days-1 year
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very late thrombus
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> 1 year
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acute thrombus
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< 24 hours
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risk of thrombus is _____ in the drug eluting stent than the bear metal stent
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greater than
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why drug eluting stents
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complications of bear metal stents
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Non pacemaker cells phases
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phase 0: influenced by NA causing a sharp depolrization
phase 1: K cause a slight decrease in the AP, but the channels are open transiently phase 2: influenced by Ca to maintain the depolarization of the cell phase 3: Ca channels are closing and K channels are opening so the cell begins to repolarize phase 4: cell is repolarized by K channels to resting diastolic potential |
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are non-pacemaker cells dependent on Na for the sharp up swing
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yes
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In non-pacemaker cells what causes depolarizaiton to decrease
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the closing of Ca channels
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non-pacemaker cells are in the
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atial and ventricular myocytes
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cardiac electrical pathways and activity
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why is the resting membrane potential negative
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because K channels are open
K hyperpolarizes the cell toward -96 mV |
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equilibrium potential=
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70 mV
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Pacemaker cell phases
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phase 0: gradual upslope is dependent on Ca
phase 3: K channels open to repolarize the cell phase 4: is the pacemaker potential (this slope is what makes it a pacemaker cell) leaky Na channels phase |
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F channels
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(funny channels)
open when membrane potential becomes negative enough and allows Na to flow into the cell during phase 4 |
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non-pacemaker cell graph
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Pacemaker cell graph
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pacemaker cells are in
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the sinus and atrioventricular nodes, purkinje
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if the Kach channels are activated what happens to the heart
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decrease conduction, slope (rate of depolarization), HR
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__________ is the gateway to the ventricles
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AV node
The AP must go through the AV node to pass from the atria to the ventricles |
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Why does the AV node have a delay
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so the atria can contract before the ventricles and allow the ventricles to fully fill
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what is the pathway of the AP in the heart
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SA node--> AV node(delay)--> bundle of HIS--> purkinje fibers--> ventricular muscle (apex first)
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during diastole what ion is the heart more permeaable to
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K that is why the heart has a negative resting potential
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what is the f channel activated by
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hyperpolarization
cyclic nucleotide (cAMP) causing Na to flow into the cell |
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what channel is on the ventricles in high concentration to prevent them from becoming overstimulated
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Ik1
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Kur channel
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atria primarily-->drug target for atria selective
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are the channels different in the pacemaker cells and the non-pacemaker cells
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yes
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some ion channels sense muocardial cell status
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KATP: activated by ADP → coupled to metabolic state of cell (sense ration of ADP/ATP
- Kkp: stretch & pH-sensitive → there is an increase in EDP (HF) and a decrease in pH in ischemia and causing these channels to become activated |
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during agina what is happening to ATP
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ATP is being consumed and there will annd there is an increase in lactate acid ativating Katp and Kkp channels
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changes associted with HF
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conduction changes due to fibrosis
changes at a cellular level |
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Ion channel properties:
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• ion channels comprise:
α subunit pore-forming unit (ions pass through) β subunit modifies channel function |
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can mutations in ion channels be associated with dysrhythmias
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yes
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alterations in ion channel function can lead to dysrhythmias by altering:
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a. threshold for activation (determining how much have to stimulate cells to open)
b. availability of channels for opening |
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alterations in ion channel function can lead to dysrhythmias by altering:
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a. threshold for activation
b. availability of channels for opening |
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disease and altered ion channel function
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disease states such as ischemia can cause slower recovery of inactivated Na channels and decrease tissue responsiveness
RMP can become more + and AP duration is diminished conduction and excitability changes can occur |
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genetics can cause alterations in channel function
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mutated protein channels
for instance if K channels don't fully open the AP duration would be longer (prolonged QT interval-->torsades |
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channel protein modifications
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- glycosylation
- phosphorylation (PKA, PKC, Ca2+/calmodulin-dep. PK) - other post-translational modifications |
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If PKA induces phosphorylation of Ca2+ channels in myocardial cells:
what agonist (that you know of) would induce Ca2+ channel phosphorylation? |
B agonist induce Ca phosphorylation
In answering the question above, what would you predict that PKA-induced phosphorylation does to Ca2+ channel function? increase |
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changes in the function of other ion channels
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indirect effect by changing membrane potential
MP influences if channel opens or not indirectly modifying functions of another channel |
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ion channels cycle through different states in a manner that is:
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a. membrane potential dependent
b. time-dependent |
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what determines the state of an ion channel
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membrane potential
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what is different about the resting state and inacitvatied state of the membrane
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resting state is able to open and the inside of the cell is negative and resides at RMP
inactivated state is not able to open in response to an AP and the membrane is still depolarized |
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what is the charge of the ion channel
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positive charge resides in the ion channel making it voltage sensitive
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non-pacemaker cells in resting state
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Resting state
• Na+ channel closed (m gate closed) (= resting channel) |
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non-pacemaker cells in phase 0
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Na+ channels (m gates) open
(= activated channel) → ↑ Na+ flux into cell → depolarizes the cell |
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non-pacemaker cells phase 1
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Na+ channels are rapidly inactivated
(h gates) close (= inactivated channel) Na+ channels do not open again until reactivated by repolarization • K+ channels are transiently activated → ↑ K+ flux out of cell → initial repolarization |
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non-pacemaker cells phase 2
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Phase 2
• Ca2+ channels open → plateau of action potential L-type channels involved • Ca2+ channels slowly inactivated during plateau • K+ channels begin to open |
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non-pacemaker cells phase 3
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• K+ channels open
• Ca2+ channels inactivating → membrane repolarization to return to RMP |
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non-pacemaker cells phase 4
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Phase 4
• membrane potential constant and stable during diastole |
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pacemaker cells phase 0
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Ca2+ channels open (open when membrane reaches threshold)
→ ↑ Ca2+ flux into cell pacemaker cells do not have a phase 1 or 2 → depolarization |
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pacemaker cells phase 3
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• K+ channels open
• Ca2+ channels inactivating → membrane repolarization to return to RMP |
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pacemaker cells phase 4
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spontaneous depolarization = pacemaker potential
- "funny" channels open (when cell is hyperpolarized) → ↑ Na+ flux into cell → membrane potential drifts towards threshold during diastole "funny" channel activation facilitated by ↑ intracellular cAMP (increase slope--> increase rate) - Ca2+ channels may play role late in this phase (ie: verapamil decreases pacemaker rate and slope so Ca must affect the rate of depolrization) - K+ channels (e.g., Kr, KACh) can also be activated → ↑ K+ flux into cell → membrane potential drifts away from threshold pacemaker current is faster in SA nodal cells than AV node ⇒ SA node paces the heart hyperpolarizes the cell and decreases the rate of depolarization membranes drift further away from threshold |
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when depolarization reaches threashold-->
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AP
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firing rate (heart rate) of pacemaker cells determined by:
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a. threshold potential
b. maximal diastolic potential (how far the cell repolarizes) c. slope of phase 4 depolarization (diastolic potential) |
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what would happen if the threshold was increased
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decrease in HR because it would take longer to reach threashold
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what would happen in the slope increased
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increase in HR
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what would happen to HR if diastolic potential became more negative
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HR would decrease because it would take longer to reach threshold
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conditions like myocardial ischemia can make phase 4 unstable in non-pacemaker cells-->
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diastolic potential of phase 4 is flat so if change the sloe you can make them a pacemaker if faster than the SA node
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cardiac responsiveness
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• relates to the ability of cardiac cells to respond to an AP or other stimulus
⇒ also relates to ERP • depolarizing channels (Na+, Ca2+) must be available (i.e., in resting state) • channel recovery is membrane potential- and time- dependent |
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MEMBRANE POTENTIAL-DEPENDENCE
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- number of Na+ channels available is
dependent on RMP ⇒ more positive RMP → ↓ Na+ channels in resting state - If RMP > -55mV, all Na+ channels inactivated ⇒ APs will only occur by alterations in Ca2+ or K+ fluxes |
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ERP
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effective resting potential
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RMP
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resting membrane potential
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if the RMP is more + what state are the channels in
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inactive so less can respond
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repolarization is necessary before
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cardiac cells can develop a
normal response e.g., h gates do not open until RMP < ≈ -75mV |
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time dependence
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as membrane potential becomes more
positive, Na+ channels take longer to recover (inactive → resting) The more positive the membrane potential → fewer Na+ channels can open |
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maximal rate of depolarization in non-pacemaker cells
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(= slope of phase 0) in non-pacemaker cells is dependent upon
the availability of resting (= activable) Na+ channels |
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slope of phase ) dictates in non-pacemaker cells
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Conduction velocity
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when the MP is more + fewer channels can open-->
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↓ conduction velocity, ↓ tissue excitability
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if try to stimulate cell too soon after AP
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→ all Na+ channels haven't recovered
→ ↓ rate of depolarization, ↓ AP amplitude |
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decrease Na channels avaiable-->
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leads to a decrease in rate
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In non-pacemaker cells, normal conduction decreases only after the maximal rate of
depolarization decreases by at least ___% |
50
large safety margin for normal conduction slope of phase 0 has to decrease by 50% |
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Hyperkalemia, ischemic cell damage, Na+/K+-ATPase blockade can result in a more positive
resting membrane potential. In what state are the Na+ channels likely to be, i.e., resting, open or inactivated? |
inactivated
this would decrease tissue conduction and excitability |
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CARDIAC REFRACTORINESS
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relates to the duration of the effective refractory period (ERP)
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if give a Na channel blocking drug what happens
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conduction decreases
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Hyperkalemia, ischemic cell damage, Na+/K+-ATPase blockade can result in a more positive
resting membrane potential. In what state are the Na+ channels likely to be, i.e., resting, open or inactivated? How will this affect tissue conduction and excitability? |
relative and absolute refractory periods so cannot stimulate the nerve becuse it has not recovered
in the inactivated state |
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non-pacemeaker cells in regards to ERP and AP duration
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ERP ≈ AP duration
- recovery of Na+ channels from inactivation closely parallels repolarization, i.e., potential dependent recovery is determined by the movement of inactive channels--> resting state the cell will not respond while under going an AP |
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pace maker cells in regards to ERP and AP duration
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Ca2+ channels recover slowly from inactivation, i.e. time-dependent
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antidysrhythmic drugs tend to prolong ERP relative to AP duration which
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↓ propagation of rapid impulses
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What channels would you target to increase the ERP in non-pacemaker cells and in what state
would you want them to be? |
Na
would want them to be in the inactive state so they cannot open |
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What channels would you target to increase the ERP in pacemaker cells and in what state would
you want them to be? |
Ca
hold in the inactive state |
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automaticity of the heart
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SA node 60-100
AV node 40-60 bundle of His 25-40 Purkinje fibers 20-40 fastest pacemaker generally dictates the HR |
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limb/peripheral leads:
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I, II, III, AVR, AVL, AVF
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chest/precordial leads:
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V1, V2, V3, V4, V5, V6
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12 leads on EKG because
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each lead is looking how the impluse is moving away and towards it
the more leads the better description of the heart 12 views of the heart triangulation |
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components of the ECG include:
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P wave depolarization of both atria
PR interval time for impulse to pass through the atria and AV node and to initiate ventricular depolarization QRS complex ventricular depolarization ST segment ventricles fully depolarized T wave repolarization of ventricles |
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ECG INTERPRETATION
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atrial rate = # P waves/min
ventricular rate = # R waves/min |
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6 second method EKG
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i. count number of R waves between alternate long indicator lines
ii. multiply number by 10 (= heart rate) |
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divsion method EKG
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i. count number of large squares between two R waves
ii. divide 300 by the number (= heart rate) |
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rhythm describes
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the regularity between the complexes
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if difficult to see individual P waves on EKG
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a fib
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how will an EKG look with 3rd degree AV block
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regular P waves but the QRS complex will not be linked with the P waves because the ventricles will be going at their own rate
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rhythm
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• describes regularity of complexes
• regular rhythm Þ P-P intervals are equivalent and R-R intervals are equivalent |
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if the P-R interval is linger than 1 block
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the AV node conduction has slowed down and you may see 2 P waves in a row
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If the QRS complex is on top of the P wave
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It is a sign that the P wave is not the trigger
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P waves
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P waves
a. present? b. upright? (if inverted the AP is moving away from the electrode not toward c. look similar to each other? d. present before each QRS complex? |
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PR interval
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a. within normal range (0.1-0.2 s)?
b. similar to each other |
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QRS complex
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a. present?
b. look similar to each other? c. present after every P wave? d. within normal range (0.04-0.12 s)? |
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ST segment
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a. normal, elevated, depressed, biphasic?
b. look similar to each other? |
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T waves
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a. normal, elevated , depressed
b. look similar to each other? |
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If a P wave is inverted, what does this tell you about the movement of APs in the atria?
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reversed
impluses are moving away |
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If the QRS complex does not appear to follow a P wave, what does this tell you about the
pacemaker driving ventricular contraction? |
not the SA node, it is something else
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If the distance between the P wave and the QRS complex exceeds 1 large square (or 5 little
squares) on an ECG, what does this tell you about AP passage from the atria to the ventricles? |
slowed down
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dysrhythmias general mechanism
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• occur by a disturbance in impulse formation and/or impulse conduction
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tachycardia
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regularity: regular
bmp; > 100 |
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SITE OF FORMATION DEFINITIONS
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SITE OF FORMATION DEFINITIONS
• relative to bifurcation of bundle of His i. supraventricular (above the bundle of HIS, atria, Av node, Sa node) ii. ventricular (below the bundle of HIS) |
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flutter
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regularity: regular
bpm: 200-400 (like a fast tachycardia, Co will be decreased) |
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fibrillation
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regularity: irregular
bpm: >300 |
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extrasystole
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premature complex
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escape
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1-2 consecutive impluses from atypical pacemaker
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tiggered activity (premature complex)
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• abnormal impulse triggered by preceding AP
• caused by instability of membrane potential at end of AP → afterpotential if afterpotential reaches threshold → abnormal Ca flux |
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EAD
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early afterdepolarizations occur before the cell ha repolarized by changes in Ca fluxes
the cell contracts sooner than it would have causing tachycardia |
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DAD
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delayed after polarization
the cell is repolarized but there is a transient depolarization so there is a little depolarization after the QRS complex there is an increase in HR due to the abnormal flux in Ca there is an extra systole if the AP reaches threshold and it can lead to a self sustaining fast rhythm |
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re-entry
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• occurs when a single impulse activates the same groups of cells two or more
times → activation of entire heart • promoted by regional cardiac differences in: i. AP conduction velocity ii. tissue recovery from refractoriness takes over when the rates are faster than the SA node |
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examples of re-entry include
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examples include:
i. AV nodal re-entry ii. Wolff-Parkinson-White syndrome iii. atrial flutter |
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? What happens if a drug slows AP conduction?
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allows tissue to recover more quickly and increases the likelihood of re-entry creating a difference in conduction
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pictures of normal cells-->reentry
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in the premature impluse the impluse stops because it hits tissue that is refractory
if cells recover quickly enough can get a re-entry circuit |
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What happens if a drug increases the refractoriness of cells in the circuit?
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re-enterant rhythm stops
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fibrillation occurs when
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occurs when refractory state of cells become asynchronized
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fibrillation process
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excitation wave divides around refractory cells
→ refractory cells become responsive and become excited → APs pass from these cells to formerly refractory myocardium → fast, disorganized myocardial activation → no coordinated myocardial contraction |
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in fibrillation is the AP moving in one cordinated direction
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no, it is moving out of the re-entrant circuits in all directions to surrounding tissue that is responsive
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in fibrillation does all of the tissue recover at the same rate
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no
some of the cells are depolarized while others are in recovery or still recovering |
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picture of fibrillation
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IMPULSE CONDUCTION (slow rates)
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usually involves delay or failure of AP propagation = block
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what is worse atrial or ventricular fibrillation
|
ventricular it can cause death
atrial doesn't cause death becasue the AV node fillters some of the AP so the ventricles are not contracting at the same rate as the atria |
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causes of re-entry
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chnages in recovery of tissue
different rates of recovery changes in conduction velocity |
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DYSRHYTHMIA SIGNS & SYMPTOMS
• clinical manifestations include: |
i. patient complaints
ii. hemodynamic complications iii. neurological symptoms |
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patient complaints
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subjective
• perception of dysrhythmia varies from person to person • extrasystoles "heart turning cartwheels" "standing still for a moment" "beating very hard" • tachycardia rapid heart beat or fluttering in chest → anxiety, breathlessness, fatigue, dizziness • bradycardia rarely sensed |
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HEMODYNAMIC COMPLICATIONS of dysrhythmias
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• related to: i. severity of dysrhythmia
ii. functional states of myocardium and circulatory system |
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example of hemodynamic complications and dysrhythmias
|
tachycardias
- in healthy individual, HR up to 200 bpm → minor symptoms - in pt with severely diseased myocardium or severe CAD, HR up to 150 bpm → CHF, pulmonary edema or anginal pain bradycardias - in healthy individual, HR down to 30 bpm → well tolerated - in pt with AMI or severe chronic IHD, HR down to 30 bpm → CHF, shock |
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neurological symptoms of dysrhythmia
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• tachycardia (sometimes bradycardia) → confusion, dizziness, mental tiredness
• Stokes-Adams attacks or sudden death most serious neurological consequences (faints or come close to fainting because heart is stopping and starting) |
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ATRIAL DYSRHYTHMIAS usually involve changes in
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P wave
PR interval |
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atrial flutter
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characteristics
• regular • rate ≈ 250 - 300 bpm • originates from single atrial site (not SA node) |
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ECG changes and atrial flutter
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• normal P wave not produced → F waves
• negative F wave ⇒ atria depolarizing in abnormal pattern • "saw-toothed" appearance • ventricles usually depolarize/repolarize at normal rate • # F waves : QRS complexes indicates extent of "block" |
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causes of atrial flutter
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aging heart, heart disease, MI, drug toxicity
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symptoms of atrial flutter
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decrease MAP
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issues of atrial flutter
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• may degenerate to atrial fibrillation
• ventricular tachycardia if slow atrial rate |
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What is the atrial rate?
What is the ventricular rate? |
atrial 500 bpm (300/0.6)
ventricular 94 bmp (300/1.2) |
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atrial fibrillation characteristics
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characteristics
• rate ≈ 350 - 600 bpm • irregular originates from many atrial sites aside from SA node → many impulses not conducted → each impulse does not cause complete atrial depolarization → atria quiver rather than contract forcefully (fast and irregular, lots of pacemakers at multiple sites) |
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ECG and atrial fibrillation
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• "wavy" line between QRS complexes
• irregular R-R intervals (QRS cpmplexes) - not possible to identify which impulse conducted from atria to ventricle ⇒ no true P waves or PR intervals - controlled atrial fibrillation = ventricular rate in normal range uncontrolled atrial fibrillation = ventricular rate > 150 bpm |
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causes of atrial fibrillation
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• left atrial enlargement (by mitral valve stenosis or regurgitation) ie: HF
• aging, CAD, thyrotoxicosis, pulmonary disease • excessive use of alcohol or caffeine |
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issues and atrial fibrillation
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rapid ventricular rates → ↓ stroke volume → hypotension, pulmonary congestion
decrease in CO--> decrease BP • thrombus formation → ↑ risk of thromboemboli (because of blood be static and backed up) |
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heart block characteristics
|
partial or complete interruption in cardiac conduction system
i. in atria iii. bwn AV node and Purkinje fibers ii. bwn SA node and AV node iv. in ventricles |
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ECG changes and heart block
first degree |
- delay in conduction bwn atria and bundle of His
→ prolonged PR interval - P wave occurs for every QRS complex - P-P and R-R intervals are usually regular |
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second degree AV bolck
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second degree AV block
- intermittent failure of P wave conduction through the AV node → "missed" QRS complex - often expressed as conduction ratios (# P waves)/(# QRS complexes) |
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3rd degree AV block
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- complete interruption of AV node conduction
- SA node fires at same rate and ventricles beat at slower rate |
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what degree of heart block is this
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First degree
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what degree of av block is this
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second degree
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what degree of heart block is this
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thrid degree
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causes of heart block
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• structural defect in conduction pathway (usually AV node)
• ↑ vagal tone, transient AV nodal ischemia • drugs |
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more on second degree heart block
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some of the AP do not make it to the ventricles so do not always see a QRS
the QRS complex will not always be behind the p wave, but the atria are still driving the ventricles |
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more on third degree heart block
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complete block, ventricles and atria are doing their own thing
the atria are still driven by the sa node the ventricles are driven by something else |
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issues with heart block
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syncope in 3°
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ventricular tacycardia characteristics
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• rate ≈ 100 - 250 bpm
• commonly caused by re-entry in Purkinje fibers |
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ECG and ventricular tacycardia
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QRS complexes are: (different because starting at different locations)
i. abnormally broad ii. monomorphic or polymorphic iii. not consistently related to P waves |
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what is this ecg representative of? what is the ventricular rate?
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Ventricular tachycardia
300/1.6= 188 bpm regular rhythm so not fibrillation |
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ventricular fibrillation characteristics
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• disordered, rapid stimulation of ventricles
• caused by multiple wavelets of re-entry |
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causes of ventricular tachycardia
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• severely damaged myocardium (AMI, chronic IHD, cardiomyopathy)
• can occur in healthy individuals |
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issues with ventricular tachycardia
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• inefficient ventricular contraction → ↓CO → hypotension, loss of consciousness
• deterioration to ventricular fibrillation → sudden death |
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ECG and venrtricular fibrillation
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irregular waves of varying amplitude and morphology
no distinct QRS, ventricles are not beating in a cordinated fashion because of re-entry |
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causes of ventricular fibrillation
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causes
• severe heart disease • acute MI • electrolyte imbalance, hypoxemia, acidosis |
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issues with ventricular fibrillation
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• most life-threatening dysrhythmia
• ventricles do not contract in coordinated fashion → ↓↓↓CO if untreated → • long-term survival varies according to time and cause of V. fib i. occurs in first days of AMI → good survival (similar to patients where infarction not complicated by V. fib.) ii. occurs 2-3 wks after AMI → ↑ risk of sudden death iii. caused by chronic IHD without evidence of AMI → ↑ risk of sudden death |
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why do we shock the heart
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to depolarize all the cells at the same time
hope all cells recover at the same rate |
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torsades de pointes characteristicz
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• disordered contraction of ventricles
• caused by early afterdepolarizations in diseased tissues what sets a person up is a long QT interval (depolarization time is increased, so AP duration is increased) |
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ecg and torsades
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waves with continuously varying amplitudes → sinusoidal appearance
can see R waves but of continuous varying amplitudes |
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causes of torsades
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3° or advanced AV block
- precipitated by hypokalemia or hypomagnaesemia acquired long QT syndromes - antidysrhythmic drugs that prolong AP duration - psychotropic drugs - severe hypokalemia, subarachnoid bleeding, myxedema iii. congenital long QT syndromes - Jervell-Lange-Nielsen syndrome - Romano-Ward syndrome |
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issues with torsades
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• usually assymptomatic but may cause syncope
• may degenerate into ventricular fibrillation • untreated symptomatic congenital long QT syndrome patient → high mortality |
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what is this an ecg of
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torsades
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What is occurring in the myocardium during the ST segment?
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ventricles are fully depolarized there are no moving charges
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ST segment elevation
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transmural ischemia
commonly associated with variant angina |
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What determines ST elevation or depression
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the way the current is going
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is the ST segement actually altered
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no, there are changes around the St segment
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Q wave infarction
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- abnormal Q-wave
a. width (≥ 0.04s) b. height (> 25% of following R wave) ± T wave inversion (sign of ischemia) indicative of myocardial necrosis or fibrosis |
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picture of increase height of the Q wave (MI)
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picture of increased q wave and inversion of the T wave (MI)
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R has decreased in size
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picture of such a increased p wave there is no R wave
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non-q wave infarction
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- deep , symmetrical negative T waves
- ST segment depression - R wave reduction - positive Q wave |
