Book stuff Flashcards
Supraventricular tachycardias
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
Reentry arrthmias require what?
An area of slow conduction must be found somewhere (ischemia/blockage)
Each limb must have a different refractory period
What do automaticity Arrhythmias require?
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
Atrial flutter is defined as
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
What can be done to the patient who is suspected of atrial flutter to confirm it?
Give adenosine
Use vagal maneuvers
Diffference between isthmus-dependent clockwise atrial flutter and isthmus-dependent counterclockwise
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
WPW diagnosis
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
When you replace potassium, what electrolyte must be replaced first?
Magnesium
How to treat hyperkalemia?
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*
When is surgery indicative for aortic stenosis?
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)
Normal through severe classifications of mitral valve stenosis
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
AHA definition of CHF and cardinal signs
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”
Difference between diastolic and systolic heart failures based on AHA guidelines
Systolic = Heart failure w/ a reduced ejection fraction
Diastolic = Heart failure w/out a reduced ejection fraction
the cut off is <40% ejection fraction
Possible etiologies of heart failure
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)
Pathogenesis of Heart failure
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)
Compensatory mechanisms for LV dysfunction that prevent acute Heart failure
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*
Left ventricular remodeling biological steps
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)
Potential Biological stimuli for the progressive of LV remodeling
1) increased mechanical stress of myocytes
2) neurohormones (angiotensin and NE)
3) inflammatory cytokines
4) endothelin
5) ROS
Primary physiological issue that results in decreased contractility and depresses LV systolic function
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
Symptoms of HF
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
Labs to get for HF
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*
Imagining to get for HF
ECG:
- will show LVH
- Q waves may or may not be present
X-rays (may show any of these)
- LVH
- pulmonary effusion
- cardiac effusion
Differential diagnosis for HF
Renal failure
Acute respiratory distress syndromes
Endocarditis
Treatment of HF w/ no ejection fraction issues (diastolic HF)
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
Treatment of HF w/ ejection fraction issues (systolic HF)
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*
Coronary artery bypass grafting (CABG)
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
Dilated cardiomyopathy
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
Treatment of Chagas induced infectious endocarditis
Benzindazole and nifurtimox therapies
Peripartum cardiomyopathy
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
Takotsubo cardiomyopathy
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)
Restrictive cardiomyopathy
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)
Hypertrophic cardiomyopathy
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
What is the dominant cause of valvular heart disease in developing countries?
Rheumatic heart disease
- causes commissural fusion of the tricuspid or the aortic valves if the disease effects those valves.
What is the dominant cause of valvular disease in developed countries?
Degenerative or inflammatory processes that lead to valve thickening or calcifications
- # 1 is infectious endocarditis
- rates increase with age
Aortic stenosis
2nd most common valvular disease (1/4 of all valve diseases)
- 80% are male
Bicuspid aortic valve disease
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
4 pathologies that lead to obstructive LV outflow
HCM w/ obstruction
Fibromuscular/membranous subaortic stenosis
Bicuspid aorta valves (BAV)
aortic stenosis
What is the physiological response of the body to aortic stenosis/ LV outflow impairment?
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
Symptoms and TX of aortic stenosis
- 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
ECG findings for Aortic stenosis
LV strain
( ST segment depression w/ inverted T waves) in leads 1/aVL/ V4-6
Classification of severe and moderate Aortic stenosis
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
Pathophysiology of aortic regurgitation
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*
Symptoms and treatment of aortic regurgitation
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
Mitral stenosis
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*
Treatment of mitral stenosis
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)
5 functional components of the mitral valve apparatus that can be dysfunctional in mitral regurgitation
Leaflets
Annulus
Chordae tendineae
Papillary muscles
Myocardium
acute MR often is caused by MI, blunt trauma or a severe course of infective endocarditis
