Step Up to medicine - Cardiovascular Flashcards by Dahveed Topher

stable angina pectoris is due to __________ narrowing of _________ vessels

fixed

atherosclerotic

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what are the top 5 risk factors for stable angina pectoris

DM
HLD
HTN
Cigarette smoking
age
FHx

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what are the two prognostic indicators for CAD

Left ventricular function

vessels involved

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which of the vessels involved in CAD purports the worst prognosiss

left main

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T/F multiple vessel disease is worse that single vessel

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T/F ischemic pain changes with changes in body positioning and breathing

F ( does not change with these changes, these would indicate a different pathology for the pain)

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Any combination of Hypercholesterolemia
Hypertriglyceridemia impaired glucose tolerance
diabetes hyperuricemia
HTN
Key underlying factor is insulin resistance

Metabolic syndrome X

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exertional angina with normal coronary arteriogram

exercise testing and nuclear imaging show evidence of myocardial ischemia

syndrome X

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T/F physical exam in patients with CAD is often normal

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what is the typical outcome of resting ecg in patients with stable angina

normal

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Q waves present on resting ECG indicate

prior MI

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how does the diagnosis of angina change with presence of ST elevations or segmeental changes

unstable

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useful test for patients with an intermediate pretest probability of CAD based upon age gender and symptoms

stress test

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quick and dirty method for finding a persons maximum HR

220 - age

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patients with a positive stress test should undergo

cardiac cath

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what is the parameter by which a stress test is considered postive

ST segment depression
ventricular arrhythmia
hypotension

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stress test is 75% sensitive if patients can complete what task during the test

increase HR to 85% maximum

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when is the echo performed in stress echo

after exercise

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patients with a positive stress echo should undergo

cardiac cath

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what cardiac pathology does not allow radioactive testing in cardiac workup

left bundle branch block

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what should be done in cardiac workup if patient cannot exercise

pharmacologic testing

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how do IV adenosine and dipyramidole work with pharmacologic testing

cause coronary vasodilation which means that the vessels supplying ischemic portions of the heart are already maximally dilated therefore the shunting of blood to the areas of the heart in which the vessels still have vasodilatory capacity will lead to ischemic changes in the vessels that supply ischemic portions of the heart

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how does dobutamine work in pharmacologic testing in cardiac workup

increases HR, strength of contraction, increases BP

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can be useful for detecting silent ischemic, arrhythmias, heart rate variability and assess pacemaker/ ICD function

holter monitoring

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useful testing for unexplained dizziness and syncope if cardiovascular cause suspected

holter monitoring

definitive test for CAD

cardiac catheterization

most accurate test for detecting CAD

cardiac angiography

if CAD is severe typically with three vessel disease what should be done

surgical (CABG) repair

what medication is commonly employed in lowering cholesterol and decrease risk for CAD

statins (HMG CoA reductase inhibitors)

what types of fats should be avoided in patients with CAD

saturated

what medical therapy is indicated for all patients with CAD

aspirin

first line therapy that has been shown to decrease the number of coronary events in patients with CAD

beta blocker

relieve angina by reducing preload myocardial O2 demand | VERY COMMON

nitrates

medical therapy that induces coronary vasodilation and afterload reduction

calcium channel blockers

If CHF is present in patients with CAD then what two medications can be added on to the typical therapeutic options of aspirin beta blockers and CCbs

diuretics and ACE inhibitors

Mild disease normal EF mild angina single vessel what should be done in terms of management on top of aspirin therapy

beta blockers and nitrates consider CCBs if symptoms persist

normal EF moderate angina and two vessel disease

coronary angiography to assess for revascularization

decreased EF severe angina three vessel of left main or LAD disease

angiography to consider CABG

T/F oxygen demand is increased in unstable agina

F (only the supply is diminished)

significant because it indicates stenosis that has enlarged via throbosis hemorrhage or plaque rupture

unstable angina

chronic angina with increasing frequency duration or intensity of chest pain new onset that is severe and worsening angina at rest

unstable angina

what is the only test that determines the difference between unstable angina and NSTEMI

cardiac enzymes

in what order should testing and management be carried out in patients with unstable angina

medically stabilize symptoms first before stress testing or angiography to assess for two/three vessel disease

patients with unstable angina should undergo what global management in terms of placement, nuts and bolts medical management

admission to hospital for continuous cardiac enzyme monitoring establish IV access and give 2L fluids initially give supplemental oxygen control pain with nitrates and morphine

what is the aggressive medical management employed in a patient with unstable angina

``` supplemental oxygen IV fluid resuscitation beta blockers (if no contraindications) aspirin/clopidogrel LMWH nitrates K+ and Mg+ replacement (to avoid arrhythmia) ```

duration of aspirin and clopidogrel dual therapy in patients presenting with unstable angina

9 to 12 months

PERCENTAGE of patients that recover following initial aggressive medical management in the case of unstable angina

90%

what should be done in the management of a patient with USA that responds to initial medical management

stress ECG to assess need for catheerization

what is the immediate management in an individual that fails initial medical management in the setting of USA

immediately proceed to the cath lab

what is continued following acute treatment of USA

aspirin beta blockers and nitrate

what are the two beta blockers typically employed in the treatment of USA

metoprolol and atenolol

on top of continuing medical management what should be done in individuals with USA following acute treatment

reduce risk factors smoking cessation treat DM HTN HLD

t/F following USA a patient should be started on statin regardless of LDL level

transient ST segment elevation classically occuring at night associated with ventricular dysrhythmia

prinzmetal (variant) angina

what two medications are proven helpful with variant angina

CCBs and nitrates (those that vasodilate)

due to necrosis of myocardium as a result of an interruption of blood supply

most cases of MI are due to

acute coronary thrombosis

mortality rate associated with MI

30%

what are the two medications that are utilized in the coronary angiography when looking for variant angina

ergonovine or acetylcholine

intense substernal pressure sensation radiation to neck jaw arms back pain typically unresponsive to nitro epigastric discomfort

T/F MI can be asymptomatic in up to one third of patients

painless infarcts or atypical MI more likely in these 4 demographics

women postoperative elderly diabetics

less common symptoms of MI

``` dyspnea diaphoresis weakness fatigues nausea vomiting snese of impending doom syncope ```

very early sign of MI that is often missed

peaked T waves

ECG sign indivating transmural injury and diagnostic of acute infarct

ST segment elevation

evidence for necrosis usually seen late and typically absent acutely

Q waves

T/F T wave inversion is specific for MI

F (sensitive not specific)

ECG finding associated with subendocardial ischemia

ST segment depression

currently the diagnostic gold standard for MI versus USA

cardiac enzymes

time period over which troponins return to normal

5-14 days

when do troponins reach their peak

24-48 hours

what is the utility of CKMB enzymes

reinfarction measurement

PROVE IT TIMI 22 trial proved starting this agent should be part of maintenance therapy in MI management

statin (specifically atorvastatin 80mg)

what are the 7 agents that should be initiated in the acute treatment of MI

``` morphine oxygen nitrates aspirin ace inhibitor statin heparin ```

this ultimate treatment should be incorporated to the treatment of all patients being managed for acute MI

revascularization ASAP

what is the time period in which revascularization should be attempted in any patient presenting with acute MI

within 90 minutes

this outcome occurs with rupture of papillary muscle infarction ischemia

mitral regurg

length of time with which patients receiving a bare metal stent should be on dual platelet therapy

one month

how long should a patient be on dual platelet therapy following the placement of drug eluting stents

12 months

what is the most common cuase of inhospital mortality following MI

CHF

what is the treatment for PVCs following acute MI

conservative management (no need for antiarrhythmic agent)

what should be done in a stable patient that shows VTach that is sustained

IV amio

what should be done in an unstable patient that shows Vtach that is sustain

electrical cardioversion

what is the treatment for vfib following MI

immediate desynchronized defibrillation and CPR

sinus bradycardia management in the setting of acute MI

observation | if severe atropine may be helpful in increasing HR

asystole management in the setting of acute MI

elecrtrical defibrillation if thought to be 2/2 VFIB | transcutaneous pacing if asystole is clearly the cause

what is the typical cause for AV block in the setting of MI

infarction of the conduction tracts

second or third degree block has a terrible prognosis in the setting of what type of MI

what should be done in second or third degree heart block in the setting of anterior MI

temporary pacing (transcutaneous or transvenous)

initial management for heart block secondary to inferior MI

atropine

treatment for heart block 2/2 inferior MI that is refractory to initial treatment with atropine

pacemaker

T/F recurrent infarction is not as bad in prognosis as initial MIA

F (worse in both acute and long term prognosis)

catastrophic mechanical complication of MI that occurs within the first TWO WEEKS after MI

free wall rupture | usually within the first 1-4 days

what are the usual immediate complications of free wall rupture

hemopericardium and cardiac tamponade

what is the immediate treatment for free wall rupture

hemodynamic stabilization pericardiocentesis surgical repair

T/F interventricular septal rupture following MI is typically worse in prognosis than frree wall rupture

F (better prognostically)

what is the indication for interventricular septal rupture following MI

emergent surgery

time table for interventricular septal rupture following MI

within 10 days

new onset MR folloiwng MI cause

papillary muscle rupture

what is the immediate indication for new onset MR following MI

echo

what is the treatment for papillary muscle rupture

surgical (mitral valve replacement typically)

why are ventricular pseudoaneurysms considered surgical emergencies

tend to become free wall ruptures if left alone

acute pericarditis secondary to MI typically treated with

aspirin

what medications are contraindicated in the case of acute pericarditis following MI

NSAIDs

Immunologically based syndrome consisting of fever malaise pericarditis leukocytosis and pleuritis occuring weeks to months after an MI

dressler syndrome

what is the most effective therapy for dressler syndrome

aspirin Ibuprofen is a good secondary choice

6 main causes/systems leading to chest pain

``` Cardiac Pulmonary GI Chest wall psychiatric cocaine ```

Heart pericardium vascular causes for chest pain

stable angina USA variant angina MI Pericarditis Aortic dissection

Pulmonary causes for chest pain (3)

pulmonary embolism PNA status asthmaticus

GI causes for chest pain (4)

GERD diffuse esophageal spasm peptic ulcer disease esophageal rupture

Chest wall causes for chest pain (5)

``` costochondritis muscle strain rib fracture herpes zoster thoracic outlet syndrome ```

3 main psych causes for chest pain

anxiety panic attacks somatization

3 tests that are obtained for practically all patients presenting with chest pain

ECG troponins chest xray

clinical syndrome resulting from the hearts inability to meet the body's circulatory demands under normal physiologic conditions

CHF

what are the two most common causes for systolic CHF dysfunction

HTN and ischemia (MI)(

echocardiogram showing impaired relaxation of the left ventricle

diastolic dysfunction

which form of CHF is most common

systolic (HTN AND ISCHEMIA MUCH MORE COMMON PATHOLOGIES)

most common cause of diastolic CHF

HTN leading to hypertrophy of myocardium

aoritc stenosis mitral stenosis and aortic regurg cause what form of CHF

diastolic

``` dyspnea orthopnea paroxysmal nocturnal dyspnea nocturnal cough confusion and memory impairment in advanced forms diaphoresis and cool extremities at rest ```

CHF

difficulty breathing in the recumbent position relieved by elecation of the head with pillows

orthopnea

rapid filling phase into a noncompliant left ventricular chamber leads to what pathologic heart sound

S3 heard best in what position

apex with the bell of the stethoscope

S3 occurs at what phase in the cardiac cycle

following S2

how to remember S3 S4 and their place in the cardiac cycle

4 is more than 3 tennessee has more letters than kentucky TEN-nes-see relates S4 prior to S1 ken-tuck-Y relates S3 following S2

crackles and rales at the bases of the lungs in CHF indicates what pathologic process

pulmonary edema 2/2 fluid spilling into the alveoli

dullness to percussion and decreased tactile fremitus of the lower lung fields is a sign of

pleural effusion

``` peripheral pitting edema nocturia JVD hepatomegaly ascites right ventricular heave ``` all signs of what sidded HF

rightr

T/F given enough time left sided HF will always lead to right sided HF

short horizontal lines near periphery of the lung near the costophrenic angles and indicate pulmonary congestion secondary to dilation of pulmonary lymphatic vessels

kerley B lines

prominent interstitial markings and pleural effusion a sign of what on CXR

CHF

what is the initial test of choice in suspected CHF

transthoracic echo

what is the importance of obtaining a TTE in the diagnosis of CHF

gives us the EF

cutoff for preserved left ventricular function in patients treated for CHF

>40%

T/F ECG is often very helpful in CHF diagnosis

F (not particularly unless there is a component of MI or USA)

consider this test to rule out CAD as an underlying cause for CHF

coronary angiography

test used to assess dynamic response of HR heart rhythm and BP in the setting of CHF

stress testing

conservative management of systolic dysfunction of CHF

``` sodium restriction water restriction smoking cessation weight loss etoh decrease ```

most effective means of providing symptomatic relief to patients with moderate to severe CHF recommended for patients with systolic failure and volume overload

diuretic

T/F diuretics improve mortality in patients with CHF

F (not been shown)

most potent diuretic that is usually used

lasix

lasix is what type of diuretic

loop

HCTZ is what type of diuretic

thiazide

T/F spironolactone has been shown to have survival benefits in patients with CHRF

spironolactone used in what types of CHF

advanced forms

which aldosterone antagonist does not cause gynecomastia

eplerenone

usual initial treatment for symptomatic CHF patients

ACE inhibitor and diuretic

T/F ACE inhibitors have reduced mortality benefit

CONSENSUS and SOLVD trials proved what point

ACE inhibitors reduce mortality in patients with CHF

T/F all patients with CHF should be on a ACE inhibitor regardless of symptomatology

ACE inhibitors should be started at a low dose to avoid

hypotension

patients that experience dry cough with ACE inhibitors can be switched to what type of medication

ARBs (-sartans)

beta blockers are shown to decrease mortality in CHF for what specific patient demographic

post MI CHF

stable patients with mild to moderate CHF should be given

beta blockers

what are the three beta blockers known to be safe in CHF

metoprolol bisoprolol carvedilol

useful agent in patients with EF <40%, severe CHF or severe Afib

digitalis

typically employed for patients with refractory symptoms despite being on diuretic ACE inhibitor and aldosterone antagonist

digitalis

two medications commonly employed in patients who cannot tolerate ACE inhibitors

hydralazine and isosorbide dinitrates

4 medication types that are contraindicated in CHF

metformin (can cause lethal lactic acidosis) thiazolidinediones (fluid retention) NSAIDs increase risk of CHF exacerbation negative inotropic antiarrhythmics

what are the medications that reduce mortality in diastolic heart failure

none

what are the two devices that shown to reduce mortality in select patients

ICD prevents SCD

indicated for patients at least 40 days poist MI EF,35% and class II or III symptoms despite optimal medicla treatment

ICD

biventricular pacemaker in patients with QRS >120 ms

CRT

T/F most patients that meet criteria for CRT are also candidates for ICD and receive combined devices

last alternative if all else fails in CHF management

heart transplant

acute dyspnea associated with elevated left sided filling pressures with or without pulmonary edema

acute decompensated HF

what are the two most common causes for acute decomp HF

LH systolic or diastolic dysfunction

severe form of HF with rapid accumulation of fluid in the lungs

flash pulmonary edema

DIFFERENTIAL FOR RAPID RESPIRATORY DISTRESS

PULMONARY EMBOLISM ASTHMA pna AND FLASH PULMONARY EDEMA

diagnostic tests for an individual with flash pulmonary edema

``` chest xray ecg ABG BNP echo coronary angio (possibly) ```

what is the management of a patient with acute pulmonary (flash) edema

oxygenation and ventilation assistance diuretics dietary sodium restriction nitrates

present in 50% of adults who undergo holter monitoring and mean nothing in a healthy heart

PACs

what is the treatment for asymptomatic PACs

usually just observation

what is the treatment for symptomatic PACs (palpitations)

beta blockers

causes for PVCs

``` hypoxia electrolyte abnormalities stimulants caffeine medications structural heart disease ```

why is the QRS wider in PVCs than with regular electrical activity of the heart

through the ventricular muscle and not the conduction pathways, therefore takes a longer time

patients with frequent repetitive PVCs and underlying heart disease are at increased risk for

sudden death (Vfib etc)

what test should be ordered in patients with PVCs and underlying structural or physiologic heart disease

electrophysiology test (may benefit from ICD)

multiple foci in the atria firing continuously in a chaotic pattern causing a totally irregular rapid ventricular rate

atrial fib

atrial rate in afib is usually over ______bpm but are blocked at the AV node so ventricular rate ranges between ___ and ____

400 75 175

T/F PVCs in patients with normal hearts is associated with increased mortality

what are the causes for afib (9) (double H triple S triple P E)

1. Heart disease: CAD, MI, HTN, mitral valve disease 2. Pericarditis and pericardial trauma (e.g., surgery) 3. Pulmonary disease, including PE 4. Hyperthyroidism or hypothyroidism 5. Systemic illness (e.g., sepsis, malignancy 6. Stress (e.g., postoperative) 7. Excessive alcohol intake (“holiday heart syndrome”) 8. Sick sinus syndrome 9. Pheochromocytoma

acute hemodynamically unstable afib treatment

immediate cardioversion

acute afib in a hemodynamically stable patient

rate control (60-100bpm) beta blockers CCBs (alternatively)

delivery of a shock that is in synchrony with the QRS

cardioversion

delivery of shock that is NOT in conjunction with the QRS complex

defibrillation

if left ventricular dysfunction is present in the setting of afib what two medications can be considered

amio or dig

three cases of cardioversion being appropriate in afib

hemodynamically unstable those with worsening symptoms those having their first ever case of AFib

what is the use of ibutilide procainamide flecainide sotalol or amiodarone in afib

pharmacologic conversion if electrical cardioversion is unfeasible or doesnt work

when should anticoagulation be employed in the setting of atrial fibrillation

present greater than 48 hours

what are the timing parameters for anticoagulation surrounding cardioversion

3 weeks before and 4 weeks afterwards

what is the INR goal in anticoagulation in patients with afib prior to and following cardioversion

2-3

what can be done (in theory) to avoid 3 weeks of anticoagulation prior to cardioversion in the case of afib)

TEE to image the left atrium for thrombus, if none, start IV heparin and perform cardioversion within 24 hours

T/F if the TEE route is carried out to expedite cardioversion, patients still need to be anticoagulated 4 weeks following cardioversion

what are the two agents typically used in the setting of chronic afib for rate control

beta blockers | CCBs

patients with lone afib or afib in the absence of any underlying heart disease or cardiovascular risk can take what medication

aspirin

patients with afib and underlying CVD or risk factors need what type of anticoagulation

warfarin

what is the most common cause for aflutter

heart failure

ECG exhibiting a saw tooth baseling with a QRS complex appearing after every second or third tooth

aflutter

flutter waves seen best in which lead

II III AvF (inferior leads)

how many different P wave morphologies are required to make the diagnosis of MAT

MAT is identical to this separate diagnosis except that the heart rate in this other entity is between 60-100

wandering atrial pacemaker

MAT is strongly associated with what type of disease

lung disease

if LV function is not preserved in MAT what medication can be given

digoxin

T/F electrical cardioversion is often effective in MAT

F (not effective do not use)

what is the most common cause of PSVT

nodal re-entry tachycardia`

ECG will show what characteristic in PSVT

narrow complexes with no discernible P waves (P waves buried in the QRS)

what is the underlying process in orthodromic AV reentrant tachycardia

accessory pathway between the atria and ventricles that conducts retrogradely

what would be seen on ECG in orthodromic reentry AV tachy

narrow QRS complexes with P waves may or may not be discernible depending on the rate (could bne buried, re-entrant circuit takes longer the self contained AV reentry, therefore P waves have a higher chance to be revealed)

Six (6) causes of SVT

a. Ischemic heart disease b. Digoxin toxicity—paroxysmal atrial tachycardia with 2:1 block is the most common arrhythmia associated with digoxin toxicity c. AV node reentry d. Atrial flutter with rapid ventricular response e. AV reciprocating tachycardia (accessory pathway) f. Excessive caffeine or alcohol consumption

paroxysmal atrial tachycardia with 2:1 block is the most | common arrhythmia associated with ___________ toxicity

digoxin

what is the agent of choice for correcting SVT

IV adenosine

what is the reason that IV adenosine is the agent of choice in SVT

short duration of action and effectiveness in terminating SCTs works by decreasing sinoatrial and AVE nodal activity

what agents can be used in patients with SVT if left vent function is preserved as an alternative to IV adenosine

Iv verapamil and IV esmolol (less commonly digoxin)

treatment preferred if episodes of SVT are recurrent and symptomatic

radiofrequency cardiac ablation

narrow complex tachycardia and short PR interval with upward deflection seen before thje QRS complex

WPW syndrome

what is the typical treatment used for WPW syndrome

radiofrequency cardiac ablation

WHAT DRUGS should be avoided in WPW syndrome

drugs that act through blocking AV conduction (beta blockers CCBs digoxin) as they can facilitate conduction through the accessory pathway

rapid repetitive firind of three or more PVCs in a row at a rate between 100 and 250

ventricular Tachy

ventricular tachy typically originates where in the conduction structure

below the bundle of his

what is the most common cause for ventricular tachy

prior MI with CAD

causes for V tach

a. CAD with prior MI is the most common cause b. Active ischemia, hypotension c. Cardiomyopathies d. Congenital defects e. Prolonged QT syndrome f. Drug toxicity

Vtach progresses to what arrhythmia if left untreated

Vfib

T/F Vtach lasts longer than 30 seconds and is almost always symptomatic

brief limited runs of VT is an indipendent risk factor for SCD in what cases

with concurrent CAD and LV dysfunction

connan A waves in the neck secondary toi AV dissociation and variable S1 intensity commonly associated with

Vtachy

what are the more serious presentations of Vtachy

sudden death | cardiac shock

ecg showing wide and bizarre QRS complexes with tachycardia

Vtachy

all QRS complexes are identical in this form of Vtach

monomorphic

QRS complexes are different in this form of Vtach

polymorphic

T/F VT also responds to vagal maneuvers as with PSVT

F (does not)

what should be given to patients with hemodynamically stable patients with mild symptoms and systolic BP >90

IV amio IV procainamide IV sotalol (one of these)

hemodynamically unstable patients with Vtachy or with severe symptoms treatment

immediate synchronous DC cardioversion

what mnedication is given following DC cardioversion

amiodarone (sustains rhythm)

nonsustained VT with no underlying heart disease a recent MI or evidence of left ventricular dysfunction or symptomatology

order electrophysiologic study

electrophysiology study shows inducible rhythm in the case of nonsustained VT, what should be done

placement of ICD

second line treatment for unsustained Vtach

amiodarone

most episodes of Vfib happen following

Vtach

T/F if Vfib is not associated with MI we shouldnt expect it to recur

F (Vfib not associated with MI has a higher rate of recurrence)

what two treatments can be utilized in the treatment of patients with Vfib not associated with MI

prophylactic amiodarone or placement of ICD

T/F if Vfib follows MI by <48hours then the outcome is bleak and recurrence rate is high

F (prognosis is good and recurrence is low)

T/F chronic therapy is needed for patients with Vfib secondary to MI

F (not necessary)

most common cause for vfib

ischemic heart disease

cannot measure BP unconscious patient absent heart sounds and pulse

vfib

ECG no strial P waves can be identified | no QRS complexes can be identified

VFIB

what is the immediate treatment for vfib

(MEDICAL EMERGENCY) IMMEDIATE cardiac defibrillation and CPR immediate initiation of unsynchronized DC cardioversion immediately, if equipment not on hand, begin CPR immediately up to three sequential shocks to establish another rhythm

treatment for persistent vfib following sequential shocks

continue CPR consider intubation epi (1mg bolus initially and then every 3-5minutes) attempt to defibrillate again 30s-1min following first epi dose

if vfib persists past administration of epi, intubation and reshock

IV amiodarone followed by shock | lidocaine, magnesium procainamide alternatives

If cardioversion is successful in vfib, what next

maintain continuous IV infusion of the effective antiarrhythmic agent ICD mainstay of chronic therapy in these patients (those at risk for VF)

bradycardia clinically significant when persistent below what threshold

45bpm

pathologic causes for bradycardia (3)

cardiac ischemia increased vagal tone antiarrhythmic drugs

what medication can be used to raise BP in the case of persistent bradycardia

atropine

prolonged PR interval with a QRS following each P wave

1st degree heart block

progressive prolongation of PR interval until a P wave fails to conduct

Mobitz type I

T/F type I heart block is a benign condition that does not require treatment

Pwaves fail to conduct sudndenly without a preceding PR interval prolongation often progresses

Mobitz II

where is the conduction defect in a Mobits II

His-Purkinje system of conduction

what is the necessary treatment for MObitz II

placement of PCI

absence of conduction of atrial impulses to the ventricles; no correspondence between P waves and QRS complexes

complete HB

what is the treatment of choice for complete heart block

cardiac pacemaker

Most common type of cardiomyopathy

dilated cardiomyopathy

ischemia infection alcohol casuing dysfunction of left ventricular contractility leads to what type of cardiomyopathy

dilated

what is the prognosis for dilated cardiomyopathy

poor | most die within 5 years of diagnosis

what is the most common cause for dilated cardiomyopathy

idiopathic

toxins that lead to dilated cardiomyopathy

alcohol doxorubicin adriamycin

ALL CAUSES FOR dilated cardiomyopathy (>;))

a. CAD (with prior MI) is a common cause b. Toxic: Alcohol, doxorubicin, Adriamycin c. Metabolic: Thiamine or selenium deficiency, hypophosphatemia, uremia d. Infectious: Viral, Chagas disease, Lyme disease, HIV e. Thyroid disease: Hyperthyroidism or hypothyroidism f. Peripartum cardiomyopathy g. Collagen vascular disease: SLE, scleroderma h. Prolonged, uncontrolled tachycardia i. Catecholamine induced: Pheochromocytoma, cocaine j. Familial/genetic

what heart sounds are typically associated with dilated cardiomyopathy

S3 S4 and mitral regurg or tricuspid insufficiency

what is the common pathology associated with the enlarged ventricles of dilated cardiomyopathyt

cardiac arrhythmia

this type of testing might be warranted in a patient with DCM with no cause and fam hx of disease

genetic testing

what is the treatment for DCM

(similar to treatment for CHF) beta blockers diuretics dig

should be considered because DCM patients have risk of embolization

anticoagulation

Hypertrophic cardiomyopathy mode of inheritance

autosomal dominance

diastolic dysfunction due to a stiff hypertrophied ventriclewith elevated diastolic filling pressures

HTCM

what kind of obstruction can occur in patients with assymmetric hypertrophy of the ventricular septum

dynamic outflow obstruction

``` dyspnea on exertion chest pain syncope after exertion or the valsalva palpitations arrhythmias cardiac failure sudden death years without symptomatology ```

HTCM

sustained PMI loud S4 systolic ejection murmur decreases with squatting lying down or straight leg raise intensity increased with valsalve and standing (decreases LV size and increases obstruction)

HTCM

effect of the murmur with HTCM with sustained handgrip

decrease due to increased systemic resistance leading to decreased gradient across aortic valve

rapidly increasing carotic pulse with two upstrokes indicative of

HTCM

what is the test that establishes the diagnosis of HTCM

cardiac echo

T/F asymptomatic patients with HTCM do not need treatment

what is the initial drug used in symptomatic patients with HTCM

beta blockers

used in HTCM if patient nonresponsive to beta blockers

CCBs

surgery for HTCM

myomectomy

opening snap followed by a low pitched diastolic rumble and presystolic accentuation

mitral stenosis

S2 followed by opening snap

mitral stensosi

the distance between S2 and the opening snap of mitral stenosis tells us

severity of the valvular disease

long standing disease of mitral stenosis can lead to what clinical findings

``` (right heart failure) right ventricular heave JVD pulmonary congestion hepatomegaly ascites ```

most important test in confirming mitral stenosis

echocardiogram

what are the two medications commonly used in mitral stenosis

``` diuretics (if signs of RHF) beta blockers (decrease HR and CO) ```

what are t he two options surgically for mitral stenosis

perc balloon valvuloplasty | open commissurotomy and mitral valve replacement

when the aortic valve falls below what threshold is the cardiac output not able to increase with exertion, resulting in angina

0.7

what is the cause for mitral regurg with long standing aortic stenosis

LV dilation pulls the leaflets of the mitral valve apart resulting in MR

what are the three main causes for aortic stenosis

calcification of a bicuspid valve calcification in the elderly rheumatic fever

development of what symptoms would be a sign that aortic stenosis is worsening

syncope angina CHF

which of angina syncope and CHF in the setting of aortic stenosis carries the worse prognosis

CHF

``` harsh crescendo-decreascendo systolic murmur heard in second right intercostal space radiating to carotid arteries soft S2 S4 parvus et tardus sustained PMI precordial thrill ```

aortic stenosis

what is parvus et tardus

delayed and diminished carotid upstrokes

which test is diagnostic in aortic stenosis

echocardiography

what is the definitive diagnostic test in aortic stenosis

cardiac angiography

what test can measure valve gradient and calculate valve area in aortic stenosis

cardiac catheterization

what is the treatment for aortic stenosis

valvular replacement in all symptomatic patients

treatment for asymptomatic aortic stenosis

none

inadequate closure of aortic valve leaflets causing blood to flow into left ventricle during diastole

aortic regurg

what occurs in the left ventricle in response to aortic regurgitation

LV dilation and hypertrophy to maintain stroke volume

5 year survival for chronic regurgitation

75%

how long do patients typically survive following onset of angina with aortic regurg

4 years

how long do patients typically survive following onset of CHF with aortic regurg

2 years

4 main causes for acute aortic regurgitation

infective endocarditis trauma aortic dissection iatrogenic

causes for primary valvular aortic regurgitation (6)

``` rheumatic biscupid aortic valve marfans ehlers danlos ankylosing spondylitis SLE ```

causes for aortic root disease leading to aortic regurg (6)

``` syphilitic aortitis osteogenesis imperfecta aortic dissection behcet reiter syndrome systemic HTN ```

widened pulse pressure concerning for what valvular disease

aortic regurgitation

low pitched diastolic rumble due to competing flow anterograde from the LA and retrograde from the aorta

austin flint murmur | aortic regurgitation

rapidly increasing pulse that collapses suddenly as arterial pressure decreases rapidly in late systole and diastole

water hammer pulse, indicates aortic regurg

what happens to aortic regurg with handgrip sustained

increases

what is the utility of echo in aortic regurg

assess chronic patients for surgery over time

what is the treatment for chronic asymptomatic aortic regurg

``` conservative restrict salt diuretics vasodilators afterload reduction restriction of strenuous activity ```

what is the definitive treatment for aortic regurgitation

surgical replacement

abrupt elevation of left atrial pressure in the setting of normal LA size and compliance with pulmonary edema possible hypotension and shock due to decreased CO

acute MR

gradual elevation of left atrial pressure in setting of dilated LA and LV pulmonary HTN can result from chronic backflow

chronic MR

3 main acute causes for MR

endocarditis papillary muscle ruption (infarction) chordae tendinae rupture

4 main chronic causes for MR

rheumatic fever mitral valve prolapse marfans cardiomyopathy

T/F chronic MR has a worse prognosis than acute MR

F (acute is worse prognostically)

holosystolic murmur at the apex radiating to the back or clavicle

what arrhythmia is common seen with MR

afib

what diagnostic tests can show signs of MR

CXR | echo

device used as a bridge to surgery for MR

IABP

what medication outcome should be sought in patients with symptomatic MR

afterload reduction

what is the definitive treatment for MR

valvular replacement

results from a failure of the tricuspoid valve to close completely during systol causing regurgitation of blood into the RA

tricuspid regurg

TR regurg usually 2/2

RV enlargement

what is the most common cause for tricuspid regurg with LV dilation

left ventricular failure

when is tricuspid endocarditis typically seen

IV drug users

congenital malformation of the tricuspid valve in which there is a downward displacement of the valve into the RV

epstein anomaly

TR regurg usually asymptomatic unless what occurs

development of RGF or Pulmonary HTN

what would be expected to be some of the symptoms of tricuspid regurg

``` ascites hepatomegaly edema JVD pulsatile liver prominent V waves in jugular venous pulse with rapid y descent inspiratory S3 along LLSB blowing holosystolic murmur at LLSB increased with inspiration reduced during expiration or valsalva ```

how is the diagnosis of tricuspid regurg made

echo

treatment for volume overload and venous congestion/edema of TR regurg

diuretics

what needs to be absent in order for tricuspid valve resplacement surgery to be an available option

pulmonary hypertension

typical mid systolic click and murmuer

mitral valve prolapse

common valvular disease in patients with connective tissue disorders

MVP

most common cause of MR in developed countried

MVP

what do standing and valsalva do in regard to the murmur involved with MVP

increase

what does squatting down have in terms of effect on MVP

decrease

what is the most useful diagnostic tool for MVP

echo

what should be used for the atypical chest pain that can accompany MVP

beta blockers shown to be helpful

T/F MVP often requires surgery

F (often benign, asymptomatic for peoples entire lives)

most common valvular abnormality 2/2 rheumatic heart disease

mitral stenosis

what are the major signs of acute rheumatic fever

``` migratory arthritis acute myocarditis subcutaneous Nodules erythema marginatum syndenham chorea ```

what medication should be given to patients with streptococcal pharyngitis to avoid rheumatic fever

penecillin or rythromycin

how is acute rheumatic fever treated

NSAID

what marker is used to track treatment progress

C-RP

infection of the endocardial surface of the heart

endocarditis

acute endocarditis most commonly caused by

staph aureus

acute endocarditis happens on what type of heart valve

normal

if acute endocarditis is left untreated what is the outcome

fatal in 6 weeks

subacute endocarditis caused by

strep viridans and enterococcus

subacute endocarditis occurs on what type of valves

previously injured

what are the more rare forms of native valve endocarditis

HACEK organisms (Haemophilus, Actinobacillus, Cardiobacterium, Eikenella, and Kindella)

most common organism for prosthetic valve endocarditis

staph epi (and then staph aureus)

Endocarditis in IV drug users

Right sided endocarditis

what valve is typically involved in right sided endocarditis

tricuspid

which bug is most common in right sided endocarditis

staph aureus

what are the four main complications from endocarditis

cardiac failure myocardial abscess various solid organ damage from showered emboli glomerulonephritis

what combination of Duke criteria is necessary for the diagnosis of endocarditis

2 major 1 major 3 minor 5 minor

what are the major DUKE criteria

sustained bacteremia | endocardial involvement diagnosed by echo or by new valvular murmur on clinical exam

what are the minor DUKE criteria for endocarditis

predisposing condition (abnormal valve or abnormal risk) fever vascular phenomena (septic arterial or pulmonary emboli mycotic aneurysms intracranial hemorrhage janeway lesions) Immune phenomena (Glomerulonephritis, Osler nodes, Roth spots, rheumatoid factor) Positive blood cultures not meeting major crit Positive echo not meeting major crit

what is the treatment for endocarditis

extended parenteral antibiotics (4-6 weeks)

what are the two factors necessary to warrant endocarditis antibiotic prophylaxis

``` qualifying cardiac indication: prosthetic heart valve history of infective endocarditis congenital heart disease cardiac transplant with vulvulopathy ``` Qualifying procedure Dental procedures procedures involving biopsy or incision of respiratory mucosa procedures involving infected skin or musculoskeletal tissue

associated with debilitating illnesses susch as metastatic cancer sterile deposits of fibrin and platelets forming along the closure line of cardiac valve leaflets vegetations can embolize to the brain or periphery

marantic endocarditis (nonbacterial thrombotic endocarditis)

typically involving the aortic valves in individuals with SLE characterized by the formation of small warty vegetations on both sides of valve leaflets and may present with regurgitant murmurs can be a source of systemic embolization

libmann sacks endocarditis

what is the most common type of atrial septal defect

ostium secundum

what are the three types of ASDs

``` ostium secundum (central portion opening) ostium primum (low in septum) Sinus venosus (high in the septum) ```

what is the rare but serious complication that can occur with ASD

pulm HTN

what is the tell tale sign on clinical exam for ASD

fixed split S2

what is the diagnostic test for ASD

TEE with bubble study (bubbles can be seen crossing through the defect often used and can aid in the Dx)

what are the CXR findings c/w ASD

Large pulm arteries | increased pulm markings

pulmonary HTN for ASD typically occurs after what age if at all

late complication of ASD in which irreversible pulm HTN leads to reversal of shunt, HF and cyanosis

eisenmenger syndrome

most common of the congenital cardiac malformations

VSD

what happens to the shunt in VSD if PVR becomes larger than SVR

reversal of shunt and potential eisenmenger syndrome

sign symptoms of eisenmenger syndrome

``` high PVR SOB dyspnea on exertion chest pain syncope cyanosis ```

harsh blowing holosystolic murmur with thrill at fourth left intercostal space that decreases with valsalva and handgrip

VSD

is a louder or softer VSD more concerning

softer (smaller VSD causes louder murmur)

what is the structure that is responsible for the enlarged cardiac silhouette seen on CXR in VSD

enlargement of the pulmonary artery

what are the complications associated with VSD

endocarditis progressive aortic regurg heart failure pulmonary HTN and shunt reversl (eisenmengers)

when is endocarditis PPX not recommended in VSD

uncomplicated and no prior history of endocarditis

narrowing/constriction of aorta usually at the origin of left subclavian artery near ligamentum arteriosum

coarctation of the aorta

hypertension in the upper extremities and hypotension in the lower extremitis

coarctation of the aorta

well developed upper body with underdeveloped lower bodyu

coarctation of the aorta

CXR showing notching of the ribs

coarctation of the aorta

prevalence of this cardiac malformation is increased in patients with Turner syndrome

coarctation of the aorta

what are the 4 main complications associated with coarctations of the aorta

severe HTN rupture of cerebral aneurysms infective endocarditis aortic dissections

communication between the aorta and pulmonary artery that persists after birth

patent ductus arteriosus

what are the two factors that maintain patent ductus arteriosus during fetal development

low O2 tension | prostaglandins

when does cyanosis occur in PDA

late

cardiac malformation associated with rubella syndrome high altitude premature births

PDA

continuous machine like murmur at the left second intercostal space RVH wide pulse pressure and bounding peripheral pulses

PDA

CXR showing increased pulmonary vascular markings dilated pulmonary artery enlarged cardiac silhouette calcifications in tract coming off of the aorta

PDA

If pulmonary vascular disease is absent what is the treatment for PDA

surgical ligation

when is surgery contraindicated in PDA

when there is significant right to left shunting

what is the medication that can be used for closure of PDA

indomethacin

medication used to keep PDA open in cases of transposition

PGE1

Ventricular septal defect right ventricular hypertrophy pulmonary artery stenosis overriding aorta

tetrology of fallot

tetrology of fallot arise secondary to defects in the development of what structure

infundibular septum

most common symptom of tetrology of fallot

cyanosis

degree of symptoms in tetrology of fallot depends on

degree of pulmonary outflow obstruction

three substances that can be used in patient with frequent tet spells that are refractory to mechanical position to correct

oxygen morphine beta blockers

what is the diagnostic modality of choice in tet of fallot patient

echo

CXR showing boot shape to the heart

TOF

what is the treatment for TOF

surgery

two most common causes of death following surgery for TOF

sudden cardiac death and CHF

hypertensive emergency defined as

systolic above 220 diastolic above 120 in addition to end organ damage

elevated BP levels of hypertensive emergency without end organ damage

urgency

5 systems that need to be assessed in a patient with blood pressures in the emergency range

eyes : papilledema CNS: AMS or hemorrhage, confusion kidneys: failure, hematuria heart: USA, MI, CHF, aortic dissection

radiographic condition postulated to be caused by autoregulatory failure of cerebral vessels as well as endothelial dysfunction

PRES

insidious onset of headache altered level of consciousness visual changes and seizures with posterior cerebral white matter edema hypertensive or normotensive

PRES

how should BP be brought down in hypertensive emergencies

reduce MAP by 25% in 1 to 2 hours (get the patient out of danger and then decrease gradually)

rate typically sought for BP decrease in hypertensive urgency

normotensive in 24 hours

``` long standing HTN cocaine use trauma connective tissue diseases bicuspid aortic valve coarctation third trimester pregnancy ```

aortic dissection

what are the two classifications of aortic dissection

type A Ascending Type B (distal to subclavian) descending

servere tearing rippin stabbing pain typically abrupt in onset anterior or back opf chest interscapular

aortic dissection

anterior chest pain is more common with what type of aortic dissection

posterior chest pain more common with what type of aortic dissection

CXR finding typical for aortic dissection

widened mediastinum

which is more accurate for aortic dissection MRI or CT

MRI

best test for determining the extent of dissection in aorta for surgery

angiography

what medication should be initiated immediately in aortic dissection

``` beta blockers IV nitroprusside (BP below 120) ```

most type A dissections are treated as surgical emergencies to avoid

MI aortic regurg or cardiac tamponade

what is the typical management of type B dissections

lower blood pressure, IV beta blockers | morphine for pain

abnormal localized dilation of aorta typically between the renal arteries and iliac bifurcation

AAA

average ages for diagnosis of AAA

65=70

most cases of AAA what process is occuring in vessel

atherosclerosis

5 things other than atherosclerosis that predispose to AAA

HTN smoking vasculitis truama pos famHx

pulsatile mass on abdominal exam

AAA

sudden onset of severe pain in the back or lower abdomen with ecchymoses on back and flanks and ecchymoses aroiund umbilicus

AAA rupture

Grey turner sign

ecchymoses on flank/back

cullen sign

ecchymoses around umbilicus

triad of abdominal pain hypotension palpable pulsatile abdominal mass

AAA rupture

AAA rupture treatment

immediate laparotomy and repair

test of choice to evaluate location and size of AAA

test that can be used in hemodynamically stable patients with AAA for preop planning

size at which surgical repair of AAA should be recommended

>5cm diameter

most common site for peripheral vascular disease

superficial femoral artery

what is the most important risk factor for PVD

smoking

patient with PVD and intermittent claudication prognosis

best

patient with PVD and rest pain / non healing ulcers prognosis

bad

ABI above what value indicates severe PVD

1.3

claudication ABI

<0.7

rest pain ABI in PVD

<0.4

gold standard for diagnosing and locating PVD

arteriography

conservative management for PVD

``` stop smoking! graduated exercise program foot care atherosclerosis reduction avoid extreme temp aspiring +/- ticlopidine/clopidogral cilostazol ```

three indications for PVD surgery

rest pain ischemic ulcerations severe symptoms refractory to conservative therapy

two main options for surgery in PVD

angioplasty | bypass

most common site of acute arterial occlusion

common femoral artery

most common site and cause for embolus of acute arterial occlusion

heart afib

6 Ps of acute arterial occlusion

``` pain pallor poikilothermia (cold blooded) paralysis paresthesias pulseless ```

three tests usually obtained in acute arterial occlusion

arteriogram ecg (MI, afib) echo (valves thrombus shunts)

amount of time that skeletal muscle can tolerate ischemia

6 hours

what is the immediate therapy for embolus causing acute arterial occlusion

immediate IV heparin | surgical embolectomy with cutdown and fogarty balloonm)

when is bypass employed for acute arterial occlusion

failure of embolectomy

small discrete areas of tissue ischemia blue black toes renal insufficiency abdominal pain or bleeding treatment

cholesterol embolization syndrome\ Do not anticoagulate control BP surgical only in very extreme circumstances

aneurysm resulting from damage to aortic wall 2/2 infection

mycotic aneurysm

what is a luetic heart

complication of spyphilitic aortitis in which the dilation of the proximal aorta blocks the aortic branches most commonly the coronaries needs surgical repair

virchows triad

venous stasis endothelial injury hypercoaguable

lower extremity swelling/pain calf pain on ankle dorsiflexion palpable cord fever

DVT

initial test for DVT

doppler and duplex US

duplex is good for what location of DVT

proximal

most accurate test for DVT of calf

venography

intermediate to high pretest probability of DVT plus Doppler +

begin anticoagulation

intermediate to high pretest prob of DVT with neg doppler

repeat doppler 2-3days for 2 weeks

low-intermediate pretest prob of DVT and soppler neg

no need for anticoagulation

painful blue swollen leg following DVT

phlegmasia cerulea dolens

indicated treatment for phlegmasia cerulea dolens

venous thrombectomy

how long should warfarin be kept following DVT

3-6 months

indicated for DVT/PE massive with hemodynamic instability

systemic thrombolytics

treatment for patient with DVT and absolute contraindication to anticoagulation

inferior vena cava filter

what is the typical preceding illness that leads to venous stasis

DVT (destroys valvs in the system)

what is the reason for the brawny induration and bron black color of sjkin in chronic venous insufficency

extrav of proteins and RBCs

what is the complication common with chronic venous stasis

venous ulceration

how does elevation of legs differ in chronic venous insufficiency versus acute arterial insufficency

provides relief in venous disease

mildly painful ulcears rapidly recurring | above the medial malleolus

chronic venous stasis

three main treatment s to combat complications of chronic venous insufficiency

leg elevation avoiding long periods of sitting and standing compression stockings

superficial thrombophlebitis in lower extremities usually associated with

Varicose veins

superficial thrombophlebitis in upper extremity usually associated with

IV placement

neoplasms of the heart are commonly of what origin

metastatis

benign helatinous growth usually pedunculated and arising from the interatrial septum of the heart in the region of the fossa ovalis

atrial myxoma

fatigue fever syncope palpitations malaise and a low pitched diastolic murmur that changes character with changing body position

atrial myxoma

tachycardia decrease in BP and malfunction of underperfused organ systems

shock

fever and possible site of infection in shock patient

septic

trauma gi bleed vomiting or diarrhea in shock patient

hypovolemic

MI angina or heart disease in shock patient

cardiogenic

JVD present in a shock patient

cardiogenic

spinal cord injury or neurologic deficits are present

neurogenic shock

initial steps in ALL shock patients

establish two large bore venous catheters +/- central line and art line fluid bolus of 2L draw CBC lytes renal funcrtion PT/pTT ECG CXR pulse ox vasopressors if still hypotensive following fluids

Changes in the following for cardiogenic shock CO SVR PCWP

- + +

Changes in the following for hypovolemic shock CO SVR PCWP

- + -

Changes in the following for neurogenic shock CO SVR PCWP

- - -

Changes in the following for septic shock CO SVR PCWP

+ - -

treatment

start with ABCs! | fluid resuscitation

most common cause for cardiogenic shock

vassopressor usually used in cardiogenic shock

dopamine

what is more important in hypovolemic shock, the rate or amount of loss

rate

``` % of blood loss in following classes of hypovolemic shock I II III IV ```

10-15% 20-30 30-40 40>

Step Up to medicine - Cardiovascular Flashcards

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