1
Q
Tachycardia arrhythmogenesis
A
- Increased Automaticity: increased sympatheric nervous system tone
>Hypovolemia
>Hypoxia
>Sympathomimetic drugs
>Pain/anixety
>Increased metabolic activity of cells - Triggered activity
>Irritable area starts firing leading to abnormal sequence of conduction - Re-entrant circuit
>Most common; self-sustaining closed-loop circuit
2
Q
Arrhythmia Classifications
A
—Tachyarrhythmia—
- Supraventricular
>Sinus tachycardia (SA too fast)
>Paroxysmal supraventricular tachycardia
–>AVNRT (re-entrant circuit in AV)
–>AVRT (re-entrant circuit through accessory pathway btw atria/vs)
>Atrial tachyarythmia (irritable area in atria; AV before SA)
–>Focal atrial tachycardia (one ectopic focus)
–>Multifocal atrial tachycardia (multiple ectopic areas firing abnormally)
–>Atrial Fibrillation (multiple ectopic areas firing fast)
–>Atrial Flutter (abnormal re-entrant circuit at tricuspid valve) - Ventricular
>Ventricular fibrillation (multiple ectopic foci in ventricle firing)
>Ventricular tachycardia
–>Monomorphic (one irritable area)
–>Polymorphic (multiple irritable areas); torsades depointed
—Bradycardias—
- Sinus bradycardia (SA too slow)
- Sick sinus syndrome (too fast & too slow)
- Heart Block (conduction block in AV)
–>1st degree
–>2nd degree
——> Mobitz I
——> Mobits II
–>3rd degree
3
Q
Atrial flutter
A
- Supraventricular tachycardia caused by re-entry circuit in RA
- Atrial rate is regular bu fast (150-400 bpm); only some reach ventricles and rest blocked by AV node
- Fixed AV block: ventricular rate constant fraction of atrial (ex. 2:1)
- Variable AV block: ventricular response irregular, may mimic fibrillation
- Are in a ring of inlets of SVC, IVC and coronary sinus called CAVO TRICUSPID ISTHMUS propogates signal slowly, allowing closed-loop
- UNLIKE ATRIAL FIBRILLATION: atria have regular rate, and are contracting
ECG:
- Inverted flutter waves in II, III, aVF (because counter clockwise circuit)
- Positive flutter waves VI (may resemble P waves)
- Sawtooth wave patterns
4
Q
Carotid sinus massage
A
- Located at bifurcation of common carotid (at level of thyroid cartilage)
- Induce stimulation of parasympathetic nerves and inhibition of sympathetic nerves (bc sense arterial BP change through barorecs)
- Slows impulse formation at SA, delays conduction across AV, decreases vascular tone
-Transient slowing of ventricular rate may allow for better diagnosis of the type of tachycardia
5
Q
Coronary circulation
A
Aortic sinus –>
1. Right coronary sinus –>
————————————-a. marginal artery –> small cardiac vein
————————————-b. posterior interventricular artery –> middle
2. Left coronary sinus –>
————————————-a. anterior interventricular artery –> great
————————————-b. circumflex –> posterior vein of LFV
–>Coronary sinus
6
Q
Arteriosclerosis
A
- Umbrella term for diseases where wall of artery becomes thicker, harder and less elastic
> Arteriolosclerosis: hardening of small vessels by HTN and diabetes
–>HTN → stiffen → lumen narrower → stiff → hypoxia → often arteriolonephrosclerosis (→ chronic renal failure)
–>Diabetes → damage endothelium
> Atherosclerosis: hardening from plaque
–> LDL, smoking, high BP damage → LDLs enter endothelial → monocytes follow → “foam cells” → releases cytokines → recruit more monocytes → fatty streak→ thrombogenic → platelets gather → release platelet-derived growth factor → smooth muscle infiltration → smooth muscle releases collagen, proteoglycans, elastin fibrous cells → fibrous cap → fatty streak + fibrous cap = plaque → deposit calcium creating crystals → stiffens walls of arteries → inflammation → C-reactive protein release
7
Q
Dx of atherosclerosis
A
> Physical exam (weakened pulse over blockage,
Bruits (whooshing sound due to turbulent flow and vibration)
Angiogram (dye in vessel) shows narrowing
8
Q
Types of Angina
A
- Decreased blood flow to the heart
1. Stable angina: subendocardium ischemia (70% block); on exertion
>Release of adenosine, bradykinin → pain
>ST depression on ECG
>Can be due to atherosclerosis (less supply), thickened heart walls (more demand)
- Unstable angina: subendocardium ischemia; at rest
>Can lead to MI
>ST depression on ECG - Vasospastic angina (prinzmetal): transmural ischemia; episodes do not correlate with exertion
>Often involves vasoconstrictors like thromboxane A2
>ST elevation on ECG
9
Q
Emergencies with chest pain
A
- Pulmonary embolism: pleuritic chest pain, tachycardia, increased HR, SOB, DVT, immobilization
- Esophageal rupture: vomiting, chest/epigastric pain, anxiety, recent instrumentation
- Tension pneumothorax: tracheal deviation, sudden SOB, pleuritic chest pain, recent instrumentation
- Myocardial infarction: retrosternal chest pain worse on exertion, radiating to arm/jaw, diaphoresis (excess sweating), decreased BP, hypotension, relieved by nitroglycerin
- Aortic dissection/rupture: tearing, upper back pain, increased blood pressure, change in blood pressure by 20mmHg
- Cardiac tamponade: SOB, Beck’s triad (hypotension, JVD, muffled heart sounds)
10
Q
Medication for atherosclerosis
A
- Aspirin: anti-platelet to reduce clotting (COX-1 inhibitor)
- Beta blockers: block effects of epinephrine; slow HR, vasodilate
>Labetalol, metoprolol - Statins: cholesterol medication; HMG-CoA reductase inhibitor
>Atorvastatin, rosuvastatin - Nitroglycerine: vasodilator
11
Q
Funny channels
A
- Funny current refers to a specific current in the heart
- Has effects opposite to those of most other heart currents
- Properties suitable for generating repetitive activity and for modulating spontaneous rate
- Degree of activation of the funny current determines steepness of phase 4 depolarization (frequency)
12
Q
Systole and diastole
A
Systole:
>End-diastolic: mitral valve closes, blood in left ventricle
>Aortic valve opens
>Ejection into aorta
Diastole:
>End-systolic: aortic valve closes, blood fills atrium
>Mitral valve opens: blood fills the ventricle
13
Q
Systolic heart failure
A
- Ventricles can’t pump hard enough (flabby)
- Decreased contractility: MI, dilated cardiomyopathy
- Increased preload: mitral/aortic regurgitation
14
Q
Diastolic heart failure
A
- Not enough blood fills the ventricles
- Normal ejection fraction, low total volume
- Heart is stiff, fibrotic, noncompliant
- Reduced preload: MI, restrictive cardiomyopathy, constrictive pericarditis, tamponade, tachyarrhythmia,
- Increased afterload: HTN, aortic stenosis, coarctation
- Can progress to systolic
15
Q
Left sided heart failure
A
- Usually occurs with underlying CVD; increased CO needed to meet higher demand
COMPENSATION: low CO = HoTN → activate sympathetic → increase HR and contractility (B1 rec on myocardium), universal vasoconstriction → JG renin release → AII → overwork of heart - Left sided HF usually systolic, often due to damage to the myocardium
>Ischemic heart disease
>Long-standing HTN (TPR increase, hypertrophy)
>Dilated cardiomyopathy (dilated to fill more blood) - Left sided diastolic:
>Long-standing HTN (hypertrophy, aortic stenosis)
>Restrictive cardiomyopathy (stiff muscles)
16
Q
Targets of angiotensin II
A
- Stimulate pituitary release of ADH → fluid retension
- Vasocontriction of arterioles → increased TPR
- Stimulate adrenal aldosterone → Na and H20
17
Q
Right-sided heart failure
A
- Blood backed up to body so congestion of veins in systemic circulation (JVP, hepatosplemomegaly, ascites, edema)
- Increased afterload: pulmonic stenosis, pulmonary HTN (PE, COPD, bronchiectasis, cor pulmonale)
- Increased preload: tricuspid/pulmonary regurgitation
- Decreased contractility: inferior MI, myocarditis
- Most often caused by left sided heart failure
18
Q
Framingham Diagnostic criteria
A
- For heart failure; 2 major or 1 major and 2 minor
MAJOR:
> Acute pulmonary edema
> Cardiomegaly
> Hepatojugular reflex
> Neck vein distention
> PND/orthopnea
> S3 heart sound
MINOR:
> Ankle edema
> Dyspnea on exertino
> Hepatomegaly
> Nocturnal cough
> Pleural effusion
> Tachycardia
19
Q
Diagnostic tools for CHF
A
- CXR
- BNP (brain natriuretic peptide; protein by heart in stress)
- Echocardiogram (ventricles dilated, stiff, etc)
- Ventriculography (cardiac catheterization)
20
Q
CHF treatment
A
- ACEi: ramipril
- ARBs: AII rec blocker
- Beta blocker: decrease HR, contractility, afterload (**never use in decompensated HF!!)
- Diuretics: furosemide (lasix), HCTZ (thiazide)
- Aldosterone antagonists (spirinolactone)
- Digoxin: increase contractility
21
Q
The layers of the heart
A
EPICARDIUM: single sheet of squamous epithelial cells overlying delicate connective tissue; in older patients, often infiltrated with fat
MYOCARDIUM: thick contractile middle layer of uniquely constructed and arranged muscle cells (bulk of the heart)
ENDOCARDIUM: white sheet of squamous epithelium that rests on a thin connective tissue layer; lines the chambers, continuous with great vessels`
22
Q
Pericardium
A
FIBROUS PERICARDIUM: outer wall; tough, dense, connective tissue that protects, anchors, and prevents overfilling
SEROUS PERICARDIUM: is thin serous membrane
> Parietal layer: lines internal surface of the fibrous pericardium
> Visceral layer/epicardium: outermost layer of the heart
> Parietal space
23
Q
Dilated cardiomyopathy (path, causes, treatment)
A
- Dysfunction of myocardium due to dilated heart chambers; ventricular dilation and thin walls (eccentric hypertrophy; added in series); S3
- CAUSES: most common idiopathic, alcohol, Beriberi (thiamine deficiency), Coxackie B myocarditis, cocaine, Chagas, Doxorubicin toxicity, , 3rd trimester pregnancy
- TREATMENT:
> Decrease preload: diuretics, fluid restriciton
> Decrease afterload: ACEi/ARBs, hydralazine (vasodilator)
> Increase contractility: digoxin
> Increase EF: pacemaker
> Decrease remodelling: BB, ACEi, aldosteron antagonist
> Anticoagulation: warfarin, DOACs
24
Q
Hypertrophic cardiomyopathy
A
- Asymmetric hypertrophy of interventricular septum; S4 (atrial kicks)
- CAUSES: genetic (mutation in HCM protein in sarcomeres; Freidreich ataxia), HTN
- Small ventricular diameter and thick walls (concentric hypertrophy; parallel)
- Decreased coronary perfusion (angina, SOBOE, vtach/vfib), decreased systemic perfusion (syncope)
- Venturi effect can lead to mitral regurgitation
- TREATMENT:
>Increase preload: no diuretics
>Increase afterload: avoid ACEi/ARBs
>Decrease contractility: BBs, CCB; avoid digoxin
25
Restrictive cardiomyopathy
- Myocardial dysfunction due to fibrosis/infiltration of cardiac tissue
- CAUSES: most common idiopathic, radiation, amyloidosis, sarcoidosis, hemochromatosis
- S3 heart sounds because rapid ventricular filling; bilateral atrial enlargement so mitral and tricuspid regurg
- TREATMENT:
> Gently decrease preload: diuretics
> Gently decrease afterload: ACEi, hydralazine
> Anticoagulation: warfarin, DOACs
26
Troponin
- Substance released into bloodstream upon death of cardiomyocytes
- Elevated early in disease process
27
Medications for MI
- Aspirin: anti-platelet
- Ticagrelor: antiplatelet medicine
- Enoxaparin: anticoagulant (Xa)
28
post-MI complications
- Decreased contractility → HoTN → less to coronary arteries → cardiogenic shock
- Electrical instability → arrhythmias
- Tissue necrosis → pericarditis, ventricular septal defect, ventricular rupture (→ tamponade), chordae tendinae (→ valve regurgitation)
29
Pericarditis (acute v chronic)
- Acute: less than 3months
> CAUSES:
--> Infectious: mostly viral, S. aureus, TB
--> Autoimmune: Ab-mediated agitation (RA, SLE)
--> Uremia: end stage renal disease, AKI
--> Neoplasia: primary cancer can seed (most likely lung cancer > non-hodgkins > leukemia > renal cell carcinoma > breast
--> Radiation: destruction of pericardial tissue
--> Post-MI: ischemia → dead myocardium → immune cell cleanup → cytokines → inflammation → leaky vessels → fluid buildup
- Chronic: more than 3 months
- Can lead to pericardial effusion → squeeze heart → reduce ventricular filling → cardiac tamponade
30
Electrical alternans
- Electrical alternans: alternating QRS amplitudes in any or all leads on an electrocardiogram (ECG) with no additional evident changes in conduction pathways of the heart
- This rhythm is typically associated with pericardial effusion from fluid surrounding the heart (fluid sloshing, messing up vectors)
31
Pericardial effusion treatment
- NSAIDS (7-10 days)
- Colchicine: inhibit neutrophils (recurrence)
- Steroids: reduce inflammatory process in TB patients and autoimmune
- Pericardiocentesis
32
MI Bloodwork
- Troponins: certain subtypes only found in heart muscle cells; most specific marker for heart damage
- Myoglobin: found elsewhere in body and heart cells
- Creatine kinase mB: more specific, sometimes looked for
33
Endocarditis (causes, Dx)
- Most cases are due to microbial infection of endocardium, often around valves because tiny vessels supply them
> Gram (+) bacteria (Viridans streptococcu, S. aurea [IV drugs], S. epidermidis [mech valves]
- Mitral and aortic valve most often affected; prosthetic valves, congenital defects, damage to valves (rheumatic heart disease), IV drug use all risks
- Non-bacterial thrombotic endocarditis → bacteremia → infective endocarditis → bacteria bind NBTE → vegetation → immune system involvement → proteases → valve destruction → regurgitation
- Septic emboli and immune complexes (osler nodes, roth spots, glomerulus) deposit around body and cause problems/symptoms
- Mitral valve regurgitation → increased preload → eccentric hypertrophy → left sided HF
34
Aortic valve
- Three leaflets, opens in systole
- STENOSIS: doesn't open all the way, hard to pump
> Chronic rheumatic fever: repeated inflammation and repair → fibrosis → leaflets fuse (commissural fusion)
>Bicuspid aortic valve: <70 y/o; congenital, 2 leafs
>Calcified aortic valve: >70 y/o; calcium deposition (HTN, hyperlipidemia, smoking, DM)
> High pressure on stiff valves → ejection click; turbulence (small opening) murmur (crescendo-decrescendo)
> Left ventricle hypertrophies
> Risk of heart failure because reduction in blood flow out of the heart to aorta (syncope and angina in exercise) → S4
- REGURGITATION: leak back to atria
> 50% cases due to aortic root dilation (root gets wider, leaflets pulled apart; mostly idiopathic, aneurysms and syphilis)
>Valvular damage such as endocarditis or chronic rheumatic fever
>Early decrescendo diastolic murmur because blood flowing back to the valve
>Ventricular blood volume increases, increasing stroke volume → more pressure to pump out, but less blood in the atrium → bigger gap between systole and diastole → increased pulse pressure (difference) = hyperdynamic circulation where pulses are very violent, can cause head bobbing and capillary beds in fingers to pulsate (Quincke’s sign)
>Increase in blood volume leads to left ventricle hypertrophies
35
Mitral valve
- Two leaflets (anterior and posterior); separate LA and LV
- STENOSIS:
> Rheumatic fever: commissural fusion makes opening smaller; higher pressure makes snap sound then diastolic rumble when blood forced to squeeze through (antibodies attacking mitral valve) → back up in left atrium → pulmonary congestion and edema → pulmonary hypertension → right ventricle hypertrophy and failure → RHF
- REGURGITATION:
> Primary: involving the leaflets, chordae tendineae, or papillary muscles
> Secondary: stretch annulus; CHF, dilated cardiomyopathy
>Leading cause is mitral valve prolapse → weakened connective tissue lead to prolapse
-->Often associated with marfan syndrome and ehlers-danlos syndrome (connective tissue disorders); infective endocarditis; MI (death of chordae tendineae or papillary muscles)
-->Usually asymptomatic, heart murmur with midsystolic click (leaflet folding into atrium and suddenly stopped by chordae tendinae), sometimes followed by systolic murmur (if regurgitation)
>Left sided heart failure leading to ventricular dilation, bigger opening
>Rheumatic fever → chronic rheumatic heart disease → leaflet fibrosis → holo-systolic murmur (lasts for duration of systole)
36
Tricuspid valve
- Three leaflets, separate RA and RV
- STENOSIS:
>Rheumatic fever: if tricuspid effected, mitral and aortic almost always also affected; commissural fusion → snapping sound when opening → RA dilation → blood back up in veins & irritation of pacemaker cells → arrhythmias
- REGURGITATION:
>Heard as holosystolic murmur (duration of systole), and sometimes also Carvallo’s Sign, where murmur gets louder on inspiration because more blood to the heart
>Extra blood leaking increases right ventricular preload → eccentric right ventricular hypertrophy → stretches the annulus (ring of valve, more leakage!) → eventually RV can’t keep up → right HF → JVP, peripheral edema, hepatosplenomegaly
-->Pulmonary hypertension, increasing RV pressure
-->Rheumatic heart disease → fibrosis
-->Damage to papillary muscles from heart attack
-->Congenital defects
37
Pulmonary valve
- 3 leaflets
-STENOSIS:
> Carcinoid syndrome: diarrhea, rash, wheezing → neuroendocrine tumor cells in heart, secretes serotonin precursor, making valve very stenotic
> Tetralogy of fallot: congenital; VSD, right ventricular hypertrophy, high riding aorta
-REGURGITATION:
>After balloon in repaired tetralogy of fallot
38
Acyanotic congenital heart defects
- Left to right shunts (increase pulmonary blood flow)
- ATRIAL SEPTAL DEFECT: LA → RA
- VENTRICULAR SEPTAL DEFECT: LV → RV
- PATENT DUCTUS ARTERIOSUS: aorta → pulm artery
- ENDOCARDIAL CUSHION DEFECT: combo ASD and VSD; only 1 leaflet for mitral and tricuspid valves
- CONSTRICTION OF AORTA: stenotic ring, restrict bloodflow to lower extremities
39
Cyanotic congenital heart defects
- TETRALOGY OF FALLOT: ventricular septal defect, right ventricular hypertrophy, pulm stenosis, overriding aorta
> Prostaglandin E1: keep ductus arteriosus patent
- TRANSPOSITION OF GREAT ARTERIES: failed spiraling so RV empties into aorta and LV into pulm arteries (DiGeorge Syndrome, maternal DM)
- TRUNCUS ARTERIOSUS: VSD and single trunk from RV and LV, bifurcates; total mixing → LHF
- TOTAL ANOMALOUS PULMONARY VENOUS RETURN: pulmonary veins don't empty into LA, pulmonary veins empty into RA via connecting veins; no O2 blood to LA, resp distress, pulm edema
- TRICUSPID ATRESIA: tricuspid valve fails to develop normally with a hypoplastic right heart and VSD
Medical School
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