Cardiology Flashcards
1
Q
What coronary artery supplies what part of heart?
A
2
Q
What are the three categories of criteria for Duke’s?
A
Pathological
Major Clinical
Minor Clinical
3
Q
If _________of the pathological criteria are met, diagnosis is definite.
A
EITHER
4
Q
What are the two pathological criteria?
A
- Microorganisms in a vegetation - culture or histological exam of a vegetation or intracardiac abscess specimen
- Pathologic Lesions - Vegetation or intracardiac abscess confirmed by histologic exam showing active endocarditis.
5
Q
What are the two major clinical criteria?
A
- blood cultures positive for endocarditis - microorganisms consistent with IE from 2 separate cultures; single positive culture for Coxiella burnetti or antiphase IgG ab titer >1:800.
- Evidence of endoardial involvement - echo positive for IE, abscess, new valvular regurgitation, dehiscence of a prosthetic valve
6
Q
How many of the major clinical criteria do you need to make a diagnosis definite?
A
BOTH
7
Q
How many of the minor clinical criteria alone do you need to make the diagnosis definite?
A
All 5
8
Q
What are the 5 minor clinical criteria?
A
- predisposing heart condition or IV drug user
- Fever
- Vascular phenomenon -major arterial emboli; septic pulmonary infarcts; mycotic aneurysm; intracranial hemorrhage; conjunctival hemorrhages; Janeway’s lesions
- Immunologic Phenomena - glomurelonephritis, Osler’s nodes, Roth’s spots and rheumatoid factor.
- Micro evidence - positive blood culture that does not meet a major criterion or serological evidence of active infection with an organism consistent with IE.
9
Q
If you have one major criteria and one or two minor criteria, the diagnosis is __________?
A
Possible
10
Q
If you have one major criteria and three minor criteria, the diagnosis is ___________?
A
Definite
11
Q
What procedure should you do if Possible?
A
A TEE to see if you can make it definite
12
Q
IF you have three minor criteria, the diagnosis is ___________?
A
Possible
13
Q
What are Janeway lesions?
A
They are small, bruise-like spots on the palms of the hands and soles of the feet.
Osler’s nodes are similar but they are tender
14
Q
How much fluid is in the pericardium?
A
20-30 ml
15
Q
What is cardiac tamponade and how do you treat it?
A
When blood escapes from the heart due to injury, fills up the pericardium, thereby restricting the heart.
Pericardiocentsis: insert a needle in the left infrasternal angle toward the left shoulder in order to avoid puncturing the left lung, and remove excess pericardial fluid.
16
Q
What is the difference between a right dominant
and left dominant heart?
A
Right dominant (90%) the posterior descending artery PDA comes from the right coronary artery
Left dominant (10%) the posterior descending artery PDA comes from the circumflex branch of the left coronary artery
NOTE: the PDA runs along the atrioventricular groove
17
Q
What are the five great vessels of the heart?
A
Superior and Inferior Vena Cava
Pulmonary Artery and Vein
Aorta
(Note: from the aorta come the brachiocephalic, common carotid and subclavian arteries)
18
Q
What part of the cardiac cycle fills the coronary arteries?
A
Diastole
(During systole the huge flow of blood compresses the intramyocardial branches so that blood cannot get through to the coronary arteries.)
19
Q
What parts of the heart
do the left and right coronary arteries supply?
A
It can vary a bit from person to person, but…
Right coronary artery supplies the right atrium and most of the right ventricle, with some of the left atrium and ventricle.
Left coronary artery supplies all else, and notably the interventricular septum.
20
Q
What are the two branches of the left coronary artery?
A
Left Anterior Descending LAD
Circumflex Branch
21
Q
What is considered normal Ejection Fraction?
A
> 55%
22
Q
How does a cardiac CT work?
A
It is like a big 3D xray.
They use Gallium via IV for contrast, Metoprolol to decreases heart rate to decrease blurriness of image, dilate blood vessels to see better, and patient must hold breath for 10 seconds.
23
Q
What is a new development re Cardiac CT?
A
Prospective ECG Triggering: the CT is synched to your heartbeat so it only takes an image at diastole and this also minimizes the amount of radiation exposure.
24
Q
What are indications for Cardiac CT?
A
- Noninvasive anatomic assessment of CAD
- Evaluation of structure of heart
- Risk stratification using coronary calcium scoring
- Rapid evaluation re acute chest pain
25
What are the pros of Cardiac CT?
Very fast!
Newer developments have decreased radiation, amount of contrast needed, and enable 3-D rendering.
26
What are the cons or contraindications of Cardiac CT?
Radiation exposure
Patient must have BMI under 35
Patient must have GFR \>30 and if 30-45 must evaluate risk/benefit ratio
27
How does cardiac catheterization work
They thread a catheter through an artery in your leg or arm, through aorta and into the coronary arteries to take a look.
28
What are the indications of cardiac catheterization?
Gold standard re Dx of CAD
29
What are the cons of cardiac catheterization?
1/2000 risk of
death, MI, stroke or procedural complications
30
How does a cardiac MRI work?
It uses magnets to line up the spinning, angular momentum of protons and uses "math" to translate this into images.
31
What are the indications for Cardiac MRI?
Assess:
* Myocardial viability
* Cardiomyopathy
* Inflammation/myocarditis
* Congenital Heart Disease such as septal defects
* Cardiac Tumors
* Pericardium
* Great Vessels
32
What are Cons/Contraindications of Cardiac MRI?
Can cause nephrogenic systemic fibrosis if pt has moderate to mild kidney disease
Danger re metal objects, such as shrapnel in tissues or wheelchair in room.
(Orthopedic implants, stents and valves are usually safe though)
33
Who are prime candidates for noninvasive cardiac imaging?
Those patients in the middle in terms of pretest probability.
34
What are the Cons/Contraindications of ECHO
Not sensitive to small blockages
Need a trained technician
35
What do you know if your patient has a negative ETT and a negative SPECT?
Paitne has a 4-5 year "warranty" in the absense of new Sx
36
How many heart attack patients had LDL levels at NCEP goal?
75%
37
What are the chances a 40 yo will get CAD?
1 in 3 women
1 in 2 men
(1 in 8 women will get breast cancer)
38
What is the most dangerous part of coronary artery disease/atherosclerosis?
If it ruptures and creates a thrombus
39
What are the two types of vulnerable plaques?
Erosion prone
Critically Stenotic
40
What is Chronic Stable Angina?
Stable plaque causing ischemia due to an imbalance of supply and demand
41
Which population is especially at risk for Stable Angina?
Incidence in age groups 45-65 is far higher in African American women.
42
What re the Sx of Stable Angina?
1. Substernal or left chest pain/tightness/pressure/burning, lasting less than 3 minutes (sometimes up to 15)
2. That increases with physical activity, stress and/or a big meal, and
3. Decreases with rest, Nitro.
**Typical Angina** has all three
**Atypical** has 2 of 3
**Asymptomatic** has 1 of 3
NOTE: rarely will a patient refer to angina as "pain"
43
PE findings in Stable Angina
* Levine Sign (clenched fist to chest)
* PMI shifted to left
* Apical systolic murmur at mitral valve
44
Risk Factors/Hx re Stable Angina
Hyperlipidemia
Diabetes
Smoking
45
How do you diagnos Stable Angina?
Hx + Risk Factors + EKG
Then Exercise Tolerance Test for
* Every patient with "typical" angina
* Men \>40, women \>50 60 with atypical
46
What are the four classifications of Stable Angina?
Class 0: Asymptomatic
■ Class 1: Angina with **strenuous exercise**
■ Class 2: Angina with **moderate** exertion
■ Class 3: Angina with **mild** exertion
■ Class 4: Angina **at any level of physical exertion**
47
Stable Angina Rx
**Acute/Active**: a dose of Nitro
(.3,.4, .5 mg sublingual tablet or .4 mg buccal spray)
every 3-5 minutes up to 3 doses.
If no releif after 5 minutes call 911
**Chronic**: Long term Nitroglycerin (patch),
Calcium Channel Blockers or Beta Blockers
NOTE: Nitro can go through the skin so only the patient should handle it and should be seated. Blood pressure can drop suddenly.
48
What are predictors of the severity of Angina?
* # diseased vessels
* severity and location of obstruction (LAD is bad)
* Left Ventricular funtion
* Hx of arrhythmia
* Accelerating Angina (more frequent, more severe)
* Duke Treadmill Score
49
Secondary prevention of Stable Angina?
* Risk Modification (lower cholesterol and HTN, stop smoking, take statins, wt loss, exercise/cardiac rehab)
* Long acting nitrates
* Beta Blockers
* Calcium Channel Blockers
* Ranolazine
* Aspirin or clopidogrel (post PCI, post MI)
50
What patient education is needed about Stable Angina?
* Give prognosis and explain
* Lifestyle modifications
* Information about all meds
* Instructions on Nitro usage
* Importance of secondary prevention
* CPR for family members
* Resources: online or hard copy
51
What is follow up for a patient with Stable Angina?
Every 4-6 months 1st year, then annually.
EKG when change in Sx severity/frequency.
ETT every 1-3 years depending on risk category and/or change in Sx.
Inquire about:
1. Changes in physical activity
2. Changes in frequency/severity of angina
3. Adverse effects of Tx
4. Adherence to meds and lifestyle changes
5. Knowledge about CAD
6. Changes in comorbidities
52
The coronary arteries can compenstate for atherosclerosis until they are \_\_\_% occluded
75%
53
What is the **sequence** of atherosclerosis?
○ Fatty streak formation
○ Leukocyte recruitment
○ Macrophages → Foam cells
○ Development of lipid rich core
○ Accumulation of smooth muscle cells
○ Large atheroma with fibrous surface cap
54
What is the **progression** of atherosclerosis?
**Chronic**: slowly encroaches on lumen
**Acute**: suddenly encroaches on lumen due to plaque destabilization and clot formation.
55
What are the Coronary Artery Risk Factors?
Which are modifiable?
**Major Risk Factors:** Advanced age, Family history of CAD , Male gender, Hypertension Lipid abnormality, *Diabetes mellitus, Cigarette smoking*
**Other Risk Factors:** *Physical inactivity, Abdominal obesity, Emotional stress, Low intake of fruits and vegetables , Excessive alcohol intake*
***Modifiable in italics.***
56
What is the difference between
Ischemia, Injury and Infarction?
**Ischemia**: Insufficient blood flow, cytokine release ("pain"), tissue can survive
**Injury**: occurs with sustained ischemia, release of initial cardiac biomarkers,
**Infarction**: irreversible cell death and necrosis, decrease in cardiac funtion, release of later biomarkers
57
What are the EKG findings for
Ischemia, Injury and Infarction?
**Ischemia**: ST depression +/- T wave inversion
**Injury**: ST elevation +/- hyperacute T waves,
T wave inversions, new LBBB
**Infarction**: ST elevation +/- pathologic Q waves
(2.5 deep, 2 wide in 2 contiguous leads)
58
Who automatically gets and EKG?
Every patient with a Hx of chest pain
59
What are EKG indictions of current infarction or increased risk of infarction?
○ Evidence of ischemia, injury, or infarction
○ LV Hypertrophy → hypertension → increased risk for infarction
○ Atrial fibrillation → previous infarct vs. increased risk of infarction
○ Bundle Branch Blocks → if new LBBB, increased risk of infarction, masked ischemia, injury, and infarct
60
What can an ambulatory EKG/Holter Monitor tell you?
Paroxysmal dysrhythmias (SVT, Afib)
Periods of Ischemia (in conjuntion with angina journal, detecting silent ischemia) (NOT ideal for this)
61
What is the Duke Treadmill Score?
Assessment based on Bruce Protocol time in minutes, amount of ST depression on EKG, and degree of angina. Used for insurance purposes.
Low Risk \> or = +5
High risk: \< or = -11
62
What are the cons of a Nuclear Study (Myocardial Perfusion Scan)?
Takes 4 hours
Expensive so not all centers have it
Hard to read so inter-reader variability
63
What are the indications and risks of
Coronary Angiography?
Definitive Dx of CAD but...
Contraindictions: invasive, contrast media allergy/anaphylaxis, kidney damage
Thus: indicated ONLY if PTCA/stenting or CABG is a consideration
64
Which cardiac biomarkers appear first and how long do they last?
**Myoglobin** rises first and peaks at 5 hours
**Creatine Kinase** rises second and peaks at about 15 hours
**Troponin** rises slowly until about 15 hours, then shoots up and peaks at about 25 hours and declines slowly.
Note: these enzymes are not specific to MI, but WITH chest pain, they are!
65
What is Percutaneous Coronary Intervention PCI?
Stenting and angioplasty
to reduce Sx (Recently disproven by a double blind study with 200 pts)
NO improvement in lifespan
Metal stents can cause clots or inflammatory response
Drug Alluding Stents have endothelial cells growing on them so they are hidden from the immune system
66
What is Coronary Artery Bypass Grafting CABG?
Internal mammary or saphenous vein used to bypass occluded coronary arteries. Only done if multiple vessel disease.
Mortality: 1-8% depending on health of pt
Will add years to life
67
What are complications of PCI?
Intimal dissection
Stent thrombosis
MI (esp if not on anticoag)
68
What is accelerating angina?
Change in pattern such as
* Greater ease of provocation
* Longer episodes
* Greater severity
* Longer recovery
* More frequent use of Nitro
May be unstable angina or acute coronary syndrome such as MI.
69
What do you give in the office if you realize a patient is having a STEMI?
MONA:
Morphine, oxygen, Nitro. aspirin
70
What is a coronary vasospasm?
AKA Prinzmetal Angina
AKA Variant Angina
Atherosclerotic arteries plus parasympathetic innervation
leads to coronary **vasocontriction**
(usually parasympathetic leads to nitric oxide to vasodilation)
71
What are the risk factors for Coronary Vasospasm?
Smoking
Cocaine
Hyperventilation
Provocative Agents (ACh, Ergotovine, Histamine, Serotonin)
72
What are the Signs/Sx of Coronary Vasospasm? q
Typical Anginal Sx BUT
* Occur at REST, not exertion
* Perhaps only a small lesion (25%)
May also have CAD so may also have typical angina Sx
73
What is the treatment for acute Coronary Vasospasm?
* Treat as Acute Coronary Syndrome until R/O significant atherosclerosis: Nitro, Aspirin, Statins, +/- Heparin/Integrillin, Beta 1 selective beta blockers
* Avoid nonselective Beta Blockers re risk of unopposed alpha receptor mediated coronary vasoconstriction
* Monitor with serial biomarkers (Troponin, CK), telemetry until vasospasm ends.
74
How do you treat chronic Coronary Vasospasm?
Eliminate causes (smoking, cocaine)
Vasodilators: Calcium Channel Blockers
+/- Long acting Nitrates
75
What is heart failure?
* Inability of heart to pump at sufficient rate to meet needs without abnormally high filling pressure
* Abnormality of cardiac function and neurohormonal regulation
* Effort intolerance, fluid retention and reduced longevity
* Impairment of ventricles to fill with or to eject blood
76
How common is heart failure?
Prevalence: 1% of those 50-59, 10% of those 80+ in US
Incidence: 550K per year in US
Most common caudse of hospitalization in those 65+
(1/3 are readmitted in 6 mos, 24% in 1 mo)
50% 5-year mortality
77
What are some diseases that are risk factors for heart failure?
HTN, DM, Ischemia, CAD (most common), Valve Disease, Toxins (ETOH, chemo)
78
What are the three key problems
with heart failure and what causes each one?
1. Myocardial (pump) failure: myocardial loss, increased pressure/work load, increased volume load
2. LV inflow obstruction (filling problem): mitral stenosis, decrease LV compliance (eg concentric hypertrophy)
3. Increased cardiac output: due to acute (transfusions) or chronic (eg: anemia) volume overload
4. Other: thryrotoxicosis, arrhythmias
79
What are some ways of classifying heart failure?
Right vs Left Side
Systolic vs Diastolic
Acute vs Chronic
Compensated vs Decompensated
Dilated vs Hypertrophic vs Restrictive
High Output vs Low Output
80
What are the three key mechanisms of heart failure and what is their result?
1. Increased Preload (blood volume)
2. Increased Afterload (resistance)
3. Decreased Contractility
Leading to increased stroke volume
leading to cardiac remodeling.
81
What causes Increased Afterload?
Resistance in the arterial tree that the ventricle must overcome.
AKA: Systemic Vascular Resistance
82
What causes increased preload?
Total blood volume
Skeletal Muscle exercise (venous return)
Venous Tone (volume storage)
Intrapericardial pressure
Body Position
Intrathoracic pressure
Atrial Function (CHF, HTN, Aortic Stenosis)
83
What affects Contractility?
**Increased by:** # of cardiomyocytes, strength of stimulation (Ca++), Sympathetic impulses, Circulating catecholamines, Inotropic Agents (digoxin)
**Decreased by**: Cardiomyopathy (-), MI, Anoxia, Acidosis, Hypercapnia, Medications
84
How are the four classes of heart failure patients?
I: No Sx
II. Sx during ordinary activity
III. Sx during sligh activity
IV: Sx at rest
85
What are the four stages of heart failure?
A. Risk factors but not Sx
B. Structural changes but no Sx
C. Structural changes with Sx
D. Decompensated, end stage
86
What are the goals of treatment for heart failure?
Decrease Symptoms
Prevent/Slow disease progression
Increase survival
87
What are Hemodynamic Profiles?
A simple way of classifying patients
in order to guide treatment options.
Based on level of **perfusion** and level of **congestion/pressure**:
I. Normal (Dry and Warm)
II. Congestion (Wet and Warm)
III. Hypoperfusion (Dry and Cool)
IV. Hypoperfusion and Congestion (Wet and Cool)
88
What is Left Ventricular Failure?
When the left ventricle fails and fluid backs up into the **lungs**
**Sx:** SOB, DOE, tachypnea, rales, pulmonary edema,
orthopnea, paroxysmal noctural dyspnea,
S3, Mitral Regurgitation, fatigue
89
What is Right Ventricular Heart Failure?
When the right ventricle fails and fluid backs up into the **veins**/**body**.
Signs/Sx: increased JVP (FIRST SIGN!!),
pitting, dependent edema (legs, ankles, sacrum), ascites,
hepatomegaly and hepatojugular reflex sign
parasternal heave
nocturia
90
What causes Right Side Heart Failure?
1. Left Side Heart Failure
or
2. Pulmonary HTN or Pulm Stenosis --\> Cor Pulmonale
91
What are the two kinds of Left Ventricular Heart Failure?
1. Systolic (aka Heart Failure reduced Ejection Fraction - HFrEF)
2. Diastolic: (aka Heart Failure preserved Ejection Fraction HFpEF)
92
What is HFrEF?
**Systolic Heart Failure** = pump failure
More common in men
**Signs**: large, dilated heart, low ejection fraction, S3, Normal or low BP
**Tx:** Well established
93
What is HFpEF
**Diastolic Heart Failure** = filling problem
More common in post-menopausal women
**Signs:** Concentric LV hypertrophy leading to small LV cavity, HTN, normal/increased ejection fraction, S4
**Tx**: not well established
94
What is Acute Decompensated Heart Failure?
**When a heart failure patient gets rapidly worse due to:**
**Medications that worsen HF**: CCBs, BBs, NSAIDs, Antiarrhythmics, Anti-TNF antibodies,
**Other Changes that worsen HF**: Pregnancy, alcohol, increased HTN, acute valvular insufficiency, MI, ischemia, arrhythmia, infection (pneumonia), anemia, stopping HF Tx
NOTE: the point is that HF patients are very fragile
and can easily go downhill rapidly!
95
How do you diagnose Heart Failure?
**Signs/Sx**: elevated JVP, edema, rales, S3
**2D Echo with Doppler**: decreased LV ejection fraction, LV structural problems, other structural abnormalities (valves, pericardium, RV)
**CXR:** cardiomegaly (2/3 thoracic cage), pleural effusion, enlarged pulmonary artery, engorged upper lobe veins
96
What labs help with Heart Failure Dx?
* **Initial**: CBC, UA, electrolytes (Ca++, Mg++), BUN, Creatinine, Glucose, Lipid Panel, Liver Function, TSH (treatable ETX!), ANP/BNP (best re R/O)
* **Serial Monitoring**: Electrolytes and Renal
Also depending on your location and suspicion:
HIV, hemochromatosis, pheochromocytoma,
rheumatoid diseases, amyloidosis, Chagas
97
What is Invasive Hemodynamic Monitoring
and when is it used?
Threading a catheter up to the mitral valve to measure pressure.
**Used for:** respiratory distress, impaired perfusion, decreased systolic pressure, decreased renal function,
**persistent Sx despite Tx**
Consideration for revascularization or transplant
98
When is an endocardial biopsy called for?
If you suspect an inflammatory process
**and** it would change treatment.
(this is invasive)
99
What is the pharmacological Tx for Heart Failure?
For Sx, but do not decrease mortality:
* Inotropics: (to increase contractility): digoxin, sympathomimetics, phosphodiesterase inhibs
To decrease mortality:
* Vasodilators (decrease afterload): Nitro, ACEi, ARBs, Nitro, Hydralazine,
* Aldosterone inhibitors (spironolactone) (10%)
* Beta Blockers (carvedilol): effective for severe HF (30%+)
* Neprilysin Inhibitors (LCZ696) esp w ACEi (30%+)
* Ivabradine re I(f) channels in pacemaker cells
100
What are some nonpharmacologic treatments for HF?
Weight loss, exercise
biventricular pacemakers
ventricular assist devices as bridge to transplantation
heart transplant
hospice and palliative care
101
What happens during Phase 0 of the ventricular AP?
Na+ channels open
102
What happens during Phase 1 of the ventricular AP?
K1 channels open (between -90 mv and -50 mv)
Ca2+ channels open
103
What happens during Phase 2?
Na+ channels and Ca 2+ channels
| (Plateau)
104
CO X TPR =
BP
105
HR x SR =
CO
106
SV is proportional to ___ and \_\_\_\_\_?
contractility and preload
107
Preload is proportional to _______ and \_\_\_\_\_\_\_\_?
Venous tone and blood volume
108
76 yo Pt with mechanical mitral valve presents with new onset palpitations.
EKG shows irregular R-R intervals without a distinct P wave, along with fibrillatory waves
**Atrial Fibrillation**: irregularly irregular
Tx Goal: decrease progression, tachy-mediated cardiomyopathy
Tx:
* Beta Blockers,
* Aspirin, Warfarin or novel anticoags like Dabigitran;
* Antiarrhythmics (amiotarone) to prevent cardiomyopathy in younger patients.
* Chemical or electrical cardioversion
* Catheter ablation
109
30 yo man with new onset palpitations
ECHO: normal
EKG: irregularly irregular tachycardia with wide, variable QRS with Delta Wave
**Atrial Fibrillation with Pre-Excitation**
(due to accessory pathway)
Caution: can give rise to Vtach or Vfib
Tx:
* Stable: procainamide
* Unstable: electric or chemical (abutalide) cardioversion (60% success) and catheter ablation (95% success)
110
37 yo man with presyncope/fainting
EKG: PP interval is greater than 1.6 - 2 seconds and pause is not a multiple of PP interval
Sinus Pause (aka Sinus Arrest):
SA failure of automaticity followed by SA note impulse or escape rhythm
Note: can lead to tachy brady syndrome
ETX: genetic if younger, or aging to fibrosis to pause
TX: pacemaker
111
71 yo man with intermittent lightheadedness, syncope and palpitations
EKG: combination of bradyarrhythmia, tachyarrhythmia, sinus pauses, exit blocks and/or junctional escape rhythm
**Sick Sinus Syndrome** aka **Tachy Brady Syndrome**
ETX: SA node dysfunction seen in elderly
TX: monitoring if Sx (Holter, Zeopatch), pacemaker if syncope
112
76 y o woman with lightheadedness and weakness
EKG: regular RR interval, P waves are all over the place (before, during and after QRS), HR 40-60 bpm, QRS is narrow
**Juncional Escape Rhythm**
Rhythmn originating from the AV junction
**Risk Factors/ETX:** athletes with increased vagal tone, sick sinus, acute rheumatic fever, Lyme, digitalis, poast cardiac or valve surgery, isoproterenol IV, during MI
**Note:** Junctional rhythms can be brady \<40, accelerated 60-100, tachy \>60
113
55 y o man with prior A-fib ablation in hospital with palpitations
EKG: narrow complex tachycardia with P waves that all look different, isoelectric baseline, long R-P intervals, atrial rate of 100-240
**(multifocal) Atrial Tachycardia**
SVT originating in atria but outside SA node
**ETX:**
* **Unifocal:** Digitalis
* **Multifocal:** COPD, asthma due to hypoxia and irritation of SA node
114
57 yo man with new onset tachycardia
EKG: narrow and wide QRS,
long RR interval followed by short RR interval
**Atrial Tachycardia with Aberrancy**
Atrial Tach w wide QRS due to depolarization during long refractory period (refractory period influenced by rate and preceding cycle length)
**Ashman Phenomenon:** long R-R, then short R-R, then aberrant QRS waves
NOTE: can tell it is not Vtach because some of the QRS are narrow.
115
46 yo woman who drinks lots of coffee presents with sudden onset palpiations
EKG: Narrow complex tachycardia at 150 bpm with short RP interval (less than 1/2 R-R)
**AV Nodal Re-Entry Tachycardia AVNRT**
aka Supraventricular Tachy SVT
**ETX:** genetic abnormality having dual node pluse exposure + coffee/stress --\> PACs or PVCs --\> AV node loop
**Tx:**
* Acute: vagal maneuver + IV adenosine or diltiazam pill to stop AV node
* Recurrent: catheter ablation of slow pathway of dual node
116
50 yo woman with palpitations
EKG: narrow complex tachycardia
with inverted P wave in aVF, long R-P interval.
**AV Re-Entry Tachycardia AVRT**
Re-entrant tachicardia involving the AV node and an accessory pathway
* **Orthodromic**: narrow QRS with anterograde conduction via VA node and His-Perkinje system to ventricle
* **Antridromic:** wide QRS with anterograde conduction via a bypass tract and retrograde vis AV node
**TX:** interrupt AV nodal conduction to end tachy (diltiazem CCB or beta blocker) but with crashcart nearby bc can lead to Vfib via accessory pathway in 3/100.
117
48 yo woman with episodes of sustained tachycardia
EKG: normal P wave axis and morphology, short PR interval (
**Wolff-Parkinson-White** pattern
pre-excitation of ventricles by bypassing AV node
via Bundle of Kent accessory pathway
**Tx:** catheter ablation if Sx due to risk of sudden death
Can locate accessory tract based upon
where delta waves are seen on EKG
118
53 yo man with aortic stenosis
EKG: narrow complex tachycardia with regular R-R intervals and uniform sawtooth P waves (4:1 rato of P:R)
**Atrial Flutter**
Macro-re-entrant atrial tachycardia originating in the rightr atrium aroung the cavo-tricuspid isthmus
* **Typical/ Counterclockwise** (90%): Inverted F waves in inferior leads, everted in V1
* **Atypical/Clockwise** (10%): Everted F waves in inferior leads, inverted in V1
**Tx:** rate control and anticoags; Catheter ablatio in typical
Ratio of P:R tends to be 2:1 or 4:1
119
53 yo woman with non-ischemic cardiomyopathy
EKG: broad complex tachycardia \>100 bpm
**Ventricular Tachycardia**
Sustained (.30 sec) vs Non-sustained (3+ beats, \<30 secs)
**Tx:**
* **Stable** (re pulse, BP, Sx): amiodarone to control arrhythmia or lidocaine if CAD or cannot take amiodarone
* **Unstable:** defibrillation
120
57 yo ma with recent MI
EKG: polymorphic ventricular tachycardia with characteristic twisting beat-by-beat QRS changes
**Torsades de Pointes**
**ETX:** long QT (often caused by medications) + PVS (prolonged repolarization leads to early after depolarization EADs)
**Tx:**
* Avoid provocative agents (meds, ETOH, electrolytes)
* Suppress long QT using magnesium sulfate
* Emergency: defibrillation
121
598 yo alcoholic woman with hypocalcemia and hypomagnesemia
EKG: QTc interval \> 460 ms
**Long QT Interval**
QTc\>440 in men, 460 in women
ETX: genetic +/- hypocalcemia, hypothyroid, meducations (mathodone, haloperidol, etc)
TX:
* Low Risk of sudden death: avoid provocative agents
* Sx/Med risk: BB, Na+ channel blockers
* Hi risk: implanted cardio defibrillator (ICD)
122
66 yo man with CAD presents with syncope and collapse, BP = 0, unresponsive, no previous heart disease
EKG: chaotic, irregular waves without identifiable P, QRS or T
Amplitude decreases with duration (course to fine)
**Ventricular Fibrillation**
**ETX:** R on T PVC (at vulnerable period), baseball to the chest during T wave, often preceded by Vtach
**TX:** chest compressions and defribrillation with antiarrhythmics (amiodarone, lidocaine)
123
79 yo asymptomatic man comes into the office for a checkup.
EKG: Long PR (\>.2), every P followed by QRS, narrow QRS
**1st Degree AV Block**
Abnormal prolongation of PR interval
ETX: excess CCB or BB, age, AV or aortic valve surgery
TX: none
124
46 yo man with sleep apnea comes in for check up
EKG: progressive prolongation of PR interval along with shortening RR interval until P wave is blocked (no QRS)
**2nd Degree AV Block Mobitz Type I (Wenckebach)**
ETX: Digitalis, CCD, BB, AMI, Rheumatic Fever, Myocarditis, Sleep Apnea
TX: none
125
72 yo man with chest pain for 3 hours
EKG: sinus rhythm with intermittent nonconductant P waves and consistent PR interval, wide QRS
**2nd Degree AV Block: Mobitz II**
TX: pacemaker because it can turn into
3rd degree complete heart block or MI
126
89 yo woman with lightheadedness
EKG: two P waves for every QRS
**2:1 AV Block**
Cannot know whether it is 2nd degree type II or 3rd degree
127
63 yo woman presents with lightheadedness
EKG: complete absense of AV conduction resulting in independent atrial and ventricular rhythms, PR interval varies but PP and RR intervals are constant
**3rd Degree/Complete Heart Block**
ETX: Lyme (treatable!), infiltration (amyloid, sarcoid), digitalis, endocarditis, advanced hyperkalemia
TX: permanent pacemaker
128
What are the major complications associated with anticoagulant therapy?
Blow to the head
Cannot stop bleeding
Internal bleeding
129
What are the absolute contra-indications for anticoagulant therapy?
Intracranial bleeding
Severe active bleeds
Recent (\<72 hrs) surgery, especially eye, brain, spine
pregnancy or \<48 hrs post partum
malignant HTN
Esophageal varices
Severe Renal Disease
Thrombocytopenia
130
What are the three key types of cardiomyopathy?
DilatedHypertrophicRestrictive
131
What kind of cardiomyopathy involves increased left ventricular volume, decreased ejection fraction and systolic dysfunction?
Dilated Cardiomyopathy aka Congestive Heart Failure
132
What type of cardiomyopathy involves thick cardiac muscle, decreased ventricular volume and decreased compliance?
Hypertrophic Cardiomyopathy
133
What type of cardiomyopathy involves myocardial and/or pericardial stiffness and decreased compliance?
Restrictive Cardiomyopathy
134
What is the pathophysiology of dilated cardiomyopathy?
* **Genetic factors** which can lead to **DNA mutation** and **Altered immune system**
* **Viral infection** which can lead to **myocarditis**
* The above factors can lead to **altered myocardial function**
* Which leads to **dilated cardiomyopathy**
135
What are some causes of dilated cardiomyopathy?
* Idiopathic
* Infections such as myocarditis, coxsackie, parvo
* Ischemia: MI leading to scar tissue
* Toxins from alcohol, uremia, cobalt, chemo
* Peripartum (7th month of preg to 3 mos after)
* Metabolic Ds: Diabetes, Beriberi
* Arrhythmogenic RV Dysplasia
136
What are the Signs/Sx of dilated cardiomyopathy?
SOB and exercise intolerance, rales
tachycardia, S3, holosystolic murmur, JVD, displaced PMI, precordial heave
pallor, cyanosis, cachexia
ascites, hepatomegaly
Decreased cardiac output
137
What do you see on a CXR re dilated cardiomyopathy?
Bilateral pulmonary edema
Large heart silhouette
Enlarged ventricles
138
How do you treat dilated cardiomyopathy (CHF)?
Diuretics (Sx only, no increased survival)
Inotropes to increase contractility
ACEi and ARBs to decrease afterload to decrease work
Beta Blockers to increase LV systolic fcn and increase survival
Hydralazine + Nitrates for African Americans
NOTE: No beta blockers if in decompensated heart failure!!
139
What is hypertrophic cardiomyopathy?
Genetic form of hypertrophy of the heart
that is **without** an underlying cause.
Due to mutation of sarcomeric proteins
Prevalence: .26%
140
What is the most common cause
of sudden death in athletes?
Hypertrophic cardiomyopathy (44%)
141
How do you Dx hypertrophic cardiomyopathy?
Heart has thick muscle, decreased volume and decreased compliance
Myocardial fiber disarray
**Asymmetrical** LV hypertrophy (large **septum**)
LV outflow obstruction
142
What are the Signs/Sx of hypertrophic cardiomyopathy?
Often no Sx but FHx of sudden death at young age
Syncopy, chest pain, dyspnea
Prominent apical pulse
Grade 2/6 midsystolic murmur at left sternal border
Possible arrhythmia
143
What would you find in an Echocardiogram of
hypertrophic cardiomyopathy?
Thick muscle
Large septum
Tiny heart chamber
Possible valve problems
High velocity of blood
144
How do you treat hypertrophic cardiomyopathy?
NO inotropes or diuretics!
CCB and B blockers to increase size of ventricle and decrease obstruction
Septal myotomy/myectomy or nonsurgical septal ablation
Implanted defibrillator
145
What is the pathophysiology
of restrictive cardiomyopathy?
* Myocardial infiltration or hypertrophy leading to decrease myocardial compliance
* Pericardial effusion leading to increased intrapericardial pressure
* Pericardial constriction leading to decreased pericardial compliance
* All of the above leading to increased ventricular diastolic pressure
* Leading to elevated diastolic pressure and suboptimal ventricular filling
146
What are some causes of myocardial infiltration?
Idiopathic
Amyloidosis, Sarcoidosis
Fibrosis
Tumor(s)
Radiation
Heart transplant
147
What are two causes of pericardial stiffness?
Pericardial effusion
Pericardial constriction
148
How do myocardial infiltration and myocardial hypertrophy differ in terms of **voltage**?
Both conditions result in a large, stiff heart but...
**Myocardial hypertrophy** causes **high voltage** on an EKG (high amplitude) because the increased size is muscle
**Myocardial infiltration** causes **low voltage** because the increased size is due to infiltrates like sarcoid.
149
What is Tako-Tsubo Cardiomyopathy?
aka Broken Heart Syndrome
Temporary condition where the heart muscle is suddenly weakend or stunned resulting in apical ballooning
It is a form of stress cardiomyopathy
150
What are Epidemiology, Sx, Dx, Tx
of Tako-Tsubo Cardiomyopathy?
**Epidemiology**: 90% women, thought to be due to estrogen conversion to catecholamines and glucocorticoids
**Sx**: chest pain, SOB, collapse (palpitations, N/V)
**Dx**: EKG, blood test, angiogram, Echo, cardiac MRI
**Tx:** just monitor w serial echos
151
What are the ETX, Sx, Dx and Tx
of infectious myocarditis?
ETX: viruses, URI, Lyme
SX: SOB upon exertion 7-10 days post infection, nocturnal dyspnea, fatigue, palpitations, chest pain/pressure, edema, (lightheadedness, arrhythmias, loss of consciousness)
Can lead to **dilated cardiomyopathy**
DX: EKG, CXR, Echo, cardiac MRI, heart biopsy
Tx: rest, decreased salt, steriods,
If severe: pacemaker, defibrillation
152
What are the Signs/Sx, ETX and Tx of
Acute Pericarditis?
Signs/Sx: sudden onset, sharp, anterior chest pain (\<6 wks), worse with inspiration and coughing or lying down,
better if sit forward
Pericardial friction rub at Left sternal border ("squeaky")
ETX: idiopathic/viral (90%), CT dz (SLE), cancer
Tx: NSAIDs, colchicine, corticosteriods
Pericardiocentesis is severe
153
What are two complications of acute pericarditis?
Cardiac Tamonade
Constrictive Pericarditis
154
What are the ETX of
Pericardial Effusion?
ETX: idiopathic or infectious pericarditis, trauma,
neoplasm (breast, lung, lymphoma, melanoma),
metabolic dz (uremia, hemorrhagic states, myxedema)
problems from contiguous areas (aortic dissection, myocardial rupture, hemopericardium from anticoags)
155
What are the Sx, Dx and TX of
Pericardial Effusion?
Sx: chest pain/pressure
(Dyspnea, decreased BP and muffled heart sounds
if moving toward cardiac tamponade)
Dx: waterbottle sign (looks like a flask on CXR)
Tx: NSAIDs, colchicine, corticosteriods
Pericardiocentesis if severe
156
What is pericardial/cardiac tamponade?
Hemodynamic compromise of diastolic filling due to compressive intrapericardial pressue from pericardial effusion
157
What are the Sx, Etx, and Tx of cardiac tamponade?
Sx: **JVD, muffled heart sounds, decreased BP**
**pulsus paradoxus**, tachycardia, tachypnea,
patient looks terrified!
EKG: ST elevation on nearly every lead
CXR: HUGE pericardium
Echo: dark space around heart with collapsing chambers
Tx: pericardiocentesis
(or pericardiotomy/pericardial window or pericardiectomy)
158
What are some causes of constrictive pericarditis
aka pericardial constriction?
Idiopathic
Infectious (viral, TB)
CT diseases (RA, SLE, scleroderma)
Neoplasm: Primary (mesothelioma, sarcoma), or secondary
Trauma (penetrating or not)
Radiation
Post Pericardiotomy from CABG
Uremia
159
What are some Sx and Tx of Constrictive Pericarditis?
**Sx:** fatigue, dyspnea, JVD, ascites, peripheral edema, hepatomegaly, Kussmaul's sign, pleural effusion,
**pericardial knock**
EKG: low voltage
Chest CT: thick pericardium
CXR: pericardial calcification, small heart, pleural effusion
**Tx:** Pericardial stripping (entire pericardium removed)
160
What is bacterial/infective endocarditis?
Bacteria enter the blood stream
and settle in the heart lining, valves or blood vessels
Bacteria comes mainly from the mouth re poor dental hygeine
Acute: (days) sudden, life threat
Subacute/chronic: (months) less serious
161
What are Sx of bacterial endocarditis?
Fever, chills, night sweats, fatigue, tachycardia,
aching muscles and joints,
cough, pedal edema, ascites, weight loss, anemia
162
What are the risk factors for bacterial endocarditis?
Cardiac birth defects such malformed valves or septal defect
Valve surgery
Dental or medical procedures
Narcotics
163
What are the longterm sequelae of acute bacterial endocarditis?
Vegetations break loose and travel to the
brain, lungs, abdominal organs, kidneys, limbs
causing heart murmur, valve damage, HF,
stroke, seizure
PE, kidney damage, splenomegaly
paralysis
abscesses in heart, brain, lungs
Can cause **hypertrophic cardiomyopathy**
164
How do you treat bacterial endocarditis?
2-6 weeks of IV antibiotics!
165
What is the similarities and differences
between hypertrophic cardiomyopathy
and hypertensive heart disease?
Both: ventricular hypertrophy and decreased chamber size
Hypertrophic cardiomyopathy is genetic and causes asymmetrical hypertrophy with a large septum
Hypertensive heart disease is caused by long-standing hypertension and causes symmetrical hypertrophy. Associated with Heart Failure with preserved Ejection Fraction HFpEF
166
What is the difference between
intrinsic and extrinsic causes
of sinus node dysfunction?
**Intrinsic:** (problem within the heart )ideopathic, ischemic, infiltrative, inflammatory, CT disease, post op, genetic
**Extrinsic:** (problem outside of the heart, part of another system): medications, drugs, electrolyte imbalance, hypothyroid, neural reflexes, neural syncope, intracranial HTN, hypothermia
167
What is the resting membrane potential in cardomyocytes compared to pacemaker cells?
Cardiomyocytes: -90 mV
Pacemakers: -60 mV
168
What feature allows pacemaker cells to continually fire at a consistent rate?
If channel slowly leaks Na+ so it gradually increases from -60 resting membrane potential to -40 threshold at which point slow Ca++ channels open and begin to depolarize.
It is the If channels that are the "clock" that never stops ticking and keeps the pacemaker in a consistent loop.
169
What are the inherent rates of the SA node, AV node, and His-Purkinje system? Why are they different from one another?
SA node: 60-100
AV node: 40-60
His-Purkinje system: 30-40
They are different so that the AV node can serve as a back-up or fail-safe for the SA node
and the His-Purkinje as a backup for the AV node
170
What are the key mechanisms of arrhythmia?
Problems with A**utomaticity:**
* Abnormal impulse **formation**: more or less frequently than normal
* Abnormal impulse **conduction**: slowed or blocked such as in heart block
Problems with **Triggered Activity**
* **Early AfterDepolarization (EAD)**: think Long QT or Torsades
* **Delayed AfterDepolarization (DAD)**: think Digitalis or hypercalcemia
171
What are some causes of Bradycardia?
Failure of SA node
Conduction block (permanent or transient)
Uni or bidirectional
Drugs/medications
Ischemia
Fibrosis (eg: calcification in elderly)
Electrolyte imbalance (Na+, K+, Ca++)
Trauma
172
What mechanism causes Re-Entry Tachycardia?
1. **Two pathways**, either due to an accessory pathway or damage to atrial cardiomyocytes
2. Each pathway has **different electrical properties** pertaining to rate of depolarization and repolarization
3. One side is **momentarily blocked**
This creates a **continuous loop** and is the MOST important mechanism of tachy arrhythmias!
173
In a nutshell how do you treat Bradycardia?
Reverse the cause, such as fixing electrolyte imbalances
If this does not work, then pacemaker.
174
In a nutshell, how do you treat tachycardia?
Reverse the cause
Try vagal maneuvers to control SVT
Cardioversion/defibrillation
Medications
Catheter ablation
Implanted defibrillator
Surgery
175
What are two kinds of Superventricular Tachycardia SVT and how do they affect treatment?
Automatic: treat the cause
Re-Entrant: need to fix with meds, catheter, cardioversion
176
What forms of tachycardia do not require heart medications or treatment?
Automatic problems:
* **Sinus tachy**: it is normal to be tachycardic in response to pain, infection, blood less, etc. If you fix the problems (with pain meds, antibiotics, etc), the tachy stops
* **Atrial tachy and Multifocal Atrial Tachy (MAT)**: usually in response to hypoxia from lung disease. Treat the lungs and the tachy will stop.
* **Junctional Tachy:** usually due to ischemia, acid-base, electrolytes. Correct the problem and the tachy will stop.
177
What is the difference between **stable** and **unstable** tachycardia and how does that affect Tx?
**Stable**: no Sx, so you can take your time
**Unstable**: Serious Sx such as chest pain, altered mental status, hypotension, so do electrical cardioversion (defibrillation)
178
What is syncope?
A symtom, not a disease
Sudden temporary loss of consciousness, loss of postural tone, with variable onset (some with warning) and spontaneous, complete recovery.
Caused by abrupt reduction in cerebral blood flow.
1-6% of all hospital admissions
179
What affect does syncope have on a patient?
Anxiety
Decrease in activities of daily living
Driving restrictions
Loss or change of employment/profession
180
What are common causes of Syncope?
34%: unknown cause
24%: Neurally-Mediated (vasovagal, carotid sinus, situational)
11%: Orthostatic (drug induced, autonomic nervous system fail)
**14%: Cardiac Arrhythmia (brady, tachy, long QT)**
12%: Non-cardiovascular: psychogenic, metabolic, neurological
**4%: Structural Cardiac: (aortic stenosis, hypertrophic cardiomyopathy, pulm HTN, PE, tamonade)**
181
What are the more likely causes for younger patients as compared to older patients?
**Younger:** vasovagal, situational, psychiatric, genetic heart conditions such as Long QT, Brugada, WPW, hypertrophic cardiomyopathy
**Older:** mechanical or arrhythmic cardiac conditions, orthostatic hypotension, medications, neural, multifactorial
182
What is the most serious/deadly cause of syncope?
Cardiac
183
What are the key components of a workup for a patient with syncope?
Hx
PE
EKG
Echo
will be sufficient for 90% of patients
184
What is the relevant Hx for a patient with syncope?
Details of syncopal episode from pt and observers
Precipitating factors
Prodrome/warning signs
Duration and frequency of episodes
Recovery Sx
Cardiac Hx
FH of cardiac, syncope and sudden death
Medications (cause or clue to Dx)
185
What do you look for in terms of PE for a patient with syncope?
orthostatics
cardiac exam (re CHF, valves)
neuro exam
carotid sinus massage
186
How do you do carotid sinus massage test?
* Massage R carotid artery below the thyroid cartilage for 5-10 seconds
* Pause
* Massage the Left side
**Postive test** = 3 seconds of asystole or 50 mm Hg drop in BP
187
What might you look for on an EKG for a patient with syncope?
Brady or tachycardia
PR interval
Delta waves (WPW)
Long QT
**Patterns** re Brugada, Q waves, ST-T waves, Hypertrophic cardiomyopathy, ARVC, IVCD, Complete heart block
188
Why would you need an ambulatory EKG and what are some examples?
Unless you can get the patient to faint on command, you will need an ambulatory EKG to see what their heart is doing before/during syncope.
* Holter Monitor: 24-48 hours, good for frequent syncope
* Event Recorder: credit-card shaped item you press to your chest when you are feeling faint to capture the EKG.
* Implantable Loop Recorder (ILR): implantable under the skin, can last 3 years. Great for very infrequent syncope
* Zeopatch: like a bandaid on the chest to monitor for 14 days
189
What is a Head Up Tilt Test and how does it work?
When you go from laying down to standing, your sympathetic nerves fire initially, then your parasympathetic adjusts down. Some people's parasympathetic system adjusts too much.
The Tilt Test moves the patient back and forth from nearly vertical to nearly horizontal, reproducing the pre-syncopal Sx so the patient can learn how to recognize them and control the syncope using vagal maneuvers.
190
How do you know when to admit a patient with syncope?
Unless they have at least one of the following, you do not need to admit them:
* Hx of CHF
* Hct \< 30%
* EKG abnormal
* SOB
* Systolic BP \<90
191
List three types of permanent pacemakers
Pacemakers are names based on (1) what chamber(s) are paced, (2) which are sensed, and (3) what action it takes. (R) means the rate changes based on activity.
**DDD (R):** Dual chambers paced, sensed, and acted upon
**VVI (R)** ventricle paced and sensed, and pacing Inhibited if it senses a rhythm
**AAI (R)**: atrium paced and sensed, and pacing Inhibited if it senses a rhythm
192
What are the indications for pacing?
**Symtomatic Bradycardia**
1. HR \< 60
2. Symptoms: syncope, presyncope, SOB, chest pain, confusion, palpitations, CHF, exercise intolerance
3. Cause is not reversible
193
How do you decide whether the patient needs a single pacer or a dual pacer?
1. Can the atrium be paced or sensed?
2. Is there an AV block?
3. Is there chronotropic incompetence? (natural pacemakers do not raise heart rate when needed such as exercise)
**Examples:**
If everything is working fine except the patient cannot increase heart rate when needed, then atrial pacer needed.
If the atrial rate is meeting needs, but there is AV block then a dual pacer is needed (to sense SA and pace ventricles)
194
What is vasovagal syncope and what causes it?
Emotions and/or stress cause a drop in preload which causes decreased flow to the brain.
If the patient does not lie down quickly, they will faint, and will experience 24 hours of fatigue afterwards.
195
How do you treat vasovagal syncope?
Acute: recognize the predromal signs, lie down, elevate feet and do isometric exercises such as clenching fists.
Chronic: stay hydrated, avoid triggers, get regular exercise (preload), wear support hose (preload), eat salty foods (if young without HTN).
Rx: Midodrine, a short-acting alpha agonist
No pacemaker needed.
196
How do you treat a patient
with orthostatic hypotensive syncope?
Tell them to never lie down!
Typically they have high BP when lying down, but low BP when sitting or standing. If you give them HTN meds, their BP will be too low most the time. So stop the BP meds and get the to use a hospital-type bed at 45 degrees or elevate the head of the bed.
197
What is shock?
Circulatory failure
198
What is the cellular mechanism of shock?
1. Inadequate O2 delivery or utilization or too much consumption
2. Cellular/tissue hypoxia
3. cell membrane ion pump dysfunction -\> intracellular edema -. leakage to extracellular -\> inadequate regulation of pH
4. systemic acidosis, endothelial dysfunction, inflammatory cascade -\> ant-inflammatory cascade
5. Decreased tissue perfusion
199
What are the four key types of shock?
Distributive
Cardiogenic
Hypovolemic
Obstructive
(plus Combination)
200
Which forms of shock are primarily
due to decreased systemic vascular resistance?
Distributive Shock
201
Which forms of shock are primarily due to
decreased cardiac output?
Cardiogenic
(late) Hypovolemic
(late) Obstrucitve
202
What can cause shock (decreased perfusion) but with normal cardiac output and normal systemic vascular resistance ?
Carbon monoxide poisoning
Cyanide poisoning
Mitochondrial disease
203
What are the three stages of shock and what are they symptoms of each?
**Pre-shock** aka **Compensated Shock** aka **Cryptic Shock**:
SX: tachycardia, cool skin, hypotension
**Shock:** compensatory mechanisms inadequate
SX: tachycardia, dyspnea, restlessness, diaphoresis, N/V, thirst, pallor, narrow pulse pressure, decreased mental status, hypotension, oliguria, cool clammy skin
**Decompensated Shock** aka **End Organ Dysfunction**
SX: hypotension, anuria, labored irregular breathing, thready, weak or absent peripheral pulses, ashy/cyanotic skin, decreased body temp and mental status, dilated pupils
204
A patient has an infection and then develops signs and Sx of shock. What is the likely type of shock?
Septic
which is a kind of distributive shock
205
A patient suffering from severe aortic stenosis develops signs/Sx of shock. What type of shock is likely?
Mechanical Cardiogenic
206
A patient with the flu who has severe N/V/D for several days followed by shock Sx. Which is the likely type of shock?
Non-Hemorrhagic Hypovolemic
207
A patient develops trouble breathing after a long flight from Kenya, and then develops Sx of shock. Which type is likely?
Pulmonary Vascular Obstructive Shock
| (from a PE)
208
What type of shock is anaphylaxis?
Non-septic distributive shock
209
A patient has complete heart block and develops shock Sx. Which kind?
Arrhythmogenic Cardiogenic shock
210
A patient is in a car accident and develops pericardial tamonade and Sx of shock. Which kind?
Mechanical Obstructive
211
What is the pathophysiology of cardiogenic shock
caused by an MI as pertains to Systolic and Diastolic function?
**Systolic:**
* Decreased cardiac output and stroke volume -\> hypotension -\> decreased coronary perfusion -\> ischemia -\> progressive myocardial dysfunction -\> Death
* Decreased cardiac output and stroke volume -\> decreasesd systemic perfusion -\> compensatory vasoconstriction -\> progressive myocardial dysfunction
**Diastolic:**
* Increased LVEDP and pulmonary congestion -\> hypoxemia -\> ischemia -\> progressive myocardial dysfunction -\> Death
212
How do you work up a patient with shock?
* Cover your ABCs: airway, breathing, circulation
* Determine the underlying cause (may need tests)
* Initiate life-saving maneuvers re underlying cause (Chest tube for tension pneumothorax, Epinephrine for anaphylaxis, IV antibiotics for sepsis, coronary revascularization for MI, steriods for adrenal crisis)
* Once stable do focussed Hx and PE, general and targetted lab studies, plus possible Echo and pulmonary artery catheterization for definitive Dx and Tx
* Treat the cause (eg: steriods for adrenal crisis, IV ABX for sepsis)
*
213
What are some causes of cardiogenic shock?
Ischemia or MI
LV failure
Ventricular Septal Rupture
Papillary m or chordea t. rupture re severe mitral regurg
ventricular free wall rupture
214
How to you treat cardiogenic shock?
* **General:** ventilation, IV fluids, sodium bicarb re acidosis, aspirin, IV heparin, possible glycoprotein IIb/IIIa Inhib, possible insertion of pulmonary artery catheter
* **Specific**:
* **Meds**: sympathomimetic inotropes, Norepi
* **Revascularization**: PCI, CABG, thrombolytics
* **Mechanical**: intra-aortic balloon pump, left ventricular or biventricular assist device, percutaneous cardiopulmonary bypass
215
What is the 30-day survival rate for patients with cardiogenic shock?
about 50%
216
What are the Sx and ETX of orthostatic hypotension?
**Sx:** dizziness, blurred vision, weakness, syncope, confusion, nausea upon standing
**ETX:**
**Acute**: dehydration, prolonged bedrest, hypoglycemia, overheated, post-prandial
**Chronic**: heart problems (rate, valve, HF), endocrine (DM, thryroid, adrenal), regulation problems (neuro or baroreceptor)
217
How do you diagnose and treat orthostatic hypotension?
**Dx:** Orthostatic blood pressure testing, blood tests re anemia, hypoglycemia, EKG/Holter, Echo re structure, ETT, Tilt Table, Valsalva maneuver
**Tx**: depends on cause
* **Lifestyle** changes: hydration, less alcohol, more salt, elevate head of bed
* Compressive stockings
* **Medications**: fludrocortisone, midodrine
218
What is cardiogenic syncope?
Sudden drop in heart rate and BP causing fainting causes by cardiac arrhythmia or structural heart problem
219
What are the Sx of cardiogenic syncope
Fainting plus possibly:
Chest tightness
SOB
Sweating
Apprehension
Palpiation
220
Who is likely to get cardiogenic syncope?
Older patients with heart disease
221
How do you diagnose and treat cardiogenic syncope?
**Dx**: EKG, Holter or Event Recorder and possible electrophysioligy testing
**Tx:** depends on cause:
**Bradycardia**: pacemaker
**Tachycardia**: meds, ablation, implanted defribrillator
222
What is the definition of regurgitation/insufficiency of a heart valve?
leaking (backflow) across a closed valve
223
What is the definition of stenosis of a heart valve?
obstruction of forward flow across and opened valve
224
What are common etiologies of stenosis of heart valves?
rheumatic fever
congenital
degenerative
225
What are common causes of valvular regurgitation?
myocardial dysfunction (MI)
infective endocarditis
rheumatic
congenital
Marfan's
syphilis
anklyosing spondylitis
trauma
226
What is the most common cause of aortic stenosis?
age-related degenerative changes (calcification)
227
When you see the presentation of aortic stenosis in someone \<65, what is the most common developmental defect?
bicuspid aortic valve
228
What happens to the left ventricle as a result of aortic stenosis?
Left ventricular hypertrophy (earlier)
later, dilatation
then, CHF (left heart failure)
229
What is the survival at 2 years after the onset of symptoms in aortic stenosis?
50%
230
What is the definitve therapy for aortic stenosis?
valve replacement?
231
what are the pros and cons of mechanical heart valves?
last longer than bio (20-30 years)
requires chest-opening surgery and need anti-coags
232
What are the findings on physical exam for aortic stenosis?
* slow, diminished pulses
* single S2
* palpable systolic thrill
* harsh systolic ejection murmur (radiates to neck)
* forceful PMI
233
What are the findings on EKG in aortic stenosis?
left ventricular hypertrophy
234
What are the findings on chest x-ray in aortic stenosis?
aortic valve calcification
dilated aorta
normal or increased heart size
235
What is the most common cause of mitral stenosis?
rheumatic fever (50% \>20 years prior to presentation)
236
What conditions increase mitral valve flow and pressure?
* hypervolemia
* hyperthyroidism
* pregnancy
237
What are the key symptoms of mitral stenosis?
* fatigue on exertion
* dyspnea (on exertion at first)
* venous stasis in LA - strokes and clots forming
* LA and RV hypertrophy (dilatation late)
238
What are the signs of mitral stenosis on PE?
* RV lift
* loud S1 in mild
* quiet S1 in severe
* diastolic rumble at apex
* opening snap
239
What are the signs of mitral stenosis on ECG?
* normal sinus or a fib
* right ventricular hypertrophy
* left atrial enlargement
240
What are the signs of mitral stenosis on CXR and Echo?
left atrial enlargement and right ventricular dilatation
calcified mitral valve
241
What is the Rx for mitral stenosis?
* diuretics
* If in A fib: rate control and anticoagulation
242
What happens to the heart to compensate in mitral regurgitation?
LV dilates to increase total stroke volume, compensating for "backward" flow through the incompetent valve.
243
What can cause acute mitral regurgitation?
* reputure of the chordae tendinae due to acute MI or endocarditis
244
What is the end result of mitral regurgitation if untreated?
left heart failure (due to dilatation of the LV)
245
What is the Rx for mitral regurgitation
diuretics
valve repair/replacement
246
What is a surgical repair of mitral regurgitation called and what does it do?
annuloplasty and it shores up edges of leaflet so it closes during systole
247
What are the PE findings with mitral regurgitation?
pansystolic murmur and an S3 gallop
248
What are the ECG findings with mitral regurgitation?
LVH and LA dilatation
249
What are the findings on CXR and Echo in mitral regurgitation?
CXR - cardiomegaly
Echo - dilated LV, LA, MVP, ruptured chord, vegetation, thickening
250
What extra heart sounds do you hear in mitral valve prolapse?
midsystolic click and late systolic murmur
251
What happens to the heart as a result of aortic regurgitation?
the LV gets volume overloaded and dilates
252
What happens to the entire CV system as a result of aortic regurgitation?
* Peripheral vasodilation to minimize pressure and regurgitation
* low arterial diastolic pressure
* increased systolic pressure
* widened pulse pressure as a result of above
253
What are the signs of aortic regurgitation on PE?
* bounding pulses
* wide pulse pressure
* diastolic blowing murmur, diastolic rumble
* systolic ejection murmur
254
What are the signs of aortic regurgitation on ECG?
LVH
255
What are the signs of aortic regurgitation on CXR/Echo?
LV dilatation
aortic root dilatation
dilated LV, valve thickening, vegetation, dilated aorta
diastolic fluttering of the MV
256
Why is nitro contraindicated in severe aortic stenosis?
Patients with severe aortic stenosis already have a reduced cardiac output and LV strain, from trying to push blood through the narrowed valve to the circulation. Nitro will produce venous dilation, reducing preload and further reducing cardiac output through the narrowed valve. In addition it will reduce coronary artery filling.
Main problems are syncope and angina.
257
What are additional problems, other than aortic stenosis, of a congenital bicuspid valve?
* Bicuspid aortic valves also put patients at increased risk for aortic enlargement and dissection and are associated with coarctation of the aorta.
258
What is the most common cause of tricuspid stenosis?
rheumatic heart disease
259
What are the symptoms aortic stenosis?
* angina
* syncope
* heart failure
(ordered from least to most severe)
NB: People are typically asymptomatic for a long time
260
What are the two most common causes of acute **aortic** regurgitation?
* aortic dissection
* endocarditis
261
what are the symptoms of tricuspid stenosis?
usually occurs with mitral valve disorders, so hard to distinguish
edema and ascites with normal RV function
262
What are some of the PE findings with tricuspid stenosis?
* prominent a wave on inspection of jugular venous pulsations.
* An opening snap may be audible.
* A soft diastolic-flow rumble may be identified by placing the bell of a stethoscope at the right parasternal border but may be inaudible.
* The key to distinguishing murmurs of right-sided origin is the respiratory variation in intensity, which augments with inspiration.
263
What is the Rx for tricuspid stenosis?
Diuretics, but you get increasing fatigue and dyspnea
264
How common is pulmonary valve stenosis/regurgitation?
Rare - usually identified in childhood and results from congenital disorders (Noonan's Syndrome)
265
What physical exam findings might you see with pulmonary stenosis/regurgitation?
RV lift
and a diastolic decrescendo murmur
266
What is the most common congential heart defect?
VSD
(also believed 1/2 of these repair themselves and never come to medical attention)
267
What is an atrial septal defect?
persistent opening in the interatrial septum after birth that allows for direct communication between the l. and r. atria
268
What is the prevalence of ASD?
1:1500 live births
10% of all congenital heart disease
269
What is the consequence of an ASD?
blood ordinary shunted from left--\>right
volume overload in right atrium
270
What is Einsemenger Syndrome?
When a shunt that was formerly left-to-right becomes right-to-left
271
What is the common presentation for ASD?
* May be asymptomatic
* DOE
* Fatigue
* Recurrent lower respiratory tract infections
272
What are the exam/test findings with ASD?
RV heave along LSB
S2 wide, fixed splitting
murmur is mid-systolic left USB
cardiac cath - measures higher O2 in right atria
echo - shows shunt on doppler
273
Rx for ASD?
Surgical-
* direct suture closure
* pericardial or synth patch
* percutaneous apporahc with septal occluder device
274
How prevalent is VSD?
1.5-3.5:1000 live births
275
How do you diagnose VSD?
echocardiography
276
What are the symptoms and signs of VSD?
* depends upon the size of the defect ranges from no symp. to heart failure
* harsh, holosystolic murmur along LSB
* systolic thrill
* if reversed shunt, cyanosis and dyspnea
277
What is the Rx for VSD?
* 1/2 close spontaneously by age 2
* closure indicated with s/sx of CHF or pulmonary vascular disease
* same as ASD methods for closure
278
What is the tetraology of Fallot?
4 Defects:
1. VSD
2. pulmonic stenosis
3. overridng aorta (communicates with right ventricle through VSD)
4. RVH
279
How common is tetralogy of Fallot?
Pretty rare: 5:10k live births
but most common cyanotic heart disease in childhood
280
What are the s/sx of tetralogy of Fallot?
* "Tet" Spells - hyperventilation, cyanosis, syncope and squatting after exertion, feeding, crying
* dyspnea on exertion
* mild cyanosis and clubbing
* RV heave
* systolic ejection murmur at left USB
281
What is the Rx for tetralogy of Fallot?
surgery-close VSD and increase pulmonary artery width
\*if necessary, temporarily create connection between aorta and pulmonary artery to reduce hypertension
282
What is transposition of the great vessels?
aorta arises from the RV
pulmonary artery arises from the LV
so, aorta pumps deoxygenated blood and the pulmonary artery carries oxygenated blood to the heart
283
What is the prevelence of transposition of the great vessels?
40:100k births (7% congenital)
most common neonatal cyanosis
284
What are the s/sx of transposition of the great vessels?
blue baby - extremely hypoxic and cyanotic
285
How do you diagnose transposition of the great vessels?
echocardiogram
286
What is the Rx for transposition of the great vessels?
arterial switch surgery is definitive
until that can occur, use prostaglandins to keep ductus arteriosis open (only way to get some oxygenated blood circulating)
287
Who still gets pre-dental/surgical antibiotic prophylaxis with congenital heart disease?
unreparid cyanotic heart disease
post-repair for six months
post-repair with residual defects
288
What is coarctation of the aorta?
narrowing of the aortic lumen
(can be postductal -98% or preductal - 2% for the DA)
289
how common is coarctation of the aorta?
1:6k live births
290
What are the s/sx of coarctation of the aorta?
* most asymptomatic, but severe will be evident in a newborn
* preductal has cyanosis in LE
* femoral pulses weak and delayed
* midsystolic murmur
* elevated UE BP
