Book stuff

Question 1

Supraventricular tachycardias

Answer 1

Rapid rhythm disturbances origin in from the atria or the AV node
- often are considered paroxysmal SVTs (since they come and go in episodes)

Can occur in 3 mechanisms

• reentry (most common)
• enhanced automaticity
• triggered activity

Question 2

Reentry arrthmias require what?

Answer 2

An area of slow conduction must be found somewhere (ischemia/blockage)

Each limb must have a different refractory period

Question 3

What do automaticity Arrhythmias require?

Answer 3

Either a single or multiple foci firing independently from the SA node

• enhanced = foci fires spontaneously either within the sinus node or not. Does not have a disease associated with it
• abnormal = same as enhanced except a diseases process does exist

Question 4

Atrial flutter is defined as

Answer 4

Heart rate usually 150-300

P wave rates hover around 250-340

• shows in a “sawtooth” pattern
• usually 2-4:1 ratio of f waves: QRS complexes

R-P relation is undefined since the P waves are actually f waves and moving too fast

can also show neck venous pulsation of about 300/min

Question 5

What can be done to the patient who is suspected of atrial flutter to confirm it?

Answer 5

Give adenosine

Use vagal maneuvers

Question 6

Diffference between isthmus-dependent clockwise atrial flutter and isthmus-dependent counterclockwise

Answer 6

Clockwise:

• Positive f waves in leads 2,3, and aVF
• negative f waves in lead V1

Counter wise:

• positive f waves in lead V1
• negative f waves in leads 2,3 and aVF

Question 7

WPW diagnosis

Answer 7

Genetic issues where bypass tracts are present, but may or may not mean tachyarrhythmia

• show a short PR interval
• Wide QRS complex
• secondary repolarization abnormalities
• presence of delta waves

Tx:

• vagal maneuvers
• adenosine
• BBs or CBBs

Question 8

When you replace potassium, what electrolyte must be replaced first?

Answer 8

Magnesium

Question 9

How to treat hyperkalemia?

Answer 9

Give calcium (stabilize the myocardium)

Give glucose/insulin (to uptake the excess potassium)

• NEVER give calcium to a patient with hyperkalemia due to digoxin-induced, will kill*

Question 10

When is surgery indicative for aortic stenosis?

Answer 10

1) symptomatic patients w/ severe obstruction marked by any of the following
- valve area <1cm
- LV systolic dysfunction (<50% EF)
- aneurysmal aortic root/ascending aorta

2) asymptomatic patients with aortic stenosis who are also required to get CABG (coronary artery bypass grafts)

Question 11

Normal through severe classifications of mitral valve stenosis

Answer 11

Normal: No treatment

• 0 mmHg pressure gradient
• > 4.0 cm valve area

Mild: no treatment

• 1-5 mmHg pressure gradient
• 2.5-4.0 cm valve area

Moderate: no treatment except *

• 6-10 mmHg pressure gradient
• 1.0-2.5 cm valve area
• *pulmonary capillary pressure >25mmHg w/ exercise (requires percutaneous mitral balloon valvotomy(PMBC/V)

Severe: requires surgery unless no atrial fibrilation is present

• > 10 mmHg
• <1.0 mitral valve area
• usually presents w/ atrial fib
• can be asymptomatic or symptomatic
• surgery includes PMBV unless patient is not a high surgical risk, then Mitral valve replacement

Question 12

AHA definition of CHF and cardinal signs

Answer 12

Complex clinical syndrome that results from structural or functional impairment of ventricular filling and/or ejection of blood.

• cardinal signs include
  1) dyspnea
  2) fatigue/syncope
  3) systemic edema
  4) rales in lungs “crackling sounds in lungs”

Question 13

Difference between diastolic and systolic heart failures based on AHA guidelines

Answer 13

Systolic = Heart failure w/ a reduced ejection fraction

Diastolic = Heart failure w/out a reduced ejection fraction

the cut off is <40% ejection fraction

Question 14

Possible etiologies of heart failure

Answer 14

1) any conditions that alter left ventricular structure and function
- HCM
- DCM
- MI
- patient ductus arteriosis
- endocarditis
- mitral/aortic stenosis or regurgitation
- CAD most common cause 75%
- HTN induced LVH second most common cause 70%
- diabetes
- duchennes, Becker’s and limb girdle dystrophies (causes DCM)
- rheumatic heart disease (causes valvular defects and LVH)

Question 15

Pathogenesis of Heart failure

Answer 15

Progressive disorder that is almost always initiated after an “index event”

• index event is one of 2 things:
  1) damage to myocytes w/ loss-of-function
  2) disruptions in the ability for the heart to generate force (RCM, valvular diseases, ETC)

Question 16

Compensatory mechanisms for LV dysfunction that prevent acute Heart failure

Answer 16

1) activation of RAAS system
2) activation of nervous system
3) increases in myocontractility (concentric hypertrophy in LVH)
4) increases in natriuretic peptides
5) increases a in bradykinin, prostaglandins and nitric oxide production (natural vasodilation to decrease SVR)
* all of these cause many patients with LV dysfunction to remain asymptomatic until clinical heart failure is present*

Question 17

Left ventricular remodeling biological steps

Answer 17

The official title for the process in which asymptomatic HF becomes symptomatic HF

1) individual myocyte hypertrophy
2) alterations in contractile properties of myocytes
3) progressive less of total myocytes
4) B-adrenergic desensitization
5) abnormal myocardial metabolism (increases in oxygen demand)
6) changes in ECM that do not provide strucutre support for myocytes (unorganized new collagen)

Question 18

Potential Biological stimuli for the progressive of LV remodeling

Answer 18

1) increased mechanical stress of myocytes
2) neurohormones (angiotensin and NE)
3) inflammatory cytokines
4) endothelin
5) ROS

Question 19

Primary physiological issue that results in decreased contractility and depresses LV systolic function

Answer 19

Decreased adenosine triphosphate (SERCA2A)

Causes the following
- decreases calcium reabsorption to the SR inside myocytes

• hyperphosphylation of ryanodine receptors (causes the receptors to stay open and leak, as well as up-regulate more leaky ryanodine receptors)
• decreased a-myosin chains

Question 20

Symptoms of HF

Answer 20

Cardinal:

• dyspnea
• fatigue
• syncope
• systemic edema

Other symptoms:

• orthopnea
• paroxysmal nocturnal dyspnea
• anorexia/ cachexia
• nausea
• satiety w/ ab pain
• hepatomegaly w/ tenderness
• sinus tachycardia
• cyanosis
• rales
• pleural effusions
• displaced PMI to the lateral side
• S3 and/or S4 sound

Question 21

Labs to get for HF

Answer 21

CBC

CMP

Creatinine and troponin levels

Hepatic enzymes

Urinalysis

Naturetic peptide levels

• Lipid panel and thyroid abnormalities if expected to be a cause*
• diabetes testing (glucose levels) only if expected to be a cause*

Question 22

Imagining to get for HF

Answer 22

ECG:

• will show LVH
• Q waves may or may not be present

X-rays (may show any of these)

• LVH
• pulmonary effusion
• cardiac effusion

Question 23

Differential diagnosis for HF

Answer 23

Renal failure

Acute respiratory distress syndromes

Endocarditis

Question 24

Treatment of HF w/ no ejection fraction issues (diastolic HF)

Answer 24

1) should focus tx on lower blood pressure and increase exercise tolerance
- diuretics
- ACEIs/ ARBs
- Clonidine or a-Methyldopa

• BBs, dobutamine/dopamine, digoxin and CBBs dont work as well for diastolic HF*
• dont overuse direct vasodilators (no more than 1)*
  2) treatment of sleep issues and correction of underlying iaschemia should also be focused on if present

Question 25

Treatment of HF w/ ejection fraction issues (systolic HF)

Answer 25

1) treatment should be focused on stabilizing heart rate and increase contractility - first line BBs (except bucindolol) ACEIs (PRILS) and ARBs (SARTANs) - second line Diuretics Digoxin (only if needed) * must monitor dosage w/ all drugs since all CHF requires different doses in different people* * NO statins*

Question 26

Coronary artery bypass grafting (CABG)

Answer 26

Usually only used when someone has multi vessel CAD w/ an ischemic cardiomyopathy (due to decently high mortality rates (10%)) Revascularization to ischemic cardiac tissue via grafting-an artery or vein (artery preferred) and attaching it to the coronary circulation mostly seen in left ventricular failure and unstable angina w/ CAD

Question 27

Dilated cardiomyopathy

Answer 27

Systolic failure marked by an enlarged eccentric left ventricle w/ reduced systolic function/ejection fraction - can also do right ventricle as well, but most acute shows left ventricle affected 1st. Commonly seen with mitral valve regurgitation as well *most commonly treated with BBs and either ACEIs/ARBs combo therapies*

Question 28

Treatment of Chagas induced infectious endocarditis

Answer 28

Benzindazole and nifurtimox therapies

Question 29

Peripartum cardiomyopathy

Answer 29

Develops during the last trimester of within 6 months after pregnancy Risk factors are: - increased maternal age - malnutrition - twin pregnancy - being preeclampsia during pregnancy - toximeia during pregnancy

Question 30

Takotsubo cardiomyopathy

Answer 30

Apical ballooning of ventricles during very high stress situations - typically occurs in older women Symptoms: - hypotension - pulmonary edema - angina - ECG mimics acute MI Treatment - labetalol/ carvedilol - nitrates (if pulmonary edema is present)

Question 31

Restrictive cardiomyopathy

Answer 31

Abnormal diastolic function with decreased contractility, ventricular compliance and ejection fractions. Also called diastolic heart failure. - often seen with bilateral atrial enlargement - major cause is amyloidosis,but can also be progressive fibrosis due to mechanical stress Symptoms: Usually right sided based - systemic edema - abdominal discomfort - ascites - S4 may be present - kussmauls sign may be present (increased IJV during inspiration)

Question 32

Hypertrophic cardiomyopathy

Answer 32

Left ventricular concentric hypertrophy that is caused by hemodynamic factors - also called hypertrophic obstructive cardiomyopathy (HOA) or diastolic heart failure. Is very autosomal dominant genetically tied where a sarcomere mutation is 60% of the time the cause - these mutations usually result in gain-o-function mutations in myocyte calcium sensitivity. Myocytes are hyper sensative to calcium and often impairs relaxation. - if family members have it, its likely the offspring has it

Question 33

What is the dominant cause of valvular heart disease in developing countries?

Answer 33

Rheumatic heart disease | - causes commissural fusion of the tricuspid or the aortic valves if the disease effects those valves.

Question 34

What is the dominant cause of valvular disease in developed countries?

Answer 34

Degenerative or inflammatory processes that lead to valve thickening or calcifications - #1 is infectious endocarditis - rates increase with age

Question 35

Aortic stenosis

Answer 35

2nd most common valvular disease (1/4 of all valve diseases) - 80% are male

Question 36

Bicuspid aortic valve disease

Answer 36

Most common congenital heart valve defect - autosomal dominance w/ incomplete penetrance The gene that causes this mutation is the NOTCH1 gene Most common degenerative effect of this is ascending aortic aneurysm since the patients aorta is naturally enlarged. - obstructs the left ventricular outflow leading to LVH as well

Question 37

4 pathologies that lead to obstructive LV outflow

Answer 37

HCM w/ obstruction Fibromuscular/membranous subaortic stenosis Bicuspid aorta valves (BAV) aortic stenosis

Question 38

What is the physiological response of the body to aortic stenosis/ LV outflow impairment?

Answer 38

Concentric LV hypertrophy - this is to combat the reduced stroke volume and increased pressure gradient the LV must now overcome *may also lead to some eccentric LV hypertrophy as well*

Question 39

Symptoms and TX of aortic stenosis

Answer 39

* NOTE: most aortic stenosis goes asymptomatic until the radius has dipped below 1.0cm* - if occurring, usually lasts till about age 60 unless BAV occurs then around 40 Symptoms: - exertional dyspnea - angina pectoris - syncope Physical findings: - HTN - pulsus parvus et tardus (carotid pulse rises slowly and beats slower than the radial pulse) - S4 noice - S2 paradoxical splitting - Mid systolic cresendo-decresendo murmur (3-4/6) w/ a mid click If symptoms develop, Aortic valve replacement is indicated 100% of the time. Surgical Treatment: - TAVR for severe patients and/or low EF (<50%) - PABV for moderate patients w/ mild symptoms - use CABG if multiple CAD present - no physical activity for severe AS Medication treatment: - for angina: nitroglycerin - for CAD or HTN: BBs and ACEIs

Question 40

ECG findings for Aortic stenosis

Answer 40

LV strain | ( ST segment depression w/ inverted T waves) in leads 1/aVL/ V4-6

Question 41

Classification of severe and moderate Aortic stenosis

Answer 41

Severe - velocity = 4m/s or greater - pressure gradient > 40mmHg - symptoms are usually present - area = <1.0cm moderate - velocity = 3-3.9m/s - pressure gradient = 20-39mmHg - symptoms may or may not be present - area = 1.1-1.9cm

Question 42

Pathophysiology of aortic regurgitation

Answer 42

Total stroke volume ejected is increased or unchanged in patients - this leads to increased afterload and dilation (eccentric hypertrophy) of the LV * note the heart also will concentrically hypertrophy, but only during the end stages and patients are near death*

Question 43

Symptoms and treatment of aortic regurgitation

Answer 43

Symptoms - decresendo diastolic murmur - low exercise tolerance - bobbing of head or large arteries at rest (severe only) - strange pulse sounds systemically - quincke’s pulse (push down on the fingertips, the blanching will pulse instead of remain constant) Treatment: - use vasodilators and/or diuretics to control blood pressure and combat increased afterload - AVR/TAVR is required

Question 44

Mitral stenosis

Answer 44

Leading cause is rheumatic fever Results in reduction of mitral valve area (down from 4-6cm -> <2cm) - severe is considered <1.5cm Usually results in normal ejection fractions and LV diastolic pressure Processes a cresendo-decresendo diastolic murmur w/ a rumbling (grade 1-2/6) Symptoms: - pulmonary hypertension (may also result in RV enlargement) - malar flush w/ blue facies - dilation of both atria - dyspnea - tachycardia - hemoptysis - pulmonary edema - dysphasia * note the dilation of atria can result in a fib/flutter rates being higher than normal*

Question 45

Treatment of mitral stenosis

Answer 45

Penicillin (if caused by rheumatic fever or suspected rheumatic fever) Small doses of BBs or digoxin if a fib/flutter is present Warfarin is required for life in patients with MS that have A fib/flutter or has a history of Requires mitral valve replacement in severe cases or very symptomatic cases. PMBV is in patients who are less severe but have a low area and ejection fraction (Also used in high risk surgical patients)

Question 46

5 functional components of the mitral valve apparatus that can be dysfunctional in mitral regurgitation

Answer 46

Leaflets Annulus Chordae tendineae Papillary muscles Myocardium *acute MR often is caused by MI, blunt trauma or a severe course of infective endocarditis*