Unit 4 Flashcards
Name 2 Types of Antihypertensive Drugs
- Diuretics
- Sympatholytic
What do diuretics do; what diseases are they used for? Name examples and list adverse effects
Increase excretion of Na+ and H2O, reduce fluid in system and work on heart. Used for HTN and CHF. Thiazides, loop diuretics
(Lasix), and K+ sparing. Orthostatic hypo, weakness, confusion
What are sympatholytics? What are they used for? Name examples and adverse effects
Beta blockers. Bind to heart and block E/NE functions, so decrease HR and contraction force (reduce symp. responses). Used
for HTN, angina, arrhythmias, HF, recovery from MI, migraines, Reynaud’s, situation anxiety. Propanolol (noncardioselective)
and metoprolol (cardioselective). Bronchoconstriction (esp with asthma and COPD), orthostatic hypo, psychotropic effects
(depression and lethargy), reduced max exercise capacity
How do vasodilators affect peripheral vasculature?
Act directly on vascular smooth muscle by inhibiting contraction. Used for HTN and HF. Adverse FX: reflex tachycardia,
orthostatic hypo, dizziness, headaches, edema. Avoid systemic heat.
Explain how drugs that control the renin-angiotensin system are useful for treating HTN and HF
The RAS helps to control BP- when it drops, angiotensinogen -> AngI (with renin) -> AngII (with ACE) -> powerful
vasoconstriction to increase BP. Drugs like ACE inhibitors, AngII receptor blockers, and renin inhibitors prevent acute
vasoconstriction, help reduce BP, and prevent chronic FX of vascular hypertrophy from AngII. Lisinopril (ACE inhibitor) often
causes dry cough from bradykinin, while Sartans (AngII receptor blockers) have fewer side FX
Explain why calcium channel blockers can help reduce blood pressure and/or treat certain cardiac dysrhythmias
Calcium causes the heart and arteries to contract more strongly. By blocking calcium entry into cardiac cells, calcium channel
blockers can slow down the electrical activity of the heart, which can be useful in treating certain arrhythmias, and allows
blood vessels to dilate, reducing BP.
What are Ca2+ channel blockers used for and what are adverse FX?
Used for HTN, angina, arrhythmias “-ipine drugs” but adverse FX include swelling in feet, orthostatic hypo, altered
HR/arrhythmia. Avoid systemic heat. May increase risk of MI?
Justify the use of nitroglycerin when treating angina pectoris.
It dilates peripheral vasculature, reducing preload via venous dilation and reducing afterload via arterial dilation, thereby
reducing workload and oxygen demand on the heart. Can relieve angina within 1-3 mins, though only lasts 30-60 mins
sublingually. Adverse fx: headache, dizziness, orthostatic hypo. No systemic heat.
Categorize the drugs used to control arrhythmias
I. Sodium channel blockers – used for PVCs and Vtach. Stabilizes excitability by inhibiting abnormal sodium channel opening in
cardiac cells. (includes lidocaine and apoquin)
II. Beta blockers – Afib, Vtach
III. Drugs that prolong repolarization – used for Afib, Vfib, and Vtach. Lengthen time between Aps to allow heart to rest prob
by reducing K+ efflux in repolarization. (includes amiodarone)
IV. Calcium channel blockers – Afib, supraventricular tachycardias
*these drugs can have a proarrhythmic effect so monitor HR and symptoms, look for fatigue and dyspnea especially during
exercise
Name the classes of drugs commonly used to treat HF that work to reduce the workload of the heart, slow the progression,
and increase the contractility of the heart
Diuretics, beta blockers, vasodilators, renin-ang drugs, and positive inotropic drugs
Differentiate the positive effects of digitalis from possible negative effects when treating heart failure.
It increases CO and reduces symptoms especially in systolic HF by inhibiting the sodium potassium pump in heart cells – Na+
accumulates, less Ca2+ leaves and builds up -> stronger contraction. Also reduces HR by stimulating vagus n to increase fill
time. However, 25% of pts will develop digitalis toxicity even in normal serum range: GI distress, cramps, nausea, vomiting,
fatigue, confusion, depression, blurred vision, arrhythmia
2 other drugs given in severe/acute HF
Phosphodiesterase inhibitors and dopamine/dobutamine – given parenterally (IV) and not more effective than digitalis. Both
increase contractility
In the clotting cascade, both extrinsic and intrinsic eventually get to CFX which converts prothrombin to thrombin, and
thrombin converts fibrinogen to fibrin. But how are each of the diff systems activated?
Intrinsic: CFXII activated by contact with damaged vessel
Extrinsic: CFVII activated by thromboplastin
Explain how clots are broken down
Tissue plasminogen activator (tPA) activates plasminogen which turns into plasmin and breaks down the clot
Differentiate conventional (unfractionated) heparin from low molecular-weight heparin.
Unfractionated is administered via IV, several times a day
Low molecular weight is administered subcutaneously once a day and has a more predictable, safer response “-parin” drugs
What kind of clots are anticoagulants used primarily for?
Venous thrombosis (like DVT)
How is heparin diff from warfarin?
Hep is given via injection/IV (parenterally), increases effects of antithrombin III, (slows down clotting) has rapid effects
Warfarin AKA coumadin is given orally, inhibits vit K fxn in liver so reduces synthesis of clotting factors, has a time lag 3-4 days
What’s cool about aspirin?
Can be used to prevent arterial clots in MI and stroke but also prevent DVT after surgery (antiplatelet drug)
What are the primary drugs used to treat arterial thrombosis? (decrease platelet-induced clots like MI/stroke)
Aspirin, ADP inhibitors (Plavix = clopidogrel), and glycoprotein inhibitors (block fx of fibrinogen on platelet)
How does aspirin work as a platelet inhibitor?
Inhibits prostaglandins and thromboxane (which stimulates platelet aggregation) biosynthesis by inhibiting the COX enzyme
Explain how thrombolytic drugs can be used to reduce morbidity and mortality in myocardial infarction and ischemic stroke.
tPA and other agents break down clots by activating plasmin. Can restore blood flow, prevent/reverse damage during MI and
ischemic stroke. Can reduce mortality in MI by 50% if given within 1 hr after onset of symptoms, still beneficial if given 3-12
hours after onset. Need to rule out hemorrhagic stroke 1st, but tPA can be used within 2 hours after symptom onset
Give an example of a thrombolytic drug
Urokinase AKA u-plasminogen activator
What is a rehab concern with anti-thrombotics?
Risk of hemorrhage: be gentle when changing dressings, debriding, performing joint mobility and chest percussion
Address the primary methods used to treat inadequate blood clotting.
Replace clotting factors, inhibit fibrinolysis (slow the breakdown of clots “Amicar”), and supplement with vit K (used for
warfarin OD)
Differentiate the primary drug strategies used to treat blood lipid disorders
Statins: reduce cholesterol synthesis, decrease LDL and VLDL, may reduce triglycerides and increase HDL
Fibric acids: reduce triglycerides and increase VLDL breakdown
Others: Niacin reduces VLDL and LDL synthesis, reduces triglycerides
Ezetimibe inhibits chol. Absorption from GI tract
Bile acid binding drugs increase GI excretion of bile acids and reduce plasma chol
What are predisposing factors to statin-induced myopathy?
women, adv. Age, genetics, renal or liver disease, other cholesterol meds, high dose, heavy exercise, lipophilic strain
What are rehab concerns for anti-lipid drugs?
Myopathy (can lead to rhabdo), arrhythmias, pancreatitis, liver toxicity, bloating, diarrhea, nausea
What controls HR, BP, and contractility after heart transplant?
Since the heart is denervated, the adrenals and thyroid glands produce hormones that affect the heart (slow). Meds like
calcium channel blockers and beta blockers can reduce HR and contractility. The SA node’s intrinsic rate is 96-110 bpm. These
patients rely first on the Frank-Starling mechanism to augment SV and then on the catecholamine response to augment both
HR and SV. Resting HR and BP are elevated. Sympathetic reinnervation can happen ~4 years later.
What are common reasons for heart transplants?
Viral cardiomyopathy, ischemic cardiomyopathy, congenital heart disease, amyloidosis, sarcoidosis, chagas
What are the 2 types of heart transplants?
Orthotopic (OHT) – typical; heterotopic (HHT) – uncommon, involves 2 hearts
What are the types of lung transplants?
SLT (single) – COPD, pulmonary fibrosis; DLT (double) – CF, bronchiectasis, COPD, infectious dz; HLT (heart-lung) – pulmonary
HTN, CF, rare cases of COPD, sarcoidosis, amyloidosis, cor pulmonale; living donor – from parent to child
What are the 2 biggest complications with organ transplants?
Rejection, infection
Name 2 anti-rejection drugs
OKT3 and cyclosporine
What are signs of rejection in heart and lung transplant?
Heart: Fever, SOB, fatigue, swelling in legs, flu-like symptoms reduced exercise tolerance
Lungs: Fever, fatigue, malaise, myalgia, resp. difficulty, dyspnea, crackles reduced exercise tolerance
What are some good inpatient goals for heart/lung transplants?
Independent mobility, >20 min aerobic activity, 3+ strength, improve posture and flexibility, independent in pulm. Hygiene.
Exercise parameters: RPE 12-14, HR not to exceed 120 at rest, increase no more than 40
SBP not to exceed 170mmHg at rest, increase no more than 30
DBP not to exceed 120mmHg at rest, increase or decrease no more than 20
Can heart transplant pts feel angina with ischemia?
No b/c heart is denervated (so don’t use that as an endpoint to exercise testing).
What is heart rate inertia?
May fatigue rapidly with increased RPE. need a longer initial anaerobic component until the HR “catches up”
Heart rate slows more gradually with rest.
Post heart transplant, what does SBP and DBP look like?
Both higher than normal
Why would DBP be higher than normal?
Increased stiffness of ventricles from myocardial scarring and fibrosis impairs filling
How can you help your pt post-heart transplant?
Allow time to adapt to position changes (orthostatic hypo), extend warmup and cooldown by 5-10 mins
What are 3 major losses with lung transplants?
Denervation (loss of cough reflex and RR may not increase as much during exercise), Loss of lymphatics (post-op swelling and
mild restrictive disease increase work of breathing), loss of bronchial arteries (not a big deal)
Name some helpful treatments post lung transplant
Teach volitional coughing on a schedule, incentive spirometry, Acapella for clearance, frequent position changes, breathing
exercises especially thoracic mobility. Goals: improving gas exchange, airway clearance, pt positioning, reduce pain, reduce
mob restrictions
Name 4 prerequisites to being a lung donor
<40 yo, no infection, excellent gas exchange, clear CXR
What are exercise benefits for all transplant patients?
Increase aerobic function of skeletal muscle, increase maximal muscle force production, increase endothelial function,
increase BMD
Post-heart transplant, what are patients at risk for?
Graft failure, cancer, hyperlipidemia, diabetes, and HTN
Name some drugs used to quit smoking
Nicotine replacement, Buproprion (Wellbutrin) which prolongs FX of dopamine and NE in brain, Chantix which is a partial
agonist at nicotine receptors
