July 2023 Flashcards
Case Study: Constructive Pericarditis
Constructive pericarditis is scarring and calcification of the pericardium result in loss of normal elasticity—this limits diastolic relaxation of the heart and causes congestive heart failure.
How to Diagnose
• LV discordance due to the “ventricular interdependence” (will be caught during RHC).
• Since the ventricles in the setting of constrictive pericarditis are unable to expand, the variation in intracardiac pressure during the respiratory cycle exerts changes only between the right and left ventricles = does not occur in restrictive cardiomyopathy.
• With inspiration, intrathoracic pressure decreases and the right ventricle fills. This causes the right ventricular pressure to increase, pushing the interventricular septum towards the left ventricle and impairing left ventricular filling.
• With expiration, intrathoracic pressure increases and right ventricular filling is decreased. The left ventricle fills and pushes the interventricular septum towards the right and impairs right ventricular filling.
• RV and LV end-diastolic pressures elevated and equal. Low or normal BNP levels (restrictive has elevated BNP, due to myocardium stretching).
Etiology
1. Tuberculosis, which is the most common cause worldwide.
2. Viral infection.
3. Radiation therapy (occurred frequently in the late 1970s and early 1980s when high doses were given for non-Hodgkin’s lymphoma—constrictive pericarditis can present decades later).
4. Trauma.
5. Post-cardiac surgery.
H&P
• 20 yo Arab male. Cash pay. Upper respiratory infection from Middle East (Hajj, Umrah, Dubai, Qatar, etc.) in 12/22. Ascites presentation lead to negative biopsy of cirrhosis. Finally got cardiology referral seven months later, due to presenting symptoms of RS failure.
Symptoms
• SOB, ascites, leg edema, large RA, tricsupid valve buldging into RV due to pressure, JVD—typical RS failure symptoms.
• IVC plethora (high pressure in RA).
• Large pleural infusion.
Diagnostics
• TTE (initially thought of Ebstein Analomy due to large RA and age): Septal bouncing due to pressure from the RV, so LV has less space as a result of stiff pericarditis. Ventricular interdependence increases in constrictive pericarditis and presents as septal bounce. Diastology issue.
• Hepatic vein doppler (JVD):?
• RHC (atrial pressure): clear ventricular interdependence on RV LV pressures. Augmented V-wave (on pressure wave form) with Y descent suggestive of RA non-compliance. Normal filling pressures on left side. Intra-thoraic intracardiac dissociation on PCW-LVEDP pressures.
• MRI: Positive (inflammation present).
Treatment
• High dose aspirin and colchicine.
• Presidone.
• Control inflammation prior to pericardiectomy.
Case Study: Aortic Dissection
Aortic dissection is the tearing and/or widening of artery’s internal layer, followed by blood entering vessel wall,causing pain.
• Tear forms in tunica intima of aorta→high pressure blood flows between tunica
intima/tunica media→layer separation
false lumen→dilate aorta.
• Most aneurysms develop in first 10 cm of
the aorta.
Types: Stanford Classification
• Type A
◦ Dissection involves ascending aortaand/or aortic arch; sometimes descendingaorta.
• Type B
◦ Dissection involves descendingaorta/aortic arch without involvement ofascending aorta.
Causes
•Weakness in vessel wall due to chronic
hypertension, blood vessel coarctation (narrowing of aorta),connective tissue disorders, aneurysms.
•Pregnancy, previous open heart surgery,
vasculitis, trauma, family history of aortic.
dissection, Turner’s syndrome, cocaine use.
• Cystic medial necrosis (cyst-like on aorta).
Complications
•Pericardial tamponade
◦ Most common cause of death (compression of the fluid surrounding the sac around heart).
• Blood flow tears tunica media/tunica
externa→severe internal bleeding→death.
• Blood flow tears tunica intima again, returnto true lumen (not severe).
• Obstruction of arterial branches off aorta,
leading to ischemia of individual organs.
• Blood tunnels, creates false lumen that
extends to aortic branch→obstruction.
Signs and Symptoms
•Sudden, intense, tearing chest pain
radiating to back; nausea, vomiting,diaphoresis.
• Chronic dissection, painless.
• Decreased peripheral pulses, asymmetric
pulses.
• Hypertension/hypotension depending on
location of dissection.
• Diastolic decrescendo murmur
◦Ascendingaortic dissections→ aortic regurgitation.
• Neurological deficients
◦Stroke, hemiplegia (half side paralysis), syncope.
• Abnormal Chest X-ray
◦Widening of mediastinum consistent withdissection, but inadequate as sole evidencefor diagnosis.
• Abnormal Transesophageal echocardiogram
◦Best for hemodynamically-unstableindividuals.
◦High sensitivity for identifying dissection, complications like aortic regurgitatior cardiac tamponade. Involvement ofcoronary arteries.
• Abnormal CT angiography
◦Best for hemodynamically-stable individuals.
◦High sensitivity for identifying dissection,can provide anatomic information useful in planningsurgical repair: visualize/locatedissection.
Treatment
•Stanford Type B: lower heart rate, blood
pressure.
• Beta-blockers (first line).
• Calcium channel blockers (second line).
• Pain management for acute dissection.
• Stanford type A: medical emergency,surgical repair indicated.
• Stanford type B: surgical repair indicated
when dissection acute, complications arisemedication ineffective.
H&P
• White male, 70 years of age in the ER
Symptoms
• Pressure on chest (no fluttering); shortness of breath; chest, back, and shoulder pain—that did not get better with rest.
• Left atrium scarring, LVH.
• Elevated creatinine, lactic acid, and troponin.
• Leaky value, hypoperfusing.
• Presented with acute syndrome in the ER; they did not rule out acute aortic dissection.
• Wide mediastinum on X-Ray that was not caught in time, when in the ER.
Treatment
• Proposed treatment was cardioversion (which was initially declined), but he was seen with an aortic dissection; thus, he was sent to getstat CTA.
• Underwent emergent type A-B aortic repair with arch replacement and AV replacement w/ Kathryn Harrington @ Baylor Heart Plano.
Prognosis
• Passed away two days after surgery—was extubated.
Pulmonary Hypertension Classes
Pulmonary hypertension is increased blood pressure in pulmonary circulation.
• Mean pulmonary arterial pressure →
25mmHg (normal ~15mmHg).
• Pulmonary hypertension is excess fluid in pulmonary interstitium (pulmonary edema) → impaired gas exchange.
• Pulmonary hypertension → strain on right heart → hypertrophy → right heart oxygen demand eventually exceeds supply → right-sided heart failure.
◦Right heart failure caused by lung disease → cor pulmonale → backup of blood in venous system → signs, symptoms of right heart failure.
Symptoms
• Raised jugular venous pressure.
• Fluid build up in liver (hepatomegaly).
• Fluid build up in legs (leg edema).
• Left ventricle receives less blood → compensation → pumps harder, faster (tachycardia).
• Heptaojugular reflex.
• Ascites.
• Loud pulmonic component of second heart sound (P2).
• Dyspnea, syncope, fatigue, chest pain, poor effort tolerance, loss of appetite lightheadedness, orthopnea (left-sided heart failure).
• Tachycardia. cyanosis, parasternal heave.
Risk Factors
• Family history, prior pulmonary embolic events, HIV/AIDS, sickle cells disease, cocaine use, COPD, sleep apnea, living at high altitude, mitral valve pathology.
Types
Group I
• Pulmonary arterial hypertension, pulmonary veno-occlusive disease, pulmonary capillary hemangiomatosis.
• Abnormal increase in pulmonary arteriolar resistance = increased strain on right heart (pumping fluid through narrower pipe).
• Damage to endothelial cells lining pulmonary arteries → release of endothelin-1 serotonin, thromboxane, produce less nitric oxide and prostacyclin → constriction of arterioles, hypertrophy of smooth muscle → pulmonary hypertension.
• Over time affected vessels become stiffer, thicker (fibrosed) due to vasoconstriction, thrombosis, vascular remodeling → greater increase in blood pressure in lungs, more strain on right heart.
• Idiopathic, inherited, drug/toxin associated causes connective tissue disease, HIV infection, portal hypertension congenital heart disease (shunting).
Group II
• Pulmonary hypertension secondary to left heart isease.
• Pulmonary hypertension due to left heart disease (heart failure, valvular dysfunction)
→ left heart fails to pump blood efficiently
→ backup of blood in pulmonary veins, capillary beds → increased pressure in pulmonary artery → pulmonary edema, pleural effusion
• Raised back pressure may trigger secondary vasoconstriction → increased right heart strain
• Common causes include:
◦Left ventricular systolic/diastolic dysfunction.
◦Valvular heart disease.
◦Congenital/acquired in/out-flow tract obstruction.
◦Congenital cardiomyopathy.
◦Pulmonary venous stenosis.
Group III
• Pulmonary hypertension due to lung disease/chronic hypoxia
• Low oxygen levels in alveoli pulmonary arteries constrict.
• Chronic lung disease → region of diseased lung → inefficient/total lack of gas exchange → hypoxic vasoconstriction (pulmonary arterioles) → shunting of blood away from damaged areas.
• Prolonged alveolar hypoxia across wide portion of pulmonary vascular bed → increase in pulmonary arterial pressure thickening of pulmonary vessel walls → greater effort required from right heart → sustained pulmonary hypertension.
• Causes include:
◦COPD
Group IV
• Chronic arterial obstruction
thromboembolic disease.
• Recurrent blood clots in pulmonary vasculature.
• Blockage/narrowing of pulmonary vessel wIth unresolved obstruction (e.g. clot) increased pressure, shear stress (turbulence) in pulmonarv circulation → vessel wall remodeling → sustained pulmonary hypertension.
• Causes endothelium to release histamine,
serotonin → constriction of pulmonary
arterioles → rise in pulmonary blood
pressure → chronic thromboembolic
pulmonary hypertension.
• Other causes of arterial obstruction:
◦Angiosarcoma, arteritis, congenital pulmonary artery stenosis, parasitic
infection.
Group IV
• Unclearmultitactor mechanisms.
• Hematologic disease e.g. hemolytic anemia.
• Systemic disease (e.g. sarcoidosis, vasculitis).
• Metabolic disorders (e.g. glycogen storage disease, thyroid disease.
• Other (e.g. microangiopathy, chronic kidney
disease).
Diagnostics
• Chest X-ray
◦ Enlarged pulmonary arteries.
◦ Lung helds may or may not be clear dependent on underying cause.
• Echocardiogram
◦Increased pressure in pulmonary arteres riant ventricies → dilated pulmonary artery
◦Dilatation/hypertrophy of right atrium, right ventricle.
◦Large right ventricle → bulging septum
• Ventilation/perfusion scan
◦Identity exclude ventilation-perfusion mismatches.
• Right heart catheterization (gold standard)
◦Catheter into right heart → most accurate measure of pressures.
• ECG
◦Right heart strain pattern: T wave inversior in right precordial (V -V), and inferior leads (II, Ill, aVF).
• Spirometer
◦Unidentified underlying cause
Diuretics
• Thiazide group (e.g. Indapamide and Bendroflumethiazide).
• Diuretics are used in the treatment of both hypertension and heart failure. Thiazides are used in hypertension.
◦Diuretics increase fluid loss from the body therefore lowering BP, making them useful in the treatment of hypertension. By lowering fluid levels in the body, the preload and afterload are reduced which helps to reduce the demand on the heart.
• Aldosterone antagonists (e.g. Spironolactone) or Mineralocorticoid receptor antagonists
◦This group of drugs are another type of diuretic, and are especially used in the treatment of hypertension caused by hyperaldosteronism.
◦These drugs block aldosterone receptors, therefore reducing the reabsorption of sodium and water from the kidney to reduce BP.
◦They can also be used as an adjunct along with ACEi or ARBs in primary hypertension.
Steal Syndromes
Coronary Steal Syndrome
• Narrowed/obstructed coronary vessel + vasodilator alters cardiac circulation
→ blood shunted away from area distal to narrowing/obstruction exacerbating ischemia
• Artery narrowing/obstruction → dilation of distal arteries to compensate for decreased blood flow → addition of vasodilator → dilation of resistance vessels → blood supplying ischemic zone shunted away to areas of least resistance → more ischemia
• Narrowing of coronary arteries + vasodilator (e.g. dipyridamole, adenosine)
→ blood flows to non-obstructed vessels
→ exacerbating ischemia
◦Dipyridamole: antiplatelet, vasodilator
→ all coronary vessels dilate when in individual with partial obstruction of coronary artery.
◦Vasodilator may steal blood from deprived region distal to obstruction.
• Dilation of resistance vessels → blood shunted away from coronary vessels.
Causes
• Coronary artery bypass grafting surgery
(CABG)
◦Due to left internal mammary artery
(LIMA) graft.
◦Retrograde flow from LIMA to left subclavian artery.
• Drugs
◦Dipyridamole, nitroprusside, isoflurane (inhaled anesthetic), vasodilators.
◦Coronary arteriovenous fistula between coronary artery, cardiac chamber.
Subclavian Steal Syndrome
• Stenosis/occlusion in subclavian artery → reversal of blood flow in vertebral artery
• Occlusion/narrowing in subclavian artery
→ blood drawn away from head, flows retrogradely to supply oxygen to upper extremities (e.g. blood to brain stolen to supply left upper limb)
• Blood flows up right brachiocephalic → right subclavian → right vertebral artery
→ basilar artery, left vertebral joins → blockage of left vertebral upstream → blood from right vertebral artery enters left vertebral → left subclavian → flows back to right arm.
Causes
• Atherosclerosis is most common
• Takayasu disease is least common (chronic inflammation of aorta, large vessels)
• Giant cell arteritis.
• Blalock Taussig shunt (surgical procedure to increase blood flow to lungs; tube placed between subclavian, pulmonary arteries).
• Thoracic aortic dissection.
• Thoracic outlet compression.
• Interrupted aortic arch.
• Congenital aortic coarctation.
RAAS
Renin-Angiotensin-Aldosterone System (RAAS)
• Baroreceptors (pressure-sensitive receptors) in arterial vessels detect low BF/BP or kidneys detect low NA + decrease in renal perfusion [juxtaglomercular apparatus] → JG Cells + in kidney release Renin → Angiotensinogen in liver is converted to A.T. I → ACE in lungs then converts to A.T. II…
Renin Release
• Renin released from granular cells of the renal juxtaglomerular apparatus (JGA) in response to one of three factors:
1. Reduced sodium delivery to the distal convoluted tubule detected by macula densa cells.
2. Reduced perfusion pressure in the kidney detected by baroreceptors in the afferent arteriole.
3. Sympathetic stimulation of the JGA via β1 adrenoreceptors.
• The release of renin is inhibited by atrial natriuretic peptide (ANP), which is released by stretched atria in response to increases in blood pressure.
- Production of Angiotensin II
• Angiotensinogen is a precursor protein produced in the liver and cleaved by renin to form angiotensin I.
• Angiotensin I is then converted to angiotensin II by angiotensin converting enzyme (ACE). Occurs in the lungs by vascular endothelial cells, but smaller quantities by renal endothelium.
Binding of Angiotensin II
• Binds to one of two G-protein coupled receptors, the AT1 and AT2 receptors. Most actions occur via the AT1 receptor.
Arterioles → Vasoconstriction.
Kidney → Stimulates Na+ reabsorption.
Sympathetic nervous system → Increased release of noradrenaline (NA).
Adrenal cortex → Stimulates release of aldosterone.
Hypothalamus → Increases thirst sensation and stimulates anti-diuretic hormone (ADH) release.
Effects of Angiotensin II
• Cardiovascular Effects
◦Angiotensin 2 acts on AT1 receptors found in the endothelium of arterioles throughout the circulation to achieve vasoconstriction. This signalling occurs via a Gq protein, to activate phospholipase C and subsequently increase intracellular calcium.
◦ The net effect of this is an + in total peripheral resistance and BP.
• Neural Effects
◦Angiotensin II acts at the hypothalamus to stimulate the sensation of thirst → increase in fluid consumption → raise the circulating volume and BP.
◦Increase the secretion of ADH from posterior pituitary gland → more concentrated urine to reduce the loss of fluid from urination (allows the circulating volume to be better maintained until more fluids can be consumed).
◦Stimulates the SNS to increase the release of noradrenaline (NA), in fight or flight: → increase in cardiac output → vasoconstriction of arterioles → release of renin.
• Renal Effects
◦Renal artery and afferent arteriole → Vasoconstriction = Voltage-gated calcium channels open and allow an influx of calcium ions.
◦Efferent arteriole → Vasoconstriction (greater than the afferent arteriole) = Activation of AT1 receptor.
◦Mesangial cells → Contraction, leading to a decreased filtration area = Activation of Gq receptors and opening of voltage-gated calcium channels.
◦Proximal convoluted tubule → Increased Na+ reabsorption = Increased Na+/H+ antiporter activity and adjustment of the Starling forces in peritubular capillaries to increase paracellular reabsorption.
◦Angiotensin II is also an important factor in tubuloglomerular feedback, which helps to maintain a stable glomerular filtration rate. The local release of prostaglandins, which results in a preferential vasodilation to the afferent arteriole in the glomerulus, is also vital to this process.
Aldosterone
• Angiotensin II acts on the adrenal cortex to stimulate the release of aldosterone. Aldosterone is a mineralocorticoid, a steroid hormone from the zona glomerulosa of the adrenal cortex.
• Aldosterone acts on the principal cells of the collecting ducts in the nephron (increases the expression of apical epithelial Na+ channels (ENaC) to reabsorb urinary sodium + activity of the basolateral Na+/K+/ATPase is increased.
• Additional sodium reabsorbed through ENaC to be pumped into blood by the sodium/potassium pump = potassium is moved from the blood into the principal cell of the nephron → potassium exits the cell into the renal tubule to be excreted into the urine → increased levels of aldosterone cause reduced K+.
ACEi/ARBs
Angiotensin Converting Enzyme Inhibitors (ACEi)
• -pril (e.g. Ramipril, Lisinopril)
• These drugs inhibit the action of ACE, blocks the amount of angiotensin II formed from angiotensin I.
• Reduced activity of RAAS by decreased arteriolar resistance, decreased arteriolar vasoconstriction, decreased cardiac output, reduced potassium excretion in the kidneys → all results in vasodilation, reduced aldosterone release, reduced ADH release.
◦No vasoconstriction (as no angiotensin II), instead there is vasodilation → increased diameter of lumen and less resistance (lower TPR) → lower blood pressure.
◦Angiotensin II stimulates posterior pituitary gland to make ADH—with less stimulation → less water reabsorbed → drop in blood volume → lower blood pressure (as water retention increase BP, heart works harder).
◦Zona glomerulosa of the adrenal cortex produces aldosterone—with decrease Angiotensin II → less of aldosterone → decrease in sodium and water reabsorption → decrease in BV and BP → no excreted potassium, which may lead to hyperkalemia (potential side effect of ACEi)—aldosterone causes kidneys to excrete potassium.
◦Help to treat hypertension as they decrease the TPR (total peripheral resistance—if the area available for blood to flow through is reduced then pressure will increase) and help to increase fluid loss—helps heart failure as it reduces the hearts workload.
◦Taken after MI→ increase perfusion of heart to prevent further damage.
◦Heart isn’tstrong enough to pump out an enoughblood→ decreased vasoconstriction leads to decreased peripheral vascular resistance→heart doesn’tpump as hard with medication.
• Cannot be taken during pregnancy→ congenital defects of fetus (Potter Syndrome).
• Side effect of a dry cough.
◦This is as ACE also breaks down bradykinin in the lungs. Inhibiting ACE allows bradykinin to build up in the lungs which causes a dry cough.
◦Bradykinin accumulation can lead to painful swelling in the airway (angiodemia).
◦This can alter compliance with treatment, especially as hypertension is a mostly silent condition i.e. the drug induces symptoms when there were none previously. Patients with this side effect may be switched to an angiotensin receptor blocker.
Angiotensin Receptor Blockers (ARBs)
• -sartan (e.g. Losartan, Valsartan, Candesartan)
• Used in both the treatment of hypertension and heart failure.
◦They block angiotensin receptor 1 which prevents angiotensin II from binding. This leads to a reduced effect of angiotensin II.
◦ARBs essentially have the same effects as ACEi, however one difference is that the ACE enzyme is not affected. This means that ACE can still break down bradykinin and therefore dry cough is not a side effect of ARBs.
◦ARBs are used in patients who cannot tolerate ACEi.
• A.T II → Vasoconstriction → increased TPR → increased after-load → more stress on the heart.
• A.T II → increased ADH + increased aldosterone → increased Na/H2O → increased BV → increased preload (amount of blood that returns to the heart) → increased EDV → more stress on the heart.
◦With ACEi/ARB, the opposite happens.
Beta-Adrenoreceptor Blockers
• -lol (e.g. atenolol and bisoprolol)
◦Beta blockers are used as an add on in hypertension and are not generally first line.
Class I: Sodium Channel Blockers
• Membrane-stabilizing drugs that block fast sodiumchannels, slowing conduction in fast-channeltissues (working atrial and ventricularmyocytes, His-Purkinje system)
• Must take with a heart slowing medicine likeBetaBlockerorCalcium Channel Blocker
•Proarrhythmiarisk
◦All class I drugs mayworsen VTs (tend to depressventricular contractility)→more likely to occur in patients with astructural heart disorder→NOT for patients with congestive heart failure,cardiomyopathy, history of stent, or coronary arterydisease
•Can take only upon onset of symptoms as “pill-in-pocket” approach
- Class la drugshave intermediate kinetics
•Block repolarizingpotassium channels + prolongs refractoryperiods of fast-channel tissues→slows conduction velocity
• On the ECG, thiseffect is reflected as QT-interval prolongation (evenat normal rates)
•Indications aresupraventricular & ventricular tachycardias→may causetorsades de pointeandventricular tachycardia
•Disopyramide,Procainamide,Quinidine - Class Ib drugs have fast kinetics
• Expresseffects only at fast heart rates→ no effect on conduction velocity + shorten APD (action potential duration)
•Used for the suppression ofventriculararrhythmias
◦Ventricular prematurebeats, ventricular tachycardia, ventricularfibrillation
•Lidocaine, Mexiletine,Phenytoin - Class Ic drugs have slow kinetics
•Expresseffects at all heart rates→ slows conduction
•Potentantiarrhythmics (better than other class drugs)
• Suppressionof atrialpremature beats, ventricular premature beats,supraventricular tachycardia, ventriculartachycardias, atrial fibrillation, atrial flutter, andventricular fibrillation
• Flecainide,Propafenone
Medications
• Flecainide
◦Blurring of vision; headache
• Propafenone
◦Metallic taste; constipation
Class II: Beta Blockers
• Affectspredominantly slow-channel
tissues (SA/AVnodes)→decrease rate of
automaticity, slow conduction velocity, and
prolong refractoriness→heart rateis slowed, the PR interval is lengthened, and the AVnode transmits rapid atrial depolarizations at alower frequency
• Fatigue; insomnia; impotence; gastrointestinal upset
• Weak AAD for AFib →used for rate control orwith Class I or Class Ill drugs
•Can be used in most patients unless very slowheart rate or very low blood pressure→induce bradycardia
• Can worsen severe lung disease like asthma andCOPD→fatigue or impotence
Medications
• Acebutalol
• Atenolol
• Bisoprolol
• Carvedilol
• Esmolol
• Metoprolol
• Nebivolol
• Propranolol
Class III: Potassium Channel Blockers
•Prolongaction potential duration and refractoriness inslow and fast-channel tissues→capacity of cardiac tissues to transmitimpulses at high frequencies reduced +conduction velocity not affected
• Treat supraventricular tachycardia and ventricular tachycardia
•All Class Ill drugs require QTC monitoring on ECG
• Avoid low potassium or low magnesium whichprolongs QTC
•QTC prolongation can cause a fatal heart rhythm (proarrthrymia) →Torsade de pointes (TaP)
Medications
• Sotalol
◦Needs dose adjustment as kidney function declined;started in thehospital for 3-6 doses for QTC monitoring
• Dofetilide
• Amiodarone
◦Safe inpatients with heartdisease and kidneydysfunction includingdialysis; needs dose adjustment as kidney function declines;started in thehospital for 3-6 doses for QTC monitoring
• Dronedarone
◦Weaker version of Amiodaronebutcan’t be used incardiomyopathy orcongestive heart failure
Class IV: Calcium Channel Blockers
•Nondihydropyridine calcium channel blockers→depress calcium-dependent actionpotentials in slow-channel tissues and thusdecrease the rate of automaticity, slowconduction velocity, and prolongrefractoriness
• Weak AAD for AFib → for rate control or withClass I or Class Ill drugs
•Avoid in patients with congestive heart failure orleft ventricular ejection fraction LVEF < 35%
•Can excessively slow normal heart rate
• Constipation; leg edema
Medications
•Verapamil
◦Left septal or Belhassen VT
• Diltiazem
Articles
https://www.ahajournals.org/doi/pdf/10.1161/CIRCULATIONAHA.118.035455
https://www.medschool.lsuhsc.edu/cardiology/docs/Antiarrhythmic%20Drugs.pdf
Calcium Channel Blockers
• Dihydropyridine
◦-dipine (e.g. Amlodipine, Nifedipine, Nicardipine)
• Start AA on CC blockers and hydrochlorothiazide.
◦Work by peripheral vascular—relaxing atrial smooth muscle, inhibiting vasoconstriction → increased vasodilation → dropping total peripheral resistance (don’t want to increase afterload) → decrease overall pressure.
◦Widen blood vessel too much→swelling in the legs.
◦Binds to and blocks Ca+ channels in the smooth muscle cell of arterial blood vessel → so instead of Ca+ entry leading to muscle contraction, it increases vasodilation → lowers BP.
◦More effect on vasodilation, less effect on heart function.
• Non-dihydropyridine
• -amil, -mez (e.g. Verapamil, Diltiazem)
◦CCBs from the dihydropiridine group are mainly used in the treatment of hypertension due to the effect on the peripheral vasculature to reduce TPR.
◦Decrease contractility by inhibiting calcium from going in.
◦Inhibitory effect on SA/AV nodes →slows cardiac conduction and contracting.
◦Less effect on vasodilation, more effect on heart function.
• Class IV Antiarrhythmics
• Verapamil (Calan, Isoptin)
◦Decrease myocardial contractility
◦More cardioselective→ potent anti-arrhythmic (slows heart rhythms).
• Diltiazem (Cardizem)
◦Decrease myocardial contractility.
◦More effective for vasodilation (lower blood pressure; not a lot of effect on heart).
Alpha Adrenoreceptor Blockers
• -osin (e.g. doxazosin and prazosin).
• Selectively antagonise α1-receptors cause vasodilation and decreasing the total peripheral resistance, therefore lowing BP.
◦Block effect of sympathetic nerves on blood vessels by binding to alpha-adrenoceptors on the vascular smooth muscle.
◦Selective alpha-1 adrenergic antagonists prevent norepinephrine (NE) from being released by sympathetic nerves synapsing on smooth muscle causing vasodilation = sympatholytics (antagonize sympathetic activity).
Digoxin Toxicity
• Being on Digoxin + low level of magnesium (as magnesium transports potassium into the heart) may cause toxicity.
• Worsened by hypokalemia—digoxin binds to the K+ site of the Na+/K+-ATPase pump, low serum potassium levels increase the risk of digoxin toxicity.
• Hyperkalemia diminishes digoxin’s effectiveness; most are elderly, often with K+ imbalances and poor renal function, toxicities are not uncommon.
Symptoms
• Non-specific with cardiac (dysrhythmia), gastrointestinal (nausea, vomiting, abdominal pain), neurological (confusion, weakness, delirium) symptoms, visual disturbances (green or yellow halos, “fuzzy shadows”—like driving at night with dirty glasses).
• Confusion and yellow vision, cardiac (atrioventricular blockade, bradycardia, and ventricular arrhythmias).
Risk Factors
• Renal impairment: digoxin is eliminated in the urine; the half-life of digoxin is prolonged in patients with kidney disease.
• Concomitant medicines: Inducers/inhibitors of P-glycoprotein and electrolyte abnormalities (eg, diuretics).
• Age: the incidence of digoxin toxicity increases with age.
Mechanism of Digibind Antidote
• Inhibition of Na/K ATPase on the cell surface → increased intracellular Na+ and increased extracellular K+ → increased intracellular Ca2+ due to Na+/Ca2+ antiporter → calcium-mediated inotropy and increased automaticity, as well as negative dromotropy due to decreased intracellular K+ (DIRECT)
• Increased vagal tone—vagomimetic effect (INDIRECT)
Beer Potomania
RHC
Cardiac Output
Cardiac output (ml/min) = stroke volume (ml/beat) × heart rate (beats/min)
• Commonly 5L/min (0.07 mL/min x 70 bpm)
• Stroke volume = the amount of blood put out by the left ventricle of the heart in one contraction (EDV - ESV = SV).
eFick Principle
• Calculate cardiac output by measuring myocardial oxygen consumption.
Cardiac Output = Total O2 Consumption / (O2 pulmonary vein) - (O2 pulmonary artery) OR arteriovenus O2 difference
Example: 250 mL/min / 0.3 mL - 0.25 mL = 5 L/min or 5000 mL/min
• Pulmonary veins: peripheral arterial blood
• Pulmonary arteries: Mixed veinous blood from pulmonary artery/ right ventricle
• O2 in pulmonary veins - O2 in pulmonary arteries = O2 body has used.
• Model used to measure cardiac output (CO)
◦Output of left = right ventricles equal during normal cardiac function.
• Steady state: rate of O2 consumption = (amount of O2 leaving lungs via pulmonary vein) - (amount of O2 returning via
pulmonary arteries) × CO
• Pulmonary blood flow of right heart = CO of left heart, which is used to calculate CO.
• 250mL/minute = total O2 consumption (70kg, biological-male individual): pulmonary venous O2 content = 0.20/mL AND pulmonary arterial O2 content = 0.15/mL
Cardiac Output = (250mL/min) / (0.20mL - 0.15mL) = 5000mL/min or 5L/min
• Also measures blood flow to individual organs:
◦Renal blood flow now = renal O2 consumption / (renal arterial O2) - (renal venous O2)
Thermodiluation Technique
• Swan-Ganz catheter is inserted from venous to pulmonary artery. A cold saline solution of known temperature and volume is injected into the RA. The injectate mixes with the blood as it passes through the ventricle and into the pulmonary artery, thus cooling the blood. The blood temperature is measured by a thermistor at the catheter tip, which lies within the pulmonary artery, and a computer is used to acquire the thermodilution profile and a computer calculates flow (cardiac output from the right ventricle) using the blood temperature information, and the temperature and injected volume. Injections are repeated a few times and the cardiac output averaged. Because cardiac output changes with respiration, it is important to inject the saline at a consistent time point during the respiratory cycle.
Eisenmenger Syndrome (ASD)
EKG (Q: how often is AFIB misdiagnosed with fib waves being P waves)?
• Prolonged PR interval = 1st degree heart block (P waves followed by QRS, with delay of AP from atria to ventricle causes longer PR)
2nd degree HB (only some have QRS after P waves).
• Morbitz 1 (Progressively longer PR til no P wave)
• Morbitz 2 (PR constant with intermittent non-conducted P waves). Dangerous as it can lead to complete HB (structural causes).
• 3rd degree AV block; p-waves not correlated with QRS, no association between atria and ventricles
• Absent P waves with irregularly irregular rhythm = AFIB (rvr vs svr); narrow QRS + fib waves
• Tall tent T waves = hyperkalemia.
• Saw tooth between QRS complexes = atrial flutter.
• PAC: early P and narrow QRS
• ST elevation in leads II, III, aVF = inferior STEMI (RCA) w/ recipocal depression in I, V5, V6, and aVL (if no depression = pericarditis).
• LBBB (WilliaM); wide QRS, deep S in V1 and prolonged R in V6. Tall T waves (LVH has ST elevations too, use echo to differentiate).
• RBBB (MarroW); wide QRS, RSR in V1 and prolonged S in V6.
P wave = SA node (atrial depolarization, atria contracts to ventricles)
QRS = (ventricular depolarization, ventricle contracts to lungs/body)
T wave = (ventricle repolarization, ventricle relaxes).
R-R intervals evenly spaced = regular.
