FirstAid-Cardiovascular

VAN
Internal jugular vein (lateral)
Common carotid artery (medial)
Vagus nerve (posterior)

Right coronary artery > marginal artery > posterior descending artery
Left coronary artery > left anterior descending artery > circumflex artery

The right coronary artery.

posterior descending artery

It arises from either the RCA (80%) or the CFX (20%).

The left atrium; enlargement may cause dysphagia (esophageal n.) or hoarseness (recurrent laryngeal n.).

CO = (stroke volume) x (heart rate)

CO = (rate of O2 consumption)/(arterial O2 content - venous O2 content)

MAP = (CO) x (total peripheral resistance)

MAP = 2/3 diastolic pressure + 1/3 systolic pressure

systolic pressure - diastolic pressure

stroke volume

increase in SV, then an increase in HR. Heart contractility can increase initially and is followed by an increase in heart rate.

In ventricular tachycardia, diastolic filling is incomplete and cardiac output goes down.

SV increases

SV decreases.

1. Catecholamines cause ↑ activity of Ca2+ pump in sarcoplasmic reticulum
2. ↑ intracellular calcium
3. ↓ extracellular sodium (↓ activity of Na+/Ca2+ exchanger)
4. Digitalis (↑ intracellular Na+, resulting in ↑ Ca2+)

1. beta1 blockers
2. heart failure
3. acidosis
4. hypoxia/hypercapnea
5. non-dihydropyridine Ca2+ channel blockers.

The stroke volume decreases.

1. anxiety
2. exercise
3. pregnancy

1. ↑ afterload
2. ↑ contractility
3. ↑ heart rate
4. ↑ heart size (wall tension)

Ventricular end diastolic volume

mean arterial pressure

It is a venodilator that decreases preload.

It is a vasodilator that decreases Afterload and Arterial pressure.

The force of contraction is proportional to the initial lenght of cardiac muscle fibers (preload).

The exercise curve shifts up and to the left giving an increased CO (SV) at any given preload. This is due to sympathetic innervation increasing contractility.

The curve will shift up and to the left, with an increase in CO (SV) at any given preload due to increased contractility.

1. Catecholamines
2. Digitalis
3. Sympathetic stimulation

1. Pharmacologic depressants
2. Loss of myocardium

SV/EDV

>55%

ΔP=QR

viscosity; radius to the fourth power

series: Pt=P1+P2...
parallel: 1/Pt=1/P1+1/P2...

The hematocrit

Arterioles

1. Polycythemia
2. Hyperproteinemic states such as MM
3. Hereditary spherocytosis

1. Isovolumetric contraction
2. Systolic ejection
3. Isovolumetric relaxation
4. Rapid filling
5. Reduced filling

Isovolumetric contraction of the left ventricle.

S1-4

Mitral and tricuspid valve closure.

In the mitral valve area.

Aortic and pulmonary valve closure.

At the left sternal border

Rapid ventricular filling in early diastole. Associated with increased filling pressures and more common in dilated ventricles.

In children and pregnant women.

Atrial kick in late diastole: always pathological.

Hypertrophic cardiomyopathy leads to ventricular hypertrophy and the LA must push against a thickened LV wall.

a-wave: atrial contraction
c-wave: RV contraction
v-wave: RA filling

When the aortic valve closes before the pulmonic valve.

Inspiration.

Pulmonary stenosis or a right bundle branch block.

Atrioseptal defects.

Splitting decreases upon inspiration. This indicates either aortic stenosis or left bundle branch block.

Inspiration ↓ intrathoracic P, ↑pulmonary circulation so pulmonic valve closes late and aortic valve closes early.

Conditions that delay RV emptying delays the pulmonic sound.

Left to right shunting increases the amount of blood being pumped through pulmonic valve regardless of breath leading to delayed pulmonic valve closure.

These conditions delay LV emptying and aortic valve closure, leading to splitting which actually decreases with inspiration because delayed pulmonic valve closure gets closer to aortic valve closure.

Mitral/tricuspid valve regurgitation.

Techniques that increase afterload (squatting) or LA return (expiration).

Manuevers that increase RA return (inspiration).

Ischemic heart disease, mitral valve prolapse, or LV dilation.

RV dilation or endocarditis, both may be caused by rheumatic heart disease.

Aortic stenosis.

Radiation to the carotid arteries.

VSD

Mitral valve prolapse.

Because of sudden tensing of the chordae tendinae.

Aortic regurgitation.

Mitral valve stenosis.

Patent ductus arteriosus.

extracellular calcium which induces Ca release from the sarcoplasmic reticulum.

Cardiac muscle AP has a plateau phase which is due to Ca2+ influx.

If channels that permit influx of sodium.

Cells are linked together by gap junctions which facilitates cell to cell contraction.

Ventricular and pacemaker potentials.

notes

Phase 0, Phase 1, Phase 2, Phase 3, Phase 4, Phase 5

rapid upstroke due to voltage-gated sodium channel (Ina) opening.

Initial repolarization due to inactivation of Ina channels. Voltage-gated sodium channels start to open (IK+).

Plateau phase caused by Ca influx through voltage-gated Ca-channels (ICa), balancing K efflux. Ca influx triggers Ca release from sarcoplasmic reticulum inducing contraction.

Rapid repolarization due to massive K efflux due to opening of voltage gated slow K channels and closure of voltage-gated Ca channels.

Resting potential due to high K permeability through K channels.

In the SA and AV nodes.

Pacemaker APs do not have fast voltage-gated Na channels, rather, the opening of voltage gated Ca channels results in slow conduction velocity.

The slope of phase 4 which represents the If sodium channels.

notes

ACh ↓ depolarization and ↓ HR; catecholamines ↑ depolarization and ↑ HR; sympathetic stimulation ↑ chance that If channels are open and ↑ HR.

atrial depolarization.

conduction delay through the AV node (normal < 200 msec)

ventricular depolarization

mechanical contraction of the ventricles

ventricular repolarization

recent MI

Because it is masked by the QRS complex.

isoelectric region where the ventricles are depolarized.

Purkinje fibers.

The SA node.

100msec to allow for ventricular filling during diastole.

Ventricular tachycardia characterized by shifting sinusoidal waveforms on ECG.

Ventricular fibrillation.

Anything that prolongs the QT interval, specifically congenital disorders such as cardiac sodium or potassium channel disorders (Jervell and Lange-Nielsen syndrome).

Torsades de Pointe

Wolff-Parkinson-White syndrome

Because an accessory conduction pathway from the atria to the ventricles (bundle of kent) is present, giving rise to a characteristic delta wave on ECG.

A reentry current may result leading to supraventricular tachycardia.

Chaotic and erratic baseline (irregularly irregular) with no discrete P waves in between irregularly spaced QRS complexes.

Atrial stasis and subsequent stroke.

With beta-blocker or calcium channel blocker; prophylaxis against thromboembolism with warfarin or coumadin.

A rapid succession of identical, back to back atrial depolarization waves.

Sawtooth pattern on ECG.

Attempt to convert to sinus rhythm using class IA, IC, or III antiarrhythmics.

The PR interval is prolonged (>200 msec).

Wenckebach (Mobitz Type I) and Mobitz Type II

Progressive lengthening of the PR interval unitl a beat is "dropped" (a P wave not followed by a QRS complex).

Wenckebach (Mobitz Type I) 2nd degree AV block

Dropped beats which are not preceded by a change in the PR interval length.

A 2:1 block, where there are 2 P-waves to every one QRS response.

It may convert to a 3rd degree block.

The PR interval increases in Wenckebach until a QRS complex is skipped, whereas the PR interval remains constant in Mobitz Type II.

Mobitz Type II 2nd degree block.

The atria and ventricles beat independently of each other.

The P waves will bear no relation to the QRS complexes. Typically the atrial rate is faster than the ventricular rate.

Lyme disease.

Pacemaker

Third degree AV block

A completely erratic rhythm with no identifiable waves.

Fatal arrhythmia will occur without immediate CPR and defibrillation.

Ventricular fibrillation

Renin-angiotensin system in the kidneys and the baroreceptor/sympathetic response.

Study this figure from Robbins

1. ↓ MAP
2. ↓ baroreceptor firing
3. ↑ sympathetic activity
4. β1 (↑HR, ↑contractility = ↑CO); α1 (venoconstriction = ↑CO); α1 (arteriolar constriction = ↑TPR)

1. ↓ MAP
2. Juxtaglomerular apparatus (JGA) senses
3. ↑ RAA system
4. Angiotensin II (vasoconstriction = ↑TPR); Aldosterone (↑ blood volume = ↑CO)

Atrial natriuretic peptide released by the atria in response to ↑ blood volume and atrial pressure.

It is involved in "escape from aldosterone" and causes vascular relaxation by constricting efferent renal arterioles and dilating afferent arterioles.

Baroreceptors and Chemoreceptors

Through the vagus nerve; they only respond to increased BP.

Through the glossopharyngeal nerve; they respond to increase/decrease in BP.

Increases pressure on carotid artery, increasing stretch or baroreceptors, leading to decreased HR.

Peripheral (carotid and aortic bodies) and Central.

They respond to decreased PO2, increased PCO2, and decreased blood pH.

Respond to changes in pH and PCO2 of brain interstitial fluid.

Central chemoreceptors: ↑ICP, cerebral ischemia, HTN (sympathetic), reflex bradycardia

HTN, bradycardia, respiratory distress

The liver.

The kidney.

The heart.

By the coronary circulation.

Pulmonary capillary wedge pressure (PCWP).

PCWP>LV diastolic pressure

RA: <5
RV: <25/<5
Pulmonic artery: <25/10
PCWP: <12
LA: <12
LV: <130/10
Aorta: <130/90

A Swan-Ganz catheter.

Hypoxia causes vasoconstriction so that only well ventilated areas are well perfused.

O2, adenosine, NO

CO2 and pH

Myogenic and tubuloglomerular feedback.

Hypoxia causes vasoconstriction

Lactate, adenosine, potassium

Sympathetic stimulation mediating temperature control.

1. Pc = capillary pressure
2. Pi = interstitial fluid pressure
3. πc = plasma collid osmotic pressure
4. πi = interstitial fluid colloid osmotic pressure

In: Pi and πc
Out: Pc and πi

Pnet = (Pc-Pi) - (πc-πi)

The filtration constant which is affected by the capillary permeability.

Net fluid flow = (Pnet)(Kf)

Excessive fluid outflow into the interstitium.

1. ↑ capillary pressure (↑Pc; heart failure)
2. ↓plasma proteins (↓πc; nephrotic syndrome, liver failure)
3. ↑ capillary permeability (↑ Kf; toxins, infections, burns)
4. ↑ interstitial fluid colloid osmotic pressure (↑ πi; lymphatic blockage)

The 5 T's: Tetralogy of Fallot (most common), Transposition of great vessels, Truncus arteriosus, Tricuspid atresia, TAPVR (total anomalous pulmonary venous return)

Tricuspid atresia is characterized by absence of tricuspid valve and presence of a hypoplastic right ventricle. It requires both ASD and VSD for viability.

1. VSD (most common cardiac anomaly).
2. ASD (loud S1; wide fixed split S2)
3. PDA (close with indomethacin)

VSD>ASD>PDA

Increased pulmonary resistance due to arteriolar thickening.

In kids with left to right shunts, over time the pulmonary resistance increases until progressive pulmonary HTN reverse to a right to left shunt.

PROVe
Pulmonary stenosis, Right ventricular hypertrophy, Overriding aorta, Ventricular septal defect.

A right to left shunt across the VSD. Because pulmonic valve stenosis restricts outflow tract of RV.

Boot-shaped because of RV hypertrophy.

Anterosuperior displacement of the infundibular septum.

Squat.

Compression of femoral arteries increases afterload. This decreases the right to left shunt, directing more blood from the RV to the lungs.

The aorticopulmonary septum fails to spiral in embryogenic development so the aorta leaves the RV and the pulmonic valve leaves the LV.

A shunt such as VSD, ASD or patent foramen ovale.

Infantile (IN close to the hear; preductal) and Adult (Distal to the ductus).

Notching of the ribs (due to collateral circulation), HTN in upper extremities, weak pulses in lower extremities.

Turner's syndrome

Aortic regurgitation.

In fetal period, shunt is right to left. In neonatal period, lung resistance decreases and DA closes.

A left to right shunt occurs from the aorta through the pulmonic valve.

A continuous machine like murmur.

Open: PGE[E] kEEps it open and low pO2
Closed: [E]NDomethacin

In transposition of the great vessels.

Truncus arteriosus and tetralogy of fallot.

ASD, VSD, AV septal defect (endocardial cushion defect)

Septal defects, PDA, pulmonary artery stenosis.

Coarctation of the aorta.

Aortic insufficiency.

Transposition of the great vessels.

BP greater than 140/90.

age, obesity, diabetes, smoking, genetics, ethnicity (black>white>asian)

Primary: 90%, essential HTN related to increased CO or increased TPR
Secondary: 10%, usually secondary to renal disease

Severe and rapidly progressing HTN.

Atherosclerosis, LVH, stroke, CHF, renal failure, retnopathy, and aortic dissection.

Atheromas, xanthomas, tendinous xanthomas, corneal arcus.

Monckeberg, arteriolosclerosis, atherosclerosis

Calcification in the media of arteries especially radial and ulnar arteries. It commonly occurs in the radial or ulnar arteries. Typically benihn forming pipestem arteries that do not obstruct blood flow and intima is not involved.

Hylaine thickening of small arteries in essential HTN or diabetes mellitus. Causes hyperplastic onion-skinning in malignant HTN.

Fibrous plaques and atheromas form in the intima of arteries.

Arteriolosclerosis

Atherosclerosis

A longitudinal intraluminal tear forming a false lumen.

HTN or cystic medial necrosis.

Marfan's syndrome.

Myocardial infarction. AD presents with tearing chest pain radiating to the back.

It can result in aortic rupture and death.

Elastic arteries and large and medium muscular arteries.

Smoking, HTN, diabetes mellitus, hyperlipidemia, family history

Endothelial cell dysfunction → macrophage and LDL accumulation → foam cell formation → fatty streaks → smooth muscle cell migration → fibrous plaque → complex atheroma

aneurysms, ischemia, infarcts, peripheral vascular disease, thrombus, emboli

abdominal aorta > coronary artery > popliteal artery > carotid artery

Angina, myocardial infarction, sudden cardiac death, and chronic ischemic heart disease.

Narrowing of the coronary arteries by 75% or more.

Stable, Prinzmetals variant, and unstable/crescendo.

Atherosclerosis.

ST depression

Retrosternal chest pain with exertion.

Coronary artery spasm.

ST elevation

Worsening chest pain at rest or with minimal exertion.

ST depression

Acute thrombosis due to coronary artery atherosclerosis.

Death from cardiac causes within 1 hour of onset of symptoms, most commonly due to a lethal arrhythmia (V-fib)

LAD>RCA>circumflex

diaphoresis, nausea, vomiting, severe retrosternal pain, pain in left arm and/or jaw, shortness of breath, fatigue, adrenergic symptoms

Arrhythmia

None, because the cellular damage is reversible.

Dark mottling and coagulative necrosis, contraction band necrosis.

1-3 days following the event.

Arrhythmias.

Free wall rupture, tamponade, papillary muscle rupture, interventricular septal rupture.

Gray-white scar morphologically and increased collagen deposition with decreased cellularity microscopically.

Ventricular aneurysm.

ECG changes.

ST elevation (transmural infarct)
ST depression (subendocardial infarct)
pathologic Q waves (transmural infarct)

Cardiac Troponin I

Cardiac troponin I and CK-MB

Transmural and subendocardial

Ischemic necrosis of <50% of the ventricle wall. This occurs because there are fewer collaterals in the subendocardium making it more susceptible to MI.

Cardiac arrhythmia.

1. Cardiac arrhythmia; 2. LV failure/pulmonary edema; 3. Cardiogenic shock; 4. Ventricular free wall rupture; 5. Aneurysm formation; 6. Postinfarction fibrinous pericarditis; 7. Dressler's syndrome

Dilated, hypertrophic, and restrictive.

Dilated cardiomyopathy

S3 heart sound, dilated heart on ultrasound, balloon appearance on chest x-ray.

Systolic dysfunction leading to CHF.

AB3CD: Alcohol, wet Beriberi, Coxsackie B virus myocarditis, chronic Cocaine use, Chagas' disease, Doxorubicin toxicity, hemochromatosis, peripartum cardiomyopathy

A hypertrophied IV septum interferes with LV outflow, and hypertrophied LV has reduced compliance.

Hypertrophic cardiomyopathy due to disoriented hypertrophied myocardial fibers.

Hypertrophic cardiomyopathy.

Hypertrophic cardiomyopathy.

Friedreich's ataxia

S4 heart sound, apical impulses, and a systolic murmur.

Treat with beta-blocker or non-dihydropyridine calcium channel blocker (verapamil).

Sarcoidosis, amyloidosis, postradiation fibrosis, endocardial fibroelastosis, loffler's syndrome, and hemochromatosis.

Dilated: systolic dysfunction
Hypertrophic: diastolic dysfunction
Restrictive: diastolic dysfunction

A clinical syndrome that occurs in patients with an inherited or acquired abnormality of cardiac structure or function, who develop a constellation of clinical symptoms (dyspnea, fatigue) and signs (edema, rales).

Failure of LV output to increase during exercise.

Greater ventricular end-diastolic volume.

LV failure leads to increased pulmonary venous pressure and subsequent transudation of fluid into the alveoli.

Heart failure cells which are hemosiderin laden macrophages gobbling up iron from microhemorrhages in the lungs due to the increased capillary pressure.

Shortness of breath when supine.

Increase in venous return (preload) exacerbates pulmonary vascular congestion.

Hepatomegaly (nutmeg liver).

Increased central venous pressure causes and increased resistance to portal flow

RV failure causes increased venous pressure and fluid transudation.

Right heart failure causing increased venous pressure.

Cor pulmonale

Acute: Staphylococcus aureus (high virulence)
Subacute: Streptococcus viridans (low virulence)

Mitral valve

Tricuspid valve endocarditis (don't Tri drugs)

chordae rupture, glomerulonephritis, supparative pericarditis, emboli.

Bacteria FROM JANE: Fever, Roth's spots, Osler's nodes, Murmur, Janeway lesions, Anemia, Nail-bed hemorrhage, Emboli

Endocarditis may be non-bacterial in origin and may occur secondary to malignancy or a hypercoagulable state.

HACEK: Haemophilus, Aggregatibacter, Cardiobacterium, Eikenella, Kingella

SLE causes LSE.

Wartlike sterile vegetations occurring on both sides of the valve.

A consequence of pharyngeal infection with group A beta-hemolytic streptococci.

Vegetations and fibrosis of heart valves (mitral>aortic>>tricuspid)

Aschoff bodies in myocardium (granuloma with giant cells), activated histiocytes, elevated ASO titers

FEVERSS: Fever, Erythema marginatum, Valvular damage, ↑ ESR, Red-hot joints (migratory polyarthritis), Subcutaneous nodules (Aschoff bodies), St. Vitus' dance (chorea)

Compression of heart by fluid (blood or effusions) in the pericardium, leading to ↓ CO and eventual equilibration of diastolic pressures in all four chambers.

hypotension, ↑ venous pressure (JVD), distant heart sounds, ↑ HR, pulsus paradoxus

An exaggerated ↓ in ampliturde of pulse during inspiration. Seen in severe cardiac tamponade, asthma, obstructive sleep apnea, pericarditis, and croup

Serous, fibrinous, and hemorrhagic

An autoimmune response to cardiac antigens following an MI which results in a pericardial friction rub and pericardial effusion.

SLE, rheumatoid arthritis, viral infection, uremia

Uremia, Dressler's syndrome, rheumatic fever

TB, malignancy (e.g., melanoma)

Pericardial pain, friction rub, pulsus pradoxus, and distant heart sounds.

ST-segment elevation in multiple leads

Without scarring or lead to chronic adhesive or chronic constrictive pericarditis.

Disruption of the vasa vasorum of the aorta with consequent dilation of the aorta and valve ring.

Aneurysm of the ascending aorta or aortic arch and aortic valve incompetence as calcification of the aortic root (tree bark appearance).

Myxomas, rhabdomyomas, and metastases.

A myxoma

Myxomas, usually in the left atrium

Rhabdomyomas, associated with tuberous slcerosis.

Metastases (e.g., melanoma, lymphoma)

An arteriovenous malformation in small vessels.

Dilated vessels on skin and mucous membranes.

It is an autosomal-dominant inherited disorder that presents with recurrent epistaxis, skin discolorations, mucosal telangiectasias, and GI bleeds.

Dilated, tortuous superficial veins due to chronically ↑ venous pressure.

Poor wound healing and varicose ulcers.

No

↓ blood flow to the skin due to arteriolar vasospasm in response to cold temperature or emotional stress.

Connective tissue disease, SLE, or CREST syndrome (systemic sclerosis scleroderma).

A triad of focal necrotizing vasculitis in small vessels, necrotizing granulomas in the lung and upper airway, and necrotizing glomerulonephritis.

Heomptysis, hematuria, perforation of nasal septum, chronic sinusitis, otitis media, mastoiditis, cough, dyspnea.

c-ANCA (anti-neutrophil Abs), chest X-ray with multiple nodular densities, heaturia and RBC casts

Microscopic polyarteritis nodosa, pauci-immune crescentic glomerulonephritis, and Churg-Strauss syndrome

MPN lacks the granulomas seen in Wegener's

The vasculitis is limited to the kidney, and there is a relative paucity of antibodies.

A congenital vascular disorder that affects capillary-sized blood vessels.

It manifests with port-wine stain (nevus flammeus) on face, ipsilateral leptomeningeal angiomatosis, seizures, and early-onset glaucoma.

It is the most common form of childhood systemic vasculitis.

Skin, joints, GI; all lesions of approximate same age.

Skin rash on buttocks and legs (palpable purpura), arthralgia, intestinal hemorrhage, abdominal pain, and melena.

IgA immune complexes.

Also know as thromboangiitis obliterans. It is idiopathic, segmental, thrombosing vasculitis of small and medium peripheral arteries and veins

Heavy smokers

Intermittent claudication, superficial nodular phlebitis, Raynaud's phenomenon, severe pain in affected part. May lead to gangrene and auto-amputation of digits.

Smoking cessation

An acute, self-limiting necrotizing vasculitis in infants and children. Associated with Asian ethnicity.

Fever, conjunctivitis, changes in lips/oral mucosa (Strawberry tongue), lymphadenitis, desquamative skin rash. May develop coronary aneurysms.

IV immunoglobulin, aspirin

Immune complex-mediated transmural vasculitis with fibrinoid necrosis.

Hep B + in ~30% of patients. Multiple aneurysms and constrictions on arteriogram.

It is know as "pulseless disease" and is associated with thickening of aortic arch and/or proximal great vessels.

FAN MY SKIN On Wednesday: Fever, Arthritis, Night sweats, MYalgia, SKIN nodules, Ocular disturbances, Weak pulses in upper extremities

The most common vasculitis affecting medium and large arteries, usually branches of carotid artery. (Giant cell arteritis)

TEMporal arteritis has signs near TEMples

Unilateral headache, jaw claudication, impaired vision (occlusion of ophthalmic artery that may lead to irreversible blindness)

Increased ESR. Half of patients have systemic involvement and polymyalgia rheumatica.

A benign capillary hemangioma of infancy. Initially grows with child, then spontaneously regresses.

Benign capillary hemangioma of the elderly. Does not regress and frequency increases with age.

A polypoid capillary hemangioma that can ulcerate and bleed. It is associated with trauma and pregnancy.

A cavernous lymphangioma of the neck, associated with Turner's syndrome.

A benign, painful, red-blue tumor under the fingernails. Arises from modified smooth muscle cells of glomus body.

Benign capillary skin papules found in AIDS patients. Caused by Bartonella henselae infections and frequently mistaken for Kaposi's sarcoma.

A highly lethal malignancy of the liver. It is associated with vinyl chloride, arsenic, and ThO2 (Thorotrast) exposure.

Lymphatic malignancy associated with persistent lymphedema (e.g., post-radical mastectomy).

An endothelial malignancy of the skin associated with HHV-8 and HIV. It is frequently mistaken for bacillary angiomatosis.

Diuretics, ACE inhibitors, angiotensin II receptor blockers (ARBs), calcium channel blockers.

Diuretics, ACE inhibitors/ARBs, beta-blockers (compensated CHF), potassium-sparing diuretics

ACE inhibitors/ARBs, calcium channel blockers, diuretics, beta-blockers, alpha-blockers

If the CHF is decompensated (ie, CO is decreased).

ACE inhibitors are protective against diabetic nephropathy.

It vasodilates arterioles and veins by increasing cGMP and thus causing smooth muscle relaxation.

Afterload reduction.

Treating severe HTN and CHF. It is the first-line therapy for HTN in pregnancy with methyldopa. It is frequently coadministered with a beta-blocker to prevent reflex tachycardia.

Reflex tachycardia.

In patients with angina or coronary artery disease.

To treat severe HTN.

It is a potassium channel opener. It hyperpolarizes and relaxes vascular smooth muscle.

Nifedipine, verapamil, and diltiazem.

They block voltage-dependent L-type calcium channels of cardiac and smooth muscle and thereby reduce muscle contractility.

Verapamil = Ventricle
Heart: verapamil>diltiazem>nifedipine
Vascular: nifedipine>diltiazem>verapamil

Treatment of HTN, angina, arrhythmias (except nifedipine), Prinzmetal's angina, and Raynaud's

Cardiac depression, AV block, and peripheral edema.

They cause vasodilation by releasing nitric oxide in smooth mucle, causing and increase in cGMP and smooth mucle relaxation. The dilate veins >> arteries therefore decreasing preload.

For treating angina and pulmonary edema.

Reflex tachycardia and hypotension.

A person who is exposed to nitroglycerin during the work week develops resistance, then loses resistance over the weekend. On the following Monday, the patient feels symptoms.

Nitroprusside, fenoldopan, and diazoxide.

It is short acting and increases levels of cGMP via direct release of NO. It may release cyanide.

It is a dopamine D1 receptor agonist that causes relaxation of renal vascular smooth muscle.

Potassium channel opener that hyperpolarizes and relaxes vascular smooth muscle. Can cause hyperglycemia by reducing insulin release.

Reduction of myocardial oxygen consumption (MVO2) by decreasing one or more of the determinants of MVO2.

end diastolic volume, blood pressure, heart rate, contractility, ejection time

Nifedipine is similar to Nitrates in effect. verapamil is similar to beta-blockers in effect.

They are partial beta-agonists, so they will actually increase contractility and ionotropy.

notes

Answers

notes

1) sodium potassium ATPase
2) sodium calcium exchanger
3) voltage gated (L-type) calcium channels
4) calcium pump in SR
5) ryanodine receptors and calcium release channels in SR closely coupled to SR
6) site of action of calcium on troponin-tropomyosin

They are coupled to Gs and activate protein kinase A, which phosphorylates L-type calcium channels and phospholamban, both of which increase intracellular calcium during contraction.

Digoxin.

Direct inhibition of sodium/potassium ATPase leading to indirect inhibition of sodium/calcium antiporter. It increases calcium leading to increased inotropy. It also stimulates the vagus nerve.

CHF (increase contractility)
atrial fibrillation (decrease conduction at AV node and depress SA node)

Cholinergic effects (nausea, vomiting, diarrhea, blurry yellow vision)
ECG changes, arrhythmia, hyperkalemia

Renal failure, hypokalemia, and quinidine

slowly normalize potassium, add lidocaine, cardiac pacer, anti-digitoxin Fab fragments, Mg

Notes

Slow or block conduction
decrease slope of phase 4 depolarization
increase threshold for firing in abnormal pacemaker cells

"The Queen Proclaims Diso's pyramid"
Quinidine, Procainamide, Disopyramide

↑ AP duration, ↑ effective refractory period, ↑ QT interval

Both atrial and ventricular arrhythmias, especially reentrant and ectopic supraventricular and ventricular tachycardia.

Quidine: cinchonism (headache, tinitus), thrombocytopenia, torsades de pointes (↑QT interval)
Procainamide: reversible SLE-like syndrome.

"I'd Buy Lidy's Mexican Tacos"
Lidocaine, Mexiletine, Tocainide

Decrease AP duration.

Ischemic or deplarized purkinje and ventricular tissue.

Acute ventricular arrhythmias (post MI) and digitalis induced arrhythmias.

Local anesthetic, CNS stim/depress, cardiovascular depression

"Chipotle's Food has Excellent Produce"
Flecainide, Encainide, Propafenone

As a last resort in refractory tachycardias and for patients without structural abnormalities.

Proarrhythmias, especially after MI.

IB is Best
IC is Contraindicated

It increases toxicity for all class I drugs.

beta-blockers: Propranolol, esmolol, metoprolol, atenolol, timolol

↓ cAMP, ↓ Ca currents, ↓ slope of phase 4, ↑ PR interval

The AV node is particularly sensitive.

Ventricular tachycardia, supraventricular tachycardia, slowing ventricular rate during atrial fibrillation and atrial flutter.

Cardiovascular depression, CNS effects, dyslipidemia (metoprolol).

They may mask the signs of hypoglycemia.

Sotalol, ibutilide, bretylium, dofetilide, amiodarone.

↑ AP duration, ↑ ERP, ↑ QT interval

When other antiarrhythmatics fail.

Excessive beta-block could lead to torsades de pointes.

Pulmonary fibrosis, hepatotoxicity, hyper/hypothyroidism (40% w/v iodine).

To check the PFTs, LFTs, and TFTs

Because it alters the lipid membrane.

notes

Bradycardia, heart block, and CHF

Verapamil and diltiazem.

They primarily affect AV nodal cells, ↓ conduction velocity, ↑ ERP, ↑ PR interval.

To prevent nodal arrhythmias such as supraventricular tachycardia.

Constipation, flushing, edema, CV effects (CHF, AV block, sunus node depression).

notes

It increases potassium efflux, causing hyperpolarization and ↓ ICa.

Diagnosisng and abolishing supraventricular tachycardia.

Flushing, hypotension, and chest pain. This can be clocked by theophylline.

Depress ectopic pacemakers in hypokalemia (digoxin toxicity).

Treating torsades de pointes and digoxin toxicity.

answer

Study

notes

notes